Chloroquine-induced cardiomyopathy: a reversible cause of heart failure.

Chloroquine (CQ) and hydroxychloroquine (HCQ) are anti-rheumatic medications frequently used in the treatment of connective tissue disorders. We present the case of a 45-year-old woman with CQ-induced cardiomyopathy leading to severe heart failure. Electrocardiographic abnormalities included bifascicular block, while structural disease consisted of severe biventricular and biatrial hypertrophy. Appropriate diagnosis via endomyocardial biopsy led to cessation of CQ and subsequent dramatic improvement in symptoms and structural heart disease. Cardiac toxicity is an under-recognized adverse effect of CQ/HCQ leading to cardiomyopathy with concentric hypertrophy and conduction abnormalities, with the potential for significant morbidity and mortality. Predisposing factors for CQ/HCQ-induced cardiomyopathy have been proposed. CQ/HCQ cardiomyopathy is a phenocopy of Fabry disease, and α-galactosidase A polymorphism may account for some heterogeneity of disease presentation.

Contemporary review of drug-induced pancreatitis: A different perspective.

Although gallstone and alcohol use have been considered the most common causes of acute pancreatitis, hundreds of frequently prescribed medications are associated with this disease state. The true incidence is unknown since there are few population based studies available. The knowledge of drug induced acute pancreatitis is limited by the availability and the quality of the evidence as the majority of data is extrapolated from case reports. Establishing a definitive causal relationship between a drug and acute pancreatitis poses a challenge to clinicians. Several causative agent classification systems are often used to identify the suspected agents. They require regular updates since new drug induced acute pancreatitis cases are reported continuously. In addition, infrequently prescribed medications and herbal medications are often omitted. Furthermore, identification of drug induced acute pancreatitis with new medications often requires accumulation of post market case reports. The unrealistic expectation for a comprehensive list of medications and the multifactorial nature of acute pancreatitis call for a different approach. In this article, we review the potential mechanisms of drug induced acute pancreatitis and provide the perspective of deductive reasoning in order to allow clinicians to identify potential drug induced acute pancreatitis with limited data.

A trial of discontinuation of empiric vancomycin therapy in patients with suspected methicillin-resistant Staphylococcus aureus health care-associated pneumonia.

Healthcare-associated pneumonia (HCAP) guidelines recommend de-escalating initial antibiotic therapy based on results from lower-respiratory-tract cultures. In the absence of adequate lower respiratory cultures, physicians are sometimes reluctant to discontinue empirical vancomycin, which is given for suspected methicillin-resistant Staphylococcus aureus (MRSA) HCAP. We evaluated a strategy of discontinuing vancomycin if both nasal and throat cultures were negative for MRSA when lower-respiratory-tract cultures were not available. An antimicrobial stewardship team identified patients receiving empirical vancomycin for suspected or proven HCAP but for whom adequate lower-respiratory-tract cultures were not available. Nasal and throat swab specimens were obtained and plated on MRSA selective media. If both nasal and throat MRSA cultures were negative, the stewardship team recommended discontinuation of empirical vancomycin. Demographic and clinical aspects, a clinical pulmonary infection score (CPIS) on the day of the stewardship recommendation, and mortality of patients for whom vancomycin was discontinued were obtained by retrospective chart review. A convenience sample of 91 patients with nasal and throat cultures negative for MRSA in the absence of adequate respiratory cultures had empirical vancomycin therapy discontinued. A retrospective review revealed that 88 (97%) patients had a CPIS of ≤6 on the day of the stewardship recommendation. In-hospital mortality (7.7%) was similar to that of a previous study of de-escalation of antibiotics in pneumonia patients without adequate cultures. In the absence of adequate lower-respiratory-tract cultures, it is reasonable to discontinue empirical vancomycin HCAP therapy in patients with negative MRSA nasal and throat cultures and a CPIS of <6.

Early risk factors for persistent anemia after kidney transplantation.

STUDY OBJECTIVE: To identify predictors of persistent posttransplant anemia that appear within the first week after kidney transplantation in order to determine the high-risk patients who might receive the most benefit from erythropoiesis-stimulating agents. STUDY DESIGN: Retrospective cohort study. SETTING: University-affiliated hospital and outpatient clinic. PATIENTS: One hundred sixty-four adult kidney transplant recipients (January 1, 2002-June 30, 2007) with anemia on posttransplant day 7 who were followed at the clinic for at least 2 months after transplantation. MEASUREMENTS AND MAIN RESULTS: Data from deidentified electronic medical records of the kidney transplant recipients were collected and included demographic characteristics, primary cause of renal failure, pertinent laboratory data, and donor information. To detect early predictors of persistent anemia, patients with persistent posttransplant anemia, defined as a hemoglobin level below 11 g/dl for 2 months (day 60) after transplantation, were compared with those who had nonpersistent posttransplant anemia, defined as a hemoglobin level below 11 g/dl on day 7 but 11 g/dl or greater on day 60. Of the 164 patients classified as having anemia on posttransplant day 7, 39 (23.8%) had persistent posttransplant anemia on day 60. In univariate analyses, hemoglobin level of 9 g/dl or below on day 7, donor age younger than 10 years, and female sex were variables associated with increased risk of persistent posttransplant anemia. In a multivariate analysis, donor age younger than 10 years was the most significant predictor of persistent posttransplant anemia, followed by hemoglobin level of 9 g/dl or below. CONCLUSION: Patients receiving transplants from donors younger than 10 years and those with hemoglobin levels of 9 g/dl or below on postoperative day 7 were found to be at highest risk for persistent posttransplant anemia and may receive the most benefit from early initiation of erythropoiesis-stimulating agent therapy. In most of the kidney transplant recipients, posttransplant anemia resolved without the use of these agents.

Tigecycline-induced acute pancreatitis: case report and literature review.

Tigecycline is a broad-spectrum antimicrobial agent structurally related to minocycline. Pancreatitis has been associated with the tetracycline class of antibiotics and concerns about tigecycline-induced acute pancreatitis have recently been raised. We describe a 69-year-old female who received tigecycline for treatment of a complicated skin and skin-structure infection. Following 7 days of tigecycline she developed severe abdominal pain and elevated pancreatic enzymes suggesting acute pancreatitis. According to the Naranjo adverse drug reaction probability scale, tigecycline was the probable cause of her acute pancreatitis. Clinicians should be aware of this potential adverse effect of tigecycline. We recommend that clinicians monitor patients for signs and symptoms of pancreatitis, including abdominal pain, during treatment with tigecycline.