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Biomedical subjects

E M Kilbourne

Publications and source records attributed to E M Kilbourne.

15 recordsLinked to original sources
PubMed1992

Eosinophilia-myalgia syndrome in L-tryptophan-exposed patients.

OBJECTIVES: To study the incidence of eosinophilia-myalgia syndrome, the risk factors associated with the syndrome, and the clinical spectrum of illness associated with L-tryptophan use in an exposed population. DESIGN: Retrospective cohort and nested case-control studies of risk factors for eosinophilia-myalgia syndrome using inpatient and outpatient chart reviews, telephone interviews, and in-person patient interviews. Descriptive study of clinical course of L-tryptophan users. SETTING: Office practice of one psychiatrist based in a small city (population 43,467) in South Carolina. PATIENTS: Eligible subjects were all patients from the practice who used L-tryptophan during the 1989 study interval. Of these, 418 (87%) were interviewed. MAIN OUTCOME MEASURES: Clinical spectrum of illness associated with L-tryptophan use, including definite and possible cases of eosinophilia-myalgia syndrome. RESULTS: Among the 418 interviewed L-tryptophan users, we identified 47 definite cases (11%) and 68 possible cases (16%) of eosinophilia-myalgia syndrome, most of which involved patients who were using one retail brand of L-tryptophan (brand A). Among the 157 brand A users, we identified 45 definite cases (29%) and 36 possible cases (23%) of eosinophilia-myalgia syndrome, and the risk for the syndrome increased as the brand A dose increased. Fifty percent (19 of 38) of those using more than 4000 mg/day developed definite eosinophilia-myalgia syndrome, and 84% (32 of 38) developed either definite or possible eosinophilia-myalgia syndrome. On multivariate analysis, risk for definite eosinophilia-myalgia syndrome was associated with brand A dose and age of the patient; however, gender, race, and use of other medications were not associated with the syndrome. CONCLUSIONS: These results suggest that many people exposed to the agent causing eosinophilia-myalgia syndrome may develop illness, and dose of presumably contaminated L-tryptophan is the single most important predictor of eosinophilia-myalgia syndrome. The broad range of signs and symptoms reported by patients using L-tryptophan illustrates that a strict case definition may identify only about half of those affected.

Adult↗
PubMed1992

Eosinophilia-myalgia syndrome: coming to grips with a new illness.

In late October 1989, over 1,500 cases of an unusual illness involving severe myalgia and striking peripheral eosinophilia were reported in the United States and several other countries. Other clinical manifestations included pulmonary involvement (interstitial infiltrates and pleural effusions), skin rash and edema, axonal polyneuropathy, perimyositis, and possible adverse neurocognitive effects. Because of the primary manifestations of the illness, it was named "eosinophilia-myalgia syndrome" (EMS) by the Centers for Disease Control. Epidemiologic studies clearly linked illness to the ingestion of tryptophan produced by a single manufacturer in Japan, and the time course of the epidemic was most consistent with its being caused by a product contaminant. Epidemiologic analysis of plant operating conditions and data obtained from chemical analyses of case- and control-associated lots implicated 1,1'-ethylidene-bis(tryptophan) (EBT) as a candidate for the compound that causes EMS. However, the etiologic significance of EBT is still uncertain. Factors found to increase a person's risk for EMS included higher tryptophan dose and older age. Although cases occurred predominantly in women and patients had frequently been taking other medications concurrently with tryptophan, sex and use of several categories of other medications were not shown to influence the risk of illness. Few patients recovered rapidly and fully from the disease. Many were treated with glucocorticoid medications, and although they may have benefited from therapy in the short term, the development of chronic sequelae of EMS appears not to have been prevented. Public health practitioners currently depend on the reports of alert clinicians to detect this type of outbreak. In this case, state and federal government epidemiologists, once they were notified, were able to develop substantial basic information about the epidemic in a relatively short time. Control measures were introduced rapidly, effectively stopping the epidemic.

Age Factors↗
PubMed1991

Postmortem studies of the heart in three fatal cases of the eosinophilia-myalgia syndrome.

OBJECTIVE: To examine the hearts of individuals who died from the eosinophilia-myalgia syndrome associated with ingestion of L-tryptophan, with particular attention paid to the coronary arteries, the neural structures, and the conduction system of the heart because of reported terminal disturbances of cardiac rhythm and conduction. STUDY MATERIAL: Three hearts fixed in neutral formalin and well preserved with all the relevant areas of conduction system intact. METHODS: Light microscopic examination of subserial sections of the sinus node, atrioventricular node and His bundle, coronary chemoreceptor and regional nerves, ganglia, and small coronary arteries. Routine stains used were Goldner trichrome and Verhoeff-van Gieson. RESULTS: Arterial abnormalities were numerous and primarily of two types: focal fibromuscular dysplasia causing moderate to severe narrowing, as well as endarteritis and panarteritis. Extensive examples of neuritis and ganglionitis were present throughout the heart, including the conduction system, where arterial abnormalities were also abundant. In the coronary chemoreceptor there were both old and new lesions comprising focal inflammation with degeneration as well as older areas of fibrotic destruction. Within the sinus node, areas of dense fibrosis replaced all nodal tissue. These abnormalities were similar in nature and extent in all three hearts. CONCLUSIONS: The pathologic lesions present in the coronary arteries, neural structures, and conduction system of the heart in patients who died from the eosinophilia-myalgia syndrome provide a suitable anatomic substrate for substantial cardiac electrical instability, including the occurrence of sudden death. In cases of unexplained cardiac electrical instability or sudden unexpected death an inquiry should be made about previous use of L-tryptophan. In patients with the eosinophilia-myalgia syndrome, the possibility of cardiac electrical instability should be considered as part of long-range clinical management.

Aged↗
PubMed1991

Eosinophilia-myalgia syndrome. A clinical case series of 21 patients. New Mexico Eosinophilia-Myalgia Syndrome Study Group.

We reviewed 21 cases of eosinophilia-myalgia syndrome to describe the range of clinical findings in these patients. Most patients were women (20 [95%]) and middle-aged (mean, 46 years) and had taken the food supplement L-tryptophan (95%). All cases involved eosinophilia (eosinophil count, greater than or equal to 2.0 x 10(9)/L) and incapacitating myalgias. Fourteen (88%) of the 16 patients tested had mild liver function abnormalities. Aldolase levels were abnormal in all patients tested. Muscle biopsies were done in five patients; four showed eosinophilic perimyositis, and one had interstitial inflammation. No physical finding was pathognomonic or universal, but muscle tenderness, tachycardia, and rash were the most common signs found during physical examinations. Seven patients were treated with prednisone, and six showed improvement in muscle pain and a decrease in eosinophilia. The cause of this disorder is still unknown.

Biopsy↗
PubMed1991

Manufacturing processes at two French rapeseed oil companies: possible relationships to toxic oil syndrome in Spain.

The toxic oil syndrome (TOS) epidemic that occurred in Spain in spring 1981 has been associated with the consumption of rapeseed oil that was denatured with aniline for industrial use but diverted for human consumption. The precise aetiologic agent in the oil responsible for the outbreak has not been identified. To learn more about possible contaminants and how the contamination might have occurred, we visited two French companies that process rapeseed oil and that were identified in Spanish administrative and judicial records as the ones exporting aniline-denatured rapeseed oil to Spain in 1981. With the apparently full and voluntary co-operation of personnel at both companies, we reviewed the processes involved in manufacturing, treating and transporting rapeseed oil, and we have summarized the information provided to us. Of particular importance is the finding that oil exported to Spain was taken from stock, the rest of which was sold for human consumption in the French domestic market, apparently without any adverse health effects. The differences between the oil exported to Spain and the oil sold as food in France were that aniline equivalent to 2% of the weight of the oil was added to most of the Spanish oil but not to that sold in France, and that contamination of the Spanish oil may have occurred in the tank trucks used for transportation to Spain, which had previously carried industrial chemicals. There is no assurance that the trucks were cleaned appropriately for transporting a food product before the oil was loaded for the journey to Spain. Since the clinical manifestations of TOS are not those of aniline toxicity, we conclude that the aetiological agent of TOS is likely to be one of the following: (1) a contaminant in the aniline, (2) a contaminant introduced during transportation, (3) a reaction product of normal oil components or materials used in refining with either aniline or the potential contaminants mentioned under (1) or (2) above.

Aniline Compounds↗
PubMed1991

Toxic oil syndrome: a current clinical and epidemiologic summary, including comparisons with the eosinophilia-myalgia syndrome.

In the spring and summer of 1981, an epidemic of a new illness now referred to as the toxic oil syndrome occurred in central and northwestern Spain, resulting in some 20,000 cases, 12,000 hospital admissions and greater than 300 deaths in the 1st year of the epidemic. The initial onset of illness was usually acute, and patients presented primarily with a respiratory syndrome involving cough, fever, dyspnea, hypoxemia, pulmonary infiltrates and pleural effusions. While approximately 50% of patients recovered from this acute phase of the illness without apparent sequelae, the remaining patients developed an intermediate or chronic phase, or both, of illness involving severe myalgia, eosinophilia, peripheral nerve damage, sclerodermiform skin lesions, sicca syndrome, alopecia and joint contractures, among other findings. Epidemiologic and analytic chemical studies have clearly linked the toxic oil syndrome to the ingestion of oil mixtures containing rapeseed oil denatured with aniline. However, the precise identity of the etiologic agent within this oil has never been determined. Aniline itself did not cause the illness, but the causal agent may be a reaction product of aniline with some oil component. Although many aspects of disease activity in the involved patients have lessened with time, the ultimate consequences of their disease are not clear and are the subject of ongoing study. The recently described eosinophilia-myalgia syndrome in the United States clinically resembles the toxic oil syndrome.

Aniline Compounds↗
PubMed1991

The eosinophilia-myalgia syndrome: the Los Alamos Conference.

On June 12 and 13, 1990 the Los Alamos National Laboratory in cooperation with the New Mexico Department of Health and Environment, the Centers for Disease Control (CDC), the Food and Drug Administration (FDA), and the National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health (NIH) hosted a conference on the eosinophilia-myalgia syndrome. Fifty presentations covered a variety of important issues which are summarized herein.

Centers for Disease Control and Prevention, U.S.↗
PubMed1990

Mercury exposure from interior latex paint.

BACKGROUND: Many paint companies have used phenylmercuric acetate as a preservative to prolong the shelf life of interior latex paint. In August 1989, acrodynia, a form of mercury poisoning, occurred in a child exposed to paint fumes in a home recently painted with a brand containing 4.7 mmol of mercury per liter (at that time the Environmental Protection Agency's recommended limit was 1.5 mmol or less per liter). METHODS: To determine whether the recent use of that brand of paint containing phenylmercuric acetate was associated with elevated indoor-air and urinary mercury concentrations, we studied 74 "exposed" persons living in 19 homes recently painted with the brand and 28 "unexposed" persons living in 10 homes not recently painted with paint containing mercury. RESULTS: The paint samples from the homes of exposed persons contained a median of 3.8 mmol of mercury per liter, and air samples from the homes had a median mercury content of 10.0 nmol per cubic meter (range, less than 0.5 to 49.9). No mercury was detected in paint or air samples from the homes of unexposed persons. The median urinary mercury concentration was higher in the exposed persons (4.7 nmol of mercury per millimole of creatinine; range, 1.4 to 66.5) than in the unexposed persons (1.1 nmol per millimole; range, 0.02 to 3.9; P less than 0.001). Urinary mercury concentrations within the range that we found in exposed persons have been associated with symptomatic mercury poisoning. CONCLUSIONS: We found that potentially hazardous exposure to mercury had occurred among persons whose homes were painted with a brand of paint containing mercury at concentrations approximately 2 1/2 times the Environmental Protection Agency's recommended limit.

Adolescent↗
PubMed1990

Eosinophilia-myalgia syndrome. Results of national surveillance.

Eosinophilia-myalgia syndrome, a newly recognized disorder that occurred in epidemic proportions during 1989, is associated with ingestion of manufactured tryptophan. A case is defined by debilitating myalgias and absolute eosinophilia greater than or equal to 1.0 x 10(9) cells/L. As of July 10, 1990, a total of 1531 cases had been reported nationwide, including 27 deaths. The highest rates of reported illness are concentrated in the western states, 68% are non-Hispanic white women aged 35 years and older, and data on associated clinical findings suggest a multisystemic disorder. The most frequent features include arthralgia (73%), rash (60%), cough or dyspnea (59%), peripheral edema (59%), elevated aldolase level (46%), and elevations in the results of liver function tests (43%). Neuropathy or neuritis, resulting in paralysis and death in some patients, was seen in 27%, and chest roentgenogram abnormalities were noted in 21% of those tested. Ninety-one percent reported onset of symptoms during or after May 1989, and 97% reported having taken tryptophan before the onset of symptoms. Since the recall of over-the-counter preparations of tryptophan in November 1989, the number of new cases of this potentially fatal disorder has fallen dramatically.

Adolescent↗
PubMed1990

L-tryptophan and eosinophilia-myalgia syndrome in New Mexico.

On Oct 30, 1989, the New Mexico Health and Environment Department learned of 3 patients with eosinophilia and severe myalgia who had been taking L-tryptophan. Further review of these and similar cases led to the initial recognition of the eosinophilia-myalgia syndrome (EMS) epidemic. To elucidate the apparent association between L-tryptophan-containing products (LTCPs) and EMS a case-control study was done. The case definition was unexplained peripheral eosinophilia (2000/microliters or more) and incapacitating myalgia. Cases were found through review of white blood cell counts from May 1 to Oct 31, 1989, in nine medical laboratories in New Mexico. 11 cases and 22 matched controls were interviewed for information on symptoms and other clinical findings, on the use of LTCPs, and on potential confounding factors. All 11 cases (100%) used LTCPs compared with only 2 controls. These findings led to a ban on the sale of LTCPs in New Mexico, followed by a nationwide recall of such preparations in the United States.

Adult↗
PubMed1990

Participation of eosinophils in the toxic oil syndrome.

The participation of eosinophils in the Spanish toxic oil syndrome (TOS) was investigated. Eosinophil infiltration and degranulation in tissues from 52 patients with the TOS were examined by immunofluorescence staining for the eosinophil granule major basic protein (MBP). Serum MBP levels were determined in sera from 323 patients. Eosinophil infiltration and degranulation were found in several tissues, especially during the acute phase of the TOS, and serum MBP was significantly elevated during all phases of the disease, suggesting that eosinophils play a role in the pathogenesis of the TOS.

Blood Proteins↗
PubMed1990

Lethal paralytic shellfish poisoning in Guatemala.

An outbreak of paralytic shellfish poisoning occurred in Champerico, on the Pacific coast of Guatemala, July-August 1987. Of 187 people affected with characteristic neurologic symptoms, 26 died. A case study implicated a species of clam, Amphichaena kindermani, harvested from local beaches as the vehicle of the neurotoxins (saxitoxins). Children less than 6 years old had a higher fatality rate (50%) than people greater than 18 years of age (7%). The minimum lethal dose for 1 child was estimated to have been 140 mouse units of toxin/kg body weight; thus children may be more sensitive to the saxitoxins than are adults. This is the first large outbreak of paralytic shellfish poisoning recognized in Guatemala.

Adolescent↗