Hepatotoxicity to both erythromycin estolate and erythromycin ethylsuccinate

Keeffe, Emmet B.; Reis, Thomas C.; Berland, John E.

doi:10.1007/bf01393764

Cited by 24 publications

(5 citation statements)

References 8 publications

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“…Hypersensitivity from aromatic anticonvulsants might share common mechanisms and some patients could have cross-sensitivity to these drugs—cross-sensitivity frequently is observed between phenytoin and carbamazepine. 37 Cross-sensitivity has been reported from erythromycin derivatives, 38 phenothiazines, 39 haloalkane anesthetics, 40 and anti-androgens. 41 There is a case report of DILI that arose from cross-sensitivity between the propionic acid derivatives naproxen and fenoprofen.…”

Section: Nongenetic Risk Factorsmentioning

confidence: 99%

Risk Factors for Idiosyncratic Drug-Induced Liver Injury

2010

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Idiosyncratic drug-induced liver injury (DILI) is a rare disorder that is not related directly to dosage and little is known about individuals who are at increased risk. There are no suitable preclinical models for the study of idiosyncratic DILI and its pathogenesis is poorly understood. It is likely to arise from complex interactions among genetic, nongenetic host susceptibility, and environmental factors. Nongenetic risk factors include age, sex, and other diseases (eg, chronic liver disease or human immunodeficiency virus infection). Compound-specific risk factors include daily dose, metabolism characteristics, and propensity for drug interactions. Alcohol consumption has been proposed as a risk factor for DILI from medications, but there is insufficient evidence to support this. Many studies have explored genetic defects that might be involved in pathogenesis and focused on genes involved in drug metabolism and the immune response. Multicenter databases of patients with DILI (the United States Drug Induced Liver Injury Network, DILIGEN, and the Spanish DILI registry) are important tools for clinical and genetic research. A genome-wide association study of flucloxacillin hepatotoxicity has yielded groundbreaking results and many similar studies are underway. Nonetheless, DILI is challenging to investigate because of its rarity, the lack of experimental models, the number of medications that might cause it, and challenges to diagnosis.

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Section: Nongenetic Risk Factorsmentioning

confidence: 99%

Risk Factors for Idiosyncratic Drug-Induced Liver Injury

2010

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“…This issue is of clinical significance as it indicates that a history of a specific drug toxicity should serve as a red flag for potential toxicity from another structurally similar drug 39. Examples of such a class effect include aromatic anticonvulsants (phenytoin, phenobarbital and carbamezapine; rates of cross-sensitivity as high as 80%);96 ACE inhibitors (captopril and enalapril);97 NSAIDS (naproxen and fenoprofen);98 erythromycin;99 phenothiazines;100 and tricyclic antidepressants (amineptine and clomipramine) 101…”

Section: Role Of Alt Monitoringmentioning

confidence: 99%

Diagnosis, management and prevention of drug-induced liver injury

Verma

Kaplowitz

2009

Gut

166

120

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Drug-induced liver injury (DILI) is increasingly being recognised as a significant cause of both acute and chronic liver disease. The most commonly implicated agents are paracetamol, antimicrobials, non-steroidal anti-inflammatory drugs, statins, isoniazid and herbal remedies. Drug-induced hepatotoxicity is generally idiosyncratic in nature. The pathogenesis of DILI remains enigmatic, but involves exposure to the toxic agent, mitochondrial injury, failure of adaptation, and innate and adaptive immune responses. Diagnosis of drug-induced liver diseases can be difficult, but the key to causality is to diligently exclude other causes of liver injury, and to identify a characteristic clinical drug-related signature. Management of drug-induced liver injury is symptomatic, with early referral to a liver transplant unit at the first hint of liver failure, especially in those with non-paracetamol-induced liver injury. Prevention of drug hepatotoxicity includes increased vigilance during pre-clinical drug development and clinical trials, alanine aminotransferase monitoring with certain drugs, better marketing strategies, and the future identification of both diagnostic and prognostic biomarkers.

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“…There were only a handful of cases of azithromycinrelated cholestasis reported in the literature, 1,2 unlike the well-described erythromycin-related cholestasis. [3][4][5] Oral contraceptive-related cholestasis was unlikely since the patient had been taking oral contraceptive for several years without any side effects. Symptoms of oral contraceptive cholestasis usually occurred during the first few cycles of ingestion.…”

Section: Differential Diagnosismentioning

confidence: 99%

“…6 This is best documented with erythromycin estolate. 3,4 Erythromycin is known to induce its own biotransformation by enhancing microsomal enzymes in the liver and particularly some isoenzymes of the cytochrome P-450 system with high affinity to erythromycin. 7 Onset is 2 to 25 days after exposure.…”

Section: Commentsmentioning

confidence: 99%

A 33-Year-Old Woman with Jaundice after Azithromycin Use

Suriawinata¹,

Min²

2002

Semin Liver Dis

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CASE REPORTA 33-year-old woman presented with a history of migraine, and a flu-like syndrome for which she had taken a 5-day course of azithromycin followed by one day of erythromycin. She began to have dark urine and pruritus, and 3 days later, her friend noticed her to be jaundiced. Three additional days later, she presented to her primary care physician with jaundice. Her laboratory results included total and direct bilirubinof 11.3/6.8 mg/dL (normal = 0.1-1.2/0.0-0.8), alanine aminotransferase (ALT) of 583 U/L (normal = 1-53), aspartate aminotransferase (AST) of 208 U/L (normal = 1-50). She had been taking propranolol for 1 year, sumatriptan for 6 months and oral contraceptive steroids on-and-off for 15 years and for about 1 year prior to this presentation. All medications were stopped. Over the next 3 weeks, her pruritus worsened with total bilirubin of 25 mg/dL. She presented to the Mount Sinai Hospital for further management after trying cholestyramine without any relief. Review of her prior work-ups, which included ultrasound and CT scan, showed no dilatation of bile ducts. There was no history of blood transfusion or intravenous drug use. She had about one drink of alcohol per month. She worked as a computer database person. Her family history was significant for her paternal grandfather with "liver cancer." On examination, she was markedly jaundiced with numerous scratch marks over her entire body, but there were no stigmata of chronic liver disease. There was no hepatosplenomegaly, ascites or pedal edema. Her blood tests at this time showed total and direct bilirubin of 22.8/20.4 mg/dL, ALT of 42 U/L, AST of 45 U/L and alkaline phosphatase of 228 U/L (normal = 20-130). The viral serologies were all negative. These included negative IgM anti-HAV, HBsAg, IgM anti-HBc, and HCV RNA by qualitative PCR. Antismooth muscle and anti-LKM antibodies were not detectable. Anti-nuclear antibodies were "weakly positive," and serum protein electrophoresis showed normal level of gamma-globulin. Ceruloplasmin level was normal. A repeat ultrasound showed no bile duct dilatation. A liver biopsy was performed.

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Hepatotoxicity to both erythromycin estolate and erythromycin ethylsuccinate

Cited by 24 publications

References 8 publications

Risk Factors for Idiosyncratic Drug-Induced Liver Injury

Risk Factors for Idiosyncratic Drug-Induced Liver Injury

Diagnosis, management and prevention of drug-induced liver injury

A 33-Year-Old Woman with Jaundice after Azithromycin Use

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