Mary Ann Moon

An early and steep rise in circulating levels of soluble endoglin appears to predict preeclampsia, reported Dr. Richard J. Levine of the National Institute of Child Health and Human Development, Bethesda, Md., and his associates.

Pregnant women's circulating levels of soluble endoglin, an antiangiogenic protein, appears to rise markedly 2–3 months before the onset of preeclampsia. This rise is accompanied by a similar rise in the ratio of another antiangiogenic protein—soluble fms-like tyrosine kinase 1—to placental growth factor (the sFlt-1:PlGF ratio). “Taken together with experimental evidence in rodents, these data suggest that circulating soluble endoglin and sFlt-1, each of which causes endothelial dysfunction by a different mechanism, may both contribute to the syndrome of preeclampsia,” Dr. Levine and his associates said.

“Prospective longitudinal studies are needed to assess whether these biomarkers can predict the imminent onset of clinical disease.”

In an accompanying editorial comment, Dr. Marshall D. Lindheimer and Dr. Jason G. Umans said these findings puts the measurement of antiangiogenic proteins “at the forefront of tests that are potentially useful for predicting preeclampsia.” The findings also point the way to both preventing and treating the disorder, they said.

To examine gestational patterns in levels of these proteins, Dr. Levine and his associates performed a nested case-control study using data and frozen serum samples from a subset of 3,630 women who had participated in the Calcium for Preeclampsia Prevention (CPEP) trial. The CPEP study, conducted in 1992–1995, was a randomized trial that assessed the disorder in healthy nulliparous women with singleton pregnancies.

Of these subjects, 2,469 were normotensive throughout pregnancy and delivered normal-sized infants; these women served as controls in the current study. Another 225 subjects were normotensive but gave birth to small-for-gestational-age (SGA) infants, 651 had gestational hypertension, 213 had preeclampsia at or after 37 weeks (term preeclampsia), and 72 had preeclampsia before 37 weeks' gestation (preterm preeclampsia). For the case-control study, serum specimens that had been obtained during pregnancy were evaluated for 120 subjects randomly selected from the first four categories and from all 72 subjects in the last category.

Serum levels of soluble endoglin rose during the last 2 months of normal pregnancies, but rose earlier and much more steeply in women who later developed preeclampsia, “reaching a peak at the onset of clinical disease,” the researchers said (N. Engl. J. Med. 2006;355:992–1005).

Beginning at 17–20 weeks' gestation, mean serum soluble endoglin levels were significantly higher in women who later developed preterm preeclampsia (10.2 ng/mL) than in controls (5.8 ng/mL). They then showed a steep rise at 33–36 weeks. Similarly, starting at 25–28 weeks' gestation, levels were significantly higher in women who later developed term preeclampsia (8.5 ng/mL) than in controls (5.9 ng/mL). Levels also rose steeply at 33–36 weeks.

After the onset of clinical disease, mean serum levels of soluble endoglin were markedly higher in women with preterm preeclampsia (46.4 ng/mL) than in matched controls (9.8 ng/mL) and were similarly higher in women with term preeclampsia (31.0 ng/mL) than in matched controls (13.3 ng/mL).

“Elevations in soluble endoglin were particularly pronounced—therefore, potentially most useful for prediction—among women in whom preterm preeclampsia developed or women in whom preeclampsia developed who had an SGA infant,” they said.

Increased levels of soluble endoglin were usually accompanied by increased sFlt-1:PlGF ratios. In addition, women with both biomarkers in the highest quartile at 21–32 weeks' gestation had an increased risk of preterm preeclampsia, and those with levels in the highest quartile at 33–42 weeks had an increased risk of term preeclampsia.

“The data can be interpreted to imply that soluble endoglin levels and the sFlt-1:PlGF ratio both contribute to the pathogenesis of preeclampsia. Indeed, a composite measure incorporating all three molecules—the ratio of (sFlt-1 plus soluble endoglin):PlGF—was more strongly predictive of preeclampsia than were individual biomarkers,” the authors said.

An early and steep rise in circulating levels of soluble endoglin appears to predict preeclampsia, reported Dr. Richard J. Levine of the National Institute of Child Health and Human Development, Bethesda, Md., and his associates.

Pregnant women's circulating levels of soluble endoglin, an antiangiogenic protein, appears to rise markedly 2–3 months before the onset of preeclampsia. This rise is accompanied by a similar rise in the ratio of another antiangiogenic protein—soluble fms-like tyrosine kinase 1—to placental growth factor (the sFlt-1:PlGF ratio). “Taken together with experimental evidence in rodents, these data suggest that circulating soluble endoglin and sFlt-1, each of which causes endothelial dysfunction by a different mechanism, may both contribute to the syndrome of preeclampsia,” Dr. Levine and his associates said.

“Prospective longitudinal studies are needed to assess whether these biomarkers can predict the imminent onset of clinical disease.”

In an accompanying editorial comment, Dr. Marshall D. Lindheimer and Dr. Jason G. Umans said these findings puts the measurement of antiangiogenic proteins “at the forefront of tests that are potentially useful for predicting preeclampsia.” The findings also point the way to both preventing and treating the disorder, they said.

To examine gestational patterns in levels of these proteins, Dr. Levine and his associates performed a nested case-control study using data and frozen serum samples from a subset of 3,630 women who had participated in the Calcium for Preeclampsia Prevention (CPEP) trial. The CPEP study, conducted in 1992–1995, was a randomized trial that assessed the disorder in healthy nulliparous women with singleton pregnancies.

Of these subjects, 2,469 were normotensive throughout pregnancy and delivered normal-sized infants; these women served as controls in the current study. Another 225 subjects were normotensive but gave birth to small-for-gestational-age (SGA) infants, 651 had gestational hypertension, 213 had preeclampsia at or after 37 weeks (term preeclampsia), and 72 had preeclampsia before 37 weeks' gestation (preterm preeclampsia). For the case-control study, serum specimens that had been obtained during pregnancy were evaluated for 120 subjects randomly selected from the first four categories and from all 72 subjects in the last category.

Serum levels of soluble endoglin rose during the last 2 months of normal pregnancies, but rose earlier and much more steeply in women who later developed preeclampsia, “reaching a peak at the onset of clinical disease,” the researchers said (N. Engl. J. Med. 2006;355:992–1005).

Beginning at 17–20 weeks' gestation, mean serum soluble endoglin levels were significantly higher in women who later developed preterm preeclampsia (10.2 ng/mL) than in controls (5.8 ng/mL). They then showed a steep rise at 33–36 weeks. Similarly, starting at 25–28 weeks' gestation, levels were significantly higher in women who later developed term preeclampsia (8.5 ng/mL) than in controls (5.9 ng/mL). Levels also rose steeply at 33–36 weeks.

After the onset of clinical disease, mean serum levels of soluble endoglin were markedly higher in women with preterm preeclampsia (46.4 ng/mL) than in matched controls (9.8 ng/mL) and were similarly higher in women with term preeclampsia (31.0 ng/mL) than in matched controls (13.3 ng/mL).

“Elevations in soluble endoglin were particularly pronounced—therefore, potentially most useful for prediction—among women in whom preterm preeclampsia developed or women in whom preeclampsia developed who had an SGA infant,” they said.

Increased levels of soluble endoglin were usually accompanied by increased sFlt-1:PlGF ratios. In addition, women with both biomarkers in the highest quartile at 21–32 weeks' gestation had an increased risk of preterm preeclampsia, and those with levels in the highest quartile at 33–42 weeks had an increased risk of term preeclampsia.

“The data can be interpreted to imply that soluble endoglin levels and the sFlt-1:PlGF ratio both contribute to the pathogenesis of preeclampsia. Indeed, a composite measure incorporating all three molecules—the ratio of (sFlt-1 plus soluble endoglin):PlGF—was more strongly predictive of preeclampsia than were individual biomarkers,” the authors said.

An early and steep rise in circulating levels of soluble endoglin appears to predict preeclampsia, reported Dr. Richard J. Levine of the National Institute of Child Health and Human Development, Bethesda, Md., and his associates.

Pregnant women's circulating levels of soluble endoglin, an antiangiogenic protein, appears to rise markedly 2–3 months before the onset of preeclampsia. This rise is accompanied by a similar rise in the ratio of another antiangiogenic protein—soluble fms-like tyrosine kinase 1—to placental growth factor (the sFlt-1:PlGF ratio). “Taken together with experimental evidence in rodents, these data suggest that circulating soluble endoglin and sFlt-1, each of which causes endothelial dysfunction by a different mechanism, may both contribute to the syndrome of preeclampsia,” Dr. Levine and his associates said.

“Prospective longitudinal studies are needed to assess whether these biomarkers can predict the imminent onset of clinical disease.”

In an accompanying editorial comment, Dr. Marshall D. Lindheimer and Dr. Jason G. Umans said these findings puts the measurement of antiangiogenic proteins “at the forefront of tests that are potentially useful for predicting preeclampsia.” The findings also point the way to both preventing and treating the disorder, they said.

To examine gestational patterns in levels of these proteins, Dr. Levine and his associates performed a nested case-control study using data and frozen serum samples from a subset of 3,630 women who had participated in the Calcium for Preeclampsia Prevention (CPEP) trial. The CPEP study, conducted in 1992–1995, was a randomized trial that assessed the disorder in healthy nulliparous women with singleton pregnancies.

Of these subjects, 2,469 were normotensive throughout pregnancy and delivered normal-sized infants; these women served as controls in the current study. Another 225 subjects were normotensive but gave birth to small-for-gestational-age (SGA) infants, 651 had gestational hypertension, 213 had preeclampsia at or after 37 weeks (term preeclampsia), and 72 had preeclampsia before 37 weeks' gestation (preterm preeclampsia). For the case-control study, serum specimens that had been obtained during pregnancy were evaluated for 120 subjects randomly selected from the first four categories and from all 72 subjects in the last category.

Serum levels of soluble endoglin rose during the last 2 months of normal pregnancies, but rose earlier and much more steeply in women who later developed preeclampsia, “reaching a peak at the onset of clinical disease,” the researchers said (N. Engl. J. Med. 2006;355:992–1005).

Beginning at 17–20 weeks' gestation, mean serum soluble endoglin levels were significantly higher in women who later developed preterm preeclampsia (10.2 ng/mL) than in controls (5.8 ng/mL). They then showed a steep rise at 33–36 weeks. Similarly, starting at 25–28 weeks' gestation, levels were significantly higher in women who later developed term preeclampsia (8.5 ng/mL) than in controls (5.9 ng/mL). Levels also rose steeply at 33–36 weeks.

After the onset of clinical disease, mean serum levels of soluble endoglin were markedly higher in women with preterm preeclampsia (46.4 ng/mL) than in matched controls (9.8 ng/mL) and were similarly higher in women with term preeclampsia (31.0 ng/mL) than in matched controls (13.3 ng/mL).

“Elevations in soluble endoglin were particularly pronounced—therefore, potentially most useful for prediction—among women in whom preterm preeclampsia developed or women in whom preeclampsia developed who had an SGA infant,” they said.

Increased levels of soluble endoglin were usually accompanied by increased sFlt-1:PlGF ratios. In addition, women with both biomarkers in the highest quartile at 21–32 weeks' gestation had an increased risk of preterm preeclampsia, and those with levels in the highest quartile at 33–42 weeks had an increased risk of term preeclampsia.

“The data can be interpreted to imply that soluble endoglin levels and the sFlt-1:PlGF ratio both contribute to the pathogenesis of preeclampsia. Indeed, a composite measure incorporating all three molecules—the ratio of (sFlt-1 plus soluble endoglin):PlGF—was more strongly predictive of preeclampsia than were individual biomarkers,” the authors said.

Adolescent elite cross-country skiers show increased thoracic kyphosis over time, which contributes to their high incidence of low back pain and might put them at risk for hyperkyphosis.

Noting numerous reports in the literature of a high rate of low back pain in young skiers, Dr. Marie Alricsson of Mid Sweden University, Östersund, and Dr. S. Werner of the Karolinska Institute, Stockholm, hypothesized that the flexed position of the spine in classical cross-country skiing might eventually cause increased thoracic curvature in growing adolescents. They assessed possible changes in the spinal curvature of 15 adolescent members of an elite cross-country ski team before and after 5 years of intensive skiing.

The seven boys and eight girls had a mean age of 13.6 years at the start of the study. At 5-year follow-up, “the relationship between thoracic kyphosis and lumbar lordosis increased from 3.5 degrees to 13.1 degrees,” the investigators reported (Phys. Ther. Sport 2006 June 26 [Epub doi:10.1016/j.ptsp.2006.06.003]).

“This means that growing individuals [who] participate in cross-country skiing might develop a hyperkyphosis over time,” they added.

Seven subjects reported low back pain. They “showed a significantly higher relationship between thoracic kyphosis and lumbar lordosis than did those skiers without low back pain, 18.2 degrees and 10.5 degrees, respectively,” the researchers said.

Seven of the eight subjects who did not report low back pain at follow-up had participated in other sports at least once per week for the preceding 3 years. “It is likely that participating in other sports might at least to some extent prevent or reduce development of low back pain in cross-country skiers. … [It] might promote a more all-round type of body exercise, which could 'balance' the sport-specific training” of elite cross-country skiing, the researchers said.

They advised that adolescent cross-country skiers regularly participate in other physical activities or sports concurrently with their skiing.

Adolescent elite cross-country skiers show increased thoracic kyphosis over time, which contributes to their high incidence of low back pain and might put them at risk for hyperkyphosis.

Noting numerous reports in the literature of a high rate of low back pain in young skiers, Dr. Marie Alricsson of Mid Sweden University, Östersund, and Dr. S. Werner of the Karolinska Institute, Stockholm, hypothesized that the flexed position of the spine in classical cross-country skiing might eventually cause increased thoracic curvature in growing adolescents. They assessed possible changes in the spinal curvature of 15 adolescent members of an elite cross-country ski team before and after 5 years of intensive skiing.

The seven boys and eight girls had a mean age of 13.6 years at the start of the study. At 5-year follow-up, “the relationship between thoracic kyphosis and lumbar lordosis increased from 3.5 degrees to 13.1 degrees,” the investigators reported (Phys. Ther. Sport 2006 June 26 [Epub doi:10.1016/j.ptsp.2006.06.003]).

“This means that growing individuals [who] participate in cross-country skiing might develop a hyperkyphosis over time,” they added.

Seven subjects reported low back pain. They “showed a significantly higher relationship between thoracic kyphosis and lumbar lordosis than did those skiers without low back pain, 18.2 degrees and 10.5 degrees, respectively,” the researchers said.

Seven of the eight subjects who did not report low back pain at follow-up had participated in other sports at least once per week for the preceding 3 years. “It is likely that participating in other sports might at least to some extent prevent or reduce development of low back pain in cross-country skiers. … [It] might promote a more all-round type of body exercise, which could 'balance' the sport-specific training” of elite cross-country skiing, the researchers said.

They advised that adolescent cross-country skiers regularly participate in other physical activities or sports concurrently with their skiing.

Adolescent elite cross-country skiers show increased thoracic kyphosis over time, which contributes to their high incidence of low back pain and might put them at risk for hyperkyphosis.

Noting numerous reports in the literature of a high rate of low back pain in young skiers, Dr. Marie Alricsson of Mid Sweden University, Östersund, and Dr. S. Werner of the Karolinska Institute, Stockholm, hypothesized that the flexed position of the spine in classical cross-country skiing might eventually cause increased thoracic curvature in growing adolescents. They assessed possible changes in the spinal curvature of 15 adolescent members of an elite cross-country ski team before and after 5 years of intensive skiing.

The seven boys and eight girls had a mean age of 13.6 years at the start of the study. At 5-year follow-up, “the relationship between thoracic kyphosis and lumbar lordosis increased from 3.5 degrees to 13.1 degrees,” the investigators reported (Phys. Ther. Sport 2006 June 26 [Epub doi:10.1016/j.ptsp.2006.06.003]).

“This means that growing individuals [who] participate in cross-country skiing might develop a hyperkyphosis over time,” they added.

Seven subjects reported low back pain. They “showed a significantly higher relationship between thoracic kyphosis and lumbar lordosis than did those skiers without low back pain, 18.2 degrees and 10.5 degrees, respectively,” the researchers said.

Seven of the eight subjects who did not report low back pain at follow-up had participated in other sports at least once per week for the preceding 3 years. “It is likely that participating in other sports might at least to some extent prevent or reduce development of low back pain in cross-country skiers. … [It] might promote a more all-round type of body exercise, which could 'balance' the sport-specific training” of elite cross-country skiing, the researchers said.

They advised that adolescent cross-country skiers regularly participate in other physical activities or sports concurrently with their skiing.

Intra-articular injections of hyaluronic acid relieved pain and produced functional improvements lasting at least 6 months in a pilot study of 75 patients with ankle osteoarthritis, reported Dr. Shu-Fen Sun of Veterans General Hospital, Kaohsiung, Taiwan, and associates.

Researchers have reported success with hyaluronic acid injections in osteoarthritic knees, so Dr. Sun and colleagues assessed the efficacy and safety of these injections in an open-label prospective clinical trial involving 41 men and 34 women with mild to moderate unilateral ankle osteoarthritis (OA). “To date there is only limited published literature on its use in the ankle,” and it is approved for clinical use only in the knee, they noted.

OA reduces the concentration of hyaluronic acid in the synovial fluid of affected joints. Intra-articular injections are thought to restore viscosity and elasticity in that fluid, as well as to normalize endogenous synthesis of hyaluronic acid and inhibit its degradation, the investigators said (Osteoarthritis Cartilage 2006;14:867-74).

Study subjects received five weekly intra-articular injections. Beneficial effects were noted within 1 week of completing the series of injections and persisted through a 6-month follow-up. On the Ankle Osteoarthritis Scale, a patient-rated measure that addresses pain and function in the affected joint, scores decreased significantly beginning at 1 week after treatment and continuing through 1-month, 3-month, and 6-month follow-up visits.

Similarly, on the physician-rated 100-point measure of the American Orthopaedic Foot and Ankle Society, which assesses pain, function, and alignment, mean scores improved from 64 at baseline to 75 at 1 week and 78 at all subsequent follow-ups.

The treatment decreased the patients' use of rescue analgesics. Acetaminophen use dropped from an average of 14 tablets per week at baseline to 3 tablets per week at 1-month, 3-month, and 6-month follow-up visits.

Ankle sagittal range of motion did not change significantly with treatment.

Given that surgical treatment of ankle OA “is often quite painful,” intra-articular hyaluronic acid injections may offer a new option to patients who have not responded to traditional pain therapies, Dr. Sun and associates said.

These findings support the idea that the treatment's mechanism of action exceeds simple replacement of viscous joint fluid. “Temporary restoration of the rheologic homeostasis may trigger normal native hyaluronic acid metabolism. Hyaluronic acid also fulfills an anti-inflammatory role by reducing white cell aggregation and activation. With this postulated disease-modifying behavior, its clinical effects may persist beyond its physical duration within the joint,” the researchers noted.

Intra-articular injections of hyaluronic acid relieved pain and produced functional improvements lasting at least 6 months in a pilot study of 75 patients with ankle osteoarthritis, reported Dr. Shu-Fen Sun of Veterans General Hospital, Kaohsiung, Taiwan, and associates.

Researchers have reported success with hyaluronic acid injections in osteoarthritic knees, so Dr. Sun and colleagues assessed the efficacy and safety of these injections in an open-label prospective clinical trial involving 41 men and 34 women with mild to moderate unilateral ankle osteoarthritis (OA). “To date there is only limited published literature on its use in the ankle,” and it is approved for clinical use only in the knee, they noted.

OA reduces the concentration of hyaluronic acid in the synovial fluid of affected joints. Intra-articular injections are thought to restore viscosity and elasticity in that fluid, as well as to normalize endogenous synthesis of hyaluronic acid and inhibit its degradation, the investigators said (Osteoarthritis Cartilage 2006;14:867-74).

Study subjects received five weekly intra-articular injections. Beneficial effects were noted within 1 week of completing the series of injections and persisted through a 6-month follow-up. On the Ankle Osteoarthritis Scale, a patient-rated measure that addresses pain and function in the affected joint, scores decreased significantly beginning at 1 week after treatment and continuing through 1-month, 3-month, and 6-month follow-up visits.

Similarly, on the physician-rated 100-point measure of the American Orthopaedic Foot and Ankle Society, which assesses pain, function, and alignment, mean scores improved from 64 at baseline to 75 at 1 week and 78 at all subsequent follow-ups.

The treatment decreased the patients' use of rescue analgesics. Acetaminophen use dropped from an average of 14 tablets per week at baseline to 3 tablets per week at 1-month, 3-month, and 6-month follow-up visits.

Ankle sagittal range of motion did not change significantly with treatment.

Given that surgical treatment of ankle OA “is often quite painful,” intra-articular hyaluronic acid injections may offer a new option to patients who have not responded to traditional pain therapies, Dr. Sun and associates said.

These findings support the idea that the treatment's mechanism of action exceeds simple replacement of viscous joint fluid. “Temporary restoration of the rheologic homeostasis may trigger normal native hyaluronic acid metabolism. Hyaluronic acid also fulfills an anti-inflammatory role by reducing white cell aggregation and activation. With this postulated disease-modifying behavior, its clinical effects may persist beyond its physical duration within the joint,” the researchers noted.

Intra-articular injections of hyaluronic acid relieved pain and produced functional improvements lasting at least 6 months in a pilot study of 75 patients with ankle osteoarthritis, reported Dr. Shu-Fen Sun of Veterans General Hospital, Kaohsiung, Taiwan, and associates.

Researchers have reported success with hyaluronic acid injections in osteoarthritic knees, so Dr. Sun and colleagues assessed the efficacy and safety of these injections in an open-label prospective clinical trial involving 41 men and 34 women with mild to moderate unilateral ankle osteoarthritis (OA). “To date there is only limited published literature on its use in the ankle,” and it is approved for clinical use only in the knee, they noted.

OA reduces the concentration of hyaluronic acid in the synovial fluid of affected joints. Intra-articular injections are thought to restore viscosity and elasticity in that fluid, as well as to normalize endogenous synthesis of hyaluronic acid and inhibit its degradation, the investigators said (Osteoarthritis Cartilage 2006;14:867-74).

Study subjects received five weekly intra-articular injections. Beneficial effects were noted within 1 week of completing the series of injections and persisted through a 6-month follow-up. On the Ankle Osteoarthritis Scale, a patient-rated measure that addresses pain and function in the affected joint, scores decreased significantly beginning at 1 week after treatment and continuing through 1-month, 3-month, and 6-month follow-up visits.

Similarly, on the physician-rated 100-point measure of the American Orthopaedic Foot and Ankle Society, which assesses pain, function, and alignment, mean scores improved from 64 at baseline to 75 at 1 week and 78 at all subsequent follow-ups.

The treatment decreased the patients' use of rescue analgesics. Acetaminophen use dropped from an average of 14 tablets per week at baseline to 3 tablets per week at 1-month, 3-month, and 6-month follow-up visits.

Ankle sagittal range of motion did not change significantly with treatment.

Given that surgical treatment of ankle OA “is often quite painful,” intra-articular hyaluronic acid injections may offer a new option to patients who have not responded to traditional pain therapies, Dr. Sun and associates said.

These findings support the idea that the treatment's mechanism of action exceeds simple replacement of viscous joint fluid. “Temporary restoration of the rheologic homeostasis may trigger normal native hyaluronic acid metabolism. Hyaluronic acid also fulfills an anti-inflammatory role by reducing white cell aggregation and activation. With this postulated disease-modifying behavior, its clinical effects may persist beyond its physical duration within the joint,” the researchers noted.

The recent outbreak of fusarium keratitis that spread to 33 states carried “a high degree of morbidity,” with corneal transplantation required or planned for 55 of the 164 affected patients identified, reported Dr. Douglas C. Chang of the Centers for Disease Control and Prevention, Atlanta, and his associates.

The outbreak was linked to ReNu contact lens solution with MoistureLoc. The mechanism of infection remains uncertain, but researchers think that contamination of the contact lens solution occurred well after manufacturing and distribution, probably in the patients' homes.

“This outbreak may have been caused by a complex and as yet undetermined interaction between MoistureLoc, fusarium, and possibly the lens case or contact lens,” they said.

“Clinicians should be vigilant in diagnosing and treating fungal keratitis, and users of MoistureLoc should discontinue the use of this product,” the CDC investigators said (JAMA 2006;296:953–63).

In an editorial, Dr. Todd P. Margolis and Dr. John P. Whitcher of the University of California, San Francisco, said filamentous fungal keratitis is “notoriously difficult to treat,” and fusarium keratitis is “truly a therapeutic challenge.”

Many patients require adjuvant surgery ranging from recurrent corneal debridement to corneal transplantation, but the visual outcome is often dismal.”

Early treatment appears to improve the likelihood of resolving the infection. Clinicians should be alert for general signs and symptoms of keratitis, including redness, tearing, pain, light sensitivity, discharge, decreased vision, and a white corneal infiltrate, they noted (JAMA 2006;296:985–7).

Specific signs of fungal keratitis—such as a corneal stromal infiltrate with “feathery edges,” satellite lesions, a ring infiltrate, a posterior endothelial plaque, or a waxing and waning hypopyon—have been absent in some of the recent cases.

“A high index of suspicion and appropriate diagnostic studies, including cytological staining and microbiological cultures of material from the involved site” are key, they said.

Just as important is avoiding the use of topical ophthalmic corticosteroids before commencing antifungal therapy. Although corticosteroids are contraindicated in these cases, the drugs “are commonly prescribed by physicians for patients with complaints of acute red eyes, frequently by telephone and without a physical evaluation.”

Approximately one-fourth of cases assessed in earlier studies had been inappropriately treated with ophthalmic corticosteroids.

“Clinicians must immediately cease this potentially harmful practice,” the editorial writers emphasized.

Dr. Chang and his associates noted that Bausch & Lomb Inc., manufacturer of MoistureLoc contact lens solution, permanently withdrew the product from the market in May after reviewing preliminary CDC data on the outbreak, which began in June 2005 and peaked in April 2006.

The CDC began investigating the outbreak in March 2006, after a New Jersey ophthalmologist reported treating three patients who had contact-lens-associated fusarium keratitis during the preceding 2 months.

Fungal keratitis is rare, and fusarium keratitis comprises less than 5% of microbial infections in contact lens wearers. The filamental fungus is commonly found in soil, plants, and water sources in tropical or subtropical regions.

In 2004, 10 U.S. labs reported positive fusarium cultures from ocular specimens in only 12 cases.

As of June 30, the CDC had received 318 reports of fusarium keratitis in 2006. Of those, 164 cases had been confirmed and 32 had been categorized as possible. Most patients were adults, but 16 (10%) were children or adolescents.

Of the 164 confirmed cases, 37 infections (23%) had resolved with topical or systemic antifungal therapy, 65 (40%) had not yet resolved and are still being treated with antifungals, and 55 (34%) required or were awaiting corneal transplant because of active disease, residual scarring, or both.

In the month preceding infection, 69% of the keratitis patients reported using MoistureLoc contact lens solution, compared with 15% of control subjects.

At least 10 fusarium species were cultured from patient specimens and from samples from opened lens cases or bottles of solution, but no contamination was detected in unopened bottles of solution or in any of hundreds of samples taken at the manufacturing plant and distribution warehouse.

Researchers think that contamination of the contact lens solution occurred well after manufacturing and distribution, probably in the patients' homes. Yvonne Evans/Elsevier Global Medical News

The recent outbreak of fusarium keratitis that spread to 33 states carried “a high degree of morbidity,” with corneal transplantation required or planned for 55 of the 164 affected patients identified, reported Dr. Douglas C. Chang of the Centers for Disease Control and Prevention, Atlanta, and his associates.

The outbreak was linked to ReNu contact lens solution with MoistureLoc. The mechanism of infection remains uncertain, but researchers think that contamination of the contact lens solution occurred well after manufacturing and distribution, probably in the patients' homes.

“This outbreak may have been caused by a complex and as yet undetermined interaction between MoistureLoc, fusarium, and possibly the lens case or contact lens,” they said.

“Clinicians should be vigilant in diagnosing and treating fungal keratitis, and users of MoistureLoc should discontinue the use of this product,” the CDC investigators said (JAMA 2006;296:953–63).

In an editorial, Dr. Todd P. Margolis and Dr. John P. Whitcher of the University of California, San Francisco, said filamentous fungal keratitis is “notoriously difficult to treat,” and fusarium keratitis is “truly a therapeutic challenge.”

Many patients require adjuvant surgery ranging from recurrent corneal debridement to corneal transplantation, but the visual outcome is often dismal.”

Early treatment appears to improve the likelihood of resolving the infection. Clinicians should be alert for general signs and symptoms of keratitis, including redness, tearing, pain, light sensitivity, discharge, decreased vision, and a white corneal infiltrate, they noted (JAMA 2006;296:985–7).

Specific signs of fungal keratitis—such as a corneal stromal infiltrate with “feathery edges,” satellite lesions, a ring infiltrate, a posterior endothelial plaque, or a waxing and waning hypopyon—have been absent in some of the recent cases.

“A high index of suspicion and appropriate diagnostic studies, including cytological staining and microbiological cultures of material from the involved site” are key, they said.

Just as important is avoiding the use of topical ophthalmic corticosteroids before commencing antifungal therapy. Although corticosteroids are contraindicated in these cases, the drugs “are commonly prescribed by physicians for patients with complaints of acute red eyes, frequently by telephone and without a physical evaluation.”

Approximately one-fourth of cases assessed in earlier studies had been inappropriately treated with ophthalmic corticosteroids.

“Clinicians must immediately cease this potentially harmful practice,” the editorial writers emphasized.

Dr. Chang and his associates noted that Bausch & Lomb Inc., manufacturer of MoistureLoc contact lens solution, permanently withdrew the product from the market in May after reviewing preliminary CDC data on the outbreak, which began in June 2005 and peaked in April 2006.

The CDC began investigating the outbreak in March 2006, after a New Jersey ophthalmologist reported treating three patients who had contact-lens-associated fusarium keratitis during the preceding 2 months.

Fungal keratitis is rare, and fusarium keratitis comprises less than 5% of microbial infections in contact lens wearers. The filamental fungus is commonly found in soil, plants, and water sources in tropical or subtropical regions.

In 2004, 10 U.S. labs reported positive fusarium cultures from ocular specimens in only 12 cases.

As of June 30, the CDC had received 318 reports of fusarium keratitis in 2006. Of those, 164 cases had been confirmed and 32 had been categorized as possible. Most patients were adults, but 16 (10%) were children or adolescents.

Of the 164 confirmed cases, 37 infections (23%) had resolved with topical or systemic antifungal therapy, 65 (40%) had not yet resolved and are still being treated with antifungals, and 55 (34%) required or were awaiting corneal transplant because of active disease, residual scarring, or both.

In the month preceding infection, 69% of the keratitis patients reported using MoistureLoc contact lens solution, compared with 15% of control subjects.

At least 10 fusarium species were cultured from patient specimens and from samples from opened lens cases or bottles of solution, but no contamination was detected in unopened bottles of solution or in any of hundreds of samples taken at the manufacturing plant and distribution warehouse.

Researchers think that contamination of the contact lens solution occurred well after manufacturing and distribution, probably in the patients' homes. Yvonne Evans/Elsevier Global Medical News

The recent outbreak of fusarium keratitis that spread to 33 states carried “a high degree of morbidity,” with corneal transplantation required or planned for 55 of the 164 affected patients identified, reported Dr. Douglas C. Chang of the Centers for Disease Control and Prevention, Atlanta, and his associates.

The outbreak was linked to ReNu contact lens solution with MoistureLoc. The mechanism of infection remains uncertain, but researchers think that contamination of the contact lens solution occurred well after manufacturing and distribution, probably in the patients' homes.

“This outbreak may have been caused by a complex and as yet undetermined interaction between MoistureLoc, fusarium, and possibly the lens case or contact lens,” they said.

“Clinicians should be vigilant in diagnosing and treating fungal keratitis, and users of MoistureLoc should discontinue the use of this product,” the CDC investigators said (JAMA 2006;296:953–63).

In an editorial, Dr. Todd P. Margolis and Dr. John P. Whitcher of the University of California, San Francisco, said filamentous fungal keratitis is “notoriously difficult to treat,” and fusarium keratitis is “truly a therapeutic challenge.”

Many patients require adjuvant surgery ranging from recurrent corneal debridement to corneal transplantation, but the visual outcome is often dismal.”

Early treatment appears to improve the likelihood of resolving the infection. Clinicians should be alert for general signs and symptoms of keratitis, including redness, tearing, pain, light sensitivity, discharge, decreased vision, and a white corneal infiltrate, they noted (JAMA 2006;296:985–7).

Specific signs of fungal keratitis—such as a corneal stromal infiltrate with “feathery edges,” satellite lesions, a ring infiltrate, a posterior endothelial plaque, or a waxing and waning hypopyon—have been absent in some of the recent cases.

“A high index of suspicion and appropriate diagnostic studies, including cytological staining and microbiological cultures of material from the involved site” are key, they said.

Just as important is avoiding the use of topical ophthalmic corticosteroids before commencing antifungal therapy. Although corticosteroids are contraindicated in these cases, the drugs “are commonly prescribed by physicians for patients with complaints of acute red eyes, frequently by telephone and without a physical evaluation.”

Approximately one-fourth of cases assessed in earlier studies had been inappropriately treated with ophthalmic corticosteroids.

“Clinicians must immediately cease this potentially harmful practice,” the editorial writers emphasized.

Dr. Chang and his associates noted that Bausch & Lomb Inc., manufacturer of MoistureLoc contact lens solution, permanently withdrew the product from the market in May after reviewing preliminary CDC data on the outbreak, which began in June 2005 and peaked in April 2006.

The CDC began investigating the outbreak in March 2006, after a New Jersey ophthalmologist reported treating three patients who had contact-lens-associated fusarium keratitis during the preceding 2 months.

Fungal keratitis is rare, and fusarium keratitis comprises less than 5% of microbial infections in contact lens wearers. The filamental fungus is commonly found in soil, plants, and water sources in tropical or subtropical regions.

In 2004, 10 U.S. labs reported positive fusarium cultures from ocular specimens in only 12 cases.

As of June 30, the CDC had received 318 reports of fusarium keratitis in 2006. Of those, 164 cases had been confirmed and 32 had been categorized as possible. Most patients were adults, but 16 (10%) were children or adolescents.

Of the 164 confirmed cases, 37 infections (23%) had resolved with topical or systemic antifungal therapy, 65 (40%) had not yet resolved and are still being treated with antifungals, and 55 (34%) required or were awaiting corneal transplant because of active disease, residual scarring, or both.

In the month preceding infection, 69% of the keratitis patients reported using MoistureLoc contact lens solution, compared with 15% of control subjects.

At least 10 fusarium species were cultured from patient specimens and from samples from opened lens cases or bottles of solution, but no contamination was detected in unopened bottles of solution or in any of hundreds of samples taken at the manufacturing plant and distribution warehouse.

Researchers think that contamination of the contact lens solution occurred well after manufacturing and distribution, probably in the patients' homes. Yvonne Evans/Elsevier Global Medical News

Drinking cherry juice before and after exercise decreases some indicators of exercise-induced muscle damage, notably pain and loss of strength, reported Dr. Declan A.J. Connolly of the University of Vermont, Burlington, and his associates.

Tart cherries contain cyclooxygenase-inhibiting flavonoids and anthocyanins with high levels of antioxidant and anti-inflammatory activity. Moreover, “consumption of about 45 cherries a day has been shown to reduce circulating concentrations of inflammatory markers in healthy men and women,” the investigators noted.

They assessed the effects of drinking cherry juice on symptoms of muscle damage in 14 healthy men with an average age of 22 years.

The subjects drank specially formulated juice from frozen tart Montmorency cherries or a placebo drink for 8 days, then switched to the other drink for another 8 days. They drank one 12-ounce bottle in the morning and another in the evening. Each bottle of juice contained the equivalent of 50–60 cherries and provided at least 600 mg of phenolic compounds and 40 mg of anthocyanins.

After 4 days, the subjects intentionally overexercised one arm, performing a bout of elbow flexion contractions to induce later muscle soreness. The resulting loss of muscle strength was 22% with the placebo drink but only 4% with the cherry juice, the researchers said (Br. J. Sports Med. 2006;40:679–83).

The cherry drink also decreased muscle pain and shortened its duration. “Pain peaked at 24 hours in the cherry juice trial and subsequently declined, whereas pain continued to increase in the placebo trial to peak at 48 hours,” Dr. Connolly and his associates said.

“Although the results of this study indicate a protective effect of cherry juice, it is not possible to conclude that cherry juice supplementation prevented muscle damage because only two of four indirect markers of damage showed an effect.

However, there was clearly a preservation of muscle function attributable to cherry juice.

Strength was lost by 22% and 4% of theplacebo and juice groups, respectively. ELSEVIER GLOBAL MEDICAL NEWS

Drinking cherry juice before and after exercise decreases some indicators of exercise-induced muscle damage, notably pain and loss of strength, reported Dr. Declan A.J. Connolly of the University of Vermont, Burlington, and his associates.

Tart cherries contain cyclooxygenase-inhibiting flavonoids and anthocyanins with high levels of antioxidant and anti-inflammatory activity. Moreover, “consumption of about 45 cherries a day has been shown to reduce circulating concentrations of inflammatory markers in healthy men and women,” the investigators noted.

They assessed the effects of drinking cherry juice on symptoms of muscle damage in 14 healthy men with an average age of 22 years.

The subjects drank specially formulated juice from frozen tart Montmorency cherries or a placebo drink for 8 days, then switched to the other drink for another 8 days. They drank one 12-ounce bottle in the morning and another in the evening. Each bottle of juice contained the equivalent of 50–60 cherries and provided at least 600 mg of phenolic compounds and 40 mg of anthocyanins.

After 4 days, the subjects intentionally overexercised one arm, performing a bout of elbow flexion contractions to induce later muscle soreness. The resulting loss of muscle strength was 22% with the placebo drink but only 4% with the cherry juice, the researchers said (Br. J. Sports Med. 2006;40:679–83).

The cherry drink also decreased muscle pain and shortened its duration. “Pain peaked at 24 hours in the cherry juice trial and subsequently declined, whereas pain continued to increase in the placebo trial to peak at 48 hours,” Dr. Connolly and his associates said.

“Although the results of this study indicate a protective effect of cherry juice, it is not possible to conclude that cherry juice supplementation prevented muscle damage because only two of four indirect markers of damage showed an effect.

However, there was clearly a preservation of muscle function attributable to cherry juice.

Strength was lost by 22% and 4% of theplacebo and juice groups, respectively. ELSEVIER GLOBAL MEDICAL NEWS

Drinking cherry juice before and after exercise decreases some indicators of exercise-induced muscle damage, notably pain and loss of strength, reported Dr. Declan A.J. Connolly of the University of Vermont, Burlington, and his associates.

Tart cherries contain cyclooxygenase-inhibiting flavonoids and anthocyanins with high levels of antioxidant and anti-inflammatory activity. Moreover, “consumption of about 45 cherries a day has been shown to reduce circulating concentrations of inflammatory markers in healthy men and women,” the investigators noted.

They assessed the effects of drinking cherry juice on symptoms of muscle damage in 14 healthy men with an average age of 22 years.

The subjects drank specially formulated juice from frozen tart Montmorency cherries or a placebo drink for 8 days, then switched to the other drink for another 8 days. They drank one 12-ounce bottle in the morning and another in the evening. Each bottle of juice contained the equivalent of 50–60 cherries and provided at least 600 mg of phenolic compounds and 40 mg of anthocyanins.

After 4 days, the subjects intentionally overexercised one arm, performing a bout of elbow flexion contractions to induce later muscle soreness. The resulting loss of muscle strength was 22% with the placebo drink but only 4% with the cherry juice, the researchers said (Br. J. Sports Med. 2006;40:679–83).

The cherry drink also decreased muscle pain and shortened its duration. “Pain peaked at 24 hours in the cherry juice trial and subsequently declined, whereas pain continued to increase in the placebo trial to peak at 48 hours,” Dr. Connolly and his associates said.

“Although the results of this study indicate a protective effect of cherry juice, it is not possible to conclude that cherry juice supplementation prevented muscle damage because only two of four indirect markers of damage showed an effect.

However, there was clearly a preservation of muscle function attributable to cherry juice.

Strength was lost by 22% and 4% of theplacebo and juice groups, respectively. ELSEVIER GLOBAL MEDICAL NEWS

Just 2 months after the tsunami struck countries bordering the Indian Ocean almost 2 years ago, rates of depression, anxiety, and posttraumatic stress disorder were elevated among adult survivors in Thailand, according to the findings of two studies.

At 9 months after the December 2004 tragedy, those rates had declined but were still somewhat elevated in adults. In children, the rates of depression and PTSD were also elevated at 2 months and remained high at 9 months, according to the findings from two Thailand Post-Tsunami Mental Health Study Group studies.

The researchers surveyed a random sample of 371 adults and 371 children who lived in the three provinces most severely affected by the tsunami in an effort to identify vulnerable populations and to develop culturally appropriate mental health interventions

In the adult study, at 2 months after the storm, the rate of anxiety was 37%, the rate of depression, 30%, and the rate of PTSD, 12%, in those who had been displaced from their homes. For those who had not been displaced, the corresponding rates were lower at 30%, 27%, and 7%, respectively, reported Dr. Frits van Griensven of the Thailand Ministry of Public Health-U.S. Centers for Disease Control and Prevention Collaboration, Nontha- buri, Thailand, and his associates.

At the 9-month follow-up, the rates of anxiety, depression, and PTSD had declined significantly among displaced adults, at 25%, 17%, and 7%, respectively. For those who had not been displaced, less significant declines to 26%, 14%, and 2%, respectively, were observed (JAMA 2006;296:537–48).

The significant decrease over time in the prevalence of stress reactions, particularly among the displaced, may be attributable to “spontaneous recovery under improved social and environmental conditions,” the authors wrote. In the interval between the first assessment and the follow-up, numerous programs were established for mental health support, occupational training, restoration of livelihoods, and provision of more permanent housing.

The pediatric study focused on depression and PTSD. At 2 months after the storm, the rate of PTSD was 13% in children who had been displaced from their homes, and the rate of depression was 11%. For those who had not been displaced, the corresponding rates were 11% and 5%, for children who lived in affected villages, and 6% and 8% for children who lived in villages not directly affected by the tsunami (JAMA 2006;296:549–59).

At the 9-month follow-up, rates of PTSD and depression had not significantly declined in displaced children and remained high at 10% and 12%, respectively. Some of those symptoms may have been associated with the refugee camps themselves, not just with tsunami-specific trauma.

“Follow-up assessments must be conducted to assess the long-term mental health outcomes and the long-term need for mental health services” in this population, Warunee Thienkrua, also of the Thailand Ministry-CDC collaboration, and associates said.

Just 2 months after the tsunami struck countries bordering the Indian Ocean almost 2 years ago, rates of depression, anxiety, and posttraumatic stress disorder were elevated among adult survivors in Thailand, according to the findings of two studies.

At 9 months after the December 2004 tragedy, those rates had declined but were still somewhat elevated in adults. In children, the rates of depression and PTSD were also elevated at 2 months and remained high at 9 months, according to the findings from two Thailand Post-Tsunami Mental Health Study Group studies.

The researchers surveyed a random sample of 371 adults and 371 children who lived in the three provinces most severely affected by the tsunami in an effort to identify vulnerable populations and to develop culturally appropriate mental health interventions

In the adult study, at 2 months after the storm, the rate of anxiety was 37%, the rate of depression, 30%, and the rate of PTSD, 12%, in those who had been displaced from their homes. For those who had not been displaced, the corresponding rates were lower at 30%, 27%, and 7%, respectively, reported Dr. Frits van Griensven of the Thailand Ministry of Public Health-U.S. Centers for Disease Control and Prevention Collaboration, Nontha- buri, Thailand, and his associates.

At the 9-month follow-up, the rates of anxiety, depression, and PTSD had declined significantly among displaced adults, at 25%, 17%, and 7%, respectively. For those who had not been displaced, less significant declines to 26%, 14%, and 2%, respectively, were observed (JAMA 2006;296:537–48).

The significant decrease over time in the prevalence of stress reactions, particularly among the displaced, may be attributable to “spontaneous recovery under improved social and environmental conditions,” the authors wrote. In the interval between the first assessment and the follow-up, numerous programs were established for mental health support, occupational training, restoration of livelihoods, and provision of more permanent housing.

The pediatric study focused on depression and PTSD. At 2 months after the storm, the rate of PTSD was 13% in children who had been displaced from their homes, and the rate of depression was 11%. For those who had not been displaced, the corresponding rates were 11% and 5%, for children who lived in affected villages, and 6% and 8% for children who lived in villages not directly affected by the tsunami (JAMA 2006;296:549–59).

At the 9-month follow-up, rates of PTSD and depression had not significantly declined in displaced children and remained high at 10% and 12%, respectively. Some of those symptoms may have been associated with the refugee camps themselves, not just with tsunami-specific trauma.

“Follow-up assessments must be conducted to assess the long-term mental health outcomes and the long-term need for mental health services” in this population, Warunee Thienkrua, also of the Thailand Ministry-CDC collaboration, and associates said.

Just 2 months after the tsunami struck countries bordering the Indian Ocean almost 2 years ago, rates of depression, anxiety, and posttraumatic stress disorder were elevated among adult survivors in Thailand, according to the findings of two studies.

At 9 months after the December 2004 tragedy, those rates had declined but were still somewhat elevated in adults. In children, the rates of depression and PTSD were also elevated at 2 months and remained high at 9 months, according to the findings from two Thailand Post-Tsunami Mental Health Study Group studies.

The researchers surveyed a random sample of 371 adults and 371 children who lived in the three provinces most severely affected by the tsunami in an effort to identify vulnerable populations and to develop culturally appropriate mental health interventions

In the adult study, at 2 months after the storm, the rate of anxiety was 37%, the rate of depression, 30%, and the rate of PTSD, 12%, in those who had been displaced from their homes. For those who had not been displaced, the corresponding rates were lower at 30%, 27%, and 7%, respectively, reported Dr. Frits van Griensven of the Thailand Ministry of Public Health-U.S. Centers for Disease Control and Prevention Collaboration, Nontha- buri, Thailand, and his associates.

At the 9-month follow-up, the rates of anxiety, depression, and PTSD had declined significantly among displaced adults, at 25%, 17%, and 7%, respectively. For those who had not been displaced, less significant declines to 26%, 14%, and 2%, respectively, were observed (JAMA 2006;296:537–48).

The significant decrease over time in the prevalence of stress reactions, particularly among the displaced, may be attributable to “spontaneous recovery under improved social and environmental conditions,” the authors wrote. In the interval between the first assessment and the follow-up, numerous programs were established for mental health support, occupational training, restoration of livelihoods, and provision of more permanent housing.

The pediatric study focused on depression and PTSD. At 2 months after the storm, the rate of PTSD was 13% in children who had been displaced from their homes, and the rate of depression was 11%. For those who had not been displaced, the corresponding rates were 11% and 5%, for children who lived in affected villages, and 6% and 8% for children who lived in villages not directly affected by the tsunami (JAMA 2006;296:549–59).

At the 9-month follow-up, rates of PTSD and depression had not significantly declined in displaced children and remained high at 10% and 12%, respectively. Some of those symptoms may have been associated with the refugee camps themselves, not just with tsunami-specific trauma.

“Follow-up assessments must be conducted to assess the long-term mental health outcomes and the long-term need for mental health services” in this population, Warunee Thienkrua, also of the Thailand Ministry-CDC collaboration, and associates said.

Frequent drinking of fruit and vegetable juices substantially decreases the risk of Alzheimer's disease, reported Dr. Qi Dai of Vanderbilt University, Nashville, Tenn., and associates.

Results of several studies have suggested that the antioxidants and polyphenols in dietary fruits and vegetables may reduce the risk of Alzheimer's disease (AD) or delay its onset. Dr. Dai and associates hypothesized that intake of fruit and vegetable juices also might be protective. They tested their hypothesis using data from 1,836 subjects involved in the Kame Project, a large, population-based prospective study of Japanese Americans living in King County, Wash.

The subjects, aged 65 years or older at baseline (mean age 72 years), completed food frequency questionnaires and underwent periodic cognitive assessments. Over a mean of 6 years of follow-up, 81 incident cases of AD were diagnosed.

The risk of developing AD declined with increasing consumption of fruit and vegetable juices. Subjects who drank juice three times a week or more had a hazard ratio of 0.24, compared with those who drank juice less often than once a week. This protective effect was seen in subjects with all different levels of education, physical activity, and fat intake (Am. J. Med. 2006;119:751–9).

As in previous studies, the antioxidant vitamins in dietary fruits and vegetables were found to be protective, but those in vitamin supplements were not.

Although tea was the beverage most often consumed, and tea is a rich source of some polyphenols, there was no relation between tea drinking and AD risk in this study. This finding agrees with those of two previous studies of tea drinking and AD. Wine is another potent source of antioxidants, and there was a small but statistically insignificant inverse association between wine or sake drinking and AD. The lack of statistical significance may be due to the small number of subjects (6%) who drank these beverages at least once per week, the researchers noted.

The protective effect of fruit and vegetable juices is being attributed to their antioxidant properties, but it is also possible that other characteristics such as anti-inflammatory properties are at work. Moreover, in addition to possessing antioxidant vitamins and polyphenols, juices may contain other components such as folate and minerals, which contribute to the protective effect, they added.

Frequent drinking of fruit and vegetable juices substantially decreases the risk of Alzheimer's disease, reported Dr. Qi Dai of Vanderbilt University, Nashville, Tenn., and associates.

Results of several studies have suggested that the antioxidants and polyphenols in dietary fruits and vegetables may reduce the risk of Alzheimer's disease (AD) or delay its onset. Dr. Dai and associates hypothesized that intake of fruit and vegetable juices also might be protective. They tested their hypothesis using data from 1,836 subjects involved in the Kame Project, a large, population-based prospective study of Japanese Americans living in King County, Wash.

The subjects, aged 65 years or older at baseline (mean age 72 years), completed food frequency questionnaires and underwent periodic cognitive assessments. Over a mean of 6 years of follow-up, 81 incident cases of AD were diagnosed.

The risk of developing AD declined with increasing consumption of fruit and vegetable juices. Subjects who drank juice three times a week or more had a hazard ratio of 0.24, compared with those who drank juice less often than once a week. This protective effect was seen in subjects with all different levels of education, physical activity, and fat intake (Am. J. Med. 2006;119:751–9).

As in previous studies, the antioxidant vitamins in dietary fruits and vegetables were found to be protective, but those in vitamin supplements were not.

Although tea was the beverage most often consumed, and tea is a rich source of some polyphenols, there was no relation between tea drinking and AD risk in this study. This finding agrees with those of two previous studies of tea drinking and AD. Wine is another potent source of antioxidants, and there was a small but statistically insignificant inverse association between wine or sake drinking and AD. The lack of statistical significance may be due to the small number of subjects (6%) who drank these beverages at least once per week, the researchers noted.

The protective effect of fruit and vegetable juices is being attributed to their antioxidant properties, but it is also possible that other characteristics such as anti-inflammatory properties are at work. Moreover, in addition to possessing antioxidant vitamins and polyphenols, juices may contain other components such as folate and minerals, which contribute to the protective effect, they added.

Frequent drinking of fruit and vegetable juices substantially decreases the risk of Alzheimer's disease, reported Dr. Qi Dai of Vanderbilt University, Nashville, Tenn., and associates.

Results of several studies have suggested that the antioxidants and polyphenols in dietary fruits and vegetables may reduce the risk of Alzheimer's disease (AD) or delay its onset. Dr. Dai and associates hypothesized that intake of fruit and vegetable juices also might be protective. They tested their hypothesis using data from 1,836 subjects involved in the Kame Project, a large, population-based prospective study of Japanese Americans living in King County, Wash.

The subjects, aged 65 years or older at baseline (mean age 72 years), completed food frequency questionnaires and underwent periodic cognitive assessments. Over a mean of 6 years of follow-up, 81 incident cases of AD were diagnosed.

The risk of developing AD declined with increasing consumption of fruit and vegetable juices. Subjects who drank juice three times a week or more had a hazard ratio of 0.24, compared with those who drank juice less often than once a week. This protective effect was seen in subjects with all different levels of education, physical activity, and fat intake (Am. J. Med. 2006;119:751–9).

As in previous studies, the antioxidant vitamins in dietary fruits and vegetables were found to be protective, but those in vitamin supplements were not.

Although tea was the beverage most often consumed, and tea is a rich source of some polyphenols, there was no relation between tea drinking and AD risk in this study. This finding agrees with those of two previous studies of tea drinking and AD. Wine is another potent source of antioxidants, and there was a small but statistically insignificant inverse association between wine or sake drinking and AD. The lack of statistical significance may be due to the small number of subjects (6%) who drank these beverages at least once per week, the researchers noted.

The protective effect of fruit and vegetable juices is being attributed to their antioxidant properties, but it is also possible that other characteristics such as anti-inflammatory properties are at work. Moreover, in addition to possessing antioxidant vitamins and polyphenols, juices may contain other components such as folate and minerals, which contribute to the protective effect, they added.

Older men are at higher risk of fathering autistic children than are younger men, results of a large cohort study suggest.

After a man reaches his 20s, the risk of fathering an autistic boy or girl more than doubles with every 10-year increase in his age. This increase is independent of other factors such as the mother's age and the family's socioeconomic status, reported Abraham Reichenberg, Ph.D., of Mount Sinai School of Medicine, New York, and his associates.

Older paternal age at the birth of offspring is associated with several congenital disorders, and it also has been linked to schizophrenia and to decreased intellectual capacity. Previous studies examining a possible link between paternal age and autism risk have produced mixed results, but “few have systematically examined this association in rigorous designs that included adjustment for maternal age,” Dr. Reichenberg and his associates said (Arch. Gen. Psychiatry 2006;63:1026–32).

They conducted a very large population-based cohort study “specifically designed for a rigorous test of the hypothesis that advancing paternal age is associated with increased risk of ASD [autism spectrum disorder] in offspring.”

The investigators used data collected on a cohort of 378,891 Israelis born during a consecutive 6-year period in the 1980s and evaluated at age 17 by the Israeli draft board, which determines intellectual, medical, and psychiatric eligibility for the country's compulsory military service. The birth dates of both mothers and fathers were available in 132,271 members of the cohort.

The draft board also reviews detailed medical records on all Israelis with developmental disabilities, including the virtually 100% of children and adolescents diagnosed with ASDs who receive universal health care and other services through government agencies.

The overall prevalence of autism spectrum disorders in this cohort was 8.4 cases per 10,000 persons.

The risk of ASDs increased significantly with advancing paternal age and was “especially strong” in offspring of the oldest men. Compared with fathers in their late teens or twenties, the risk of fathering an autistic child was 1.6 times higher among men in their 30s, 5.7 times higher among men in their 40s, and 9.4 times higher among men aged 50 and older, Dr. Reichenberg and his associates said.

The increase in risk persisted after the data were adjusted to account for maternal age, socioeconomic status, and other potentially confounding factors. Risk was increased for both male and female offspring.

Although all ASDs were included in this study, almost all the subjects in this cohort had autism itself. The study findings therefore may not necessarily be generalizable to the other disorders in the spectrum, such as Asperger's syndrome and Rett syndrome. “The relationship of paternal age to these disorders should be specifically examined in more contemporary cohorts,” the researchers noted.

One possible mechanism for this effect of paternal age is mutagenesis. Spontaneous mutations–either point mutations or structural chromosomal anomalies–might arise and accumulate in successive generations of sperm-producing cells.

Another possible mechanism is imprinting, a form of gene regulation in which the gene of only one parental allele is expressed and the other one is silenced. It is possible that for paternally imprinted genes, biological processes may be impaired as the father ages. Imprinted genes are known to play a key role in brain development, they added.

“These hypothesized mechanisms for paternal age effects on risk of ASD are genetic. It is important to keep in mind, however, that age at paternity is influenced by the sociocultural environment and varies across societies and over time.

“In a given population, a change in the sociocultural environment could produce a change in paternal age at birth. In theory, it could thereby lead to a change in the incidence of genetic causes autism,” Dr. Reichenberg and his associates said.

One study limitation was that no information was available on possible autistic traits in the subjects' parents. It's possible that if fathers had some traits related to the autism phenotype, especially social deficits, these may have contributed to their older age at marriage and fatherhood.

Older men are at higher risk of fathering autistic children than are younger men, results of a large cohort study suggest.

After a man reaches his 20s, the risk of fathering an autistic boy or girl more than doubles with every 10-year increase in his age. This increase is independent of other factors such as the mother's age and the family's socioeconomic status, reported Abraham Reichenberg, Ph.D., of Mount Sinai School of Medicine, New York, and his associates.

Older paternal age at the birth of offspring is associated with several congenital disorders, and it also has been linked to schizophrenia and to decreased intellectual capacity. Previous studies examining a possible link between paternal age and autism risk have produced mixed results, but “few have systematically examined this association in rigorous designs that included adjustment for maternal age,” Dr. Reichenberg and his associates said (Arch. Gen. Psychiatry 2006;63:1026–32).

They conducted a very large population-based cohort study “specifically designed for a rigorous test of the hypothesis that advancing paternal age is associated with increased risk of ASD [autism spectrum disorder] in offspring.”

The investigators used data collected on a cohort of 378,891 Israelis born during a consecutive 6-year period in the 1980s and evaluated at age 17 by the Israeli draft board, which determines intellectual, medical, and psychiatric eligibility for the country's compulsory military service. The birth dates of both mothers and fathers were available in 132,271 members of the cohort.

The draft board also reviews detailed medical records on all Israelis with developmental disabilities, including the virtually 100% of children and adolescents diagnosed with ASDs who receive universal health care and other services through government agencies.

The overall prevalence of autism spectrum disorders in this cohort was 8.4 cases per 10,000 persons.

The risk of ASDs increased significantly with advancing paternal age and was “especially strong” in offspring of the oldest men. Compared with fathers in their late teens or twenties, the risk of fathering an autistic child was 1.6 times higher among men in their 30s, 5.7 times higher among men in their 40s, and 9.4 times higher among men aged 50 and older, Dr. Reichenberg and his associates said.

The increase in risk persisted after the data were adjusted to account for maternal age, socioeconomic status, and other potentially confounding factors. Risk was increased for both male and female offspring.

Although all ASDs were included in this study, almost all the subjects in this cohort had autism itself. The study findings therefore may not necessarily be generalizable to the other disorders in the spectrum, such as Asperger's syndrome and Rett syndrome. “The relationship of paternal age to these disorders should be specifically examined in more contemporary cohorts,” the researchers noted.

One possible mechanism for this effect of paternal age is mutagenesis. Spontaneous mutations–either point mutations or structural chromosomal anomalies–might arise and accumulate in successive generations of sperm-producing cells.

Another possible mechanism is imprinting, a form of gene regulation in which the gene of only one parental allele is expressed and the other one is silenced. It is possible that for paternally imprinted genes, biological processes may be impaired as the father ages. Imprinted genes are known to play a key role in brain development, they added.

“These hypothesized mechanisms for paternal age effects on risk of ASD are genetic. It is important to keep in mind, however, that age at paternity is influenced by the sociocultural environment and varies across societies and over time.

“In a given population, a change in the sociocultural environment could produce a change in paternal age at birth. In theory, it could thereby lead to a change in the incidence of genetic causes autism,” Dr. Reichenberg and his associates said.

One study limitation was that no information was available on possible autistic traits in the subjects' parents. It's possible that if fathers had some traits related to the autism phenotype, especially social deficits, these may have contributed to their older age at marriage and fatherhood.

Older men are at higher risk of fathering autistic children than are younger men, results of a large cohort study suggest.

After a man reaches his 20s, the risk of fathering an autistic boy or girl more than doubles with every 10-year increase in his age. This increase is independent of other factors such as the mother's age and the family's socioeconomic status, reported Abraham Reichenberg, Ph.D., of Mount Sinai School of Medicine, New York, and his associates.

Older paternal age at the birth of offspring is associated with several congenital disorders, and it also has been linked to schizophrenia and to decreased intellectual capacity. Previous studies examining a possible link between paternal age and autism risk have produced mixed results, but “few have systematically examined this association in rigorous designs that included adjustment for maternal age,” Dr. Reichenberg and his associates said (Arch. Gen. Psychiatry 2006;63:1026–32).

They conducted a very large population-based cohort study “specifically designed for a rigorous test of the hypothesis that advancing paternal age is associated with increased risk of ASD [autism spectrum disorder] in offspring.”

The investigators used data collected on a cohort of 378,891 Israelis born during a consecutive 6-year period in the 1980s and evaluated at age 17 by the Israeli draft board, which determines intellectual, medical, and psychiatric eligibility for the country's compulsory military service. The birth dates of both mothers and fathers were available in 132,271 members of the cohort.

The draft board also reviews detailed medical records on all Israelis with developmental disabilities, including the virtually 100% of children and adolescents diagnosed with ASDs who receive universal health care and other services through government agencies.

The overall prevalence of autism spectrum disorders in this cohort was 8.4 cases per 10,000 persons.

The risk of ASDs increased significantly with advancing paternal age and was “especially strong” in offspring of the oldest men. Compared with fathers in their late teens or twenties, the risk of fathering an autistic child was 1.6 times higher among men in their 30s, 5.7 times higher among men in their 40s, and 9.4 times higher among men aged 50 and older, Dr. Reichenberg and his associates said.

The increase in risk persisted after the data were adjusted to account for maternal age, socioeconomic status, and other potentially confounding factors. Risk was increased for both male and female offspring.

Although all ASDs were included in this study, almost all the subjects in this cohort had autism itself. The study findings therefore may not necessarily be generalizable to the other disorders in the spectrum, such as Asperger's syndrome and Rett syndrome. “The relationship of paternal age to these disorders should be specifically examined in more contemporary cohorts,” the researchers noted.

One possible mechanism for this effect of paternal age is mutagenesis. Spontaneous mutations–either point mutations or structural chromosomal anomalies–might arise and accumulate in successive generations of sperm-producing cells.

Another possible mechanism is imprinting, a form of gene regulation in which the gene of only one parental allele is expressed and the other one is silenced. It is possible that for paternally imprinted genes, biological processes may be impaired as the father ages. Imprinted genes are known to play a key role in brain development, they added.

“These hypothesized mechanisms for paternal age effects on risk of ASD are genetic. It is important to keep in mind, however, that age at paternity is influenced by the sociocultural environment and varies across societies and over time.

“In a given population, a change in the sociocultural environment could produce a change in paternal age at birth. In theory, it could thereby lead to a change in the incidence of genetic causes autism,” Dr. Reichenberg and his associates said.

One study limitation was that no information was available on possible autistic traits in the subjects' parents. It's possible that if fathers had some traits related to the autism phenotype, especially social deficits, these may have contributed to their older age at marriage and fatherhood.

Four of five different models for profiling gene expression in breast cancers produced concordant results, showing significant agreement in predicting disease outcome even though they tested for evidence of different genes.

Researchers used samples from breast cancers excised from 295 women to compare the results of five different gene-expression profiling studies. The studies assess whether given genes are expressed in the tumors, which enables clinicians to more accurately estimate the tumor's aggressiveness, wrote Dr. Cheng Fan of the University of North Carolina, Chapel Hill, and associates (N. Engl. J. Med. 2006 355:560–9).

The first model uses gene-expression profiles to identify the cancer's subtype, differentiating between tumors that originate from luminal cells or basal cells and determining if the tumor is human epidermal growth factor receptor (HER)-2 positive.

The second model identifies the levels of expression of 70 genes thought to regulate the cell cycle, invasion, metastasis, and angiogenesis. The third model calculates the likelihood of cancer recurrence in estrogen receptor (ER)-positive, node-negative tumors by assessing their expression of 21 genes. The fourth model assesses the expression of wound-response genes, which identifies tumors that are more likely to metastasize because they have activated pathways for matrix remodeling, cell motility, and angiogenesis.

All four of these models were significant predictors of relapse-free survival and overall survival.

The fifth model uses a ratio of the levels of expression of two genes: one encodes homeobox 13; the other encodes the interleukin-17B receptor. This model was not predictive of survival.

Four of five different models for profiling gene expression in breast cancers produced concordant results, showing significant agreement in predicting disease outcome even though they tested for evidence of different genes.

Researchers used samples from breast cancers excised from 295 women to compare the results of five different gene-expression profiling studies. The studies assess whether given genes are expressed in the tumors, which enables clinicians to more accurately estimate the tumor's aggressiveness, wrote Dr. Cheng Fan of the University of North Carolina, Chapel Hill, and associates (N. Engl. J. Med. 2006 355:560–9).

The first model uses gene-expression profiles to identify the cancer's subtype, differentiating between tumors that originate from luminal cells or basal cells and determining if the tumor is human epidermal growth factor receptor (HER)-2 positive.

The second model identifies the levels of expression of 70 genes thought to regulate the cell cycle, invasion, metastasis, and angiogenesis. The third model calculates the likelihood of cancer recurrence in estrogen receptor (ER)-positive, node-negative tumors by assessing their expression of 21 genes. The fourth model assesses the expression of wound-response genes, which identifies tumors that are more likely to metastasize because they have activated pathways for matrix remodeling, cell motility, and angiogenesis.

All four of these models were significant predictors of relapse-free survival and overall survival.

The fifth model uses a ratio of the levels of expression of two genes: one encodes homeobox 13; the other encodes the interleukin-17B receptor. This model was not predictive of survival.

Four of five different models for profiling gene expression in breast cancers produced concordant results, showing significant agreement in predicting disease outcome even though they tested for evidence of different genes.

Researchers used samples from breast cancers excised from 295 women to compare the results of five different gene-expression profiling studies. The studies assess whether given genes are expressed in the tumors, which enables clinicians to more accurately estimate the tumor's aggressiveness, wrote Dr. Cheng Fan of the University of North Carolina, Chapel Hill, and associates (N. Engl. J. Med. 2006 355:560–9).

The first model uses gene-expression profiles to identify the cancer's subtype, differentiating between tumors that originate from luminal cells or basal cells and determining if the tumor is human epidermal growth factor receptor (HER)-2 positive.

The second model identifies the levels of expression of 70 genes thought to regulate the cell cycle, invasion, metastasis, and angiogenesis. The third model calculates the likelihood of cancer recurrence in estrogen receptor (ER)-positive, node-negative tumors by assessing their expression of 21 genes. The fourth model assesses the expression of wound-response genes, which identifies tumors that are more likely to metastasize because they have activated pathways for matrix remodeling, cell motility, and angiogenesis.

All four of these models were significant predictors of relapse-free survival and overall survival.

The fifth model uses a ratio of the levels of expression of two genes: one encodes homeobox 13; the other encodes the interleukin-17B receptor. This model was not predictive of survival.

The recent outbreak of fusarium keratitis that spread to 33 states carried “a high degree of morbidity,” with corneal transplantation required or planned for 55 of the 164 affected patients identified, reported Dr. Douglas C. Chang of the Centers for Disease Control and Prevention, Atlanta, and his associates.

The outbreak was linked to ReNu contact lens solution with MoistureLoc. The mechanism of infection remains uncertain, but researchers think that contamination of the contact lens solution occurred well after manufacturing and distribution, probably in the patients' homes.

“This outbreak may have been caused by a complex and as yet undetermined interaction between MoistureLoc, fusarium, and possibly the lens case or contact lens,” they said.

“Clinicians should be vigilant in diagnosing and treating fungal keratitis, and users of MoistureLoc should discontinue the use of this product,” the CDC investigators said (JAMA 2006;296:953–63).

In an editorial, Dr. Todd P. Margolis and Dr. John P. Whitcher of the University of California, San Francisco, said filamentous fungal keratitis is “notoriously difficult to treat,” and fusarium keratitis is “truly a therapeutic challenge. Many patients require adjuvant surgery ranging from recurrent corneal debridement to corneal transplantation, but the visual outcome is often dismal.”

Early treatment appears to improve the likelihood of resolving the infection. Clinicians should be alert for general signs and symptoms of keratitis, including redness, tearing, pain, light sensitivity, discharge, decreased vision, and a white corneal infiltrate, they noted (JAMA 2006;296:985–7).

Specific signs of fungal keratitis—such as a corneal stromal infiltrate with “feathery edges,” satellite lesions, a ring infiltrate, a posterior endothelial plaque, or a waxing and waning hypopyon—have been absent in some of the recent cases. “A high index of suspicion and appropriate diagnostic studies, including cytological staining and microbiological cultures of material from the involved site” are key, they said.

Just as important is avoiding the use of topical ophthalmic corticosteroids before commencing antifungal therapy.

Dr. Chang and his associates noted that Bausch & Lomb Inc., manufacturer of MoistureLoc contact lens solution, permanently withdrew the product from the market in May after reviewing preliminary CDC data on the outbreak, which began in June 2005 and peaked in April 2006. The CDC began investigating the outbreak in March 2006, after a New Jersey ophthalmologist reported treating three patients who had contact-lens-associated fusarium keratitis during the preceding 2 months.

Fungal keratitis is rare, and fusarium keratitis comprises less than 5% of microbial infections in contact lens wearers. The filamental fungus is commonly found in soil, plants, and water sources in tropical or subtropical regions. In 2004, 10 U.S. labs reported positive fusarium cultures from ocular specimens in only 12 cases.

As of June 30, the CDC had received 318 reports of fusarium keratitis in 2006. Of those, 164 cases had been confirmed and 32 had been categorized as possible. Most patients were adults, but 16 (10%) were children or adolescents. Of the 164 confirmed cases, 37 infections (23%) had resolved with topical or systemic antifungal therapy, 65 (40%) had not yet resolved and are still being treated with antifungals, and 55 (34%) required or were awaiting corneal transplant because of active disease, residual scarring, or both.

In the month preceding infection, 69% of the keratitis patients reported using MoistureLoc contact lens solution, compared with 15% of control subjects. At least 10 fusarium species were cultured from patient specimens and from samples from opened lens cases or bottles of solution, but no contamination was detected in unopened bottles of solution or in any of hundreds of samples taken at the manufacturing plant and distribution warehouse.

The recent outbreak of fusarium keratitis that spread to 33 states carried “a high degree of morbidity,” with corneal transplantation required or planned for 55 of the 164 affected patients identified, reported Dr. Douglas C. Chang of the Centers for Disease Control and Prevention, Atlanta, and his associates.

The outbreak was linked to ReNu contact lens solution with MoistureLoc. The mechanism of infection remains uncertain, but researchers think that contamination of the contact lens solution occurred well after manufacturing and distribution, probably in the patients' homes.

“This outbreak may have been caused by a complex and as yet undetermined interaction between MoistureLoc, fusarium, and possibly the lens case or contact lens,” they said.

“Clinicians should be vigilant in diagnosing and treating fungal keratitis, and users of MoistureLoc should discontinue the use of this product,” the CDC investigators said (JAMA 2006;296:953–63).

In an editorial, Dr. Todd P. Margolis and Dr. John P. Whitcher of the University of California, San Francisco, said filamentous fungal keratitis is “notoriously difficult to treat,” and fusarium keratitis is “truly a therapeutic challenge. Many patients require adjuvant surgery ranging from recurrent corneal debridement to corneal transplantation, but the visual outcome is often dismal.”

Early treatment appears to improve the likelihood of resolving the infection. Clinicians should be alert for general signs and symptoms of keratitis, including redness, tearing, pain, light sensitivity, discharge, decreased vision, and a white corneal infiltrate, they noted (JAMA 2006;296:985–7).

Specific signs of fungal keratitis—such as a corneal stromal infiltrate with “feathery edges,” satellite lesions, a ring infiltrate, a posterior endothelial plaque, or a waxing and waning hypopyon—have been absent in some of the recent cases. “A high index of suspicion and appropriate diagnostic studies, including cytological staining and microbiological cultures of material from the involved site” are key, they said.

Just as important is avoiding the use of topical ophthalmic corticosteroids before commencing antifungal therapy.

Dr. Chang and his associates noted that Bausch & Lomb Inc., manufacturer of MoistureLoc contact lens solution, permanently withdrew the product from the market in May after reviewing preliminary CDC data on the outbreak, which began in June 2005 and peaked in April 2006. The CDC began investigating the outbreak in March 2006, after a New Jersey ophthalmologist reported treating three patients who had contact-lens-associated fusarium keratitis during the preceding 2 months.

Fungal keratitis is rare, and fusarium keratitis comprises less than 5% of microbial infections in contact lens wearers. The filamental fungus is commonly found in soil, plants, and water sources in tropical or subtropical regions. In 2004, 10 U.S. labs reported positive fusarium cultures from ocular specimens in only 12 cases.

As of June 30, the CDC had received 318 reports of fusarium keratitis in 2006. Of those, 164 cases had been confirmed and 32 had been categorized as possible. Most patients were adults, but 16 (10%) were children or adolescents. Of the 164 confirmed cases, 37 infections (23%) had resolved with topical or systemic antifungal therapy, 65 (40%) had not yet resolved and are still being treated with antifungals, and 55 (34%) required or were awaiting corneal transplant because of active disease, residual scarring, or both.

In the month preceding infection, 69% of the keratitis patients reported using MoistureLoc contact lens solution, compared with 15% of control subjects. At least 10 fusarium species were cultured from patient specimens and from samples from opened lens cases or bottles of solution, but no contamination was detected in unopened bottles of solution or in any of hundreds of samples taken at the manufacturing plant and distribution warehouse.

The recent outbreak of fusarium keratitis that spread to 33 states carried “a high degree of morbidity,” with corneal transplantation required or planned for 55 of the 164 affected patients identified, reported Dr. Douglas C. Chang of the Centers for Disease Control and Prevention, Atlanta, and his associates.

The outbreak was linked to ReNu contact lens solution with MoistureLoc. The mechanism of infection remains uncertain, but researchers think that contamination of the contact lens solution occurred well after manufacturing and distribution, probably in the patients' homes.

“This outbreak may have been caused by a complex and as yet undetermined interaction between MoistureLoc, fusarium, and possibly the lens case or contact lens,” they said.

“Clinicians should be vigilant in diagnosing and treating fungal keratitis, and users of MoistureLoc should discontinue the use of this product,” the CDC investigators said (JAMA 2006;296:953–63).

In an editorial, Dr. Todd P. Margolis and Dr. John P. Whitcher of the University of California, San Francisco, said filamentous fungal keratitis is “notoriously difficult to treat,” and fusarium keratitis is “truly a therapeutic challenge. Many patients require adjuvant surgery ranging from recurrent corneal debridement to corneal transplantation, but the visual outcome is often dismal.”

Early treatment appears to improve the likelihood of resolving the infection. Clinicians should be alert for general signs and symptoms of keratitis, including redness, tearing, pain, light sensitivity, discharge, decreased vision, and a white corneal infiltrate, they noted (JAMA 2006;296:985–7).

Specific signs of fungal keratitis—such as a corneal stromal infiltrate with “feathery edges,” satellite lesions, a ring infiltrate, a posterior endothelial plaque, or a waxing and waning hypopyon—have been absent in some of the recent cases. “A high index of suspicion and appropriate diagnostic studies, including cytological staining and microbiological cultures of material from the involved site” are key, they said.

Just as important is avoiding the use of topical ophthalmic corticosteroids before commencing antifungal therapy.

Dr. Chang and his associates noted that Bausch & Lomb Inc., manufacturer of MoistureLoc contact lens solution, permanently withdrew the product from the market in May after reviewing preliminary CDC data on the outbreak, which began in June 2005 and peaked in April 2006. The CDC began investigating the outbreak in March 2006, after a New Jersey ophthalmologist reported treating three patients who had contact-lens-associated fusarium keratitis during the preceding 2 months.

Fungal keratitis is rare, and fusarium keratitis comprises less than 5% of microbial infections in contact lens wearers. The filamental fungus is commonly found in soil, plants, and water sources in tropical or subtropical regions. In 2004, 10 U.S. labs reported positive fusarium cultures from ocular specimens in only 12 cases.

As of June 30, the CDC had received 318 reports of fusarium keratitis in 2006. Of those, 164 cases had been confirmed and 32 had been categorized as possible. Most patients were adults, but 16 (10%) were children or adolescents. Of the 164 confirmed cases, 37 infections (23%) had resolved with topical or systemic antifungal therapy, 65 (40%) had not yet resolved and are still being treated with antifungals, and 55 (34%) required or were awaiting corneal transplant because of active disease, residual scarring, or both.

In the month preceding infection, 69% of the keratitis patients reported using MoistureLoc contact lens solution, compared with 15% of control subjects. At least 10 fusarium species were cultured from patient specimens and from samples from opened lens cases or bottles of solution, but no contamination was detected in unopened bottles of solution or in any of hundreds of samples taken at the manufacturing plant and distribution warehouse.