Prevalence of amiodarone-related hepatotoxicity in 720 Chinese patients with or without baseline liver dysfunction.

BACKGROUND: The prevalence of hepatotoxicity after longterm oral amiodarone therapy in Chinese patients with or without elevated liver enzymes at baseline is unknown. HYPOTHESIS: Amiodarone may still be safely prescribed for Chinese patients who have baseline liver dysfunction. METHODS: This is a retrospective cross-sectional study. Significant liver dysfunction (SLD) was defined as alanine aminotransferase (ALT) > 2 times upper limit of normal range. RESULTS: Baseline liver function was checked in 628 of the 720 Chinese patients identified. The mean duration of amiodarone use was 615.9 +/- 703.1 days. Ninety patients (14.3%) had elevated baseline ALT. The prevalence of SLD was 3.7% (confidence interval [CI] 2.1-5.3%) and 4.4% (CI 0.2-8.6%) in patients with normal (n = 538) and elevated (n = 90) baseline ALT, respectively (p = 0.765). Therapy was continued in 42 patients with elevated baseline ALT until final follow-up. Eight of these (19.0%) had elevated ALT upon final follow-up, but the derangement was mild (mean ALT 134.8 +/- 145.9 IU/l, median 76 IU/l). During follow up, 24 patients developed SLD and half of these subsequently withdrew from therapy. The ALT levels at final follow-up had improved over time in both groups, but the mean difference was not significant (255.1 +/- 706.4 vs. 131.0 +/- 207.5 IU/l, p = 0.312). CONCLUSION: The prevalence of SLD in Chinese patients taking oral amiodarone with or without elevated baseline ALT was similar (4.4 vs. 3.7%). It seems that amiodarone may be safely prescribed in patients with elevated baseline ALT.

Neuroleptic malignant syndrome and dopaminergic blockade.

After receiving 90 mg of haloperidol and 100 mg of chlorpromazine hydrochloride within 25 hours, a 29-year-old man was found to have neuroleptic malignant syndrome (NMS), characterized by the acute onset of hyperpyrexia, extreme muscular rigidity, autonomic instability, and coma. Subsequently, rhabdomyolysis developed, with myoglobinuric renal failure and bilateral anterior tibial compartment syndromes. The patient's initial neuroleptic levels were in the therapeutic and nontoxic ranges. He was treated with supportive measures and his clinical improvement was paralleled by decreased neuroleptic levels, a return toward normal of an elevated prolactin level, and an increased responsiveness to a dopamine hydrochloride infusion. This supports an association between NMS and dopamine receptor blockade.

Early left ventricular lead dislodgement related to hyperpnea respiration.

Left ventricular lead dislodgement remained a problem for cardiac resynchronization therapy and is one of the major causes of repeated procedures. We report a 30-year-old lady with possible left ventricular lead dislodgement related to hyperpnea respiration.

Prolongation of atrial effective refractory period with biatrial nonexcitatory stimulation.

BACKGROUND: A nonexcitatory, nonpropagating atrial extrastimulus delivered in the refractory period of the preceding cycle can prolong the atrial effective refractory period (AERP) and prevent the induction of atrial fibrillation by another AE introduced in the vulnerable period. Whether the effect of this nonexcitatory stimulation (NE) is confined only to its application site is unknown. METHODS AND RESULTS: Sixteen consecutive patients were recruited into the study and 2 patients were excluded because of development of more sustained atrial fibrillation. NE was commenced by introduction of a 2.0 msec, 20-mA impulse at 50 msec after the preceding captured pacing impulse. AERP of right atrial septum, a distant site to NE application, was determined at baseline and after 5 minutes of steady pacing at six different protocols: protocol 1, 2, and 3 were conventional pacing at high right atrium, distal coronary sinus, and biatrial sites, respectively, and protocol 4, 5, and 6 were conventional pacing together with NE applied to the same sites as protocol 1, 2, and 3. Biatrial NE (protocol 6 with median AERP = 212.5 msec) significantly prolonged AERP compared with baseline (median AERP = 202.5 msec and P < 0.05), conventional pacing (protocol 1, 2, and 3 with median AERP = 205.0 msec, 205.0 msec, and 205.0 msec, respectively, and all P < 0.05), and single-site NE (protocol 4 and 5 with median AERP = 207.5 msec and 207.5 msec, respectively, and both P < 0.05). CONCLUSION: Biatrial NE resulted in AERP prolongation even at sites distant to NE application. The study result suggests that by adding NE to multi-sites pacing for atrial fibrillation prevention may have additional benefit.

Treatment of chlorpropamide overdose with diazoxide.

A patient who took a chlorpropamide overdose was treated for several hours with concentrated glucose solutions, with little success in maintaining adequate serum glucose concentrations. Intravenous diazoxide administration was begun with the hope of decreasing pancreatic insulin release. After diazoxide was begun, glucose requirements decreased dramatically, and serum glucose was supranormal for most of the period of diazoxide administration. The case was complicated by the fact that the patient had taken three agents that can cause hypoglycemia--chlorpropamide, alcohol, and aspirin. Drug interactions potentiating the hypoglycemic effect of the chlorpropamide were also possible. Glucose infusion is the mainstay of therapy for a sulfonylurea overdose. However, glucose acts as a further stimulus of insulin release from a sulfonylurea-primed pancreas. Administration of concentrated glucose solutions is technically difficult because of damage to veins. Metabolic consequences of high rates of glucose infusion to hyperinsulinemic patients include hypokalemia and hypophosphatemia. Diazoxide appeared to decrease the glucose requirement in this patient, as it did in three other reported cases. Diazoxide is approved for certain hypoglycemic, hyperinsulinemic conditions. Sulfonylurea overdose represents a hypoglycemic, hyperinsulinemic condition; diazoxide appears to be an effective treatment.

Acute renal failure after acetaminophen overdose: report of two cases.

Two cases of acute tubular necrosis without hepatic failure following acetaminophen overdose are reported. A 19-year-old Caucasian woman ingested 100 500-mg capsules of acetaminophen. She was admitted to a hospital 68 hours after ingestion, and serum acetaminophen concentration 70 hours after ingestion was 3 microgram/ml. Liver-function test results were markedly elevated, and urinalysis was abnormal on admission. Liver function improved over the next five days, but the patient's renal function deteriorated. Her condition initially was diagnosed as prerenal azotemia, but was later consistent with acute tubular necrosis. Hemodialysis was begun on the fifth day of hospitalization. On the eleventh hospital day, the patient's renal function began to improve, and she was subsequently discharged. In the second case, a 19-year-old Spanish-American woman ingested 30 500-mg capsules of acetaminophen. She was seen in an emergency room 16 hours after the ingestion; her serum acetaminophen concentration was 32 microgram/ml 19 hours after ingestion. Oral acetylcysteine therapy was begun, and liver-function test results were elevated and peaked on the third hospital day. Renal function began to decline on the fifth hospital day; her condition was consistent with acute tubular necrosis. She was hemodialyzed once, and her renal function improved on the tenth hospital day. She was subsequently discharged. It is concluded that acute renal failure without prior hepatic failure may occur after acetaminophen overdose.

Acquired methemoglobinemia and hemolytic anemia after usual doses of phenazopyridine.

Two patients developed symptomatic methemoglobinemia and hemolytic anemia after treatment with phenazopyridine. Methemoglobinemia appears to be a rare occurrence after commonly used doses of phenazopyridine; phenazopyridine-associated hemolytic anemia has been reported both after overdose and after usual doses. The presentation of methemoglobinemia in the first patient and the response to treatment with methylene blue in the second patient were unusual, suggesting that the patients had a red cell defect or were exposed to other oxidizing substances. One of the major metabolites of phenazopyridine is aniline, a known cause of methemoglobinemia. Aniline-induced methemoglobinemia is less responsive to treatment with methylene blue than nitrate- or nitrite-induced methemoglobinemia. This may explain, in part, the poor response to methylene blue by one of our patients.

Brugada syndrome unmasked by febrile illness.

The ionic mechanisms responsible for the electrocardiographic phenotype of the Brugada syndrome are temperature dependent. This report describes a healthy young man with ECG changes typical of Brugada syndrome that were unmasked during a febrile illness.