Trazodone-induced hepatotoxicity: a case report with comments on drug-induced hepatotoxicity

Trazodone (Desyrel) is a second-generation, nontricyclic antidepressant that has been in use in North America since the early 1980s. It has the advantage of being more sedating and having less anticholinergic side effects than other secondary amines in the piperazine class, namely, desipramine and nortriptyline. Five previous cases of trazodone hepatotoxicity have been reported in the literature, one describing chronic damage and the others, more acute cellular and cholestatic injury. We describe a case of acute reversible liver injury with the use of trazodone. This case is unique in that injury occurred after protracted (18 months) drug use and while the patient was on corticosteroids. Moreover, the diagnosis was confirmed by an inadvertent challenge with trazodone. This case reports not only a well documented instance of trazodone-induced liver injury, but also serves as a basis for a brief discussion of mechanisms, clinical monitoring, and therapy in drug-induced hepatotoxicity.     

Bee sting therapy-induced hepatotoxicity: A case report

The use of bee venom as a therapeutic agent for the relief of joint pains dates back to Hippocrates,and ref-erences to the treatment can be found in ancient Egyp-tian and Greek medical writings as well.Also known as apitherapy,the technique is widely used in Eastern Europe,Asia,and South America.The beneficial effects of bee stings can be attributed to mellitinin,an anti-in-flammatory agent,known to be hundred times stronger than cortisone.Unfortunately,certain substances in the bee venom trigger allergic reactions which can be life threatening in a sensitized individual.Multiple stings are known to cause hemolysis,kidney injury,hepatotoxicity and myocardial infarction.The toxicity can be immedi-ate or can manifest itself only weeks after the exposure.We describe hepatotoxicity in a 35-year-old female,following bee sting therapy for multiple sclerosis.She presented to our clinic 3 wk after therapy with a his-tory of progressive jaundice.The patient subsequently improved,and has been attending our clinic now for the last 9 mo.     

Quinidine hepatotoxicity. A report of a case and review of the literature.

A case is described of presumed quinidine hepatotoxicity, characterized by the development of fever, abnormal serum transaminase values, which improved after cessation of the drug but recurred after a challenge dose, and centrizonal hepatocellular necrosis detected on liver biopsy. Morphological changes on electron microscopy, consistent with a drug reaction, are also described. Pertinent features of previous case reports are analyzed, and the histological findings by light microscopy of the present and past cases are discussed. It is suggested that the development of unexplained fever within 1 month of quinidine administration should lead to consideration of possible hepatotoxicity.     

Sertraline hepatotoxicity: a case report and review of the literature on selective serotonin reuptake inhibitor hepatotoxicity

The causal role of sertraline in rare cases of liver failure in patients taking the drug has not been proven in a manner consistent with usually accepted standards. We describe an individual who developed clinically significant hepatitis while being treated with sertraline. This case is significant because it is the only one of which we are aware in which the diagnosis of sertraline hepatotoxicity was confirmed when inadvertent rechallenge with the medication resulted in recurrent hepatitis. We review this case and the general role of this widely prescribed class of drugs in causing hepatitis.     

Terbinafine hepatotoxicity. A case report and review of literature

We report a 53-year old Mexican female who developed liver dysfunction following a seven-day course of treatment with terbinafine for onychomycosis. She presented with jaundice and abdominal pain. Her serum bilirubin levels showed a peak value of 23.2 mg/dL seven weeks after discontinuing the medication. Infectious causes (hepatitis viruses A, B and C) were excluded. Imaging studies of the abdomen did not reveal any abnormalities. Serum iron and ceruloplasmin levels were normal. Autoantibodies were negative. A liver biopsy revealed necrosis and mononuclear infiltration of the parenchyma, mainly along the sinusoids and surrounding the portal spaces and biliary ducts. Eosinophil infiltration of the portal spaces was also noted. Treatment with ursodeoxycholic acid and ademethionine was started. Her liver tests normalized in the sixth months after stopping terbinafine.     

Metronidazole-induced hepatotoxicity in a patient with xeroderma pigmentosum: A case report

Rationale:Whereas metronidazole-induced hepatotoxicity is quite rare in the general population, in individuals carrying a nucleotide excision repair disorder, namely Cockayne syndrome, there is a high risk of developing this complication.Patient concerns:We report the case of a 44-year-old man, affected by xeroderma pigmentosum, who was admitted to the hospital presenting aspiration pneumoniae caused by worsening dysphagia and with severe hepatotoxicity during the hospitalization.Diagnoses:Acute hepatitis, which was leading to acute liver failure, occurred during antibiotic treatment with metronidazole and ceftazidime with an elevation of liver enzymes consistent with hepatocellular damage pattern.Interventions:Hydration with glucose 5% solution, pantoprazole and vitamin K were administered, meanwhile other causes of hepatitis were ruled out and the ongoing antibiotic treatment was stopped suspecting a drug-induced liver injury.Outcomes:Liver function nearly completely recovered 1 month later with a first rapid improvement, within few days, of aminotransferases and coagulation studies, and slower of cholestatic enzymes.Lessons:We describe the first case available in the literature of hepatotoxicity associated with metronidazole treatment in a xeroderma pigmentosum patient. Clinicians therefore, based on this report and according to the possible underlying mechanism shared by other genetic diseases characterized by alterations in the pathway of DNA-repair, should consider such adverse event also in patients affected by this rare disease.     

Hepatic decompensation associated with lamivudine: a case report and review of lamivudine-induced hepatotoxicity

We report a case of a 62-yr-old man with chronic hepatitis B virus (HBV)-related cirrhosis who developed hepatic decompensation after being started on lamivudine requiring liver transplantation. Decompensated liver disease while on lamivudine has been previously reported on two occasions, both HIV coinfected patients on a combination of nucleoside analogues. Our patient is alive and well nearly 2 yr after successful liver transplantation.     

Myonecrosis caused by Edwardsiella tarda: a case report and case series of extraintestinal E. tarda infections.

Edwardsiella tarda is an unusual human pathogen. It is primarily associated with gastrointestinal disease, although recent reports of extraintestinal disease are broadening the current understanding of the clinical spectrum of E. tarda. A series of 11 cases of extraintestinal E. tarda infection is presented, including the first reported case of myonecrosis in an immunocompetent patient. Wound infections were the most common manifestation, and 3 of 5 patients with infected wounds had been exposed to a marine environment. One patient had bacteremia, and the remaining 5 patients developed abscesses that required surgical drainage. Four patients had E. tarda isolated in pure culture, including the patient with myonecrosis. Although it is often difficult to ascertain the contribution of E. tarda to infection when it is isolated as part of a mixed culture, this case series suggests that E. tarda is singularly capable of causing limb- and life-threatening infections.     

Fatal hepatotoxicity after re-exposure to isoflurane: a case report and review of the literature

A 76-year-old Caucasian woman developed fulminant hepatic necrosis 6 days after an uneventful operation under isoflurane anaesthesia. Laboratory findings included elevated bilirubin, grossly elevated transaminases and prolonged prothrombin time. Radiological investigation showed no evidence of extra-hepatic disease. Serological studies were negative for acute viral hepatitis and autoimmune disease. The patient may have been previously sensitized by exposure to isoflurane 3 years previously but antibodies to tri-fluoro acetate, present in 70% of cases of halothane hepatitis, were not detected in pre-operative or postoperative samples of blood. On the seventh postoperative day the patient died and postmortem examination demonstrated centrilobular necrosis of the liver, with a histological pattern similar to changes associated with halothane hepatitis.     

Acute interstitial pneumonia: report of a series.

Four cases of acute interstitial pneumonia (AIP) are described with special emphasis on clinical background, lung imaging and bronchoalveolar lavage findings. A retrospective chart review of four patients with histologically-proven AIP, diagnosed between 1998 and 2000, was carried out. Clinical data, bronchoalveolar lavage (BAL) findings, high-resolution computed tomography (HRCT) and histological features were analysed. Three patients died and only one is in follow-up. HRCT showed areas of ground glass attenuation and alveolar consolidation in all patients. Histology, documented by open lung biopsy or autopsy specimens, was consistent with the organising form of diffuse alveolar damage pattern. BAL findings were characteristic, with a huge neutrophilia associated with scattered atypical type II pneumocytes collected in clusters with extracellular amorphous material (fragments of hyaline membranes) observed in two out of three cases. In this paper, four cases of acute interstitial pneumonia are reported in detail. The poor prognosis associated with this entity has been confirmed and the possible diagnostic role of the bronchoalveolar lavage is emphasised.     

Tocilizumab in glucocorticoid-resistant graves orbitopathy. A case series report of a mexican population

PurposeTo describe pre- to post-treatment changes in clinical activity score (CAS) and exophthalmometry in patients with Graves orbitopathy treated with tocilizumab (TCZ).Material and methodsEight Mexican patients presenting with active Graves orbitopathy (CAS > 3/7) previously treated with glucocorticoids received 1 monthly dose of TCZ for 6 months. CAS, EUGOGO severity assessment and exophthalmometry were used to evaluate clinical status, with serum measurement of thyroid-stimulating hormone receptor antibodies (TR-Ab) for biochemical evaluation before and after application of TCZ.ResultsEight patients were analyzed: 6 male (75%), 2 female (25%): mean age, 45.9 ± 11.2 years; mean weight, 85 ± 18.3 kg. Mean TR-Ab level at treatment outset was 291.9 ± 96.4%, mean CAS 4.1 ± 0.3 and mean exophthalmometry 21.2 ± 3.2 mm. After TCZ treatment, mean TR-Ab level fell to 172.7 ± 54% (P = 0.001), mean CAS to 1.1 ± 0.6 (P = 0.001) and mean exophthalmometry to 19.3 ± 2 mm (P = 0.02).ConclusionsTCZ is a therapeutic option for glucocorticoid-resistant orbitopathy, and should be considered in second line due to the cost of treatment or in first line in patients with contraindications to intravenous GC pulse therapy.     

Heroin-related noncardiogenic pulmonary edema : a case series.

STUDY OBJECTIVES: To examine the current clinical spectrum of noncardiogenic pulmonary edema (NCPE) related to heroin overdose. DESIGN: Retrospective chart review of all identified patients from August 1994 through December 1998. SETTING: Urban academic hospital. PATIENTS OR PARTICIPANTS: Heroin-related NCPE was defined as the syndrome in which a patient develops significant hypoxia (room air saturation < 90% with a respiratory rate > 12/min) within 24 h of a clinically apparent heroin overdose. This should be accompanied by radiographic evidence of diffuse pulmonary infiltrates not attributable to other causes, such as cardiac dysfunction, pneumonia, pulmonary embolism, or bronchospasm, and which resolve clinically and radiographically within 48 h. INTERVENTIONS: None. MEASUREMENTS AND RESULTS: Twenty-seven patients were identified during this 53-month period, with a majority being male patients (85%; average age, 34 years). Twenty patients (74%) were hypoxic on emergency department arrival, and 6 patients (22%) had symptoms develop within the first hour. One patient had significant hypoxia develop within 4 h. Nine patients (33%) required mechanical ventilation, and all intubated patients but one were extubated within 24 h. Eighteen patients (66%) were treated with supplemental oxygen alone. Hypoxia resolved spontaneously within 24 h in 74% of patients, with the rest (22%) resolving within 48 h. Twenty patients (74%) had classical radiograph findings of bilateral fluffy infiltrates, but unilateral pulmonary edema occurred in four patients (15%) and more localized disease occurred in two patients (7%). CONCLUSION: NCPE is an infrequent complication of a heroin overdose. The clinical symptoms of NCPE are clinically apparent either immediately or within 4 h of the overdose. Mechanical ventilation is necessary in only 39% of patients. The incidence of NCPE related to heroin overdose has decreased substantially in the last few decades.     

A case of meglumine iodipamide hepatotoxicity.

There have been only two reports of severe hepatotoxic reaction caused by meglumine iodipamide. Lately we experienced such a reaction in an 66-year old female with chronic intrahepatic cholestasis. After drip infusion cholangiography was performed by infusing 40 ml. of 50% meglumine iodipamide (Biligrafin) intravenously, the patient developed nausea and abdominal pain. Her serum transaminase rose to more than 2,000 K-A units on the third day and gradually returned to normal by the 18th day. The macrophage migration inhibition test of her blood was positive for meglumine iodipamide. Accordingly some delayed type of hypersensitivity in the above reaction could be considered. When a larger amount than a recommended dose of meglumine iodipamide is infused in cholangiography, a severe hepatotoxic reaction might be induced, especially in icteric cases.     

Hydroxycut hepatotoxicity： A case series and review of liver toxicity from herbal weight loss supplements

Dietary supplements represent an increasingly common source of drug-induced liver injury. Hydroxycut is a popular weight loss supplement which has previously been linked to hepatotoxicity, although the individual chemical components underlying liver injury remain poorly understood. We report two cases of acute hepatitis in the setting of Hydroxycut exposure and describe possible mechanisms of liver injury. We also comprehensively review and summarize the existing literature on commonly used weight loss supplements, and their individual components which have demonstrated potential for liver toxicity. An increased effort to screen for and educate patients and physicians about supplement-associated hepatotoxicity is warranted.