Am J Gastroenterol 2002 May;97(5):1198-203
Internal Medicine, Community Health Care, Inc, Davenport, Iowa, USA.
OBJECTIVES: Southeast Asian immigrants, with a high prevalence of both hepatitis B and latent tuberculosis, constitute a large proportion of immigrants to the United States. Isoniazid hepatotoxicity may be associated with hepatitis B. This study was conducted to document the prevalence and interaction of hepatitis B, latent tuberculosis, and isoniazid toxicity. METHODS: Hepatitis B surface antigen (HBsAg) and tuberculin skin testing was done on 743 Vietnamese immigrants to the Midwest between January, 1991 and December, 1999. HBsAg positive cases were tested for hepatitis B e antigen (HBeAg). All tuberculin skin test-positive patients were treated with isoniazid, unless contraindicated. Complications of isoniazid treatment and compliance with hepatitis B virus immunization recommendations were evaluated. RESULTS: One hundred three subjects (13.86%) had HBsAg, and 43 (5.7%) HBeAg. Prevalences of latent tuberculosis were similar in HBsAg positive (53%) and HBsAg negative (45%) subjects. Sixty-two percent of HBeAg positive versus 19% of HBeAg negative subjects had hepatotoxic side effects requiring discontinuation of treatment (relative risk [RR] = 11.38, CI = 5.49 < RR < 23.59, p < 0.001). Three cases of severe isoniazid hepatitis occurred in 21 HBeAg positive subjects, versus no cases in 121 HBeAg negative cases treated with isoniazid (RR = 7.72, CI = 5.02 < RR < 11.88, p < 0.001). Only 58% of subjects at risk of developing hepatitis B virus infection were appropriately immunized. CONCLUSIONS: Vietnamese immigrants have a high prevalence of hepatitis B and latent tuberculosis. HBeAg positive cases have a 7.7-fold increased risk of serious isoniazid toxicity and an 11.3-fold increased risk of isoniazid side effects requiring discontinuation of treatment. HBeAg represents an important risk factor for severe isoniazid hepatitis.
PMID: 12014728, UI: 22008885
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Ann Intern Med 2002 May 21;136(10):780; discussion 780-1
Publication Types:
PMID: 12020152, UI: 22014989
Ann Pharmacother 2001 Dec;35(12):1677
PMID: 11793648, UI: 21651736
Ann Pharmacother 2001 Dec;35(12):1674-5
PMID: 11793645, UI: 21651733
Ann Pharmacother 2001 Dec;35(12):1672-3
PMID: 11793643, UI: 21651731
Ann Pharmacother 2001 Dec;35(12):1584-7
Department of Dermatology, Eulji Hospital University of Medicine, 280-1, Hagye-1-dong, Nowon-gu, Seoul 139-711, South Korea. lay5103@eulji.or.kr
OBJECTIVE: The most important goal in the management of photosensitive drug eruptions, as in other types of drug eruptions is identification of the causative drugs to prevent reexposure to them. CASE SUMMARIES: Seven patients whose lesions were mainly distributed on sun-exposed areas underwent laboratory tests, phototests, and photopatch tests with suspected drugs. Phototests were done with ultraviolet A (UVA), UVB, and visible light. Drugs used in the photopatch tests were usually prepared as 10% concentrations in petroleum base, which did not produce reactions in 10 control subjects, followed by irradiation of suberythema doses of UVA. Systemic provocation by oral administration of small doses of causative drugs with irradiation of suberythema doses of UVA was performed to confirm the results of skin tests in four patients. Two patients were not rechallenged with the causative drugs. None of the patients had systemic lupus erythematosus, porphyria, or pellagra. All showed positive reactions to photopatch testing. Systemic provocation confirmed the results of photopatch tests in four patients. The two patients who were not rechallenged had no recurrence of lesions. One patient ingested only one drug at the time of eruptions, and provocation or avoidance was not attempted. A photoallergic mechanism was considered in five cases. CONCLUSIONS: Although there is no information about the appropriate concentrations or vehicles for suspected drugs, photopatch testing could be reliable for identification of causes of photosensitive drug eruptions. Besides piroxicam (a well-known photosensitizer) and carbamazepine, isoniazid and triflusal were identified as the causes of the reactions.
PMID: 11793626, UI: 21651714
Ann Pharmacother 2001 Dec;35(12):1559-61
School of Pharmacy, University of Connecticut, St. Francis Hospital Burgdorf Primary Care Clinic, Hartford, CT, USA. k.rettman@att.net
OBJECTIVE: To report a case of severe hepatotoxicity from a four-day course of trazodone in a patient being treated according to protocol in a detoxification center. CASE SUMMARY: A 46-year-old HIV-positive man with a past medical history of intravenous drug abuse and hepatitis C, who was well controlled with HIV medications, was admitted for cocaine withdrawal. The patient was started on a standard protocol at the detoxification center with methadone 50 mg/d, clonidine 0.1 mg twice daily for four days, and trazodone 200 mg/d for four days. Laboratory results showed acute hepatitis and cholestasis five days following admission. Trazodone and clonidine were discontinued at that time. His methadone and HIV regimens remained unchanged. Liver function test results were greatly improved 10 days after trazodone and clonidine discontinuation. DISCUSSION: This is the first case report of trazodone-induced liver damage after only a few days of therapy. Previous reports describe hepatitis developing after weeks to months of trazodone therapy. All comorbidities thought to affect the described laboratory abnormalities were ruled out as a cause by a hepatologist. The observation of the sudden rise and fall of liver enzymes is characteristic of a drug reaction in the absence of trauma and severe shock. CONCLUSIONS: Due to the temporal relationship of the introduction and withdrawal of trazodone in the medication regimen and the elevations in liver enzymes, we conclude that this patient experienced acute hepatitis induced by trazodone 200 mg/d therapy for four days. The findings of this case warrant caution and closer monitoring in a patient with multiple risk factors for liver damage.
PMID: 11793619, UI: 21651707
Forensic Sci Int 2002 May 23;126(3):203-9
Department of Forensic Medicine, University of Helsinki, P.O. Box 40, 00014, Helsinki, Finland
[Medline record in process]
Compilation of mortality statistics from death certificate data is based on international and national conventions which in certain situations result in the underlying cause-of-death other than that established and reported by the physician.The present study compares all fatal alcohol poisonings in 1997 as registered on forensic toxicological grounds at the accredited central laboratory and as presented in the national cause-of-death statistics, according to the underlying cause-of-death, by applying international statistical rules and principles in ICD-10.Four groups were formed, and case frequencies in each group were obtained from forensic toxicological data, group "T51" for acute poisonings due to alcohol alone, and group "Comb" for acute alcohol poisonings combined with some drug, medicament or other biological substance, and from cause-of-death statistics data, group "X45", for deaths from alcohol poisoning, and group "F102" for those medico-legal fatal alcohol poisoning deaths which at the statistics office were inferred to be due to alcoholism.The study shows that in Finland the officially compiled statistics on fatal alcohol poisonings, when compared with medico-legal statements based on forensic toxicological examinations, were underrepresented by 31.4% in 1997. About two-thirds of this underrepresentation is explained by preferring, as the underlying cause-of-death, alcoholism to acute alcohol poisoning, and about one-third by preferring, in cases of acute combined poisonings, the drug component to the alcohol. From 1998 onwards, more emphasis has been put on the alcohol component when coding medico-legally proven accidental deaths from simultaneous poisoning with alcohol and a medicinal agent. This change in coding practices presumably explains the subsequent decline in the annual underrepresentation rate of alcohol poisoning in mortality statistics to the level of 15-16%.It is concluded that the present ICD rules inevitably lead to underrepresentation of alcohol poisonings in the mortality statistics, and conceptual and practical proposals for future procedures are made.
PMID: 12062942, UI: 22057864
Gastroenterol Clin Biol 2002 Feb;26(2):181-3
PMID: 11938073, UI: 21935214
Gastroenterol Clin Biol 2002 Feb;26(2):179-80
PMID: 11938071, UI: 21935212
J Clin Psychiatry 2002 May;63(5):447-50
Department of Psychiatry, Chinese University of Hong Kong. cmleung@ha.org.hk
BACKGROUND: Carbon monoxide (CO) poisoning by burning charcoal has become one of the most common ways of committing suicide in Hong Kong since late 1998. The evolution of the phenomenon was explored in the current study. METHOD: Information about completed suicides between January 1996 and December 1999 was obtained from the Hong Kong death registry and hospital authority, and information about ambient temperature and humidity was obtained from the Hong Kong Observatory. News on completed suicides by burning charcoal was collected by computer search using the data bank of 6 major Hong Kong newspapers. The data were analyzed. RESULTS: CO poisoning by burning charcoal rose from 0% of all Hong Kong suicides in 1996 and 1997 to 1.7% in 1998 and 10.1% in 1999. The monthly incidence rate bore a reciprocal relationship with the ambient temperature. Suicidal pacts were overrepresented, and past history of mental illness was uncommon. Both demographic and clinical features of suicides by burning charcoal resembled those of suicides by domestic gas poisoning. The overall suicide rate remained unchanged in the above period. CONCLUSION: Suicide by burning charcoal is a new variant of domestic gas poisoning. A host of biopsychosocial and ethnological factors are responsible for the birth and indigenization of the method.
PMID: 12019670, UI: 22014444
Med J Aust 2002 May 20;176(10):495
Centre for Clinical Effectiveness, Monash Institute of Health Services Research, Clayton, VIC. cce@med.monash.edu.au
PMID: 12065016, UI: 22061116
Med J Aust 2002 Jun 3;176(11):561-3
Department of Social Medicine, Canynge Hall, Whiteladies Road, Bristol, BS8 2PR, UK. d.j.gunnell@bristol.ac.uk
PMID: 12064993, UI: 22061151
Pediatr Emerg Care 2002 Jun;18(3):200-202
Departments of Pediatric Emergency Medicine (J.C. Clifton II) and Pediatric Gastroenterology and Nutrition (R.H. Sandler), Rush Children's Hospital, and Rush Emergency Services (J.B. Leikin), Rush-Presbyterian-St. Luke's Medical Center (RPSLMC), Toxikon Consortium, University of Illinois/Cook County Hospital/RPSLMC, Chicago, Illinois; Illinois Poison Center, Chicago, Illinois (T. Sigg, A.M. Burda); and Department of Pediatric Gastroenterology and Nutrition, Hope Children's Hospital, Oak Lawn, Illinois (C.J. Smith).
[Record supplied by publisher]
PMID: 12066009
Pediatr Emerg Care 2002 Jun;18(3):185-188
Departments of Emergency Medicine (S.R. White, G. Dy) and Pediatrics (S.R. White), Wayne State University School of Medicine, Detroit, Michigan; Division of Analytical Toxicology, Department of Clinical Pathology, William Beaumont Hospital, Royal Oak, Michigan (J.M. Wilson).
PMID: 12066005
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