RESUMO
Hepatotoxicity caused by chronic oral amiodarone is well documented with around 15-20% incidence rate. However, acute liver failure due to intravenous (IV) amiodarone is rare clinical presentation with 3% incidence rate. Incidence of concomitant renal failure is even rarer. There is no full explanation for the underlying mechanism. Herein, we are presenting a rare case of concomitant acute hepatic failure and acute-on-chronic renal injury induced by use of IV amiodarone. A 67-year-old man with past medical history of coronary artery disease s/p coronary artery bypass graft (CABG), history of alcoholism, and chronic kidney disease stage 3 presented with chest pain for 1 week. In the emergency department (ED), he was found to have atrial flutter. Due to unresponsiveness to IV ß-blocker and diltiazem, the patient was loaded with IV amiodarone and continued IV amiodarone drip. His liver function tests (LFTs) and renal functions at the time of administration of IV amiodarone were aspartate transaminase (AST) 176 (10 - 42 IU/L) and alanine transaminase (ALT) 208 (10 - 60 IU/L), international normalized ratio (INR) 1.39 (reference value 2 - 3), blood urea nitrogen (BUN) 37 (5 - 25 mg/dL), and creatinine 1.85. Sixteen hours later patient developed acute hepatic failure with AST 4,250 (reference value 10 - 42 IU/L), ALT 2,422 (10 - 60 IU/L), INR 2.28, and acute renal failure with creatinine of 3.2 mg/dL (0.44 - 1.0 mg/dL), and BUN of 44 mg/d (5 - 25 mg/dL). Patient was intubated due to acute hepatic encephalopathy and sent to intensive care unit (ICU). IV amiodarone was stopped immediately. All workup for other causes of acute hepatic failure came back negative. He was started on IV N-acetylcysteine and required hemodialysis for acute-on-chronic renal failure. LFTs peaked 72 h after discontinuation of amiodarone. Kidney functions started to improve 5 days after discontinuation of amiodarone and patient came off hemodialysis. Acute hepatic failure as result of IV amiodarone is a rare presentation; however, it has a high mortality. Risk factors include low ejection fraction, hepatic congestion and pre-existing hepatic dysfunction. No obvious underlying mechanism to this presentation has been fully explained. Acute renal failure can be associated with this presentation which is even rarer. Stopping IV amiodarone, administering N-acetylcysteine and good supportive care can lead to favorable outcome.
RESUMO
Henoch-Schonlein purpura (HSP) is known as a leukocytoclastic vasculitis of small vessels, resulting in skin, joint, gastrointestinal (GI) and renal involvement. It is the most common acute vasculitis in children but is relatively uncommon in adults. The pathogenesis of HSP remains unclear, but a wide variety of conditions such as bacterial or viral infections, vaccinations, drugs and other environmental exposures may be responsible for the onset. A few previous case reports have described an association between gastric Helicobacter pylori (HP) infection and HSP. A 30-year-old Indian man who migrated to the USA from India 3 years prior to this presentation with a past medical history of psoriasis on remission, not on any medications presented to the emergency department with sudden onset constant abdominal pain for 5 days. The pain was in the right upper quadrant, spasmodic in nature. The abdominal examination was normal. The patient was evaluated with complete blood count, comprehensive metabolic panel, urinalysis, computed tomography scan of abdomen and pelvis, and right upper quadrant ultrasound, all of which were negative except for leukocytosis. He was discharged on pantoprazole and tramadol. Pain continued despite treatment. Patient was readmitted 2 days later, when he noticed a new maculopapular rash on both legs. Upper GI endoscopy was done showing non-bleeding small gastric ulcer with multiple duodenal erosions. Gastric biopsy came back positive for HP and he was started on clarithromycin, amoxicillin and lansoprazole. Pain persisted after finishing antibiotic course. Rash continued to spread to involve the thighs, flanks, around the umbilicus and extensor surfaces of arms. Immunological workup was negative. A skin biopsy of the skin rash came back positive for leukocytoclastic vasculitis. HSP diagnosis was made by exclusion. Patient was started on prednisone 40 mg daily and improved drastically on the following day. He was continued steroids taper for 8 weeks. Rash as well as abdominal pain resolved completely. In conclusion, HSP involves the skin, GI tract, joints and kidneys. It is a pediatric disease and rarely occurs in adults. It can be associated with underlying malignancy in adults. HP infection can trigger HSP in pediatric and adult patients. Detection of the carrier state is crucial in HSP patients in areas where HP is endemic. Eradication of HP infection is usually associated with the resolution of HSP. In resistant cases with GI and renal involvement, corticosteroids use results in resolution of symptoms and reduction of the duration of mild nephritis.
