Ayurvedic drug induced liver injury.

Drug induced liver injury is responsible for 50% of acute liver failure in developed countries. Ayurvedic and homeopathic medicine have been linked to liver injury. This case describes the first documented case of Punarnava mandur and Kanchnar guggulu causing drug induced liver injury. Drug induced liver injury may be difficult to diagnosis, but use of multi-modalities tools including the ACG algorithms, causative assessment scales, histological findings, and imaging, is recommended. Advanced imaging, such as magnetic resonance cholangiopancreatography, may possibly have a greater role than previously reported in literature.

Rate and Predictors of Interval Esophageal and Gastric Cancers after Esophagogastroduodenoscopy in the United States.

BACKGROUND AND AIMS: In the United States, little is known about the rates of interval upper gastrointestinal (GI) cancer (possibly missed out) after an esophagogastroduodenoscopy (EGD) is performed. Data from non-US studies reported interval cancer rates of 7-26%. We aimed to study the rate and predictors of interval upper GI cancers in the United States. METHODS: Using the random 5% sample of Medicare beneficiaries in the Surveillance, Epidemiology, and End Results-Medicare linked database, we identified patients diagnosed with esophageal or gastric cancer during 2000-2007. EGD performed within 36 months prior to cancer diagnosis was identified using CPT codes. Cancers diagnosed 6-36 months after EGD were defined as interval (vs. detected) cancers. The chi-square test and the multivariate logistic model were used in statistical analysis. RESULTS: Of 751 patients diagnosed with upper GI cancer, 52 patients (6.9%) were diagnosed with interval cancers 6-36 months after EGD. The rate of interval cancers was 5.5% (31/568) for gastroenterologists and 11.5% (21/183) for non-gastroenterologists (p < 0.01). In multivariate logistic regression, EGDs performed by gastroenterologists (vs. non-gastroenterologists: OR 0.46, 95% CI 0.25-0.83) and those in inpatient setting (vs. outpatient: OR 0.53, 95% CI 0.28-0.997) were associated with a lower likelihood of interval cancers. Sensitivity analyses limited to outpatient EGDs or interval cancers 6-30 months after EGDs led to similar results. CONCLUSIONS: The rate of interval cancers after EGD is the same as the rate of colonoscopy among Medicare patients in the United States. EGDs performed by gastroenterologists and in in-patient settings were associated with a lesser likelihood of interval cancers.

Necrolytic acral erythema: an expanding spectrum.

Hepatitis C virus (HCV) infection is the most common chronic blood-borne viral infection in the United States. Well-described cutaneous manifestations of HCV infection include polyarteritis nodosa, porphyria cutanea tarda, type II cryoglobulinemia-associated vasculitis, pruritus, erythema nodosum, urticaria and urticarial vasculitis, lichen planus, and erythema multiforme. First described in 1996, necrolytic acral erythema (NAE) is now recognized as a cutaneous acral eruption uniquely associated with HCV infection. Most patients present with chronic, acral, erythematous, and psoriasiform lesions. Acute presentations of NAE are rare and patients may present with atypical clinical features; in these cases, suspicion for HCV infection may be delayed for weeks to months until more classic chronic lesions develop. In many cases, NAE presents before the patient has been diagnosed with HCV infection, which allows dermatologists the unique opportunity to suspect and diagnose HCV infection based on skin findings alone.

Metformin-induced cholestatic hepatitis.

OBJECTIVE: To report a case of metformin-induced cholestatic hepatitis. METHODS: We present a detailed case report, including laboratory and biopsy findings. In addition, similar cases from the literature are reviewed. RESULTS: In a 68-year-old man with newly diagnosed diabetes mellitus, metformin therapy was begun. The dosage initially was 500 mg twice daily and later was increased to 850 mg twice a day. Four weeks after met-formin treatment was initiated, jaundice, pruritus, and liver enzyme abnormalities were noted. The patient underwent an extensive work-up, including a hepatitis screen, ultrasonography, magnetic resonance imaging, and endoscopic retrograde cholangiopancreatography, all of which showed normal findings. A liver biopsy revealed severe cholestasis and mild portal inflammation. Treatment with metformin was discontinued, and the liver enzymes normalized except for a persistently increased level of alkaline phosphatase, most likely related to a prolonged cholestatic effect of metformin. CONCLUSION: Although rare, metformin can be responsible for inducing liver damage, and patients and physicians should be aware of this side effect.

Orlistat: its current status as an anti-obesity drug.

Orlistat is a non-centrally acting anti-obesity agent that acts locally in the gastrointestinal tract to inhibit lipase, an enzyme that is crucial for the digestion of long-chain triglycerides. At the recommended dose of 120 mg three times daily, orlistat inhibits dietary fat absorption by about 30%. Over a 1-year period, obese patients taking orlistat in combination with a hypocaloric diet show a reduction of 2-5 kg over the weight decrease with placebo. When continued for a second year in combination with a weight maintenance diet, orlistat reduces weight regain compared to placebo-treated patients. Orlistat in combination with dietary intervention is also associated with beneficial effects on cardiovascular risk factors including total and low-density lipoprotein cholesterol, blood pressure and plasma glucose. It is not known if orlistat has any impact on clinical outcomes such as myocardial infarction, stroke and sudden death. Orlistat has not been compared with other anti-obesity agents.