JACKSONVILLE, FLA. – An enhanced recovery protocol after colorectal surgery nearly eliminated differences in hospital stays between black and white patients, according to a study based on data from the University of Alabama at Birmingham.

Dr. Tyler S. Wahl, a resident at UAB reported on the institution’s experience with the Enhanced Recovery After Surgery (ERAS) pathway at the Association of Academic Surgery/Society of University Surgeons Academic Surgical Congress. “ERAS has been shown to reduce length of stay, cost, and perioperative complications without compromising readmission or mortality rates,” Dr. Wahl said. Dr. Daniel Chu was senior author.

Surgical literature has increasingly demonstrated disparities among black patients undergoing major surgery: longer lengths of stay, more readmissions, increased postoperative mortality and lower survival rates after colorectal cancer resections, Dr. Wahl said. The UAB investigators set out to determine whether the ERAS pathway would reduce disparities in length of stay among black and white patients when compared to the traditional pathway.

Before UAB started using ERAS for colorectal patients, the average length of stay for patients undergoing colorectal surgery was 6.7 days with significant differences between black and white patients: 8 days vs. 6.1 days, respectively. However, after implementation of the ERAS pathway in January 2015, average length of stay declined to 4.7 days overall. Black patients had dramatic reductions in length of stay, compared with white patients, with stays of 3.9 days vs. 5 days, respectively.

“Not only were patients leaving much earlier, but their length of stay was also shorter than predicted using the American College of Surgeons Risk Calculator,” Dr. Wahl said.

The UAB study was a retrospective, matched cohort analysis of 258 patients – 129 patients from pre-ERAS years were compared with 129 ERAS patients from January to October 2015.

Study subjects were similar in many patient- and procedure-specific factors; however, differences in operative approach, indication, ostomy formation, and operative time did not change the predicted length of stay among races, Dr. Wahl said.

Dr. Wahl said the racial makeup of the study differs from most ERAS literature in colorectal patients. “The overall percentage of the African American population was 30% within our study, as most ERAS literature has 10% or less,” he added.

“Further work needs to be pursued to find what’s driving these dramatic results among the black population,” he said.

Dr. Wahl and coauthors had no disclosures.

JACKSONVILLE, FLA. – An enhanced recovery protocol after colorectal surgery nearly eliminated differences in hospital stays between black and white patients, according to a study based on data from the University of Alabama at Birmingham.

Dr. Tyler S. Wahl, a resident at UAB reported on the institution’s experience with the Enhanced Recovery After Surgery (ERAS) pathway at the Association of Academic Surgery/Society of University Surgeons Academic Surgical Congress. “ERAS has been shown to reduce length of stay, cost, and perioperative complications without compromising readmission or mortality rates,” Dr. Wahl said. Dr. Daniel Chu was senior author.

Surgical literature has increasingly demonstrated disparities among black patients undergoing major surgery: longer lengths of stay, more readmissions, increased postoperative mortality and lower survival rates after colorectal cancer resections, Dr. Wahl said. The UAB investigators set out to determine whether the ERAS pathway would reduce disparities in length of stay among black and white patients when compared to the traditional pathway.

Before UAB started using ERAS for colorectal patients, the average length of stay for patients undergoing colorectal surgery was 6.7 days with significant differences between black and white patients: 8 days vs. 6.1 days, respectively. However, after implementation of the ERAS pathway in January 2015, average length of stay declined to 4.7 days overall. Black patients had dramatic reductions in length of stay, compared with white patients, with stays of 3.9 days vs. 5 days, respectively.

“Not only were patients leaving much earlier, but their length of stay was also shorter than predicted using the American College of Surgeons Risk Calculator,” Dr. Wahl said.

The UAB study was a retrospective, matched cohort analysis of 258 patients – 129 patients from pre-ERAS years were compared with 129 ERAS patients from January to October 2015.

Study subjects were similar in many patient- and procedure-specific factors; however, differences in operative approach, indication, ostomy formation, and operative time did not change the predicted length of stay among races, Dr. Wahl said.

Dr. Wahl said the racial makeup of the study differs from most ERAS literature in colorectal patients. “The overall percentage of the African American population was 30% within our study, as most ERAS literature has 10% or less,” he added.

“Further work needs to be pursued to find what’s driving these dramatic results among the black population,” he said.

Dr. Wahl and coauthors had no disclosures.

JACKSONVILLE, FLA. – An enhanced recovery protocol after colorectal surgery nearly eliminated differences in hospital stays between black and white patients, according to a study based on data from the University of Alabama at Birmingham.

Dr. Tyler S. Wahl, a resident at UAB reported on the institution’s experience with the Enhanced Recovery After Surgery (ERAS) pathway at the Association of Academic Surgery/Society of University Surgeons Academic Surgical Congress. “ERAS has been shown to reduce length of stay, cost, and perioperative complications without compromising readmission or mortality rates,” Dr. Wahl said. Dr. Daniel Chu was senior author.

Surgical literature has increasingly demonstrated disparities among black patients undergoing major surgery: longer lengths of stay, more readmissions, increased postoperative mortality and lower survival rates after colorectal cancer resections, Dr. Wahl said. The UAB investigators set out to determine whether the ERAS pathway would reduce disparities in length of stay among black and white patients when compared to the traditional pathway.

Before UAB started using ERAS for colorectal patients, the average length of stay for patients undergoing colorectal surgery was 6.7 days with significant differences between black and white patients: 8 days vs. 6.1 days, respectively. However, after implementation of the ERAS pathway in January 2015, average length of stay declined to 4.7 days overall. Black patients had dramatic reductions in length of stay, compared with white patients, with stays of 3.9 days vs. 5 days, respectively.

“Not only were patients leaving much earlier, but their length of stay was also shorter than predicted using the American College of Surgeons Risk Calculator,” Dr. Wahl said.

The UAB study was a retrospective, matched cohort analysis of 258 patients – 129 patients from pre-ERAS years were compared with 129 ERAS patients from January to October 2015.

Study subjects were similar in many patient- and procedure-specific factors; however, differences in operative approach, indication, ostomy formation, and operative time did not change the predicted length of stay among races, Dr. Wahl said.

Dr. Wahl said the racial makeup of the study differs from most ERAS literature in colorectal patients. “The overall percentage of the African American population was 30% within our study, as most ERAS literature has 10% or less,” he added.

“Further work needs to be pursued to find what’s driving these dramatic results among the black population,” he said.

Dr. Wahl and coauthors had no disclosures.

A 69-year-old man is evaluated for fatigue. He undergoes a colonoscopy and is found to have a right-sided colon cancer. His hematocrit is 33 with an MCV of 72. His ferritin level is 3. What do you recommend to help with his iron deficiency?

A. Ferrous sulfate 325 mg daily.

B. Ferrous sulfate 325 mg b.i.d.

C. Ferrous sulfate 325 mg t.i.d.

Treatment of iron deficiency with oral iron has traditionally been done by giving 150-200 mg of elemental iron (which is equal to three 325 mg tablets of iron sulfate).¹ This dosing regimen has considerable gastrointestinal side effects. Recent research into iron absorption suggests that the higher the dose of iron given, the more absorption may be hindered. In a study of 54 women who had low ferritin levels, lower daily doses of iron – and not giving it multiple times a day – led to better iron absorption.²

In a study of elderly patients with iron deficiency, 90 hospitalized elderly patients older than 80 years with iron deficiency anemia were randomized to receive elemental iron as 15 mg or 50 mg of liquid ferrous gluconate, or 150 mg of ferrous calcium citrate for 60 days.³ Two months of iron treatment raised hemoglobin and ferritin levels to a similar degree in all groups, with no significant differences between the 15-mg, 50-mg, and 150-mg groups.

There was a significant difference in abdominal discomfort, with much less (20%) in the patients who received 15 mg of ferrous gluconate, compared with 60% in those who received 50 mg and 70% in those receiving 150 mg (P less than .05 comparing 15 mg with 50 mg and 150 mg). Statistically significant differences were also seen for nausea/vomiting, constipation, and dropout, with much lower rates seen in the low-dose (15-mg) group.

In a study of iron supplementation in individuals undergoing blood donation, a single daily dose of iron was used (37.5 mg of elemental iron) in half of the subjects, with the rest of the subjects receiving no iron.⁴ The mean age of the participants was 48 years.

Subjects who received the once-daily low-dose iron recovered much more quickly toward predonation hematocrit than did those who did not receive the low-dose iron (time to 80% hemoglobin recovery, 32 days vs. 92 days in the non–iron treated patients, P = .02). The effect was more dramatic in subjects who started with a low ferritin level (defined as less than 26), where time to 80% hemoglobin recovery was 36 days in the iron-treated patients vs. 153 days for the no-iron group.

The results of this study are in line with what we know about avid iron absorption in iron deficient patients, and the success of low doses in a younger patient population is encouraging.

In a small study looking at two different doses of elemental iron for the treatment of iron deficiency, 24 women (ages 18-35 years) with iron deficiency were randomized to 60 mg or 80 mg of elemental iron or placebo for 16 weeks.⁵ There was no difference in normalization of ferritin levels in the women who received either dose of iron. There was also no difference in side effects between the groups.

This study is small and had minimal difference in iron dose. In addition, the dosing was given once a day for both groups. I suspect that the lack of difference in side effects was due to both the small size of the study and the minimal difference in iron dose.

What does this all mean? I think that the most appropriate dosing for oral iron replacement is a single daily low-dose iron preparation. Whether that dose is 15 mg of elemental iron to 68 mg of elemental iron (the amount in a 325-mg ferrous sulfate tablet) isn’t clear. Low doses appear to be effective, and avoiding high doses likely decreases side effects without sacrificing efficacy.

References

1. Fairbanks V.F., Beutler E. Iron deficiency, in “Williams Textbook of Hematology, 6th ed. Beutler E., Coller B.S., Lichtman M.A., Kipps T.J., eds. (New York: McGraw-Hill; 2001, pp. 460-2).

2. Blood. 2015 Oct 22;126(17):1981-9.

3. Am J Med. 2005 Oct;118(10):1142-7.

4. JAMA. 2015 Feb 10;313(6):575-83.

5. Nutrients. 2014 Apr 4;6(4):1394-405.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at dpaauw@uw.edu.

A 69-year-old man is evaluated for fatigue. He undergoes a colonoscopy and is found to have a right-sided colon cancer. His hematocrit is 33 with an MCV of 72. His ferritin level is 3. What do you recommend to help with his iron deficiency?

A. Ferrous sulfate 325 mg daily.

B. Ferrous sulfate 325 mg b.i.d.

C. Ferrous sulfate 325 mg t.i.d.

Treatment of iron deficiency with oral iron has traditionally been done by giving 150-200 mg of elemental iron (which is equal to three 325 mg tablets of iron sulfate).¹ This dosing regimen has considerable gastrointestinal side effects. Recent research into iron absorption suggests that the higher the dose of iron given, the more absorption may be hindered. In a study of 54 women who had low ferritin levels, lower daily doses of iron – and not giving it multiple times a day – led to better iron absorption.²

In a study of elderly patients with iron deficiency, 90 hospitalized elderly patients older than 80 years with iron deficiency anemia were randomized to receive elemental iron as 15 mg or 50 mg of liquid ferrous gluconate, or 150 mg of ferrous calcium citrate for 60 days.³ Two months of iron treatment raised hemoglobin and ferritin levels to a similar degree in all groups, with no significant differences between the 15-mg, 50-mg, and 150-mg groups.

There was a significant difference in abdominal discomfort, with much less (20%) in the patients who received 15 mg of ferrous gluconate, compared with 60% in those who received 50 mg and 70% in those receiving 150 mg (P less than .05 comparing 15 mg with 50 mg and 150 mg). Statistically significant differences were also seen for nausea/vomiting, constipation, and dropout, with much lower rates seen in the low-dose (15-mg) group.

In a study of iron supplementation in individuals undergoing blood donation, a single daily dose of iron was used (37.5 mg of elemental iron) in half of the subjects, with the rest of the subjects receiving no iron.⁴ The mean age of the participants was 48 years.

Subjects who received the once-daily low-dose iron recovered much more quickly toward predonation hematocrit than did those who did not receive the low-dose iron (time to 80% hemoglobin recovery, 32 days vs. 92 days in the non–iron treated patients, P = .02). The effect was more dramatic in subjects who started with a low ferritin level (defined as less than 26), where time to 80% hemoglobin recovery was 36 days in the iron-treated patients vs. 153 days for the no-iron group.

The results of this study are in line with what we know about avid iron absorption in iron deficient patients, and the success of low doses in a younger patient population is encouraging.

In a small study looking at two different doses of elemental iron for the treatment of iron deficiency, 24 women (ages 18-35 years) with iron deficiency were randomized to 60 mg or 80 mg of elemental iron or placebo for 16 weeks.⁵ There was no difference in normalization of ferritin levels in the women who received either dose of iron. There was also no difference in side effects between the groups.

This study is small and had minimal difference in iron dose. In addition, the dosing was given once a day for both groups. I suspect that the lack of difference in side effects was due to both the small size of the study and the minimal difference in iron dose.

What does this all mean? I think that the most appropriate dosing for oral iron replacement is a single daily low-dose iron preparation. Whether that dose is 15 mg of elemental iron to 68 mg of elemental iron (the amount in a 325-mg ferrous sulfate tablet) isn’t clear. Low doses appear to be effective, and avoiding high doses likely decreases side effects without sacrificing efficacy.

References

1. Fairbanks V.F., Beutler E. Iron deficiency, in “Williams Textbook of Hematology, 6th ed. Beutler E., Coller B.S., Lichtman M.A., Kipps T.J., eds. (New York: McGraw-Hill; 2001, pp. 460-2).

2. Blood. 2015 Oct 22;126(17):1981-9.

3. Am J Med. 2005 Oct;118(10):1142-7.

4. JAMA. 2015 Feb 10;313(6):575-83.

5. Nutrients. 2014 Apr 4;6(4):1394-405.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at dpaauw@uw.edu.

A 69-year-old man is evaluated for fatigue. He undergoes a colonoscopy and is found to have a right-sided colon cancer. His hematocrit is 33 with an MCV of 72. His ferritin level is 3. What do you recommend to help with his iron deficiency?

A. Ferrous sulfate 325 mg daily.

B. Ferrous sulfate 325 mg b.i.d.

C. Ferrous sulfate 325 mg t.i.d.

Treatment of iron deficiency with oral iron has traditionally been done by giving 150-200 mg of elemental iron (which is equal to three 325 mg tablets of iron sulfate).¹ This dosing regimen has considerable gastrointestinal side effects. Recent research into iron absorption suggests that the higher the dose of iron given, the more absorption may be hindered. In a study of 54 women who had low ferritin levels, lower daily doses of iron – and not giving it multiple times a day – led to better iron absorption.²

In a study of elderly patients with iron deficiency, 90 hospitalized elderly patients older than 80 years with iron deficiency anemia were randomized to receive elemental iron as 15 mg or 50 mg of liquid ferrous gluconate, or 150 mg of ferrous calcium citrate for 60 days.³ Two months of iron treatment raised hemoglobin and ferritin levels to a similar degree in all groups, with no significant differences between the 15-mg, 50-mg, and 150-mg groups.

There was a significant difference in abdominal discomfort, with much less (20%) in the patients who received 15 mg of ferrous gluconate, compared with 60% in those who received 50 mg and 70% in those receiving 150 mg (P less than .05 comparing 15 mg with 50 mg and 150 mg). Statistically significant differences were also seen for nausea/vomiting, constipation, and dropout, with much lower rates seen in the low-dose (15-mg) group.

In a study of iron supplementation in individuals undergoing blood donation, a single daily dose of iron was used (37.5 mg of elemental iron) in half of the subjects, with the rest of the subjects receiving no iron.⁴ The mean age of the participants was 48 years.

Subjects who received the once-daily low-dose iron recovered much more quickly toward predonation hematocrit than did those who did not receive the low-dose iron (time to 80% hemoglobin recovery, 32 days vs. 92 days in the non–iron treated patients, P = .02). The effect was more dramatic in subjects who started with a low ferritin level (defined as less than 26), where time to 80% hemoglobin recovery was 36 days in the iron-treated patients vs. 153 days for the no-iron group.

The results of this study are in line with what we know about avid iron absorption in iron deficient patients, and the success of low doses in a younger patient population is encouraging.

In a small study looking at two different doses of elemental iron for the treatment of iron deficiency, 24 women (ages 18-35 years) with iron deficiency were randomized to 60 mg or 80 mg of elemental iron or placebo for 16 weeks.⁵ There was no difference in normalization of ferritin levels in the women who received either dose of iron. There was also no difference in side effects between the groups.

This study is small and had minimal difference in iron dose. In addition, the dosing was given once a day for both groups. I suspect that the lack of difference in side effects was due to both the small size of the study and the minimal difference in iron dose.

What does this all mean? I think that the most appropriate dosing for oral iron replacement is a single daily low-dose iron preparation. Whether that dose is 15 mg of elemental iron to 68 mg of elemental iron (the amount in a 325-mg ferrous sulfate tablet) isn’t clear. Low doses appear to be effective, and avoiding high doses likely decreases side effects without sacrificing efficacy.

References

1. Fairbanks V.F., Beutler E. Iron deficiency, in “Williams Textbook of Hematology, 6th ed. Beutler E., Coller B.S., Lichtman M.A., Kipps T.J., eds. (New York: McGraw-Hill; 2001, pp. 460-2).

2. Blood. 2015 Oct 22;126(17):1981-9.

3. Am J Med. 2005 Oct;118(10):1142-7.

4. JAMA. 2015 Feb 10;313(6):575-83.

5. Nutrients. 2014 Apr 4;6(4):1394-405.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at dpaauw@uw.edu.

PHOENIX – Cadaveric allograft sternal replacement has proven to be safe, providing optimal stability to the chest wall and protection of surrounding organs, an analysis of 18 cases demonstrated.

“The allograft was biologically well tolerated, allowing a perfect integration into the host,” Dr. Giuseppe Marulli said at the annual meeting of the Society of Thoracic Surgeons. “Donor cryopreserved sternochondral allograft may become the ideal way for anterior chest wall reconstruction, particularly for wide resections.”

Dr. Marulli, a thoracic surgeon at the University of Padova, Italy, noted that prior experimental studies have demonstrated that cryopreserved bone allografts preserve osteoconduction and osteoinduction capacity (Eur Spine J. 2001 Oct;10:S96-101). “Therefore, they form the basis for new bone tissue formation, allowing for the capillary and perivascular blood supply,” he said.

Limitations of current materials used for sternal reconstruction include “excessive rigidity with risk of erosion and insufficient support for large chest wall defects,” he said. Perceived advantages of using cadaveric bone allograft include easy incorporation, no risk of rejection, and a low risk of infection. For each procedure used in the current analysis, cadaveric allograft sternums with costal cartilages were harvested with an aseptic method and treated with an antibiotic solution for 72 hours. Next, they were cryopreserved at –80º C and underwent microbiologic testing for at least 1 month to ensure sterility and absence of immunogenic capacity.

Dr. Marulli reported results from 18 patients who underwent the procedure between January 2009 and January 2015, 13 of whom were female. Their median age was 59 years, their median tumor diameter was 4.75 cm, most (88%) had undergone preoperative needle biopsy, and 50% had undergone induction therapy. The main indication for sternectomy was a single-site sternal metastasis (nine patients), primary chondrosarcoma (four cases), sternal dehiscence after cardiac surgery (two cases), malignant fibrous tumor (one case), radioinduced soft-tissue sarcoma (one case), and a thymic carcinoma invading the sternum (one case).

All patients were extubated in the OR, and one patient died in the hospital from a pulmonary embolism. Two patients (11%) developed postoperative complications: one case of Candida urinary infection and one case of bleeding at the site of the muscle flap. The median postoperative length of stay was 11 days.

To date, no infections or rejections of the grafts have occurred, Dr. Marulli said. After a median of 36 months, 13 patients are alive and 4 are dead (3 from a metastatic recurrence and 1 from an unrelated cause). One patient required removal of a clavicular screw for dislocation 4 months after the operation.

Dr. Marulli reported having no financial disclosures.

dbrunk@frontlinemedcom.com

PHOENIX – Cadaveric allograft sternal replacement has proven to be safe, providing optimal stability to the chest wall and protection of surrounding organs, an analysis of 18 cases demonstrated.

“The allograft was biologically well tolerated, allowing a perfect integration into the host,” Dr. Giuseppe Marulli said at the annual meeting of the Society of Thoracic Surgeons. “Donor cryopreserved sternochondral allograft may become the ideal way for anterior chest wall reconstruction, particularly for wide resections.”

Dr. Marulli, a thoracic surgeon at the University of Padova, Italy, noted that prior experimental studies have demonstrated that cryopreserved bone allografts preserve osteoconduction and osteoinduction capacity (Eur Spine J. 2001 Oct;10:S96-101). “Therefore, they form the basis for new bone tissue formation, allowing for the capillary and perivascular blood supply,” he said.

Limitations of current materials used for sternal reconstruction include “excessive rigidity with risk of erosion and insufficient support for large chest wall defects,” he said. Perceived advantages of using cadaveric bone allograft include easy incorporation, no risk of rejection, and a low risk of infection. For each procedure used in the current analysis, cadaveric allograft sternums with costal cartilages were harvested with an aseptic method and treated with an antibiotic solution for 72 hours. Next, they were cryopreserved at –80º C and underwent microbiologic testing for at least 1 month to ensure sterility and absence of immunogenic capacity.

Dr. Marulli reported results from 18 patients who underwent the procedure between January 2009 and January 2015, 13 of whom were female. Their median age was 59 years, their median tumor diameter was 4.75 cm, most (88%) had undergone preoperative needle biopsy, and 50% had undergone induction therapy. The main indication for sternectomy was a single-site sternal metastasis (nine patients), primary chondrosarcoma (four cases), sternal dehiscence after cardiac surgery (two cases), malignant fibrous tumor (one case), radioinduced soft-tissue sarcoma (one case), and a thymic carcinoma invading the sternum (one case).

All patients were extubated in the OR, and one patient died in the hospital from a pulmonary embolism. Two patients (11%) developed postoperative complications: one case of Candida urinary infection and one case of bleeding at the site of the muscle flap. The median postoperative length of stay was 11 days.

To date, no infections or rejections of the grafts have occurred, Dr. Marulli said. After a median of 36 months, 13 patients are alive and 4 are dead (3 from a metastatic recurrence and 1 from an unrelated cause). One patient required removal of a clavicular screw for dislocation 4 months after the operation.

Dr. Marulli reported having no financial disclosures.

dbrunk@frontlinemedcom.com

PHOENIX – Cadaveric allograft sternal replacement has proven to be safe, providing optimal stability to the chest wall and protection of surrounding organs, an analysis of 18 cases demonstrated.

“The allograft was biologically well tolerated, allowing a perfect integration into the host,” Dr. Giuseppe Marulli said at the annual meeting of the Society of Thoracic Surgeons. “Donor cryopreserved sternochondral allograft may become the ideal way for anterior chest wall reconstruction, particularly for wide resections.”

Dr. Marulli, a thoracic surgeon at the University of Padova, Italy, noted that prior experimental studies have demonstrated that cryopreserved bone allografts preserve osteoconduction and osteoinduction capacity (Eur Spine J. 2001 Oct;10:S96-101). “Therefore, they form the basis for new bone tissue formation, allowing for the capillary and perivascular blood supply,” he said.

Limitations of current materials used for sternal reconstruction include “excessive rigidity with risk of erosion and insufficient support for large chest wall defects,” he said. Perceived advantages of using cadaveric bone allograft include easy incorporation, no risk of rejection, and a low risk of infection. For each procedure used in the current analysis, cadaveric allograft sternums with costal cartilages were harvested with an aseptic method and treated with an antibiotic solution for 72 hours. Next, they were cryopreserved at –80º C and underwent microbiologic testing for at least 1 month to ensure sterility and absence of immunogenic capacity.

Dr. Marulli reported results from 18 patients who underwent the procedure between January 2009 and January 2015, 13 of whom were female. Their median age was 59 years, their median tumor diameter was 4.75 cm, most (88%) had undergone preoperative needle biopsy, and 50% had undergone induction therapy. The main indication for sternectomy was a single-site sternal metastasis (nine patients), primary chondrosarcoma (four cases), sternal dehiscence after cardiac surgery (two cases), malignant fibrous tumor (one case), radioinduced soft-tissue sarcoma (one case), and a thymic carcinoma invading the sternum (one case).

All patients were extubated in the OR, and one patient died in the hospital from a pulmonary embolism. Two patients (11%) developed postoperative complications: one case of Candida urinary infection and one case of bleeding at the site of the muscle flap. The median postoperative length of stay was 11 days.

To date, no infections or rejections of the grafts have occurred, Dr. Marulli said. After a median of 36 months, 13 patients are alive and 4 are dead (3 from a metastatic recurrence and 1 from an unrelated cause). One patient required removal of a clavicular screw for dislocation 4 months after the operation.

Dr. Marulli reported having no financial disclosures.

dbrunk@frontlinemedcom.com

Adjunctive dexamethasone not only failed to decrease mortality, it actually induced more disability and adverse events than placebo in patients with HIV-associated cryptococcal meningitis, according to a report published online Feb. 11 in the New England Journal of Medicine.

Glucocorticoids are inexpensive, readily available, and relatively safe for patients with central nervous system infections, and they are widely used for HIV-associated cryptococcal meningitis in regions where the burden of the infection is highest. Glucocorticoids are even recommended for this indication in some international guidelines, as they are thought to reduce intracranial pressure and inflammatory complications. But evidence of their usefulness from randomized controlled trials is sparse, said Dr. Jeremy Day of Oxford University Clinical Research Unit, Wellcome Trust Major Overseas Programme Vietnam, Ho Chi Minh City, and his associates.

alexskopje/ThinkStock

They performed a double-blind, randomized trial to compare the effectiveness and safety of adjunctive dexamethasone against placebo, which involved 451 patients treated for 6 weeks at 13 hospitals in Indonesia, Laos, Thailand, Vietnam, Malawi, and Uganda. The study participants also received standard antifungal therapy including amphotericin B and fluconazole, as well as antiretroviral therapy and Pneumocystis prophylaxis with trimethoprim-sulfamethoxazole.

The trial was stopped prematurely when the safety committee found “dexamethasone was causing harm across key outcomes, including fungal clearance, adverse events, and disability outcomes.” Consequently, the study didn’t have the statistical power to show an effect of dexamethasone on the primary outcome measure – mortality at 10 weeks after randomization (4 weeks after study treatment ended).

Dexamethasone did reduce intracranial pressure more rapidly than placebo, but this effect didn’t translate into improved survival. Mortality at 10 weeks was 47% for the 224 patients assigned to dexamethasone and 41% for the 226 patients assigned to placebo, a nonsignificant difference. However, the drug’s effects changed over time: Hazard ratios for death were 0.77 at days 1-22 but rose to 1.94 at days 23-43 and to 2.50 at days 44-71. By 6-month follow-up, mortality risk showed a trend toward harm with dexamethasone, and was 9% higher in the intention-to-treat population and 11% higher in the per-protocol population analyses, Dr. Day and his associates said (N. Engl J Med. 2016 Feb 11;374[6]: doi:10.1056/NEJMoa1509024). The rate of disability or death was significantly higher with dexamethasone than with placebo at both 10 weeks and 6 months, with odds ratios for a good outcome of only 0.42 and 0.49, respectively. Infections or infestations developed in 48 patients (21%) taking dexamethasone but only 25 (11%) of those taking placebo. Gastrointestinal disorders (13% vs. 7%), renal or urinary disorders (10% vs. 3%), and cardiac disorders (4% vs. 0%) also were significantly more frequent with dexamethasone, as were episodes of hyperglycemia, hypercreatinemia, hyperkalemia, and hyponatremia.

This study was supported by the United Kingdom Department for International Development, the Wellcome Trust, and the U.K. Medical Research Council through the Joint Global Health Trials Program. Dr. Day and his associates reported having no relevant financial disclosures.

Adjunctive dexamethasone not only failed to decrease mortality, it actually induced more disability and adverse events than placebo in patients with HIV-associated cryptococcal meningitis, according to a report published online Feb. 11 in the New England Journal of Medicine.

Glucocorticoids are inexpensive, readily available, and relatively safe for patients with central nervous system infections, and they are widely used for HIV-associated cryptococcal meningitis in regions where the burden of the infection is highest. Glucocorticoids are even recommended for this indication in some international guidelines, as they are thought to reduce intracranial pressure and inflammatory complications. But evidence of their usefulness from randomized controlled trials is sparse, said Dr. Jeremy Day of Oxford University Clinical Research Unit, Wellcome Trust Major Overseas Programme Vietnam, Ho Chi Minh City, and his associates.

alexskopje/ThinkStock

They performed a double-blind, randomized trial to compare the effectiveness and safety of adjunctive dexamethasone against placebo, which involved 451 patients treated for 6 weeks at 13 hospitals in Indonesia, Laos, Thailand, Vietnam, Malawi, and Uganda. The study participants also received standard antifungal therapy including amphotericin B and fluconazole, as well as antiretroviral therapy and Pneumocystis prophylaxis with trimethoprim-sulfamethoxazole.

The trial was stopped prematurely when the safety committee found “dexamethasone was causing harm across key outcomes, including fungal clearance, adverse events, and disability outcomes.” Consequently, the study didn’t have the statistical power to show an effect of dexamethasone on the primary outcome measure – mortality at 10 weeks after randomization (4 weeks after study treatment ended).

Dexamethasone did reduce intracranial pressure more rapidly than placebo, but this effect didn’t translate into improved survival. Mortality at 10 weeks was 47% for the 224 patients assigned to dexamethasone and 41% for the 226 patients assigned to placebo, a nonsignificant difference. However, the drug’s effects changed over time: Hazard ratios for death were 0.77 at days 1-22 but rose to 1.94 at days 23-43 and to 2.50 at days 44-71. By 6-month follow-up, mortality risk showed a trend toward harm with dexamethasone, and was 9% higher in the intention-to-treat population and 11% higher in the per-protocol population analyses, Dr. Day and his associates said (N. Engl J Med. 2016 Feb 11;374[6]: doi:10.1056/NEJMoa1509024). The rate of disability or death was significantly higher with dexamethasone than with placebo at both 10 weeks and 6 months, with odds ratios for a good outcome of only 0.42 and 0.49, respectively. Infections or infestations developed in 48 patients (21%) taking dexamethasone but only 25 (11%) of those taking placebo. Gastrointestinal disorders (13% vs. 7%), renal or urinary disorders (10% vs. 3%), and cardiac disorders (4% vs. 0%) also were significantly more frequent with dexamethasone, as were episodes of hyperglycemia, hypercreatinemia, hyperkalemia, and hyponatremia.

This study was supported by the United Kingdom Department for International Development, the Wellcome Trust, and the U.K. Medical Research Council through the Joint Global Health Trials Program. Dr. Day and his associates reported having no relevant financial disclosures.

Adjunctive dexamethasone not only failed to decrease mortality, it actually induced more disability and adverse events than placebo in patients with HIV-associated cryptococcal meningitis, according to a report published online Feb. 11 in the New England Journal of Medicine.

Glucocorticoids are inexpensive, readily available, and relatively safe for patients with central nervous system infections, and they are widely used for HIV-associated cryptococcal meningitis in regions where the burden of the infection is highest. Glucocorticoids are even recommended for this indication in some international guidelines, as they are thought to reduce intracranial pressure and inflammatory complications. But evidence of their usefulness from randomized controlled trials is sparse, said Dr. Jeremy Day of Oxford University Clinical Research Unit, Wellcome Trust Major Overseas Programme Vietnam, Ho Chi Minh City, and his associates.

alexskopje/ThinkStock

They performed a double-blind, randomized trial to compare the effectiveness and safety of adjunctive dexamethasone against placebo, which involved 451 patients treated for 6 weeks at 13 hospitals in Indonesia, Laos, Thailand, Vietnam, Malawi, and Uganda. The study participants also received standard antifungal therapy including amphotericin B and fluconazole, as well as antiretroviral therapy and Pneumocystis prophylaxis with trimethoprim-sulfamethoxazole.

The trial was stopped prematurely when the safety committee found “dexamethasone was causing harm across key outcomes, including fungal clearance, adverse events, and disability outcomes.” Consequently, the study didn’t have the statistical power to show an effect of dexamethasone on the primary outcome measure – mortality at 10 weeks after randomization (4 weeks after study treatment ended).

Dexamethasone did reduce intracranial pressure more rapidly than placebo, but this effect didn’t translate into improved survival. Mortality at 10 weeks was 47% for the 224 patients assigned to dexamethasone and 41% for the 226 patients assigned to placebo, a nonsignificant difference. However, the drug’s effects changed over time: Hazard ratios for death were 0.77 at days 1-22 but rose to 1.94 at days 23-43 and to 2.50 at days 44-71. By 6-month follow-up, mortality risk showed a trend toward harm with dexamethasone, and was 9% higher in the intention-to-treat population and 11% higher in the per-protocol population analyses, Dr. Day and his associates said (N. Engl J Med. 2016 Feb 11;374[6]: doi:10.1056/NEJMoa1509024). The rate of disability or death was significantly higher with dexamethasone than with placebo at both 10 weeks and 6 months, with odds ratios for a good outcome of only 0.42 and 0.49, respectively. Infections or infestations developed in 48 patients (21%) taking dexamethasone but only 25 (11%) of those taking placebo. Gastrointestinal disorders (13% vs. 7%), renal or urinary disorders (10% vs. 3%), and cardiac disorders (4% vs. 0%) also were significantly more frequent with dexamethasone, as were episodes of hyperglycemia, hypercreatinemia, hyperkalemia, and hyponatremia.

This study was supported by the United Kingdom Department for International Development, the Wellcome Trust, and the U.K. Medical Research Council through the Joint Global Health Trials Program. Dr. Day and his associates reported having no relevant financial disclosures.

Clonal immunoglobulin reactive to lyso-glucosylceramide (LGL1), which is elevated in Gaucher disease, was found in patients with Gaucher disease as well as in one third of patients with sporadic monoclonal gammopathies.

Antigen-specific immunoblots showed that 17 of 20 patients with Gaucher disease had clonal immunoglobulin against LGL1, researchers reported (N Engl J Med. 2016 Feb 10).

Analysis of immunoglobulin gene mutations has provided evidence for antigen-driven clonal expansion of plasma cells in multiple myeloma and monoclonal gammopathy of undetermined significance (MGUS), but the underlying antigens remained unknown. Myeloma risk is increased with lipid disorders such as Gaucher disease and obesity, suggesting lipid involvement in pathogenesis.

“These studies set the stage for newer approaches to lower the levels of these lipids in patients with Gaucher disease and others with precursors for myeloma. Potentially, this could be achieved with drugs or lifestyle changes to reduce the levels of lipids to lower the risk of cancer,” senior author Dr. Madhav Dhodapkar, chief of hematology at Yale Cancer Center, New Haven, Conn., said in a press release.

All six mouse models with Gaucher-like disease had clonal immunoglobulin against LGL1. Gaucher disease–associated gammopathy in mouse models can be targeted by the reduction of the underlying antigen. Feeding eliglustat to the mice with clonal immunoglobulins reduced anti-LGL1 antibodies detected by immunoblot and reduced clonal immunoglobulin in vivo.

Dysregulated lipids are sometimes present in sporadic myeloma, and M spikes on LGL1-specific blotting were LGL1-reactive in 22 of 66 patients (33%). These clonal immunoglobulins also were cross reactive to lysophosphatidylcholine. Patients with polyclonal gammopathies not associated with Gaucher disease did not react to the lysolipids.

“Understanding the antigenic reactivity of clonal immunoglobulin not only has direct implications for antigenic origins of myeloma but also may lead to new strategies to prevent or treat clinical cancer by targeting the underlying antigen,” wrote Shiny Nair, Ph.D., of Yale University and colleagues.

Clonal immunoglobulin reactive to lyso-glucosylceramide (LGL1), which is elevated in Gaucher disease, was found in patients with Gaucher disease as well as in one third of patients with sporadic monoclonal gammopathies.

Antigen-specific immunoblots showed that 17 of 20 patients with Gaucher disease had clonal immunoglobulin against LGL1, researchers reported (N Engl J Med. 2016 Feb 10).

Analysis of immunoglobulin gene mutations has provided evidence for antigen-driven clonal expansion of plasma cells in multiple myeloma and monoclonal gammopathy of undetermined significance (MGUS), but the underlying antigens remained unknown. Myeloma risk is increased with lipid disorders such as Gaucher disease and obesity, suggesting lipid involvement in pathogenesis.

“These studies set the stage for newer approaches to lower the levels of these lipids in patients with Gaucher disease and others with precursors for myeloma. Potentially, this could be achieved with drugs or lifestyle changes to reduce the levels of lipids to lower the risk of cancer,” senior author Dr. Madhav Dhodapkar, chief of hematology at Yale Cancer Center, New Haven, Conn., said in a press release.

All six mouse models with Gaucher-like disease had clonal immunoglobulin against LGL1. Gaucher disease–associated gammopathy in mouse models can be targeted by the reduction of the underlying antigen. Feeding eliglustat to the mice with clonal immunoglobulins reduced anti-LGL1 antibodies detected by immunoblot and reduced clonal immunoglobulin in vivo.

Dysregulated lipids are sometimes present in sporadic myeloma, and M spikes on LGL1-specific blotting were LGL1-reactive in 22 of 66 patients (33%). These clonal immunoglobulins also were cross reactive to lysophosphatidylcholine. Patients with polyclonal gammopathies not associated with Gaucher disease did not react to the lysolipids.

“Understanding the antigenic reactivity of clonal immunoglobulin not only has direct implications for antigenic origins of myeloma but also may lead to new strategies to prevent or treat clinical cancer by targeting the underlying antigen,” wrote Shiny Nair, Ph.D., of Yale University and colleagues.

Clonal immunoglobulin reactive to lyso-glucosylceramide (LGL1), which is elevated in Gaucher disease, was found in patients with Gaucher disease as well as in one third of patients with sporadic monoclonal gammopathies.

Antigen-specific immunoblots showed that 17 of 20 patients with Gaucher disease had clonal immunoglobulin against LGL1, researchers reported (N Engl J Med. 2016 Feb 10).

Analysis of immunoglobulin gene mutations has provided evidence for antigen-driven clonal expansion of plasma cells in multiple myeloma and monoclonal gammopathy of undetermined significance (MGUS), but the underlying antigens remained unknown. Myeloma risk is increased with lipid disorders such as Gaucher disease and obesity, suggesting lipid involvement in pathogenesis.

“These studies set the stage for newer approaches to lower the levels of these lipids in patients with Gaucher disease and others with precursors for myeloma. Potentially, this could be achieved with drugs or lifestyle changes to reduce the levels of lipids to lower the risk of cancer,” senior author Dr. Madhav Dhodapkar, chief of hematology at Yale Cancer Center, New Haven, Conn., said in a press release.

All six mouse models with Gaucher-like disease had clonal immunoglobulin against LGL1. Gaucher disease–associated gammopathy in mouse models can be targeted by the reduction of the underlying antigen. Feeding eliglustat to the mice with clonal immunoglobulins reduced anti-LGL1 antibodies detected by immunoblot and reduced clonal immunoglobulin in vivo.

Dysregulated lipids are sometimes present in sporadic myeloma, and M spikes on LGL1-specific blotting were LGL1-reactive in 22 of 66 patients (33%). These clonal immunoglobulins also were cross reactive to lysophosphatidylcholine. Patients with polyclonal gammopathies not associated with Gaucher disease did not react to the lysolipids.

“Understanding the antigenic reactivity of clonal immunoglobulin not only has direct implications for antigenic origins of myeloma but also may lead to new strategies to prevent or treat clinical cancer by targeting the underlying antigen,” wrote Shiny Nair, Ph.D., of Yale University and colleagues.

Caplacizumab induces faster resolution of acute episodes of acquired thrombotic thrombocytopenic purpura than does conventional therapy by blocking further platelet aggregation mediated by von Willebrand factor, according to a report published online Feb. 11 in the New England Journal of Medicine.

Faster normalization of the platelet count “prevents further consumption of platelets into microthrombi, and the consequent progression of tissue ischemia.” This in turn should prevent further ischemic injury to the brain, heart, and kidneys in both the short and the long term, said Dr. Flora Peyvandi of the Angelo Bianchi Bonomi Hemophilia and Thrombosis Center, Ospedale Maggiore Policlinico, Milan, and her associates.

Wikimedia Commons/ Erhabor Osaro/CC-SA 3.0

The investigators assessed caplacizumab, an anti–von Willebrand factor immunoglobulin, as a potential treatment for acquired TTP in a manufacturer-sponsored phase II trial involving 75 patients treated at 56 medical centers worldwide. All the study participants received standard treatment – daily plasma exchange and immunosuppressive therapy. In addition, they were randomly assigned to receive daily caplacizumab (36 patients) or placebo injections (39 patients) after each plasma exchange procedure and for 30 days following the final procedure, for a maximum of 90 days.

“Caplacizumab rapidly neutralized its target as indicated by suppression of von Willebrand factor–ristocetin cofactor activity to a mean of less than 20% by day 1 and throughout the treatment period,” Dr. Peyvandi and her associates said. These values returned to baseline levels within 1 week of treatment cessation.

The primary endpoint of the study, median time to normalization of the platelet count, was significantly reduced by 39% with caplacizumab compared with placebo. Among the 69 patients who had not undergone an initial plasma-exchange session before study enrollment, the median time to response was 3.0 days with caplacizumab and 4.9 days with placebo. And among the six patients who had undergone an initial plasma-exchange session before enrollment, the median time to response was 2.4 days with caplacizumab and 4.3 days with placebo, Dr. Peyvandi and her associates said (N Engl J Med. 2016 Feb 11;374[6]. doi:10.1056/NEJMoa1505533).

At 1-month follow-up, 81% of the caplacizumab group showed complete remission, compared with 46% of the placebo group. Three patients in the caplacizumab group had TTP exacerbations, compared with 11 in the placebo group. Post hoc analyses showed that the mean number of plasma-exchange days (5.9 vs. 7.9) and the mean volume of plasma administered (19.9 liters vs. 28.3 liters) were lower with caplacizumab than with placebo. And post hoc analyses of markers of end-organ damage, such as lactate dehydrogenase, troponin T, troponin 1, and creatinine levels, showed more rapid normalization with caplacizumab.

As expected, the number of patients who had bleeding-related adverse events was higher with the active treatment (19 patients) than with placebo (14 patients), but these events “were generally mild” and didn’t require treatment. Serious bleeding events occurred in 2 patients in each study group and included subarachnoid hemorrhage, retinal hemorrhage, and metrorrhagia in the caplacizumab group and cerebral hemorrhage and hematuria in the placebo group.

The study was supported by Ablynx, maker of caplacizumab, which also designed and conducted the study, analyzed the data, and prepared the manuscript. Dr. Peyvandi reported ties to Ablynx, Alexion, Biotest, Kedrion Biopharma, Novo Nordisk, Baxter, Bayer, CSL Behring, Grifols, LFB, Roche, and Sobi; her associates’ financial disclosures are available at NEJM.org.

Caplacizumab induces faster resolution of acute episodes of acquired thrombotic thrombocytopenic purpura than does conventional therapy by blocking further platelet aggregation mediated by von Willebrand factor, according to a report published online Feb. 11 in the New England Journal of Medicine.

Faster normalization of the platelet count “prevents further consumption of platelets into microthrombi, and the consequent progression of tissue ischemia.” This in turn should prevent further ischemic injury to the brain, heart, and kidneys in both the short and the long term, said Dr. Flora Peyvandi of the Angelo Bianchi Bonomi Hemophilia and Thrombosis Center, Ospedale Maggiore Policlinico, Milan, and her associates.

Wikimedia Commons/ Erhabor Osaro/CC-SA 3.0

The investigators assessed caplacizumab, an anti–von Willebrand factor immunoglobulin, as a potential treatment for acquired TTP in a manufacturer-sponsored phase II trial involving 75 patients treated at 56 medical centers worldwide. All the study participants received standard treatment – daily plasma exchange and immunosuppressive therapy. In addition, they were randomly assigned to receive daily caplacizumab (36 patients) or placebo injections (39 patients) after each plasma exchange procedure and for 30 days following the final procedure, for a maximum of 90 days.

“Caplacizumab rapidly neutralized its target as indicated by suppression of von Willebrand factor–ristocetin cofactor activity to a mean of less than 20% by day 1 and throughout the treatment period,” Dr. Peyvandi and her associates said. These values returned to baseline levels within 1 week of treatment cessation.

The primary endpoint of the study, median time to normalization of the platelet count, was significantly reduced by 39% with caplacizumab compared with placebo. Among the 69 patients who had not undergone an initial plasma-exchange session before study enrollment, the median time to response was 3.0 days with caplacizumab and 4.9 days with placebo. And among the six patients who had undergone an initial plasma-exchange session before enrollment, the median time to response was 2.4 days with caplacizumab and 4.3 days with placebo, Dr. Peyvandi and her associates said (N Engl J Med. 2016 Feb 11;374[6]. doi:10.1056/NEJMoa1505533).

At 1-month follow-up, 81% of the caplacizumab group showed complete remission, compared with 46% of the placebo group. Three patients in the caplacizumab group had TTP exacerbations, compared with 11 in the placebo group. Post hoc analyses showed that the mean number of plasma-exchange days (5.9 vs. 7.9) and the mean volume of plasma administered (19.9 liters vs. 28.3 liters) were lower with caplacizumab than with placebo. And post hoc analyses of markers of end-organ damage, such as lactate dehydrogenase, troponin T, troponin 1, and creatinine levels, showed more rapid normalization with caplacizumab.

As expected, the number of patients who had bleeding-related adverse events was higher with the active treatment (19 patients) than with placebo (14 patients), but these events “were generally mild” and didn’t require treatment. Serious bleeding events occurred in 2 patients in each study group and included subarachnoid hemorrhage, retinal hemorrhage, and metrorrhagia in the caplacizumab group and cerebral hemorrhage and hematuria in the placebo group.

The study was supported by Ablynx, maker of caplacizumab, which also designed and conducted the study, analyzed the data, and prepared the manuscript. Dr. Peyvandi reported ties to Ablynx, Alexion, Biotest, Kedrion Biopharma, Novo Nordisk, Baxter, Bayer, CSL Behring, Grifols, LFB, Roche, and Sobi; her associates’ financial disclosures are available at NEJM.org.

Caplacizumab induces faster resolution of acute episodes of acquired thrombotic thrombocytopenic purpura than does conventional therapy by blocking further platelet aggregation mediated by von Willebrand factor, according to a report published online Feb. 11 in the New England Journal of Medicine.

Faster normalization of the platelet count “prevents further consumption of platelets into microthrombi, and the consequent progression of tissue ischemia.” This in turn should prevent further ischemic injury to the brain, heart, and kidneys in both the short and the long term, said Dr. Flora Peyvandi of the Angelo Bianchi Bonomi Hemophilia and Thrombosis Center, Ospedale Maggiore Policlinico, Milan, and her associates.

Wikimedia Commons/ Erhabor Osaro/CC-SA 3.0

The investigators assessed caplacizumab, an anti–von Willebrand factor immunoglobulin, as a potential treatment for acquired TTP in a manufacturer-sponsored phase II trial involving 75 patients treated at 56 medical centers worldwide. All the study participants received standard treatment – daily plasma exchange and immunosuppressive therapy. In addition, they were randomly assigned to receive daily caplacizumab (36 patients) or placebo injections (39 patients) after each plasma exchange procedure and for 30 days following the final procedure, for a maximum of 90 days.

“Caplacizumab rapidly neutralized its target as indicated by suppression of von Willebrand factor–ristocetin cofactor activity to a mean of less than 20% by day 1 and throughout the treatment period,” Dr. Peyvandi and her associates said. These values returned to baseline levels within 1 week of treatment cessation.

The primary endpoint of the study, median time to normalization of the platelet count, was significantly reduced by 39% with caplacizumab compared with placebo. Among the 69 patients who had not undergone an initial plasma-exchange session before study enrollment, the median time to response was 3.0 days with caplacizumab and 4.9 days with placebo. And among the six patients who had undergone an initial plasma-exchange session before enrollment, the median time to response was 2.4 days with caplacizumab and 4.3 days with placebo, Dr. Peyvandi and her associates said (N Engl J Med. 2016 Feb 11;374[6]. doi:10.1056/NEJMoa1505533).

At 1-month follow-up, 81% of the caplacizumab group showed complete remission, compared with 46% of the placebo group. Three patients in the caplacizumab group had TTP exacerbations, compared with 11 in the placebo group. Post hoc analyses showed that the mean number of plasma-exchange days (5.9 vs. 7.9) and the mean volume of plasma administered (19.9 liters vs. 28.3 liters) were lower with caplacizumab than with placebo. And post hoc analyses of markers of end-organ damage, such as lactate dehydrogenase, troponin T, troponin 1, and creatinine levels, showed more rapid normalization with caplacizumab.

As expected, the number of patients who had bleeding-related adverse events was higher with the active treatment (19 patients) than with placebo (14 patients), but these events “were generally mild” and didn’t require treatment. Serious bleeding events occurred in 2 patients in each study group and included subarachnoid hemorrhage, retinal hemorrhage, and metrorrhagia in the caplacizumab group and cerebral hemorrhage and hematuria in the placebo group.

The study was supported by Ablynx, maker of caplacizumab, which also designed and conducted the study, analyzed the data, and prepared the manuscript. Dr. Peyvandi reported ties to Ablynx, Alexion, Biotest, Kedrion Biopharma, Novo Nordisk, Baxter, Bayer, CSL Behring, Grifols, LFB, Roche, and Sobi; her associates’ financial disclosures are available at NEJM.org.

University of California-San Diego med-peds hospitalist Weijen Chang, MD, SFHM, and Shawn Ralson, MD, vice chair of clinical affairs, Children's Hospital at Dartmouth-Hitchcock in Lebanon, N.H., discuss the factors that went into their hospital medicine career choices, and why they find hospitalist careers so fascinating.

University of California-San Diego med-peds hospitalist Weijen Chang, MD, SFHM, and Shawn Ralson, MD, vice chair of clinical affairs, Children's Hospital at Dartmouth-Hitchcock in Lebanon, N.H., discuss the factors that went into their hospital medicine career choices, and why they find hospitalist careers so fascinating.

University of California-San Diego med-peds hospitalist Weijen Chang, MD, SFHM, and Shawn Ralson, MD, vice chair of clinical affairs, Children's Hospital at Dartmouth-Hitchcock in Lebanon, N.H., discuss the factors that went into their hospital medicine career choices, and why they find hospitalist careers so fascinating.

Question: Doctors are more prone to lawsuits if they:

A. Have been sued before.

B. Spend fewer dollars per hospitalized patient.

C. Show poor communication skills.

D. A and C only.

E. A, B, and C.

Answer: E. Two very recent studies, one by David M. Studdert and the other by Dr. Anupam B. Jena, offer fresh insights into factors linked to the likelihood of a malpractice lawsuit.

The Studdert study concluded that doctors with prior paid claims are at increased risk of incurring yet another lawsuit.¹ Instead of simply relying on data from a single insurer or state, the researchers accessed the National Practitioner Data Bank (NPDB) from 2005 through 2014 and identified 66,426 claims paid against 54,099 physicians.

Over that 10-year period, only 1% of physicians accounted for 32% of paid claims. Of all the physicians, 84% incurred only one paid claim during the study period, and 16% had at least two. Four percent of the physicians had at least three. In adjusted analyses, the risk of recurrence increased with the number of previous paid claims.

For example, compared with physicians with a single claim, the 2,160 physicians who had three paid claims had three times the risk of incurring another (hazard ratio, 3.11); this corresponded in absolute terms to a 24% risk within 2 years.

Likelihood of recurrence also varied widely according to specialty. For example, the risk among neurosurgeons was four times greater than that of psychiatrists. As for internists, the risk of recurrence was approximately double that of neurosurgeons, orthopedic surgeons, general surgeons, plastic surgeons, or obstetrician-gynecologists. The lowest risks of recurrence were seen among psychiatrists (HR, 0.60) and pediatricians (HR, 0.71).

Male physicians had a 38% higher risk of recurrence than did female physicians, and the risk among physicians younger than 35 years was approximately one-third that of their older colleagues (after adjustment for age). Residents had a lower risk of recurrence than did nonresidents, and MDs had a lower risk than did DOs.

Using all 915,564 active physicians in the United States as a denominator, the authors calculated that over the 10-year study period, only 6% of physicians had a paid claim. Note that the 6% figure refers to paid claims reported to the NPDB, which can be expected to be lower than statistics derived from published surveys. These latter studies typically feature self-reported malpractice claims made over a given time period; but it is well known that the majority of such claims are dropped or decided in favor of the doctor, and so will not be reported to the NPDB.

For example, in 2010, the American Medical Association found that 42.2% of 5,825 physicians who responded to its Physician Practice Information survey reported having been sued, with 22.4% sued twice or more.² The report headlined that by mid career, 61% of doctor have been sued.

Rates varied by specialty, with general surgeons and obstetrician-gynecologists being most likely to be sued (69.2%). Family physicians and general internists had similar rates (38.9% and 34%), and pediatricians and psychiatrists were sued the least.

In that report, male doctors were twice as likely to be sued as were their female counterparts, and physicians in solo and specialty practices were sued more often than those in multispecialty practices. Physicians who had an ownership interest in a practice were also at greater risk, with 47.5% reporting being sued, compared with 33.4% for those with no ownership interest.

The second recent study, reported by Dr. Jena of Harvard Medical School, Boston, and his colleagues, analyzed Florida hospital admissions data covering some 24,000 physicians.³ They found that higher spending by physicians was associated with reduced malpractice claims made the following year.

This pattern held true for physicians in all specialties but one (family practice). For example, among internists, the malpractice risk probability was 1.5% in the bottom spending fifth ($19,725 per admission) and 0.3% in the top fifth ($39,379 per admission). Among obstetricians, the comparable figures were 1.9% and 0.4% respectively.

In addition, a separate subgroup analysis of cesarean-section rates revealed that malpractice claims were approximately halved among obstetricians with rates in the highest fifth, compared with the lowest fifth.

Unfortunately, the Jena study lacked information on illness severity and past malpractice history, and it remains speculative whether increased resource utilization could be attributed entirely to defensive medical practice.⁴

As interesting as these new reports may be, it is worth remembering that what prompts a lawsuit are poor communication and patient perception that the physician is uncaring and at fault for the bad result.

It is well known that quality of medical care correlates poorly with the filing of malpractice lawsuits, as illustrated in the conclusion of the landmark Harvard study that “medical malpractice litigation infrequently compensates patients injured by medical negligence and rarely identifies, and holds providers accountable for, substandard care.”⁵ The authors estimated that there was only 1 malpractice claim for every 7.6 adverse events caused by negligence.

In another retrospective chart review study, the quality of treatment as judged by independent peer review was no different in frequently sued versus never-sued obstetricians.⁶

Communication problems exist in more than 70% of malpractice cases, centering around four themes: 1) deserting the patient; 2) devaluing patient/family views; 3) delivering information poorly; and 4) failing to understand the patient/family perspective.⁷

Anger, either from the adverse result itself or perceived lack of caring, turns an injured patient into a plaintiff, and lies at the root of all malpractice claims. The patients may not even have a serious injury or a meritorious claim, but they are so frustrated with their physician or the hospital that they contact an attorney to vent their anger.

One experienced attorney volunteered that close to half his malpractice cases could have been avoided through disclosure or apology, noting: “What the patients really wanted was simply an honest explanation of what happened, and, if appropriate, an apology. Unfortunately, when they were not only offered neither, but were rejected as well, they felt doubly wronged and then sought legal counsel.”⁸

Communicating well begins with active listening. Patients want their doctors to listen to them and to explain their conditions and treatment plans in simple, understandable language. The physician should give them ample opportunity to tell their story and to ask questions.

In one well-publicized study, only 23% of patients were able to complete their opening statement before the doctor interrupted, which occurred, on the average, 18 seconds after the patient began to speak!⁹

References

1. N Engl J Med. 2016 Jan 28;374(4):354-62.

2. “Medical liability: By late career, 61% of doctors have been sued,” Aug. 16, 2010, American Medical News.

3. BMJ. 2015 Nov 4;351:h5516.

4. “Law & Medicine: Health care costs and defensive medicine,” Jan. 19, 2016, Internal Medicine News.

5. N Engl J Med. 1991 Jul 25;325(4):245-51.

6. JAMA. 1994 Nov 23-30;272(20):1588-91.

7. Arch Intern Med. 1994 Jun 27;154(12):1365-70.

8. Ann Intern Med. 1999 Dec 21;131(12):970-2.

9. Ann Intern Med. 1984 Nov;101(5):692-6.

Dr. Tan is emeritus professor of medicine and former adjunct professor of law at the University of Hawaii, and currently directs the St. Francis International Center for Healthcare Ethics in Honolulu. This article is meant to be educational and does not constitute medical, ethical, or legal advice. Some of the articles in this series are adapted from the author’s 2006 book, “Medical Malpractice: Understanding the Law, Managing the Risk,” and his 2012 Halsbury treatise, “Medical Negligence and Professional Misconduct.” For additional information, readers may contact the author at siang@hawaii.edu

Question: Doctors are more prone to lawsuits if they:

A. Have been sued before.

B. Spend fewer dollars per hospitalized patient.

C. Show poor communication skills.

D. A and C only.

E. A, B, and C.

Answer: E. Two very recent studies, one by David M. Studdert and the other by Dr. Anupam B. Jena, offer fresh insights into factors linked to the likelihood of a malpractice lawsuit.

The Studdert study concluded that doctors with prior paid claims are at increased risk of incurring yet another lawsuit.¹ Instead of simply relying on data from a single insurer or state, the researchers accessed the National Practitioner Data Bank (NPDB) from 2005 through 2014 and identified 66,426 claims paid against 54,099 physicians.

Over that 10-year period, only 1% of physicians accounted for 32% of paid claims. Of all the physicians, 84% incurred only one paid claim during the study period, and 16% had at least two. Four percent of the physicians had at least three. In adjusted analyses, the risk of recurrence increased with the number of previous paid claims.

For example, compared with physicians with a single claim, the 2,160 physicians who had three paid claims had three times the risk of incurring another (hazard ratio, 3.11); this corresponded in absolute terms to a 24% risk within 2 years.

Likelihood of recurrence also varied widely according to specialty. For example, the risk among neurosurgeons was four times greater than that of psychiatrists. As for internists, the risk of recurrence was approximately double that of neurosurgeons, orthopedic surgeons, general surgeons, plastic surgeons, or obstetrician-gynecologists. The lowest risks of recurrence were seen among psychiatrists (HR, 0.60) and pediatricians (HR, 0.71).

Male physicians had a 38% higher risk of recurrence than did female physicians, and the risk among physicians younger than 35 years was approximately one-third that of their older colleagues (after adjustment for age). Residents had a lower risk of recurrence than did nonresidents, and MDs had a lower risk than did DOs.

Using all 915,564 active physicians in the United States as a denominator, the authors calculated that over the 10-year study period, only 6% of physicians had a paid claim. Note that the 6% figure refers to paid claims reported to the NPDB, which can be expected to be lower than statistics derived from published surveys. These latter studies typically feature self-reported malpractice claims made over a given time period; but it is well known that the majority of such claims are dropped or decided in favor of the doctor, and so will not be reported to the NPDB.

For example, in 2010, the American Medical Association found that 42.2% of 5,825 physicians who responded to its Physician Practice Information survey reported having been sued, with 22.4% sued twice or more.² The report headlined that by mid career, 61% of doctor have been sued.

Rates varied by specialty, with general surgeons and obstetrician-gynecologists being most likely to be sued (69.2%). Family physicians and general internists had similar rates (38.9% and 34%), and pediatricians and psychiatrists were sued the least.

In that report, male doctors were twice as likely to be sued as were their female counterparts, and physicians in solo and specialty practices were sued more often than those in multispecialty practices. Physicians who had an ownership interest in a practice were also at greater risk, with 47.5% reporting being sued, compared with 33.4% for those with no ownership interest.

The second recent study, reported by Dr. Jena of Harvard Medical School, Boston, and his colleagues, analyzed Florida hospital admissions data covering some 24,000 physicians.³ They found that higher spending by physicians was associated with reduced malpractice claims made the following year.

This pattern held true for physicians in all specialties but one (family practice). For example, among internists, the malpractice risk probability was 1.5% in the bottom spending fifth ($19,725 per admission) and 0.3% in the top fifth ($39,379 per admission). Among obstetricians, the comparable figures were 1.9% and 0.4% respectively.

In addition, a separate subgroup analysis of cesarean-section rates revealed that malpractice claims were approximately halved among obstetricians with rates in the highest fifth, compared with the lowest fifth.

Unfortunately, the Jena study lacked information on illness severity and past malpractice history, and it remains speculative whether increased resource utilization could be attributed entirely to defensive medical practice.⁴

As interesting as these new reports may be, it is worth remembering that what prompts a lawsuit are poor communication and patient perception that the physician is uncaring and at fault for the bad result.

It is well known that quality of medical care correlates poorly with the filing of malpractice lawsuits, as illustrated in the conclusion of the landmark Harvard study that “medical malpractice litigation infrequently compensates patients injured by medical negligence and rarely identifies, and holds providers accountable for, substandard care.”⁵ The authors estimated that there was only 1 malpractice claim for every 7.6 adverse events caused by negligence.

In another retrospective chart review study, the quality of treatment as judged by independent peer review was no different in frequently sued versus never-sued obstetricians.⁶

Communication problems exist in more than 70% of malpractice cases, centering around four themes: 1) deserting the patient; 2) devaluing patient/family views; 3) delivering information poorly; and 4) failing to understand the patient/family perspective.⁷

Anger, either from the adverse result itself or perceived lack of caring, turns an injured patient into a plaintiff, and lies at the root of all malpractice claims. The patients may not even have a serious injury or a meritorious claim, but they are so frustrated with their physician or the hospital that they contact an attorney to vent their anger.

One experienced attorney volunteered that close to half his malpractice cases could have been avoided through disclosure or apology, noting: “What the patients really wanted was simply an honest explanation of what happened, and, if appropriate, an apology. Unfortunately, when they were not only offered neither, but were rejected as well, they felt doubly wronged and then sought legal counsel.”⁸

Communicating well begins with active listening. Patients want their doctors to listen to them and to explain their conditions and treatment plans in simple, understandable language. The physician should give them ample opportunity to tell their story and to ask questions.

In one well-publicized study, only 23% of patients were able to complete their opening statement before the doctor interrupted, which occurred, on the average, 18 seconds after the patient began to speak!⁹

References

1. N Engl J Med. 2016 Jan 28;374(4):354-62.

2. “Medical liability: By late career, 61% of doctors have been sued,” Aug. 16, 2010, American Medical News.

3. BMJ. 2015 Nov 4;351:h5516.

4. “Law & Medicine: Health care costs and defensive medicine,” Jan. 19, 2016, Internal Medicine News.

5. N Engl J Med. 1991 Jul 25;325(4):245-51.

6. JAMA. 1994 Nov 23-30;272(20):1588-91.

7. Arch Intern Med. 1994 Jun 27;154(12):1365-70.

8. Ann Intern Med. 1999 Dec 21;131(12):970-2.

9. Ann Intern Med. 1984 Nov;101(5):692-6.

Dr. Tan is emeritus professor of medicine and former adjunct professor of law at the University of Hawaii, and currently directs the St. Francis International Center for Healthcare Ethics in Honolulu. This article is meant to be educational and does not constitute medical, ethical, or legal advice. Some of the articles in this series are adapted from the author’s 2006 book, “Medical Malpractice: Understanding the Law, Managing the Risk,” and his 2012 Halsbury treatise, “Medical Negligence and Professional Misconduct.” For additional information, readers may contact the author at siang@hawaii.edu

Question: Doctors are more prone to lawsuits if they:

A. Have been sued before.

B. Spend fewer dollars per hospitalized patient.

C. Show poor communication skills.

D. A and C only.

E. A, B, and C.

Answer: E. Two very recent studies, one by David M. Studdert and the other by Dr. Anupam B. Jena, offer fresh insights into factors linked to the likelihood of a malpractice lawsuit.

The Studdert study concluded that doctors with prior paid claims are at increased risk of incurring yet another lawsuit.¹ Instead of simply relying on data from a single insurer or state, the researchers accessed the National Practitioner Data Bank (NPDB) from 2005 through 2014 and identified 66,426 claims paid against 54,099 physicians.

Over that 10-year period, only 1% of physicians accounted for 32% of paid claims. Of all the physicians, 84% incurred only one paid claim during the study period, and 16% had at least two. Four percent of the physicians had at least three. In adjusted analyses, the risk of recurrence increased with the number of previous paid claims.

For example, compared with physicians with a single claim, the 2,160 physicians who had three paid claims had three times the risk of incurring another (hazard ratio, 3.11); this corresponded in absolute terms to a 24% risk within 2 years.

Likelihood of recurrence also varied widely according to specialty. For example, the risk among neurosurgeons was four times greater than that of psychiatrists. As for internists, the risk of recurrence was approximately double that of neurosurgeons, orthopedic surgeons, general surgeons, plastic surgeons, or obstetrician-gynecologists. The lowest risks of recurrence were seen among psychiatrists (HR, 0.60) and pediatricians (HR, 0.71).

Male physicians had a 38% higher risk of recurrence than did female physicians, and the risk among physicians younger than 35 years was approximately one-third that of their older colleagues (after adjustment for age). Residents had a lower risk of recurrence than did nonresidents, and MDs had a lower risk than did DOs.

Using all 915,564 active physicians in the United States as a denominator, the authors calculated that over the 10-year study period, only 6% of physicians had a paid claim. Note that the 6% figure refers to paid claims reported to the NPDB, which can be expected to be lower than statistics derived from published surveys. These latter studies typically feature self-reported malpractice claims made over a given time period; but it is well known that the majority of such claims are dropped or decided in favor of the doctor, and so will not be reported to the NPDB.

For example, in 2010, the American Medical Association found that 42.2% of 5,825 physicians who responded to its Physician Practice Information survey reported having been sued, with 22.4% sued twice or more.² The report headlined that by mid career, 61% of doctor have been sued.

Rates varied by specialty, with general surgeons and obstetrician-gynecologists being most likely to be sued (69.2%). Family physicians and general internists had similar rates (38.9% and 34%), and pediatricians and psychiatrists were sued the least.

In that report, male doctors were twice as likely to be sued as were their female counterparts, and physicians in solo and specialty practices were sued more often than those in multispecialty practices. Physicians who had an ownership interest in a practice were also at greater risk, with 47.5% reporting being sued, compared with 33.4% for those with no ownership interest.

The second recent study, reported by Dr. Jena of Harvard Medical School, Boston, and his colleagues, analyzed Florida hospital admissions data covering some 24,000 physicians.³ They found that higher spending by physicians was associated with reduced malpractice claims made the following year.

This pattern held true for physicians in all specialties but one (family practice). For example, among internists, the malpractice risk probability was 1.5% in the bottom spending fifth ($19,725 per admission) and 0.3% in the top fifth ($39,379 per admission). Among obstetricians, the comparable figures were 1.9% and 0.4% respectively.

In addition, a separate subgroup analysis of cesarean-section rates revealed that malpractice claims were approximately halved among obstetricians with rates in the highest fifth, compared with the lowest fifth.

Unfortunately, the Jena study lacked information on illness severity and past malpractice history, and it remains speculative whether increased resource utilization could be attributed entirely to defensive medical practice.⁴

As interesting as these new reports may be, it is worth remembering that what prompts a lawsuit are poor communication and patient perception that the physician is uncaring and at fault for the bad result.

It is well known that quality of medical care correlates poorly with the filing of malpractice lawsuits, as illustrated in the conclusion of the landmark Harvard study that “medical malpractice litigation infrequently compensates patients injured by medical negligence and rarely identifies, and holds providers accountable for, substandard care.”⁵ The authors estimated that there was only 1 malpractice claim for every 7.6 adverse events caused by negligence.

In another retrospective chart review study, the quality of treatment as judged by independent peer review was no different in frequently sued versus never-sued obstetricians.⁶

Communication problems exist in more than 70% of malpractice cases, centering around four themes: 1) deserting the patient; 2) devaluing patient/family views; 3) delivering information poorly; and 4) failing to understand the patient/family perspective.⁷

Anger, either from the adverse result itself or perceived lack of caring, turns an injured patient into a plaintiff, and lies at the root of all malpractice claims. The patients may not even have a serious injury or a meritorious claim, but they are so frustrated with their physician or the hospital that they contact an attorney to vent their anger.

One experienced attorney volunteered that close to half his malpractice cases could have been avoided through disclosure or apology, noting: “What the patients really wanted was simply an honest explanation of what happened, and, if appropriate, an apology. Unfortunately, when they were not only offered neither, but were rejected as well, they felt doubly wronged and then sought legal counsel.”⁸

Communicating well begins with active listening. Patients want their doctors to listen to them and to explain their conditions and treatment plans in simple, understandable language. The physician should give them ample opportunity to tell their story and to ask questions.

In one well-publicized study, only 23% of patients were able to complete their opening statement before the doctor interrupted, which occurred, on the average, 18 seconds after the patient began to speak!⁹

References

1. N Engl J Med. 2016 Jan 28;374(4):354-62.

2. “Medical liability: By late career, 61% of doctors have been sued,” Aug. 16, 2010, American Medical News.

3. BMJ. 2015 Nov 4;351:h5516.

4. “Law & Medicine: Health care costs and defensive medicine,” Jan. 19, 2016, Internal Medicine News.

5. N Engl J Med. 1991 Jul 25;325(4):245-51.

6. JAMA. 1994 Nov 23-30;272(20):1588-91.

7. Arch Intern Med. 1994 Jun 27;154(12):1365-70.

8. Ann Intern Med. 1999 Dec 21;131(12):970-2.

9. Ann Intern Med. 1984 Nov;101(5):692-6.

Dr. Tan is emeritus professor of medicine and former adjunct professor of law at the University of Hawaii, and currently directs the St. Francis International Center for Healthcare Ethics in Honolulu. This article is meant to be educational and does not constitute medical, ethical, or legal advice. Some of the articles in this series are adapted from the author’s 2006 book, “Medical Malpractice: Understanding the Law, Managing the Risk,” and his 2012 Halsbury treatise, “Medical Negligence and Professional Misconduct.” For additional information, readers may contact the author at siang@hawaii.edu

I hope I am correct, but it seems to me that the “holistic” label is fading into the sunset. I never quite got what a holistic physician was doing that I wasn’t. Was I ignoring the fact that my patient came from a certain ethnic group and that his family had a particular set of religious beliefs? I may not have understood or agreed with those customs or beliefs. But I knew that I had better take them into account as I tried to find what was troubling the patient and help him search for a solution.

When the patient with frequent abdominal pains asked me for advice, did I fail to ask a social history because I didn’t think that the fact that her father had just lost his job or that her favorite grandmother was dying of cancer was important? Did I simply write prescriptions and avoid making recommendations about bedtimes, diet, exercise, and relaxation strategies? Did I stop my exam at the clavicles when the patient’s chief complaint was headache?

I’m sure that most physicians who marketed themselves as being holistic passionately believed that a good doctor must consider the whole patient. But what troubled me was the implication that the rest of us didn’t. I suspect that the fading popularity of the label reflects that patients began to realize that it was meaningless.

However, another buzzword has begun to flutter across the medical landscape. Every few days I open a magazine or journal in which someone is suggesting that I need to be more mindful. And they are more than willing to show me or sell me a technique for achieving mindfulness.

Is this just another packaging ploy, or should I begin paddling out to catch this new wave? The more I began to see mindfulness offered and promoted in a wider variety of settings, the more confused I became. So I did what anyone with a WiFi connection would do. I Googled “mindfulness” and discovered that I had good reason to feel confused.

It turns out that in some form or another mindfulness has been a practice in the Buddhist tradition with a history dating back hundreds of years. The first definition I found in Wikipedia read: “being aware moment-to-moment of one’s subjective conscious experience from a first-person perspective.” However, as I read further I discovered a reference to no fewer than 13 disparate definitions across a spectrum from attention and awareness on one end to retention and remindfulness on the other.

Some advocates feel that meditation should be used to prepare oneself to be mindful or that meditation is integral to mindfulness. Other folks don’t seem to see meditation as particularly necessary.

There is a growing body of literature reporting that something labeled mindfulness has helped patients and practitioners improve one or more aspects of wellness. Although the quality of these reports varies widely, it suggests along with the long Buddhist tradition that there is something out there called mindfulness worth investigating.

However, I wonder why it is becoming so widely ballyhooed. It seems to me that at its core, being mindful is simply just trying to do a better job of paying attention to the world around us and our fellow inhabitants. Is it simply the flip side of an attention deficiency? Or, is it an attempt to give a more exotic and mysterious Asian-influenced label to cognitive-behavioral therapy? Could it just be a less judgmental way of asking ourselves, “What were (are) you thinking?”

“Mindfulness” appears to have considerably more substance than “holistic,” but I fear that its indiscriminant use is going to damage its credibility. The overexposure has certainly triggered my skepticism.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics including “How to Say No to Your Toddler.”

I hope I am correct, but it seems to me that the “holistic” label is fading into the sunset. I never quite got what a holistic physician was doing that I wasn’t. Was I ignoring the fact that my patient came from a certain ethnic group and that his family had a particular set of religious beliefs? I may not have understood or agreed with those customs or beliefs. But I knew that I had better take them into account as I tried to find what was troubling the patient and help him search for a solution.

When the patient with frequent abdominal pains asked me for advice, did I fail to ask a social history because I didn’t think that the fact that her father had just lost his job or that her favorite grandmother was dying of cancer was important? Did I simply write prescriptions and avoid making recommendations about bedtimes, diet, exercise, and relaxation strategies? Did I stop my exam at the clavicles when the patient’s chief complaint was headache?

I’m sure that most physicians who marketed themselves as being holistic passionately believed that a good doctor must consider the whole patient. But what troubled me was the implication that the rest of us didn’t. I suspect that the fading popularity of the label reflects that patients began to realize that it was meaningless.

However, another buzzword has begun to flutter across the medical landscape. Every few days I open a magazine or journal in which someone is suggesting that I need to be more mindful. And they are more than willing to show me or sell me a technique for achieving mindfulness.

Is this just another packaging ploy, or should I begin paddling out to catch this new wave? The more I began to see mindfulness offered and promoted in a wider variety of settings, the more confused I became. So I did what anyone with a WiFi connection would do. I Googled “mindfulness” and discovered that I had good reason to feel confused.

It turns out that in some form or another mindfulness has been a practice in the Buddhist tradition with a history dating back hundreds of years. The first definition I found in Wikipedia read: “being aware moment-to-moment of one’s subjective conscious experience from a first-person perspective.” However, as I read further I discovered a reference to no fewer than 13 disparate definitions across a spectrum from attention and awareness on one end to retention and remindfulness on the other.

Some advocates feel that meditation should be used to prepare oneself to be mindful or that meditation is integral to mindfulness. Other folks don’t seem to see meditation as particularly necessary.

There is a growing body of literature reporting that something labeled mindfulness has helped patients and practitioners improve one or more aspects of wellness. Although the quality of these reports varies widely, it suggests along with the long Buddhist tradition that there is something out there called mindfulness worth investigating.

However, I wonder why it is becoming so widely ballyhooed. It seems to me that at its core, being mindful is simply just trying to do a better job of paying attention to the world around us and our fellow inhabitants. Is it simply the flip side of an attention deficiency? Or, is it an attempt to give a more exotic and mysterious Asian-influenced label to cognitive-behavioral therapy? Could it just be a less judgmental way of asking ourselves, “What were (are) you thinking?”

“Mindfulness” appears to have considerably more substance than “holistic,” but I fear that its indiscriminant use is going to damage its credibility. The overexposure has certainly triggered my skepticism.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics including “How to Say No to Your Toddler.”

I hope I am correct, but it seems to me that the “holistic” label is fading into the sunset. I never quite got what a holistic physician was doing that I wasn’t. Was I ignoring the fact that my patient came from a certain ethnic group and that his family had a particular set of religious beliefs? I may not have understood or agreed with those customs or beliefs. But I knew that I had better take them into account as I tried to find what was troubling the patient and help him search for a solution.

When the patient with frequent abdominal pains asked me for advice, did I fail to ask a social history because I didn’t think that the fact that her father had just lost his job or that her favorite grandmother was dying of cancer was important? Did I simply write prescriptions and avoid making recommendations about bedtimes, diet, exercise, and relaxation strategies? Did I stop my exam at the clavicles when the patient’s chief complaint was headache?

I’m sure that most physicians who marketed themselves as being holistic passionately believed that a good doctor must consider the whole patient. But what troubled me was the implication that the rest of us didn’t. I suspect that the fading popularity of the label reflects that patients began to realize that it was meaningless.

However, another buzzword has begun to flutter across the medical landscape. Every few days I open a magazine or journal in which someone is suggesting that I need to be more mindful. And they are more than willing to show me or sell me a technique for achieving mindfulness.

Is this just another packaging ploy, or should I begin paddling out to catch this new wave? The more I began to see mindfulness offered and promoted in a wider variety of settings, the more confused I became. So I did what anyone with a WiFi connection would do. I Googled “mindfulness” and discovered that I had good reason to feel confused.

It turns out that in some form or another mindfulness has been a practice in the Buddhist tradition with a history dating back hundreds of years. The first definition I found in Wikipedia read: “being aware moment-to-moment of one’s subjective conscious experience from a first-person perspective.” However, as I read further I discovered a reference to no fewer than 13 disparate definitions across a spectrum from attention and awareness on one end to retention and remindfulness on the other.

Some advocates feel that meditation should be used to prepare oneself to be mindful or that meditation is integral to mindfulness. Other folks don’t seem to see meditation as particularly necessary.

There is a growing body of literature reporting that something labeled mindfulness has helped patients and practitioners improve one or more aspects of wellness. Although the quality of these reports varies widely, it suggests along with the long Buddhist tradition that there is something out there called mindfulness worth investigating.

However, I wonder why it is becoming so widely ballyhooed. It seems to me that at its core, being mindful is simply just trying to do a better job of paying attention to the world around us and our fellow inhabitants. Is it simply the flip side of an attention deficiency? Or, is it an attempt to give a more exotic and mysterious Asian-influenced label to cognitive-behavioral therapy? Could it just be a less judgmental way of asking ourselves, “What were (are) you thinking?”

“Mindfulness” appears to have considerably more substance than “holistic,” but I fear that its indiscriminant use is going to damage its credibility. The overexposure has certainly triggered my skepticism.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics including “How to Say No to Your Toddler.”

The presence of rheumatoid arthritis in individuals who died from a myocardial infarction was associated with greater inflammatory burden at different levels of myocardial tissue than in those without the disease in a small, retrospective, case-control autopsy study.

“These findings support the hypothesis that RA [rheumatoid arthritis] patients are prone to develop more vulnerable plaques due to more inflammation in the coronary arteries, but also develop increased intramyocardial inflammation indicative of a higher risk of myocardial tissue damage post MI. This might not only explain the higher incidence of cardiovascular events in this population, but also the higher fatality rate after myocardial infarction,” wrote Dr. Inge A.M. van den Oever of the Amsterdam Rheumatology and Immunology Center and colleagues (Int J Cardiol. 2016 Feb 3. doi: 10.1016/j.ijcard.2016.02.065).

American Heart Association

The investigators took tissue samples from the infarcted left ventricle and microscopically determined infarct border area of five patients with RA and MI and five controls with MI but without RA. They found that RA patients had a greater burden of inflammatory cells in the adventitia of infarct-related epicardial coronary arteries, the intramyocardial vasculature, and the border area of the infarcted heart, compared with controls matched for age, sex, year of death, grade of stenosis, and infarct phase.

Specifically, the adventitial layer of the infarct-related epicardial coronary artery of RA patients had significantly more lymphocytes and mast cells. Intramyocardial arteries in infarct and infarct border areas of RA patients, compared with controls, showed significantly greater staining for advanced glycation end product N-epsilon-(carboxymethyl) lysine (CML), which is thought to reflect oxidative damage to cells, as well as noninfarcted tissues taken from the right ventricle.

The researchers included cases and controls from a postmortem tissue database of subjects who underwent autopsy within 24 hours after death at the VU University Medical Centre, Amsterdam, between January 1990 and December 2010.

The research was partly funded by a grant from the Dutch Society for Rheumatology. The authors had no conflicts of interest to declare.

jevans@frontlinemedcom.com

The presence of rheumatoid arthritis in individuals who died from a myocardial infarction was associated with greater inflammatory burden at different levels of myocardial tissue than in those without the disease in a small, retrospective, case-control autopsy study.

“These findings support the hypothesis that RA [rheumatoid arthritis] patients are prone to develop more vulnerable plaques due to more inflammation in the coronary arteries, but also develop increased intramyocardial inflammation indicative of a higher risk of myocardial tissue damage post MI. This might not only explain the higher incidence of cardiovascular events in this population, but also the higher fatality rate after myocardial infarction,” wrote Dr. Inge A.M. van den Oever of the Amsterdam Rheumatology and Immunology Center and colleagues (Int J Cardiol. 2016 Feb 3. doi: 10.1016/j.ijcard.2016.02.065).

American Heart Association

The investigators took tissue samples from the infarcted left ventricle and microscopically determined infarct border area of five patients with RA and MI and five controls with MI but without RA. They found that RA patients had a greater burden of inflammatory cells in the adventitia of infarct-related epicardial coronary arteries, the intramyocardial vasculature, and the border area of the infarcted heart, compared with controls matched for age, sex, year of death, grade of stenosis, and infarct phase.

Specifically, the adventitial layer of the infarct-related epicardial coronary artery of RA patients had significantly more lymphocytes and mast cells. Intramyocardial arteries in infarct and infarct border areas of RA patients, compared with controls, showed significantly greater staining for advanced glycation end product N-epsilon-(carboxymethyl) lysine (CML), which is thought to reflect oxidative damage to cells, as well as noninfarcted tissues taken from the right ventricle.

The researchers included cases and controls from a postmortem tissue database of subjects who underwent autopsy within 24 hours after death at the VU University Medical Centre, Amsterdam, between January 1990 and December 2010.

The research was partly funded by a grant from the Dutch Society for Rheumatology. The authors had no conflicts of interest to declare.

jevans@frontlinemedcom.com

The presence of rheumatoid arthritis in individuals who died from a myocardial infarction was associated with greater inflammatory burden at different levels of myocardial tissue than in those without the disease in a small, retrospective, case-control autopsy study.

“These findings support the hypothesis that RA [rheumatoid arthritis] patients are prone to develop more vulnerable plaques due to more inflammation in the coronary arteries, but also develop increased intramyocardial inflammation indicative of a higher risk of myocardial tissue damage post MI. This might not only explain the higher incidence of cardiovascular events in this population, but also the higher fatality rate after myocardial infarction,” wrote Dr. Inge A.M. van den Oever of the Amsterdam Rheumatology and Immunology Center and colleagues (Int J Cardiol. 2016 Feb 3. doi: 10.1016/j.ijcard.2016.02.065).

American Heart Association

The investigators took tissue samples from the infarcted left ventricle and microscopically determined infarct border area of five patients with RA and MI and five controls with MI but without RA. They found that RA patients had a greater burden of inflammatory cells in the adventitia of infarct-related epicardial coronary arteries, the intramyocardial vasculature, and the border area of the infarcted heart, compared with controls matched for age, sex, year of death, grade of stenosis, and infarct phase.

Specifically, the adventitial layer of the infarct-related epicardial coronary artery of RA patients had significantly more lymphocytes and mast cells. Intramyocardial arteries in infarct and infarct border areas of RA patients, compared with controls, showed significantly greater staining for advanced glycation end product N-epsilon-(carboxymethyl) lysine (CML), which is thought to reflect oxidative damage to cells, as well as noninfarcted tissues taken from the right ventricle.

The researchers included cases and controls from a postmortem tissue database of subjects who underwent autopsy within 24 hours after death at the VU University Medical Centre, Amsterdam, between January 1990 and December 2010.

The research was partly funded by a grant from the Dutch Society for Rheumatology. The authors had no conflicts of interest to declare.

jevans@frontlinemedcom.com