Kerri Wachter

An investigational near-infrared imaging technology in a handheld device can detect brain hematomas soon after trauma.

The Infrascanner detects hematomas based on the differential near-infrared light absorption of hemoglobin in the bleeding versus the nonbleeding area of the brain.

“The user-friendly device that maps out the location of the hematoma with graphics on a PDA screen can assist paramedics and emergency room personnel in attending to those injured in traffic and sports accidents, falls, and on the battlefield,” said Banu Onaral, Ph.D., director of the school of biomedical engineering, science, and health systems at Drexel University in Philadelphia.

The scanner unit is a handheld device based on a PDA platform with a wireless probe. The signal from the probe is digitized and transmitted by wireless link to the handheld unit.

Multicenter clinical trials are underway. Pending approval by the Food and Drug Administration, the device could be available by the end of the year.

An investigational near-infrared imaging technology in a handheld device can detect brain hematomas soon after trauma.

The Infrascanner detects hematomas based on the differential near-infrared light absorption of hemoglobin in the bleeding versus the nonbleeding area of the brain.

“The user-friendly device that maps out the location of the hematoma with graphics on a PDA screen can assist paramedics and emergency room personnel in attending to those injured in traffic and sports accidents, falls, and on the battlefield,” said Banu Onaral, Ph.D., director of the school of biomedical engineering, science, and health systems at Drexel University in Philadelphia.

The scanner unit is a handheld device based on a PDA platform with a wireless probe. The signal from the probe is digitized and transmitted by wireless link to the handheld unit.

Multicenter clinical trials are underway. Pending approval by the Food and Drug Administration, the device could be available by the end of the year.

An investigational near-infrared imaging technology in a handheld device can detect brain hematomas soon after trauma.

The Infrascanner detects hematomas based on the differential near-infrared light absorption of hemoglobin in the bleeding versus the nonbleeding area of the brain.

“The user-friendly device that maps out the location of the hematoma with graphics on a PDA screen can assist paramedics and emergency room personnel in attending to those injured in traffic and sports accidents, falls, and on the battlefield,” said Banu Onaral, Ph.D., director of the school of biomedical engineering, science, and health systems at Drexel University in Philadelphia.

The scanner unit is a handheld device based on a PDA platform with a wireless probe. The signal from the probe is digitized and transmitted by wireless link to the handheld unit.

Multicenter clinical trials are underway. Pending approval by the Food and Drug Administration, the device could be available by the end of the year.

ORLANDO — Combining intense pulsed light and heat energy appears to be an effective hair removal technique for individuals with dark skin, according to a study presented by Dr. Neil S. Sadick at the annual meeting of the American Academy of Cosmetic Surgery.

"By using two different energies … you can use less light energy, which means there is less chance of burning the skin," said Dr. Sadick, professor of dermatology at Cornell University, New York.

This is especially important when treating dark-skinned individuals, because using intense pulsed light alone can cause burning hyperpigmentation. "We try to use two energies to deliver more energy more gently," he said.

For his study, Dr. Sadick recruited 23 women and 3 men. Of these, 8 participants had Fitzpatrick skin type V and 18 had skin type VI. The participants' mean age was 36 years.

Patients underwent one treatment and were seen again at 6- and 12-week follow-ups, he said.

Mean hair clearance at 6 and 12 weeks was 42% and 36%, respectively. On average, hair removal after a single treatment was 36%. Hair clearance rates at 6 and 12 weeks were "lower than those seen with other, more classic, chromophore-targeting technologies, such as lasers of the past, but still were much more efficient than anything else in the past," Dr. Sadick explained.

In terms of side effects, "when you look at hypo- and hyperpigmentation, there was actually quite a low percentage—much lower than was noted using laser sources for dark-skinned individuals," he said. There were two cases of hypopigmentation noted at 6 weeks, which resolved by week 12.

Erythema and edema were transient, with 11 patients experiencing erythema and 2 experiencing edema at the time of treatment. Erythema and edema resolved by week 6.

For use in this study, Dr. Sadick used the Radiancy SkinStation, which utilizes a broad spectrum of light wavelengths (500–900 nm). Heat output for the device ranges between 8 and 55 J/cm

The light and heat energy are emitted from a lamp, targeting specific skin structures based on selective photothermolysis plus direct heat conduction. There is targeting of melanin in the hair follicle, along with nonspecific heating by the thermal component. The advantage of this technique is that there is an additive effect and less competitive melanin absorption in the epidermis.

Dr. Sadick is now conducting a study looking at multiple treatments in a larger group of individuals.

Right forearm of a male with skin type VI is shown at baseline.

The same patient is shown 6 weeks post treatment. Photos courtesy Dr. Neil Sadick

ORLANDO — Combining intense pulsed light and heat energy appears to be an effective hair removal technique for individuals with dark skin, according to a study presented by Dr. Neil S. Sadick at the annual meeting of the American Academy of Cosmetic Surgery.

"By using two different energies … you can use less light energy, which means there is less chance of burning the skin," said Dr. Sadick, professor of dermatology at Cornell University, New York.

This is especially important when treating dark-skinned individuals, because using intense pulsed light alone can cause burning hyperpigmentation. "We try to use two energies to deliver more energy more gently," he said.

For his study, Dr. Sadick recruited 23 women and 3 men. Of these, 8 participants had Fitzpatrick skin type V and 18 had skin type VI. The participants' mean age was 36 years.

Patients underwent one treatment and were seen again at 6- and 12-week follow-ups, he said.

Mean hair clearance at 6 and 12 weeks was 42% and 36%, respectively. On average, hair removal after a single treatment was 36%. Hair clearance rates at 6 and 12 weeks were "lower than those seen with other, more classic, chromophore-targeting technologies, such as lasers of the past, but still were much more efficient than anything else in the past," Dr. Sadick explained.

In terms of side effects, "when you look at hypo- and hyperpigmentation, there was actually quite a low percentage—much lower than was noted using laser sources for dark-skinned individuals," he said. There were two cases of hypopigmentation noted at 6 weeks, which resolved by week 12.

Erythema and edema were transient, with 11 patients experiencing erythema and 2 experiencing edema at the time of treatment. Erythema and edema resolved by week 6.

For use in this study, Dr. Sadick used the Radiancy SkinStation, which utilizes a broad spectrum of light wavelengths (500–900 nm). Heat output for the device ranges between 8 and 55 J/cm

The light and heat energy are emitted from a lamp, targeting specific skin structures based on selective photothermolysis plus direct heat conduction. There is targeting of melanin in the hair follicle, along with nonspecific heating by the thermal component. The advantage of this technique is that there is an additive effect and less competitive melanin absorption in the epidermis.

Dr. Sadick is now conducting a study looking at multiple treatments in a larger group of individuals.

Right forearm of a male with skin type VI is shown at baseline.

The same patient is shown 6 weeks post treatment. Photos courtesy Dr. Neil Sadick

ORLANDO — Combining intense pulsed light and heat energy appears to be an effective hair removal technique for individuals with dark skin, according to a study presented by Dr. Neil S. Sadick at the annual meeting of the American Academy of Cosmetic Surgery.

"By using two different energies … you can use less light energy, which means there is less chance of burning the skin," said Dr. Sadick, professor of dermatology at Cornell University, New York.

This is especially important when treating dark-skinned individuals, because using intense pulsed light alone can cause burning hyperpigmentation. "We try to use two energies to deliver more energy more gently," he said.

For his study, Dr. Sadick recruited 23 women and 3 men. Of these, 8 participants had Fitzpatrick skin type V and 18 had skin type VI. The participants' mean age was 36 years.

Patients underwent one treatment and were seen again at 6- and 12-week follow-ups, he said.

Mean hair clearance at 6 and 12 weeks was 42% and 36%, respectively. On average, hair removal after a single treatment was 36%. Hair clearance rates at 6 and 12 weeks were "lower than those seen with other, more classic, chromophore-targeting technologies, such as lasers of the past, but still were much more efficient than anything else in the past," Dr. Sadick explained.

In terms of side effects, "when you look at hypo- and hyperpigmentation, there was actually quite a low percentage—much lower than was noted using laser sources for dark-skinned individuals," he said. There were two cases of hypopigmentation noted at 6 weeks, which resolved by week 12.

Erythema and edema were transient, with 11 patients experiencing erythema and 2 experiencing edema at the time of treatment. Erythema and edema resolved by week 6.

For use in this study, Dr. Sadick used the Radiancy SkinStation, which utilizes a broad spectrum of light wavelengths (500–900 nm). Heat output for the device ranges between 8 and 55 J/cm

The light and heat energy are emitted from a lamp, targeting specific skin structures based on selective photothermolysis plus direct heat conduction. There is targeting of melanin in the hair follicle, along with nonspecific heating by the thermal component. The advantage of this technique is that there is an additive effect and less competitive melanin absorption in the epidermis.

Dr. Sadick is now conducting a study looking at multiple treatments in a larger group of individuals.

Right forearm of a male with skin type VI is shown at baseline.

The same patient is shown 6 weeks post treatment. Photos courtesy Dr. Neil Sadick

The Food and Drug Administration is reviewing proposed label changes for Hydrea and Droxia (hydroxyurea capsules) that warn of cutaneous vasculitic toxicities.

Bristol-Myers Squibb has notified health care professionals about revisions to the Warnings and Adverse Reactions sections of the prescribing information to include information about vasculitic ulcerations and gangrene that have occurred in patients with myeloproliferative disorders during therapy with hydroxyurea. The vasculitic toxicities were reported most often in patients who had received, or were currently receiving, interferon therapy.

Significant tumor response to Hydrea has been demonstrated in melanoma, resistant chronic myelocytic leukemia; and recurrent, metastatic, or inoperable carcinoma of the ovary. Used concomitantly with irradiation therapy, the drug is intended for use in the local control of primary squamous cell (epidermoid) carcinomas of the head and neck, excluding the lip.

Droxia is indicated to reduce the frequency of painful crises and to reduce the need for blood transfusions in adult patients with sickle cell anemia with recurrent moderate to severe painful crises. Hydroxyurea should be discontinued in these patients if cutaneous vasculitic ulcerations develop. Changes have also been added to the Precautions section of prescribing information to warn physicians that elderly patients may be more sensitive to the effects of Hydrea.

For more information, or to report serious adverse events suspected to be associated with Hydrea or Droxia, contact the company by calling 800-321-1335 or contact the FDA's MedWatch Reporting System by calling 800-332-1088.

The Food and Drug Administration is reviewing proposed label changes for Hydrea and Droxia (hydroxyurea capsules) that warn of cutaneous vasculitic toxicities.

Bristol-Myers Squibb has notified health care professionals about revisions to the Warnings and Adverse Reactions sections of the prescribing information to include information about vasculitic ulcerations and gangrene that have occurred in patients with myeloproliferative disorders during therapy with hydroxyurea. The vasculitic toxicities were reported most often in patients who had received, or were currently receiving, interferon therapy.

Significant tumor response to Hydrea has been demonstrated in melanoma, resistant chronic myelocytic leukemia; and recurrent, metastatic, or inoperable carcinoma of the ovary. Used concomitantly with irradiation therapy, the drug is intended for use in the local control of primary squamous cell (epidermoid) carcinomas of the head and neck, excluding the lip.

Droxia is indicated to reduce the frequency of painful crises and to reduce the need for blood transfusions in adult patients with sickle cell anemia with recurrent moderate to severe painful crises. Hydroxyurea should be discontinued in these patients if cutaneous vasculitic ulcerations develop. Changes have also been added to the Precautions section of prescribing information to warn physicians that elderly patients may be more sensitive to the effects of Hydrea.

For more information, or to report serious adverse events suspected to be associated with Hydrea or Droxia, contact the company by calling 800-321-1335 or contact the FDA's MedWatch Reporting System by calling 800-332-1088.

The Food and Drug Administration is reviewing proposed label changes for Hydrea and Droxia (hydroxyurea capsules) that warn of cutaneous vasculitic toxicities.

Bristol-Myers Squibb has notified health care professionals about revisions to the Warnings and Adverse Reactions sections of the prescribing information to include information about vasculitic ulcerations and gangrene that have occurred in patients with myeloproliferative disorders during therapy with hydroxyurea. The vasculitic toxicities were reported most often in patients who had received, or were currently receiving, interferon therapy.

Significant tumor response to Hydrea has been demonstrated in melanoma, resistant chronic myelocytic leukemia; and recurrent, metastatic, or inoperable carcinoma of the ovary. Used concomitantly with irradiation therapy, the drug is intended for use in the local control of primary squamous cell (epidermoid) carcinomas of the head and neck, excluding the lip.

Droxia is indicated to reduce the frequency of painful crises and to reduce the need for blood transfusions in adult patients with sickle cell anemia with recurrent moderate to severe painful crises. Hydroxyurea should be discontinued in these patients if cutaneous vasculitic ulcerations develop. Changes have also been added to the Precautions section of prescribing information to warn physicians that elderly patients may be more sensitive to the effects of Hydrea.

For more information, or to report serious adverse events suspected to be associated with Hydrea or Droxia, contact the company by calling 800-321-1335 or contact the FDA's MedWatch Reporting System by calling 800-332-1088.

Hanford Pharmaceuticals Inc. is recalling four lots of cefazolin for injection due to the possibility of microbial contamination, which may pose a serious or life-threatening risk for some patients.

The recall affects 379,975 vials (1 g/10 mL) in lots distributed by Sandoz Inc. (C4650 and C4537) and Watson Pharmaceuticals Inc. (C4689 and C4665).

Certain lots of the active ingredient used to manufacture the product have been shown to contain microbial contamination, including Bacillus pumilus, Staphylococcus hominis, Propionibacterium acnes, and Micrococcus luteus.

Cefazolin injection is used to treat skin and skin structure, respiratory, and other infections. Users, hospitals, and clinics should stop using the affected lots immediately.

Patients who believe that they may have experienced an adverse reaction to the recalled product are advised to seek medical help.

For more information, contact the company by calling 315-476-7418. Adverse reactions experienced by users of this product should also be reported to the Food and Drug Administration's MedWatch Program at www.fda.gov/medwatch/report.htm

Hanford Pharmaceuticals Inc. is recalling four lots of cefazolin for injection due to the possibility of microbial contamination, which may pose a serious or life-threatening risk for some patients.

The recall affects 379,975 vials (1 g/10 mL) in lots distributed by Sandoz Inc. (C4650 and C4537) and Watson Pharmaceuticals Inc. (C4689 and C4665).

Certain lots of the active ingredient used to manufacture the product have been shown to contain microbial contamination, including Bacillus pumilus, Staphylococcus hominis, Propionibacterium acnes, and Micrococcus luteus.

Cefazolin injection is used to treat skin and skin structure, respiratory, and other infections. Users, hospitals, and clinics should stop using the affected lots immediately.

Patients who believe that they may have experienced an adverse reaction to the recalled product are advised to seek medical help.

For more information, contact the company by calling 315-476-7418. Adverse reactions experienced by users of this product should also be reported to the Food and Drug Administration's MedWatch Program at www.fda.gov/medwatch/report.htm

Hanford Pharmaceuticals Inc. is recalling four lots of cefazolin for injection due to the possibility of microbial contamination, which may pose a serious or life-threatening risk for some patients.

The recall affects 379,975 vials (1 g/10 mL) in lots distributed by Sandoz Inc. (C4650 and C4537) and Watson Pharmaceuticals Inc. (C4689 and C4665).

Certain lots of the active ingredient used to manufacture the product have been shown to contain microbial contamination, including Bacillus pumilus, Staphylococcus hominis, Propionibacterium acnes, and Micrococcus luteus.

Cefazolin injection is used to treat skin and skin structure, respiratory, and other infections. Users, hospitals, and clinics should stop using the affected lots immediately.

Patients who believe that they may have experienced an adverse reaction to the recalled product are advised to seek medical help.

For more information, contact the company by calling 315-476-7418. Adverse reactions experienced by users of this product should also be reported to the Food and Drug Administration's MedWatch Program at www.fda.gov/medwatch/report.htm

WASHINGTON — Treating the HIV infection may ease the symptoms of Parkinson's disease in patients with both conditions, one expert said at the World Parkinson Congress.

Using levodopa to treat Parkinson's symptoms in an HIV-positive individual “may in fact accelerate the HIV infection and it definitely can exacerbate the psychosis that is associated with the infection,” said Dr. Cynthia L. Comella.

Parkinsonism is “increasingly recognized as being one of the neurologic complications of HIV,” said Dr. Comella, a neurologist at Rush University Medical Center in Chicago. As many as 5% of patients with HIV meet U.K. criteria for Parkinson's disease, according to the literature, and an additional 10% exhibit parkinsonian features.

Typically, parkinsonism is seen in HIV patients with the most severe immunosuppression—with CD4 cell counts less than 40, Dr. Comella said.

Parkinsonism associated with HIV is described as symmetric and mostly bradykinetic. Rigidity is also seen, as are early gait and postural instabilities. “Particularly, it's associated with other neurological or psychiatric manifestations, such as associated myoclonus and associated dystonia,” Dr. Comella said.

The etiology of parkinsonism in individuals with HIV arises from two mechanisms: direct HIV infection and opportunistic infections of the basal ganglia. HIV-infected patients are also very susceptible to drug-induced parkinsonism.

“The HIV virus seems to have a propensity to invade the basal ganglia, causing nigral degeneration,” Dr. Comella said.

There is a loss of as much as 25% of nigral neurons, even in asymptomatic patients with HIV. It has also been shown that there is a reduction of dopamine in the cerebral spinal fluid in HIV patients, even in those without neurocognitive deficits.

The highly active antiretroviral drug regimens that are effective against HIV infection are also the most effective treatment for HIV-associated parkinsonism, Dr. Comella said.

In some patients parkinsonian symptoms may resolve with effective treatment of underlying opportunistic infections. The atypical neuroleptics are recommended for psychiatric abnormalities seen in these patients, particularly because these patients are more susceptible to the development of drug-induced parkinsonism with the typical neuroleptics.

WASHINGTON — Treating the HIV infection may ease the symptoms of Parkinson's disease in patients with both conditions, one expert said at the World Parkinson Congress.

Using levodopa to treat Parkinson's symptoms in an HIV-positive individual “may in fact accelerate the HIV infection and it definitely can exacerbate the psychosis that is associated with the infection,” said Dr. Cynthia L. Comella.

Parkinsonism is “increasingly recognized as being one of the neurologic complications of HIV,” said Dr. Comella, a neurologist at Rush University Medical Center in Chicago. As many as 5% of patients with HIV meet U.K. criteria for Parkinson's disease, according to the literature, and an additional 10% exhibit parkinsonian features.

Typically, parkinsonism is seen in HIV patients with the most severe immunosuppression—with CD4 cell counts less than 40, Dr. Comella said.

Parkinsonism associated with HIV is described as symmetric and mostly bradykinetic. Rigidity is also seen, as are early gait and postural instabilities. “Particularly, it's associated with other neurological or psychiatric manifestations, such as associated myoclonus and associated dystonia,” Dr. Comella said.

The etiology of parkinsonism in individuals with HIV arises from two mechanisms: direct HIV infection and opportunistic infections of the basal ganglia. HIV-infected patients are also very susceptible to drug-induced parkinsonism.

“The HIV virus seems to have a propensity to invade the basal ganglia, causing nigral degeneration,” Dr. Comella said.

There is a loss of as much as 25% of nigral neurons, even in asymptomatic patients with HIV. It has also been shown that there is a reduction of dopamine in the cerebral spinal fluid in HIV patients, even in those without neurocognitive deficits.

The highly active antiretroviral drug regimens that are effective against HIV infection are also the most effective treatment for HIV-associated parkinsonism, Dr. Comella said.

In some patients parkinsonian symptoms may resolve with effective treatment of underlying opportunistic infections. The atypical neuroleptics are recommended for psychiatric abnormalities seen in these patients, particularly because these patients are more susceptible to the development of drug-induced parkinsonism with the typical neuroleptics.

WASHINGTON — Treating the HIV infection may ease the symptoms of Parkinson's disease in patients with both conditions, one expert said at the World Parkinson Congress.

Using levodopa to treat Parkinson's symptoms in an HIV-positive individual “may in fact accelerate the HIV infection and it definitely can exacerbate the psychosis that is associated with the infection,” said Dr. Cynthia L. Comella.

Parkinsonism is “increasingly recognized as being one of the neurologic complications of HIV,” said Dr. Comella, a neurologist at Rush University Medical Center in Chicago. As many as 5% of patients with HIV meet U.K. criteria for Parkinson's disease, according to the literature, and an additional 10% exhibit parkinsonian features.

Typically, parkinsonism is seen in HIV patients with the most severe immunosuppression—with CD4 cell counts less than 40, Dr. Comella said.

Parkinsonism associated with HIV is described as symmetric and mostly bradykinetic. Rigidity is also seen, as are early gait and postural instabilities. “Particularly, it's associated with other neurological or psychiatric manifestations, such as associated myoclonus and associated dystonia,” Dr. Comella said.

The etiology of parkinsonism in individuals with HIV arises from two mechanisms: direct HIV infection and opportunistic infections of the basal ganglia. HIV-infected patients are also very susceptible to drug-induced parkinsonism.

“The HIV virus seems to have a propensity to invade the basal ganglia, causing nigral degeneration,” Dr. Comella said.

There is a loss of as much as 25% of nigral neurons, even in asymptomatic patients with HIV. It has also been shown that there is a reduction of dopamine in the cerebral spinal fluid in HIV patients, even in those without neurocognitive deficits.

The highly active antiretroviral drug regimens that are effective against HIV infection are also the most effective treatment for HIV-associated parkinsonism, Dr. Comella said.

In some patients parkinsonian symptoms may resolve with effective treatment of underlying opportunistic infections. The atypical neuroleptics are recommended for psychiatric abnormalities seen in these patients, particularly because these patients are more susceptible to the development of drug-induced parkinsonism with the typical neuroleptics.

WASHINGTON — A procalcitonin-guided protocol can cut the duration of antibiotic use in patients with community-acquired pneumonia by roughly 50%, according to data presented at the annual Interscience Conference on Antimicrobial Agents and Chemotherapy.

“Procalcitonin seems to be a more reliable parameter for the individual tailoring and discontinuation of antibiotics as compared with commonly and routinely used clinical and laboratory parameters,” said Dr. Mirjam Christ-Crain, an endocrinologist at the University Hospital Basel (Switzerland).

She and her colleagues proposed using procalcitonin as a biomarker to guide antibiotic treatment because the propeptide of calcitonin is increased with increasing severity of bacterial infection.

For this study, patients with community-acquired pneumonia (CAP) were randomized to receive therapy of standard duration (151 patients) or therapy whose duration was guided by procalcitonin (151 patients).

Patients in both groups had an average age of 70 years. Only 20% had antibiotic pretreatment. Most patients in both groups had comorbidities. More than two-thirds of patients had severe or very severe pneumonia.

Among those in the procalcitonin group, patients with levels greater than 0.25 mcg/L were started on antibiotic therapy. Those with levels of 0.25 mcg/L or less were not given antibiotics.

Procalcitonin measurements were performed on all patients on days 0, 2, 4, 6, and 8, though the results were available only for those in the procalcitonin group.

The decision to continue or discontinue antibiotic therapy in the procalcitonin group was based on the cutoff levels described above.

Follow-up, including a chest x-ray, was performed at 4–6 weeks. In patients with clinical uncertainty, there was follow-up remeasurement of procalcitonin in 6 hours.

Patients in the standard therapy group received antibiotics initially, and almost all of them were on antibiotics for more than 8 days. In comparison, only 85% of those in the procalcitonin group initially received antibiotics. In this group, “only about 50% had antibiotics for more than 4 days and about 30% for more than 6 days,” Dr. Christ-Crain said.

Patients in the procalcitonin group received antibiotics for an average of 6 days, compared with 13 days for the standard therapy group. “This is a highly significant reduction of antibiotic use and antibiotic duration,” said Dr. Christ-Crain, at the meeting sponsored by the American Society for Microbiology.

Clinical outcomes—as assessed by using a visual analog scale and clinical parameters such as temperature, oxygen saturation, and pulse rate—were similar in both groups.

Laboratory outcomes—C-reactive protein and procalcitonin levels in the normal reference ranges—assessed at 4–6 weeks were also found to be similar.

Most experts recommend a 10- to 14-day course of antibiotic therapy to treat CAP, but the optimal duration is unknown.

“In our opinion, the correct duration of antibiotics varies from patient to patient,” Dr. Christ-Crain said.

New tests for the determination of procalcitonin levels have improved sensitivity, enabling physicians to distinguish clinically relevant bacterial infections from other infections.

Dr. Christ-Crain and her colleagues demonstrated this in a recent study involving lower respiratory tract infections (Lancet 2004;363:600–7).

WASHINGTON — A procalcitonin-guided protocol can cut the duration of antibiotic use in patients with community-acquired pneumonia by roughly 50%, according to data presented at the annual Interscience Conference on Antimicrobial Agents and Chemotherapy.

“Procalcitonin seems to be a more reliable parameter for the individual tailoring and discontinuation of antibiotics as compared with commonly and routinely used clinical and laboratory parameters,” said Dr. Mirjam Christ-Crain, an endocrinologist at the University Hospital Basel (Switzerland).

She and her colleagues proposed using procalcitonin as a biomarker to guide antibiotic treatment because the propeptide of calcitonin is increased with increasing severity of bacterial infection.

For this study, patients with community-acquired pneumonia (CAP) were randomized to receive therapy of standard duration (151 patients) or therapy whose duration was guided by procalcitonin (151 patients).

Patients in both groups had an average age of 70 years. Only 20% had antibiotic pretreatment. Most patients in both groups had comorbidities. More than two-thirds of patients had severe or very severe pneumonia.

Among those in the procalcitonin group, patients with levels greater than 0.25 mcg/L were started on antibiotic therapy. Those with levels of 0.25 mcg/L or less were not given antibiotics.

Procalcitonin measurements were performed on all patients on days 0, 2, 4, 6, and 8, though the results were available only for those in the procalcitonin group.

The decision to continue or discontinue antibiotic therapy in the procalcitonin group was based on the cutoff levels described above.

Follow-up, including a chest x-ray, was performed at 4–6 weeks. In patients with clinical uncertainty, there was follow-up remeasurement of procalcitonin in 6 hours.

Patients in the standard therapy group received antibiotics initially, and almost all of them were on antibiotics for more than 8 days. In comparison, only 85% of those in the procalcitonin group initially received antibiotics. In this group, “only about 50% had antibiotics for more than 4 days and about 30% for more than 6 days,” Dr. Christ-Crain said.

Patients in the procalcitonin group received antibiotics for an average of 6 days, compared with 13 days for the standard therapy group. “This is a highly significant reduction of antibiotic use and antibiotic duration,” said Dr. Christ-Crain, at the meeting sponsored by the American Society for Microbiology.

Clinical outcomes—as assessed by using a visual analog scale and clinical parameters such as temperature, oxygen saturation, and pulse rate—were similar in both groups.

Laboratory outcomes—C-reactive protein and procalcitonin levels in the normal reference ranges—assessed at 4–6 weeks were also found to be similar.

Most experts recommend a 10- to 14-day course of antibiotic therapy to treat CAP, but the optimal duration is unknown.

“In our opinion, the correct duration of antibiotics varies from patient to patient,” Dr. Christ-Crain said.

New tests for the determination of procalcitonin levels have improved sensitivity, enabling physicians to distinguish clinically relevant bacterial infections from other infections.

Dr. Christ-Crain and her colleagues demonstrated this in a recent study involving lower respiratory tract infections (Lancet 2004;363:600–7).

WASHINGTON — A procalcitonin-guided protocol can cut the duration of antibiotic use in patients with community-acquired pneumonia by roughly 50%, according to data presented at the annual Interscience Conference on Antimicrobial Agents and Chemotherapy.

“Procalcitonin seems to be a more reliable parameter for the individual tailoring and discontinuation of antibiotics as compared with commonly and routinely used clinical and laboratory parameters,” said Dr. Mirjam Christ-Crain, an endocrinologist at the University Hospital Basel (Switzerland).

She and her colleagues proposed using procalcitonin as a biomarker to guide antibiotic treatment because the propeptide of calcitonin is increased with increasing severity of bacterial infection.

For this study, patients with community-acquired pneumonia (CAP) were randomized to receive therapy of standard duration (151 patients) or therapy whose duration was guided by procalcitonin (151 patients).

Patients in both groups had an average age of 70 years. Only 20% had antibiotic pretreatment. Most patients in both groups had comorbidities. More than two-thirds of patients had severe or very severe pneumonia.

Among those in the procalcitonin group, patients with levels greater than 0.25 mcg/L were started on antibiotic therapy. Those with levels of 0.25 mcg/L or less were not given antibiotics.

Procalcitonin measurements were performed on all patients on days 0, 2, 4, 6, and 8, though the results were available only for those in the procalcitonin group.

The decision to continue or discontinue antibiotic therapy in the procalcitonin group was based on the cutoff levels described above.

Follow-up, including a chest x-ray, was performed at 4–6 weeks. In patients with clinical uncertainty, there was follow-up remeasurement of procalcitonin in 6 hours.

Patients in the standard therapy group received antibiotics initially, and almost all of them were on antibiotics for more than 8 days. In comparison, only 85% of those in the procalcitonin group initially received antibiotics. In this group, “only about 50% had antibiotics for more than 4 days and about 30% for more than 6 days,” Dr. Christ-Crain said.

Patients in the procalcitonin group received antibiotics for an average of 6 days, compared with 13 days for the standard therapy group. “This is a highly significant reduction of antibiotic use and antibiotic duration,” said Dr. Christ-Crain, at the meeting sponsored by the American Society for Microbiology.

Clinical outcomes—as assessed by using a visual analog scale and clinical parameters such as temperature, oxygen saturation, and pulse rate—were similar in both groups.

Laboratory outcomes—C-reactive protein and procalcitonin levels in the normal reference ranges—assessed at 4–6 weeks were also found to be similar.

Most experts recommend a 10- to 14-day course of antibiotic therapy to treat CAP, but the optimal duration is unknown.

“In our opinion, the correct duration of antibiotics varies from patient to patient,” Dr. Christ-Crain said.

New tests for the determination of procalcitonin levels have improved sensitivity, enabling physicians to distinguish clinically relevant bacterial infections from other infections.

Dr. Christ-Crain and her colleagues demonstrated this in a recent study involving lower respiratory tract infections (Lancet 2004;363:600–7).

N-methyl-[11C]2-(4′-methylaminophenyl)-6-hydroxybenzothiazole, better known as Pittsburgh Compound B (or simply PIB), has been long anticipated in Alzheimer's disease circles. The PET radiotracer allows researchers and clinicians to see amyloid plaque deposition in live human subjects, opening up a number of investigational and clinical possibilities.

Although the exact binding mechanism is unknown, the compound is derived from thioflavin T, a dye used in autopsy tissue studies to highlight amyloid fibrils in the brain, said Dr. William E. Klunk, of the department of psychiatry at the University of Pittsburgh, who—along with Chester Mathis, Ph.D., professor of radiology and director of PET at the university—developed the compound.

To assess the correlation between PIB binding and amyloid deposition in the brain, the researchers recently homogenized the tissue from several Alzheimer's disease (AD) brain samples and then split the homogenates for analysis with Aβ ELISA (amyloid-β peptide enzyme-linked immunosorbent assay). “They line up very nicely,” said Dr. Klunk. In human brains, the PIB binds in a 1:2 ratio with amyloid. They also performed in vitro binding studies (J. Neuroscience 2005;25:10598–606).

The imaging technique allows researchers and clinicians to follow disease progression over time, and may also allow researchers to identify patients earlier in the disease process.

It's unclear how early in the course of amyloid deposition PIB imaging can reveal this process. “We can see amyloid in some clinically normal elderly controls. We can see amyloid in some Down syndrome subjects who haven't developed any signs of clinical deterioration, but most interesting is the fact that we can see amyloid deposition in people who carry presenilin 1 or Aβ (A4) precursor protein gene mutations,” said Dr. Klunk. In fact, the researchers have looked at individuals with these risk factors who were as young as age 35 years, and have found amyloid deposition. The typical age of clinical onset in these individuals is the late 40s.

The exact relationship between AD and amyloid deposition in the brain remains elusive. “Not having clinical symptoms, in my mind, does not equate with not having a disease, if you have the pathology. The question is, do you care about having the pathology if you don't have the clinical symptoms?” Dr. Klunk likens the presence of amyloid in patients who will go on to develop AD to the presence of plaque in the carotid artery: The earlier you know about it, the better. The success in finding an intervention that can prevent disease progression “will determine whether this imaging technique becomes extremely important in the management of patients with AD, or remains [just] an interesting research technology,” said Dr. Klunk.

▸ B stands to play a role in the development of a drug that can halt or even prevent amyloid deposition. “We're currently using this technology in collaboration with pharmaceutical companies to look at their antiamyloid agents … to see if these drugs are having an effect on the target,” he said.

Using this technology both “to show that you can remove amyloid from a living person and to monitor that” and “to find the right people to use it on early enough” will be key, he said.

In the images of patients with mild cognitive impairment (MCI), the degree of clinical severity did not correlate with the presence or absence of amyloid deposition. (See photo.) “About 30% of [MCI patients] have no signs of amyloid deposition. That happens to be an interesting number because, in our center, about 30% of our MCI patients never develop AD. The question is, are these amyloid-negative MCI cases the same 30% who won't develop AD?”

The MCI PIB-negative cases—note particularly the MCI 1 image in the photo—are virtually indistinguishable from control subjects on PET. Similarly, the images of MCI 3 patients—who make up the majority of MCI cases—are virtually indistinguishable from the images of patients with AD. Only 15%–20% of MCI cases look like the MCI 2 image. “That transitional phase probably occurs before the MCI phase on most cases in the MCIs that are going to get amyloid deposition in AD,” said Dr. Klunk.

PIB imaging may also help researchers investigate potential risk factors. The researchers are currently using the technique to assess the relationship between depression and AD. Research indicates that many elderly patients with depression will develop AD. The researchers want to determine if the elderly depressed patients with amyloid are the ones who go on to develop AD, and whether the patients without amyloid are the ones who will recover and not develop AD. Although most of the results of PIB's promise remain down the road, the technique has clinical applications today. PIB imaging may be useful in cases of clinically confusing dementia. “We'd love to find out if there is amyloid in the brain to help root out these diagnoses,” said Dr. Klunk.

Along with their colleague Dr. Steven DeKosky, chair of the neurology department at the University of Pittsburgh, the researchers are currently using the technique in patients with dementia of unknown origin.

PET with PIB reveals differences in amyloid deposition between cognitively normal subjects (far left) and subjects with AD (far right). PET with PIB also reveals the range of amyloid accumulation in subjects with clinically mild cognitive impairment (center). Courtesy Dr. William E. Klunk, Ph.D. and Chester Mathis, Ph.D./University of Pittsburgh

N-methyl-[11C]2-(4′-methylaminophenyl)-6-hydroxybenzothiazole, better known as Pittsburgh Compound B (or simply PIB), has been long anticipated in Alzheimer's disease circles. The PET radiotracer allows researchers and clinicians to see amyloid plaque deposition in live human subjects, opening up a number of investigational and clinical possibilities.

Although the exact binding mechanism is unknown, the compound is derived from thioflavin T, a dye used in autopsy tissue studies to highlight amyloid fibrils in the brain, said Dr. William E. Klunk, of the department of psychiatry at the University of Pittsburgh, who—along with Chester Mathis, Ph.D., professor of radiology and director of PET at the university—developed the compound.

To assess the correlation between PIB binding and amyloid deposition in the brain, the researchers recently homogenized the tissue from several Alzheimer's disease (AD) brain samples and then split the homogenates for analysis with Aβ ELISA (amyloid-β peptide enzyme-linked immunosorbent assay). “They line up very nicely,” said Dr. Klunk. In human brains, the PIB binds in a 1:2 ratio with amyloid. They also performed in vitro binding studies (J. Neuroscience 2005;25:10598–606).

The imaging technique allows researchers and clinicians to follow disease progression over time, and may also allow researchers to identify patients earlier in the disease process.

It's unclear how early in the course of amyloid deposition PIB imaging can reveal this process. “We can see amyloid in some clinically normal elderly controls. We can see amyloid in some Down syndrome subjects who haven't developed any signs of clinical deterioration, but most interesting is the fact that we can see amyloid deposition in people who carry presenilin 1 or Aβ (A4) precursor protein gene mutations,” said Dr. Klunk. In fact, the researchers have looked at individuals with these risk factors who were as young as age 35 years, and have found amyloid deposition. The typical age of clinical onset in these individuals is the late 40s.

The exact relationship between AD and amyloid deposition in the brain remains elusive. “Not having clinical symptoms, in my mind, does not equate with not having a disease, if you have the pathology. The question is, do you care about having the pathology if you don't have the clinical symptoms?” Dr. Klunk likens the presence of amyloid in patients who will go on to develop AD to the presence of plaque in the carotid artery: The earlier you know about it, the better. The success in finding an intervention that can prevent disease progression “will determine whether this imaging technique becomes extremely important in the management of patients with AD, or remains [just] an interesting research technology,” said Dr. Klunk.

▸ B stands to play a role in the development of a drug that can halt or even prevent amyloid deposition. “We're currently using this technology in collaboration with pharmaceutical companies to look at their antiamyloid agents … to see if these drugs are having an effect on the target,” he said.

Using this technology both “to show that you can remove amyloid from a living person and to monitor that” and “to find the right people to use it on early enough” will be key, he said.

In the images of patients with mild cognitive impairment (MCI), the degree of clinical severity did not correlate with the presence or absence of amyloid deposition. (See photo.) “About 30% of [MCI patients] have no signs of amyloid deposition. That happens to be an interesting number because, in our center, about 30% of our MCI patients never develop AD. The question is, are these amyloid-negative MCI cases the same 30% who won't develop AD?”

The MCI PIB-negative cases—note particularly the MCI 1 image in the photo—are virtually indistinguishable from control subjects on PET. Similarly, the images of MCI 3 patients—who make up the majority of MCI cases—are virtually indistinguishable from the images of patients with AD. Only 15%–20% of MCI cases look like the MCI 2 image. “That transitional phase probably occurs before the MCI phase on most cases in the MCIs that are going to get amyloid deposition in AD,” said Dr. Klunk.

PIB imaging may also help researchers investigate potential risk factors. The researchers are currently using the technique to assess the relationship between depression and AD. Research indicates that many elderly patients with depression will develop AD. The researchers want to determine if the elderly depressed patients with amyloid are the ones who go on to develop AD, and whether the patients without amyloid are the ones who will recover and not develop AD. Although most of the results of PIB's promise remain down the road, the technique has clinical applications today. PIB imaging may be useful in cases of clinically confusing dementia. “We'd love to find out if there is amyloid in the brain to help root out these diagnoses,” said Dr. Klunk.

Along with their colleague Dr. Steven DeKosky, chair of the neurology department at the University of Pittsburgh, the researchers are currently using the technique in patients with dementia of unknown origin.

PET with PIB reveals differences in amyloid deposition between cognitively normal subjects (far left) and subjects with AD (far right). PET with PIB also reveals the range of amyloid accumulation in subjects with clinically mild cognitive impairment (center). Courtesy Dr. William E. Klunk, Ph.D. and Chester Mathis, Ph.D./University of Pittsburgh

N-methyl-[11C]2-(4′-methylaminophenyl)-6-hydroxybenzothiazole, better known as Pittsburgh Compound B (or simply PIB), has been long anticipated in Alzheimer's disease circles. The PET radiotracer allows researchers and clinicians to see amyloid plaque deposition in live human subjects, opening up a number of investigational and clinical possibilities.

Although the exact binding mechanism is unknown, the compound is derived from thioflavin T, a dye used in autopsy tissue studies to highlight amyloid fibrils in the brain, said Dr. William E. Klunk, of the department of psychiatry at the University of Pittsburgh, who—along with Chester Mathis, Ph.D., professor of radiology and director of PET at the university—developed the compound.

To assess the correlation between PIB binding and amyloid deposition in the brain, the researchers recently homogenized the tissue from several Alzheimer's disease (AD) brain samples and then split the homogenates for analysis with Aβ ELISA (amyloid-β peptide enzyme-linked immunosorbent assay). “They line up very nicely,” said Dr. Klunk. In human brains, the PIB binds in a 1:2 ratio with amyloid. They also performed in vitro binding studies (J. Neuroscience 2005;25:10598–606).

The imaging technique allows researchers and clinicians to follow disease progression over time, and may also allow researchers to identify patients earlier in the disease process.

It's unclear how early in the course of amyloid deposition PIB imaging can reveal this process. “We can see amyloid in some clinically normal elderly controls. We can see amyloid in some Down syndrome subjects who haven't developed any signs of clinical deterioration, but most interesting is the fact that we can see amyloid deposition in people who carry presenilin 1 or Aβ (A4) precursor protein gene mutations,” said Dr. Klunk. In fact, the researchers have looked at individuals with these risk factors who were as young as age 35 years, and have found amyloid deposition. The typical age of clinical onset in these individuals is the late 40s.

The exact relationship between AD and amyloid deposition in the brain remains elusive. “Not having clinical symptoms, in my mind, does not equate with not having a disease, if you have the pathology. The question is, do you care about having the pathology if you don't have the clinical symptoms?” Dr. Klunk likens the presence of amyloid in patients who will go on to develop AD to the presence of plaque in the carotid artery: The earlier you know about it, the better. The success in finding an intervention that can prevent disease progression “will determine whether this imaging technique becomes extremely important in the management of patients with AD, or remains [just] an interesting research technology,” said Dr. Klunk.

▸ B stands to play a role in the development of a drug that can halt or even prevent amyloid deposition. “We're currently using this technology in collaboration with pharmaceutical companies to look at their antiamyloid agents … to see if these drugs are having an effect on the target,” he said.

Using this technology both “to show that you can remove amyloid from a living person and to monitor that” and “to find the right people to use it on early enough” will be key, he said.

In the images of patients with mild cognitive impairment (MCI), the degree of clinical severity did not correlate with the presence or absence of amyloid deposition. (See photo.) “About 30% of [MCI patients] have no signs of amyloid deposition. That happens to be an interesting number because, in our center, about 30% of our MCI patients never develop AD. The question is, are these amyloid-negative MCI cases the same 30% who won't develop AD?”

The MCI PIB-negative cases—note particularly the MCI 1 image in the photo—are virtually indistinguishable from control subjects on PET. Similarly, the images of MCI 3 patients—who make up the majority of MCI cases—are virtually indistinguishable from the images of patients with AD. Only 15%–20% of MCI cases look like the MCI 2 image. “That transitional phase probably occurs before the MCI phase on most cases in the MCIs that are going to get amyloid deposition in AD,” said Dr. Klunk.

PIB imaging may also help researchers investigate potential risk factors. The researchers are currently using the technique to assess the relationship between depression and AD. Research indicates that many elderly patients with depression will develop AD. The researchers want to determine if the elderly depressed patients with amyloid are the ones who go on to develop AD, and whether the patients without amyloid are the ones who will recover and not develop AD. Although most of the results of PIB's promise remain down the road, the technique has clinical applications today. PIB imaging may be useful in cases of clinically confusing dementia. “We'd love to find out if there is amyloid in the brain to help root out these diagnoses,” said Dr. Klunk.

Along with their colleague Dr. Steven DeKosky, chair of the neurology department at the University of Pittsburgh, the researchers are currently using the technique in patients with dementia of unknown origin.

PET with PIB reveals differences in amyloid deposition between cognitively normal subjects (far left) and subjects with AD (far right). PET with PIB also reveals the range of amyloid accumulation in subjects with clinically mild cognitive impairment (center). Courtesy Dr. William E. Klunk, Ph.D. and Chester Mathis, Ph.D./University of Pittsburgh

Patients currently taking a glucocorticoid have nearly a fivefold increased risk of developing tuberculosis that is independent of other risk factors.

“Our results suggest that glucocorticoid use is associated with a substantially increased risk of developing tuberculosis and that the risk increases with increasing daily dose,” said Susan S. Jick, Sc.D., of Boston University, and her colleagues.

Although chronic corticosteroid use is common among patients with rheumatic diseases, the number of such patients in the study population was too small to say definitely whether use of corticosteroids specifically for arthritis and other rheumatic diseases was associated with an increased risk for TB.

Low body mass index (BMI), diabetes, current smoking, and obstructive pulmonary disorders were also determined to be important risk factors for tuberculosis in a review of 497 new cases of tuberculosis and 1,966 matched controls during the period 1990–2001 (Arthritis Rheum. 2006;55:19–26).

The researchers based their study on data available from the U.K.-based General Practice Research Database. Patients were included if they had a first-time diagnosis of tuberculosis followed by treatment with at least three different antituberculosis medications and if treatment lasted at least 6 months. As many as four control subjects were matched to each patient based on age, gender, the practice attended, and the patient's index date along with the control's visit to the practice that corresponded in time to the patient's index visit.

Assessment of glucocorticoid use was based on prescription data. Patients were classified as currently exposed if they had received a prescription for any oral glucocorticoid and if the supply had lasted until within 120 days prior to the index date. Recent exposure was defined as use that ended 121–180 days before the index date. All other use more than 180 days prior was considered past use.

The researchers also assessed current exposure to antirheumatic drugs or immunosuppressants and the presence of pulmonary disorders, rheumatic disorders, inflammatory bowel diseases, dermatitis, silicosis, renal failure, gastrectomy, and jejunoileal bypass surgery (diagnosed prior to the index date).

Patients currently using corticosteroids were 4.9 times more likely to develop tuberculosis than were nonusers, even after adjusting for the effects of BMI, smoking, disease-modifying antirheumatic drug use, and history of diabetes and pulmonary disease. The risk for tuberculosis remained elevated (OR 4.3) in patients who had recently stopped using corticosteroids.

First-time users were 3.2 times more likely to get tuberculosis than were never users. Patients with longer-term use, extending over two to nine consecutive prescriptions, saw their risk increase sevenfold.

The effect of corticosteroid use on risk for TB increased with increasing dose. The OR was 2.3 in people taking daily doses of prednisone equivalents less than 7.5 mg daily (physiologic) versus those taking supraphysiologic doses of 7.5 mg or more daily (OR 7.0, based on the highest daily dosage received by current users).

Both the American Thoracic Society and the Centers for Disease Control and Prevention agree that more than 15 mg/day of prednisone or its equivalent administered for 1 month or longer is a risk factor for tuberculosis. In light of this, the researchers evaluated the impact of daily dosage using this cutoff. The adjusted odds ratio was 2.8 for those using less than 15 mg of prednisone equivalents per day, while those using 15 mg of prednisone equivalents per day or more had an adjusted odds ratio of 7.7.

“We found that current smoking was associated with a 60% increased risk of tuberculosis. … Although this effect is relatively low, because smoking is prevalent in this study population 17% of all cases are attributable to smoking compared with only 8% of cases attributable to glucocorticoid use in this population,” the researchers said. Those with a BMI less than 20 kg/m

Prior pulmonary diagnoses were also associated with an increased risk of tuberculosis that was independent of other risk factors. A diagnosis of rheumatic disease and use of antirheumatic agents are purported to be risk factors for tuberculosis as well.

However, the number of patients taking antirheumatic drugs in this analysis was low—only 12 patients were currently exposed. Overall 17 participants (cases and controls) had rheumatoid arthritis, 1 had lupus, 12 had polymyalgia rheumatica, and 7 had arteritis. “Despite the large number of tuberculosis cases in this study, the prevalence of antirheumatic agent use was low … and therefore the independent effects for patients taking antirheumatic agents could not be reliably evaluated,” the researchers said.

In an accompanying editorial, Dr. Loreto Carmona observed that “the truth is that the report says little about the risk of TB in patients with rheumatic disease who are treated with glucocorticoids” (Arthritis Rheum. 2005;55:1–2). Dr. Carmona heads the research unit of the Spanish Foundation of Rheumatology in Madrid. It's unclear how much of the risk of tuberculosis is due to rheumatic diseases—for which corticoids are taken—and how much is due to the glucocorticoids.

Patients currently taking a glucocorticoid have nearly a fivefold increased risk of developing tuberculosis that is independent of other risk factors.

“Our results suggest that glucocorticoid use is associated with a substantially increased risk of developing tuberculosis and that the risk increases with increasing daily dose,” said Susan S. Jick, Sc.D., of Boston University, and her colleagues.

Although chronic corticosteroid use is common among patients with rheumatic diseases, the number of such patients in the study population was too small to say definitely whether use of corticosteroids specifically for arthritis and other rheumatic diseases was associated with an increased risk for TB.

Low body mass index (BMI), diabetes, current smoking, and obstructive pulmonary disorders were also determined to be important risk factors for tuberculosis in a review of 497 new cases of tuberculosis and 1,966 matched controls during the period 1990–2001 (Arthritis Rheum. 2006;55:19–26).

The researchers based their study on data available from the U.K.-based General Practice Research Database. Patients were included if they had a first-time diagnosis of tuberculosis followed by treatment with at least three different antituberculosis medications and if treatment lasted at least 6 months. As many as four control subjects were matched to each patient based on age, gender, the practice attended, and the patient's index date along with the control's visit to the practice that corresponded in time to the patient's index visit.

Assessment of glucocorticoid use was based on prescription data. Patients were classified as currently exposed if they had received a prescription for any oral glucocorticoid and if the supply had lasted until within 120 days prior to the index date. Recent exposure was defined as use that ended 121–180 days before the index date. All other use more than 180 days prior was considered past use.

The researchers also assessed current exposure to antirheumatic drugs or immunosuppressants and the presence of pulmonary disorders, rheumatic disorders, inflammatory bowel diseases, dermatitis, silicosis, renal failure, gastrectomy, and jejunoileal bypass surgery (diagnosed prior to the index date).

Patients currently using corticosteroids were 4.9 times more likely to develop tuberculosis than were nonusers, even after adjusting for the effects of BMI, smoking, disease-modifying antirheumatic drug use, and history of diabetes and pulmonary disease. The risk for tuberculosis remained elevated (OR 4.3) in patients who had recently stopped using corticosteroids.

First-time users were 3.2 times more likely to get tuberculosis than were never users. Patients with longer-term use, extending over two to nine consecutive prescriptions, saw their risk increase sevenfold.

The effect of corticosteroid use on risk for TB increased with increasing dose. The OR was 2.3 in people taking daily doses of prednisone equivalents less than 7.5 mg daily (physiologic) versus those taking supraphysiologic doses of 7.5 mg or more daily (OR 7.0, based on the highest daily dosage received by current users).

Both the American Thoracic Society and the Centers for Disease Control and Prevention agree that more than 15 mg/day of prednisone or its equivalent administered for 1 month or longer is a risk factor for tuberculosis. In light of this, the researchers evaluated the impact of daily dosage using this cutoff. The adjusted odds ratio was 2.8 for those using less than 15 mg of prednisone equivalents per day, while those using 15 mg of prednisone equivalents per day or more had an adjusted odds ratio of 7.7.

“We found that current smoking was associated with a 60% increased risk of tuberculosis. … Although this effect is relatively low, because smoking is prevalent in this study population 17% of all cases are attributable to smoking compared with only 8% of cases attributable to glucocorticoid use in this population,” the researchers said. Those with a BMI less than 20 kg/m

Prior pulmonary diagnoses were also associated with an increased risk of tuberculosis that was independent of other risk factors. A diagnosis of rheumatic disease and use of antirheumatic agents are purported to be risk factors for tuberculosis as well.

However, the number of patients taking antirheumatic drugs in this analysis was low—only 12 patients were currently exposed. Overall 17 participants (cases and controls) had rheumatoid arthritis, 1 had lupus, 12 had polymyalgia rheumatica, and 7 had arteritis. “Despite the large number of tuberculosis cases in this study, the prevalence of antirheumatic agent use was low … and therefore the independent effects for patients taking antirheumatic agents could not be reliably evaluated,” the researchers said.

In an accompanying editorial, Dr. Loreto Carmona observed that “the truth is that the report says little about the risk of TB in patients with rheumatic disease who are treated with glucocorticoids” (Arthritis Rheum. 2005;55:1–2). Dr. Carmona heads the research unit of the Spanish Foundation of Rheumatology in Madrid. It's unclear how much of the risk of tuberculosis is due to rheumatic diseases—for which corticoids are taken—and how much is due to the glucocorticoids.

Patients currently taking a glucocorticoid have nearly a fivefold increased risk of developing tuberculosis that is independent of other risk factors.

“Our results suggest that glucocorticoid use is associated with a substantially increased risk of developing tuberculosis and that the risk increases with increasing daily dose,” said Susan S. Jick, Sc.D., of Boston University, and her colleagues.

Although chronic corticosteroid use is common among patients with rheumatic diseases, the number of such patients in the study population was too small to say definitely whether use of corticosteroids specifically for arthritis and other rheumatic diseases was associated with an increased risk for TB.

Low body mass index (BMI), diabetes, current smoking, and obstructive pulmonary disorders were also determined to be important risk factors for tuberculosis in a review of 497 new cases of tuberculosis and 1,966 matched controls during the period 1990–2001 (Arthritis Rheum. 2006;55:19–26).

The researchers based their study on data available from the U.K.-based General Practice Research Database. Patients were included if they had a first-time diagnosis of tuberculosis followed by treatment with at least three different antituberculosis medications and if treatment lasted at least 6 months. As many as four control subjects were matched to each patient based on age, gender, the practice attended, and the patient's index date along with the control's visit to the practice that corresponded in time to the patient's index visit.

Assessment of glucocorticoid use was based on prescription data. Patients were classified as currently exposed if they had received a prescription for any oral glucocorticoid and if the supply had lasted until within 120 days prior to the index date. Recent exposure was defined as use that ended 121–180 days before the index date. All other use more than 180 days prior was considered past use.

The researchers also assessed current exposure to antirheumatic drugs or immunosuppressants and the presence of pulmonary disorders, rheumatic disorders, inflammatory bowel diseases, dermatitis, silicosis, renal failure, gastrectomy, and jejunoileal bypass surgery (diagnosed prior to the index date).

Patients currently using corticosteroids were 4.9 times more likely to develop tuberculosis than were nonusers, even after adjusting for the effects of BMI, smoking, disease-modifying antirheumatic drug use, and history of diabetes and pulmonary disease. The risk for tuberculosis remained elevated (OR 4.3) in patients who had recently stopped using corticosteroids.

First-time users were 3.2 times more likely to get tuberculosis than were never users. Patients with longer-term use, extending over two to nine consecutive prescriptions, saw their risk increase sevenfold.

The effect of corticosteroid use on risk for TB increased with increasing dose. The OR was 2.3 in people taking daily doses of prednisone equivalents less than 7.5 mg daily (physiologic) versus those taking supraphysiologic doses of 7.5 mg or more daily (OR 7.0, based on the highest daily dosage received by current users).

Both the American Thoracic Society and the Centers for Disease Control and Prevention agree that more than 15 mg/day of prednisone or its equivalent administered for 1 month or longer is a risk factor for tuberculosis. In light of this, the researchers evaluated the impact of daily dosage using this cutoff. The adjusted odds ratio was 2.8 for those using less than 15 mg of prednisone equivalents per day, while those using 15 mg of prednisone equivalents per day or more had an adjusted odds ratio of 7.7.

“We found that current smoking was associated with a 60% increased risk of tuberculosis. … Although this effect is relatively low, because smoking is prevalent in this study population 17% of all cases are attributable to smoking compared with only 8% of cases attributable to glucocorticoid use in this population,” the researchers said. Those with a BMI less than 20 kg/m

Prior pulmonary diagnoses were also associated with an increased risk of tuberculosis that was independent of other risk factors. A diagnosis of rheumatic disease and use of antirheumatic agents are purported to be risk factors for tuberculosis as well.

However, the number of patients taking antirheumatic drugs in this analysis was low—only 12 patients were currently exposed. Overall 17 participants (cases and controls) had rheumatoid arthritis, 1 had lupus, 12 had polymyalgia rheumatica, and 7 had arteritis. “Despite the large number of tuberculosis cases in this study, the prevalence of antirheumatic agent use was low … and therefore the independent effects for patients taking antirheumatic agents could not be reliably evaluated,” the researchers said.

In an accompanying editorial, Dr. Loreto Carmona observed that “the truth is that the report says little about the risk of TB in patients with rheumatic disease who are treated with glucocorticoids” (Arthritis Rheum. 2005;55:1–2). Dr. Carmona heads the research unit of the Spanish Foundation of Rheumatology in Madrid. It's unclear how much of the risk of tuberculosis is due to rheumatic diseases—for which corticoids are taken—and how much is due to the glucocorticoids.

WASHINGTON — As if there weren't already enough reasons to be worried about methicillin-resistant Staphylococcus aureus, the troublesome organism is now turning up in the pet population and appears to be able to move readily between animals and humans, a veterinary expert said at the annual Interscience Conference on Antimicrobial Agents and Chemotherapy.

“Methicillin-resistant Staphylococcus aureus, and Staph aureus in general, really hasn't been considered to be zoonotic, but now we're seeing that it can be transmitted between animals and people in both directions.

“As community-associated MRSA becomes more of a problem in people, it creates more potential exposure of pets,” said J. Scott Weese, D.V.M., a professor of large animal medicine at the University of Guelph in Ontario, Canada.

Methicillin-resistant Staphylococcus aureus (MRSA) appears to be endemic at a low level in the horse population worldwide, and it can be transmitted between horses and people fairly readily. During an equine outbreak in Ontario between 2000 and 2002, MRSA was isolated from 79 horses and 29 horse personnel. In addition, there were 13 clinical infections in horses and 1 clinical infection in a veterinarian.

“So there was fairly clear interspecies transmission,” Dr. Weese said. In fact, the outbreak was traced back to one individual.

To determine what was going on in the larger equine community, Dr. Weese and his colleagues performed a study using a convenience-based sample of 972 horses and 107 horse personnel in Ontario and New York. Nasal swabs were collected from horses and humans. Approximately 5% of horses—all of them on farms with previous MRSA exposures—and 13% of personnel were colonized with MRSA. “On every farm that had a colonized horse, there was at least one person who was colonized with an indistinguishable strain,” Dr. Weese said.

“I think the household pet issue is a more concerning issue because of the degree of contact that we have with our pets in most situations,” he said.

In the past year or two, there have been reports of a few hundred clinically infected pets in the United Kingdom. The numbers are lower in North America, but this may be attributable to lower rates of diagnosis and reporting. “We definitely do see them in North America.”

However, the prevalence of colonization in pets in the general population appears to be very low. “Most of the reports of household MRSA report strains that are typical of the common human strains in the area,” he said. The USA 100 strain is predominant in the United States and Canada.

Dr. Weese presented a few cases of transmission of MRSA between pets and humans that he has investigated. “These are not the worst of the worst. … They are representative of a lot of situations that we've investigated,” he said.

In one case in Washington, two kittens were brought to a veterinary clinic with chronic rhinitis. MRSA was isolated from cultures taken from both kittens. A technician at the clinic who had worked with the kittens was colonized as well. The kittens' owners, as well as the other cat in the household, were also colonized.

Upon investigation, the researchers learned that the kittens had been adopted from a rescue facility, and the head of the rescue facility was colonized, too. The isolates collected in the course of the investigation were indistinguishable.

The MRSA originated at the rescue facility and “one or more of the kittens brought it into the house, transmitted it to both owners and the other cat and one person at the veterinary clinic,” Dr. Weese said at the meeting, sponsored by the American Society for Microbiology.

In another case a few years ago, a dog was presented to a primary care veterinary clinic in New York for a postoperative infection related to a surgery performed at another facility the previous week. The culture was positive for a very aggressive strain of MRSA. The dog had necrotizing fasciitis and osteomyelitis and had to be euthanized.

During the investigation, another dog developed a serious postoperative infection. This dog was admitted for surgery after the first dog had been euthanized, so there had been no chance for direct contact.

Two personnel were found to be colonized, one of whom had been observed poking at the incision line of the second dog. The investigators determined that the first dog had acquired MRSA at the facility where surgery was performed, and had transmitted the organism to the owner and two personnel at the second facility, who then infected the other dog.

Dr. Weese and his colleagues are currently investigating the possibility of transmission from people to therapy dogs making visits to hospitals. Dogs are screened for MRSA at enrollment and are periodically rechecked.

The study is ongoing, and to date, one dog has been documented to have acquired MRSA during visitation with a colonized individual. “The concern is that if the dog is colonized and seeing other patients in the hospital … what's the risk for transmission,” he said.

When it comes to MRSA and potential transmission, different species have different issues, Dr. Weese said. With horses, there is concern about nasal/facial contamination, fecal contamination, and the greater potential for international movement.

With household pets—dogs, cats, and hamsters, among others—the degree, duration, and intensity of contact is the primary concern. “There's a lot of high-level contact within the household, creating the chance for transmission,” he said.

As a general rule, physicians “need to know what's going on in the household with pets,” he said. Find out if there are pets and how many, and if the pets are healthy. It's important to reinforce the importance of hand hygiene for people with pets, especially if the pet is sick.

It's also important to consider pets in the household if a patient has an otherwise unexplained MRSA infection or recurrent, persistent infections.

“Infection control measures are the key” to prevent household transmission of MRSA between pets and people, Dr. Weese said. Animals appear to eradicate MRSA colonizations on their own in most situations, he noted.

WASHINGTON — As if there weren't already enough reasons to be worried about methicillin-resistant Staphylococcus aureus, the troublesome organism is now turning up in the pet population and appears to be able to move readily between animals and humans, a veterinary expert said at the annual Interscience Conference on Antimicrobial Agents and Chemotherapy.

“Methicillin-resistant Staphylococcus aureus, and Staph aureus in general, really hasn't been considered to be zoonotic, but now we're seeing that it can be transmitted between animals and people in both directions.

“As community-associated MRSA becomes more of a problem in people, it creates more potential exposure of pets,” said J. Scott Weese, D.V.M., a professor of large animal medicine at the University of Guelph in Ontario, Canada.

Methicillin-resistant Staphylococcus aureus (MRSA) appears to be endemic at a low level in the horse population worldwide, and it can be transmitted between horses and people fairly readily. During an equine outbreak in Ontario between 2000 and 2002, MRSA was isolated from 79 horses and 29 horse personnel. In addition, there were 13 clinical infections in horses and 1 clinical infection in a veterinarian.

“So there was fairly clear interspecies transmission,” Dr. Weese said. In fact, the outbreak was traced back to one individual.

To determine what was going on in the larger equine community, Dr. Weese and his colleagues performed a study using a convenience-based sample of 972 horses and 107 horse personnel in Ontario and New York. Nasal swabs were collected from horses and humans. Approximately 5% of horses—all of them on farms with previous MRSA exposures—and 13% of personnel were colonized with MRSA. “On every farm that had a colonized horse, there was at least one person who was colonized with an indistinguishable strain,” Dr. Weese said.

“I think the household pet issue is a more concerning issue because of the degree of contact that we have with our pets in most situations,” he said.

In the past year or two, there have been reports of a few hundred clinically infected pets in the United Kingdom. The numbers are lower in North America, but this may be attributable to lower rates of diagnosis and reporting. “We definitely do see them in North America.”

However, the prevalence of colonization in pets in the general population appears to be very low. “Most of the reports of household MRSA report strains that are typical of the common human strains in the area,” he said. The USA 100 strain is predominant in the United States and Canada.

Dr. Weese presented a few cases of transmission of MRSA between pets and humans that he has investigated. “These are not the worst of the worst. … They are representative of a lot of situations that we've investigated,” he said.

In one case in Washington, two kittens were brought to a veterinary clinic with chronic rhinitis. MRSA was isolated from cultures taken from both kittens. A technician at the clinic who had worked with the kittens was colonized as well. The kittens' owners, as well as the other cat in the household, were also colonized.

Upon investigation, the researchers learned that the kittens had been adopted from a rescue facility, and the head of the rescue facility was colonized, too. The isolates collected in the course of the investigation were indistinguishable.

The MRSA originated at the rescue facility and “one or more of the kittens brought it into the house, transmitted it to both owners and the other cat and one person at the veterinary clinic,” Dr. Weese said at the meeting, sponsored by the American Society for Microbiology.

In another case a few years ago, a dog was presented to a primary care veterinary clinic in New York for a postoperative infection related to a surgery performed at another facility the previous week. The culture was positive for a very aggressive strain of MRSA. The dog had necrotizing fasciitis and osteomyelitis and had to be euthanized.

During the investigation, another dog developed a serious postoperative infection. This dog was admitted for surgery after the first dog had been euthanized, so there had been no chance for direct contact.

Two personnel were found to be colonized, one of whom had been observed poking at the incision line of the second dog. The investigators determined that the first dog had acquired MRSA at the facility where surgery was performed, and had transmitted the organism to the owner and two personnel at the second facility, who then infected the other dog.

Dr. Weese and his colleagues are currently investigating the possibility of transmission from people to therapy dogs making visits to hospitals. Dogs are screened for MRSA at enrollment and are periodically rechecked.

The study is ongoing, and to date, one dog has been documented to have acquired MRSA during visitation with a colonized individual. “The concern is that if the dog is colonized and seeing other patients in the hospital … what's the risk for transmission,” he said.

When it comes to MRSA and potential transmission, different species have different issues, Dr. Weese said. With horses, there is concern about nasal/facial contamination, fecal contamination, and the greater potential for international movement.

With household pets—dogs, cats, and hamsters, among others—the degree, duration, and intensity of contact is the primary concern. “There's a lot of high-level contact within the household, creating the chance for transmission,” he said.

As a general rule, physicians “need to know what's going on in the household with pets,” he said. Find out if there are pets and how many, and if the pets are healthy. It's important to reinforce the importance of hand hygiene for people with pets, especially if the pet is sick.

It's also important to consider pets in the household if a patient has an otherwise unexplained MRSA infection or recurrent, persistent infections.

“Infection control measures are the key” to prevent household transmission of MRSA between pets and people, Dr. Weese said. Animals appear to eradicate MRSA colonizations on their own in most situations, he noted.

WASHINGTON — As if there weren't already enough reasons to be worried about methicillin-resistant Staphylococcus aureus, the troublesome organism is now turning up in the pet population and appears to be able to move readily between animals and humans, a veterinary expert said at the annual Interscience Conference on Antimicrobial Agents and Chemotherapy.

“Methicillin-resistant Staphylococcus aureus, and Staph aureus in general, really hasn't been considered to be zoonotic, but now we're seeing that it can be transmitted between animals and people in both directions.

“As community-associated MRSA becomes more of a problem in people, it creates more potential exposure of pets,” said J. Scott Weese, D.V.M., a professor of large animal medicine at the University of Guelph in Ontario, Canada.

Methicillin-resistant Staphylococcus aureus (MRSA) appears to be endemic at a low level in the horse population worldwide, and it can be transmitted between horses and people fairly readily. During an equine outbreak in Ontario between 2000 and 2002, MRSA was isolated from 79 horses and 29 horse personnel. In addition, there were 13 clinical infections in horses and 1 clinical infection in a veterinarian.

“So there was fairly clear interspecies transmission,” Dr. Weese said. In fact, the outbreak was traced back to one individual.

To determine what was going on in the larger equine community, Dr. Weese and his colleagues performed a study using a convenience-based sample of 972 horses and 107 horse personnel in Ontario and New York. Nasal swabs were collected from horses and humans. Approximately 5% of horses—all of them on farms with previous MRSA exposures—and 13% of personnel were colonized with MRSA. “On every farm that had a colonized horse, there was at least one person who was colonized with an indistinguishable strain,” Dr. Weese said.

“I think the household pet issue is a more concerning issue because of the degree of contact that we have with our pets in most situations,” he said.

In the past year or two, there have been reports of a few hundred clinically infected pets in the United Kingdom. The numbers are lower in North America, but this may be attributable to lower rates of diagnosis and reporting. “We definitely do see them in North America.”

However, the prevalence of colonization in pets in the general population appears to be very low. “Most of the reports of household MRSA report strains that are typical of the common human strains in the area,” he said. The USA 100 strain is predominant in the United States and Canada.

Dr. Weese presented a few cases of transmission of MRSA between pets and humans that he has investigated. “These are not the worst of the worst. … They are representative of a lot of situations that we've investigated,” he said.

In one case in Washington, two kittens were brought to a veterinary clinic with chronic rhinitis. MRSA was isolated from cultures taken from both kittens. A technician at the clinic who had worked with the kittens was colonized as well. The kittens' owners, as well as the other cat in the household, were also colonized.

Upon investigation, the researchers learned that the kittens had been adopted from a rescue facility, and the head of the rescue facility was colonized, too. The isolates collected in the course of the investigation were indistinguishable.

The MRSA originated at the rescue facility and “one or more of the kittens brought it into the house, transmitted it to both owners and the other cat and one person at the veterinary clinic,” Dr. Weese said at the meeting, sponsored by the American Society for Microbiology.

In another case a few years ago, a dog was presented to a primary care veterinary clinic in New York for a postoperative infection related to a surgery performed at another facility the previous week. The culture was positive for a very aggressive strain of MRSA. The dog had necrotizing fasciitis and osteomyelitis and had to be euthanized.

During the investigation, another dog developed a serious postoperative infection. This dog was admitted for surgery after the first dog had been euthanized, so there had been no chance for direct contact.

Two personnel were found to be colonized, one of whom had been observed poking at the incision line of the second dog. The investigators determined that the first dog had acquired MRSA at the facility where surgery was performed, and had transmitted the organism to the owner and two personnel at the second facility, who then infected the other dog.

Dr. Weese and his colleagues are currently investigating the possibility of transmission from people to therapy dogs making visits to hospitals. Dogs are screened for MRSA at enrollment and are periodically rechecked.

The study is ongoing, and to date, one dog has been documented to have acquired MRSA during visitation with a colonized individual. “The concern is that if the dog is colonized and seeing other patients in the hospital … what's the risk for transmission,” he said.

When it comes to MRSA and potential transmission, different species have different issues, Dr. Weese said. With horses, there is concern about nasal/facial contamination, fecal contamination, and the greater potential for international movement.

With household pets—dogs, cats, and hamsters, among others—the degree, duration, and intensity of contact is the primary concern. “There's a lot of high-level contact within the household, creating the chance for transmission,” he said.

As a general rule, physicians “need to know what's going on in the household with pets,” he said. Find out if there are pets and how many, and if the pets are healthy. It's important to reinforce the importance of hand hygiene for people with pets, especially if the pet is sick.

It's also important to consider pets in the household if a patient has an otherwise unexplained MRSA infection or recurrent, persistent infections.

“Infection control measures are the key” to prevent household transmission of MRSA between pets and people, Dr. Weese said. Animals appear to eradicate MRSA colonizations on their own in most situations, he noted.

SAN JUAN, P.R. — Seizures in older adults have a different presentation than they do in younger patients, with these events resembling many other conditions and making diagnosis difficult, but there are a few keys that can help make the right diagnosis, said one expert speaking at the annual meeting of the American Association for Geriatric Psychiatry.

Seizures in older adults often are a by-product of stroke and/or hemorrhage, said Dr. Joseph I. Sirven, of the department of neurology at the Mayo Clinic in Phoenix, Arizona, who spoke from anecdotal experience. In addition, neurodegenerative conditions, such as dementia, also cause problems that lead to seizures.

In general, partial seizures are most commonly seen in older adults because there is a specific area of injury or damage involved, said Dr. Sirven. In older adults, the foci of seizures usually occur in the frontal or parietal lobes.

“We also know that simple partial seizures, in which there is not a loss of consciousness, tend to have more focal and/or sensory symptoms [such as] tremor or a sense of numbness,” said Dr. Sirven. Auras—primarily dizziness—may also be present. Complex partial seizures often present with altered mental activity, staring, blackouts, and confusion.

The key to seizure recognition is episodic frequency of symptoms that are stereotypic. In particular, episodes may present with loss of consciousness, dizziness, confusion, or language change. “If you see transient episodes of certain behaviors that are stereotypic, the first test really is the EEG,” said Dr. Sirven. Other diagnostic tests to consider include MRI, laboratory tests, cardiovascular testing, ambulatory EKG, and tilt table testing.

Seizure medication should be considered only if the seizures are truly impacting the patient's quality of life. “Why I'm making a big deal about it is that the moment you start someone on seizure medication … you've branded that person and no one down the road is going to stop that medication,” said Dr. Sirven.

He listed three points to consider in choosing a seizure drug for an older patient:

▸ Efficacy. Try to use monotherapy whenever possible. Choose a medication that is appropriate for the seizure type. If the seizure type is unspecified, choose a broad-spectrum agent.

▸ Safety and tolerability. First, minimize drug interactions. In addition, choose a drug with a favorable safety profile that minimizes the inhibition of cognitive function and has a minimal effect on gait, balance, and orthostatic blood pressure.

▸ Simplification. Once-daily dosing helps with patient compliance. Choose a drug with a quick onset of action. Reduce interacting drugs, especially psychoactive ones.

SAN JUAN, P.R. — Seizures in older adults have a different presentation than they do in younger patients, with these events resembling many other conditions and making diagnosis difficult, but there are a few keys that can help make the right diagnosis, said one expert speaking at the annual meeting of the American Association for Geriatric Psychiatry.

Seizures in older adults often are a by-product of stroke and/or hemorrhage, said Dr. Joseph I. Sirven, of the department of neurology at the Mayo Clinic in Phoenix, Arizona, who spoke from anecdotal experience. In addition, neurodegenerative conditions, such as dementia, also cause problems that lead to seizures.

In general, partial seizures are most commonly seen in older adults because there is a specific area of injury or damage involved, said Dr. Sirven. In older adults, the foci of seizures usually occur in the frontal or parietal lobes.

“We also know that simple partial seizures, in which there is not a loss of consciousness, tend to have more focal and/or sensory symptoms [such as] tremor or a sense of numbness,” said Dr. Sirven. Auras—primarily dizziness—may also be present. Complex partial seizures often present with altered mental activity, staring, blackouts, and confusion.

The key to seizure recognition is episodic frequency of symptoms that are stereotypic. In particular, episodes may present with loss of consciousness, dizziness, confusion, or language change. “If you see transient episodes of certain behaviors that are stereotypic, the first test really is the EEG,” said Dr. Sirven. Other diagnostic tests to consider include MRI, laboratory tests, cardiovascular testing, ambulatory EKG, and tilt table testing.

Seizure medication should be considered only if the seizures are truly impacting the patient's quality of life. “Why I'm making a big deal about it is that the moment you start someone on seizure medication … you've branded that person and no one down the road is going to stop that medication,” said Dr. Sirven.

He listed three points to consider in choosing a seizure drug for an older patient:

▸ Efficacy. Try to use monotherapy whenever possible. Choose a medication that is appropriate for the seizure type. If the seizure type is unspecified, choose a broad-spectrum agent.

▸ Safety and tolerability. First, minimize drug interactions. In addition, choose a drug with a favorable safety profile that minimizes the inhibition of cognitive function and has a minimal effect on gait, balance, and orthostatic blood pressure.

▸ Simplification. Once-daily dosing helps with patient compliance. Choose a drug with a quick onset of action. Reduce interacting drugs, especially psychoactive ones.

SAN JUAN, P.R. — Seizures in older adults have a different presentation than they do in younger patients, with these events resembling many other conditions and making diagnosis difficult, but there are a few keys that can help make the right diagnosis, said one expert speaking at the annual meeting of the American Association for Geriatric Psychiatry.

Seizures in older adults often are a by-product of stroke and/or hemorrhage, said Dr. Joseph I. Sirven, of the department of neurology at the Mayo Clinic in Phoenix, Arizona, who spoke from anecdotal experience. In addition, neurodegenerative conditions, such as dementia, also cause problems that lead to seizures.

In general, partial seizures are most commonly seen in older adults because there is a specific area of injury or damage involved, said Dr. Sirven. In older adults, the foci of seizures usually occur in the frontal or parietal lobes.

“We also know that simple partial seizures, in which there is not a loss of consciousness, tend to have more focal and/or sensory symptoms [such as] tremor or a sense of numbness,” said Dr. Sirven. Auras—primarily dizziness—may also be present. Complex partial seizures often present with altered mental activity, staring, blackouts, and confusion.

The key to seizure recognition is episodic frequency of symptoms that are stereotypic. In particular, episodes may present with loss of consciousness, dizziness, confusion, or language change. “If you see transient episodes of certain behaviors that are stereotypic, the first test really is the EEG,” said Dr. Sirven. Other diagnostic tests to consider include MRI, laboratory tests, cardiovascular testing, ambulatory EKG, and tilt table testing.

Seizure medication should be considered only if the seizures are truly impacting the patient's quality of life. “Why I'm making a big deal about it is that the moment you start someone on seizure medication … you've branded that person and no one down the road is going to stop that medication,” said Dr. Sirven.

He listed three points to consider in choosing a seizure drug for an older patient:

▸ Efficacy. Try to use monotherapy whenever possible. Choose a medication that is appropriate for the seizure type. If the seizure type is unspecified, choose a broad-spectrum agent.

▸ Safety and tolerability. First, minimize drug interactions. In addition, choose a drug with a favorable safety profile that minimizes the inhibition of cognitive function and has a minimal effect on gait, balance, and orthostatic blood pressure.

▸ Simplification. Once-daily dosing helps with patient compliance. Choose a drug with a quick onset of action. Reduce interacting drugs, especially psychoactive ones.