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Review Acute renal failure and hepatitis following ingestion of carp gallbladder. 2008
Kung SW, Chan YC, Tse ML, Lau FL, Chau TL, Tam MK. · Hong Kong Poison Information Centre, Room 2A, Block K, United Christian Hospital, 130 Hip Wo Street, Kwan Tong, Hong Kong, Administrative Region. · Clin Toxicol (Phila). · Pubmed #19238734 No free full text.
Abstract: INTRODUCTION: Fish gallbladder has long been used as folk remedy in China. Poisoning due to carp gallbladder ingestion has been reported in many countries but the majority of cases are in Chinese journals. We report a case of grass carp gallbladder poisoning and review the literature, including the Chinese reports. CASE REPORT: A 67 year old woman ingested a grass carp gallbladder and complained of nausea and epigastric pain in two hours, and had elevated alanine aminotransferase by 8 hours. She developed oliguria on day three and hemodialysis was performed on day five, following which she gradually recovered and was discharged on day 26. DISCUSSION: Carp gallbladder contains 5 alpha-cyprinol sulphate, which is hepatotoxic and nephrotoxic. The exact mechanism of toxicity is unknown. Mild poisoning causes only gastroenteritis, liver and kidneys are affected in moderate poisoning, and multi-organ failure occurs in severe poisoning. The initial symptoms are nausea, vomiting, diarrhea and abdominal pain, which usually occur 5 to 12 hours after ingestion. Raised liver enzymes or jaundice occurs in 75% to 87% of patients. Acute renal impairment occurs in 72% to 87% of patients, usually on day 3 to 6. Treatment is supportive and often included hemodialysis. CONCLUSION: The ingestion of grass carp gallbladder may result in transient hepatitis with subsequent acute renal failure. This case also illustrated the importance of understanding the use and potential serious complications of alternative medicines. Fish gallbladder poisoning should be considered in unexplained acute renal failure in Chinese and Asian patients.
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Article Comparison of PCR-based genotyping methods for hepatitis B virus. 2007
Lim CK, Tan JT, Ravichandran A, Chan YC, Ton SH. · School of Arts and Sciences, Monash University Sunway Campus, Selangor Darul Ehsan, Malaysia. · Malays J Pathol. · Pubmed #19108399 No free full text.
Abstract: Hepatitis B virus (HBV) is classified into eight genotypes (A to H). In this study, three genotyping methods were compared for their sensitivity and accuracy, namely PCR-RFLP on the S region, PCR-RFLP on the pre-S region and nested PCR with type specific primers. Sixty HBV samples from infected sera were genotyped. The nested PCR with type specific primers was found to be the most sensitive and produced substantial numbers of co-infections by genotypes B and C. The sensitivities for both PCR-RFLP methods were lower and did not reveal co-infections. Generally, the three methods produced consistent genotyping results in samples infected by single genotypes but for co-infections by genotypes B and C, the two PCR-RFLP methods yielded only single genotypic results. For the cases of single genotypic infections, genotypes ascertained by sequencing were in concordance across all three methods. However, when co-infections occurred, PCR analysis on clones revealed only single genotypic infections.
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Article Hepatitis induced by Teucrium viscidum. 2008
Poon WT, Chau TL, Lai CK, Tse KY, Chan YC, Leung KS, Chan YW. · Toxicology Reference Laboratory, Department of Pathology, Princess Margaret Hospital, Hong Kong, Hong Kong. · Clin Toxicol (Phila). · Pubmed #18608288 No free full text.
Abstract: INTRODUCTION: In Hong Kong, Chinese medicine is popular and coexists with orthodox Western medicine. Despite a long history of use, many herbs have not been submitted to rigorous scientific testing and there are reports of hepatotoxicity. We describe a woman who developed acute hepatitis after drinking an herbal remedy containing Teucrium viscidum. CASE REPORT: A previously healthy 51-year-old woman was admitted to a regional hospital because of jaundice, with complaints of nausea, vomiting, and tea-colored urine for three days prior to admission. She denied any recent ingestion of known hepatotoxins, but she had consumed an herbal remedy for low back pain for three days before the onset of symptoms. She was icteric and had a serum total bilirubin level of 11.4 mg/dL, alanine aminotransferase of 2620 U/L, aspartate aminotransferase of 1876 U/L, and alkaline phosphatase level of 186 U/L. Discontinuation of the herbal remedy resulted in normalization of the liver enzymes two months later. DISCUSSION: This is the first report of hepatitis probably related to use of Teucrium viscidum. The herb is infrequently used in Chinese medicine for treatment of rheumatic and bleeding disorders. T. viscidum contains teucvin, similar to other Teucrium species and is related to T. chamaedrys, commonly known as germander, which is a well documented cause of hepatotoxicity. CONCLUSIONS: Our findings suggest that Teucrium viscidum can cause hepatotoxicity similar to that of germander.
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Article Correlations of HBV genotypes, mutations affecting HBeAg expression and HBeAg/ anti-HBe status in HBV carriers. free! 2006
Lim CK, Tan JT, Khoo JB, Ravichandran A, Low HM, Chan YC, Ton SH. · School of Arts and Sciences, Monash University Malaysia, Petaling Jaya 46150, Malaysia. · Int J Med Sci. · Pubmed #16421626 links to free full text
Abstract: This study was carried out to determine the effects of hepatitis B virus genotypes, core promoter mutations (A1762G1764-->T1762A1764) as well as precore stop codon mutations (TGG-->TAG) on HBeAg expression and HBeAg/ anti-HBe status. Study was also performed on the effects of codon 15 variants (C1858/ T1858) on the predisposition of precore stop codon mutations (TGG-->TAG). A total of 77 sera samples were analyzed. Fifty one samples were successfully genotyped of which the predominant genotype was genotype B (29/ 51, 56.9 %), followed by genotype C (16/ 51, 31.4 %). Co-infections by genotypes B and C were observed in four samples (7.8 %). To a lesser degree, genotypes D and E (2.0 % each) were also observed. For core promoter mutations, the prevalence was 68.8 % (53/ 77) for A1762G1764 wild-type and 14.3 % (11/ 77) for T1762A1764 mutant while 9.1 % (7/ 77) was co-infected by both strains. The prevalence of codon 15 variants was found to be 42.9 % (33/ 77) for T1858 variant and 16.9 % (13/ 77) for C1858 variant. No TAG mutation was found. In our study, no associations were found between genotypes (B and C) and core promoter mutations as well as codon 15 variants. Also no correlation was observed between HBeAg/ anti-HBe status with genotypes (B and C) and core promoter mutations.
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Article Allopurinol hypersensitivity syndrome and acute myocardial infarction--two case reports. 2002
Chan YC, Tay YK, Ng SK. · National Skin Centre, 1 Mandalay Road, Singapore 308205. · Ann Acad Med Singapore. · Pubmed #11957564 No free full text.
Abstract: INTRODUCTION: Allopurinol hypersensitivity syndrome is an idiosyncratic drug reaction characterised by an acute and severe multiorgan disease. It usually begins 2 to 6 weeks after starting allopurinol. The most important and critical characteristics are the presence of visceral involvement and haematological abnormalities; hepatitis, interstitial nephritis and eosinophilia are most frequently seen. However, cardiac involvement has not been previously reported. CLINICAL PICTURE: Two previously well young Chinese men presented with fever, rash and hepatitis 3 weeks after taking allopurinol. The clinicopathological presentation was typical of allopurinol hypersensitivity syndrome. TREATMENT AND OUTCOME: Both men received systemic corticosteroid therapy and had full recovery. A few months later, they each had an acute myocardial infarction with a fatal outcome, despite minimal cardiac risk factors and no family history of coronary artery disease. CONCLUSION: The immunologic process in allopurinol hypersensitivity syndrome may have caused coronary vasculitis and subsequent myocardial infarct. Alternatively, the idiosyncratic reaction may have damaged myocardium, with the resultant myocarditis masquerading as coronary artery disease. Patients with allopurinol hypersensitivity syndrome should be followed up for cardiac involvement.
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