Leukopenia Associated with Long-Term Colchicine Adminsitration

Purpose A case of leukopenia in a patient receiving colchicine for calcium pyrophosphate dihydrate deposition disease, or pseudogout, is reported. Summary An 85-year-old man experienced leukopenia likely due to colchicine. His medical history included chronic lymphocytic leukemia (CLL), pseudogout, osteoarthritis, and hypertension. In February 2011, his white blood cell (WBC) count was 2700 cells/μL, and his absolute neutrophil count (ANC) was 2200 cells/μL. Colchicine 0.6 mg orally daily was initiated in March for the prophylaxis of pseudogout. His WBC count decreased, and his colchicine dosage was reduced to 0.6 mg every other day. Despite this decreased dosage, his WBC count and ANC were 600 and 100 cells/μL, respectively, in September. In October, the patient received chemotherapy for presumed worsening of his CLL. One month later, his WBC count and ANC were 400 and 200 cells/μL, respectively. Subcutaneous filgrastim was administered, and colchicine was discontinued. At the end of November, he received another cycle of chemotherapy followed by pegfilgrastim. On the day of pegfilgrastim administration, the patient\u27s WBC count and ANC were 2000 and 1300 cells/μL, respectively. Two weeks later, his WBC count was 8800 cells/μL, and his ANC was 8300 cells/μL. Daily colchicine was restarted at the end of December. Two months later, his WBC count and ANC were 800 and 500 cells/μL, respectively. Given the symptomatic relief with colchicine, therapy was continued with close monitoring. Conclusion A patient with CLL developed leukopenia in association with colchicine administration for pseudogout

Delayed-Onset Malignant Hyperthermia in Association with Rocuronium Use

Purpose Two cases of malignant hyperthermia suspected to be related to the use of a nondepolarizing neuromuscular blocker are reported. Summary A pharmacogenetic disorder that may occur in as many as 1 in 3000 anesthesia procedures, malignant hyperthermia has been linked to the use of certain anesthetic gases and depolarizing neuromuscular blocking agents (e.g., succinylcholine). Although nondepolarizing neuromuscular blockers were cited as contributing to the development of malignant hyperthermia in a small number of published reports, the agents are generally considered safe for use in at-risk patients. Here investigators report two cases in which the nondepolarizing agent rocuronium is thought to have triggered malignant hyperthermia in patients with no known history of the disorder. In one case, a critically ill 27-year-old man undergoing an induced-hypothermia protocol developed a fever about 4 days after receiving rocuronium infusions, with temperatures rising over 11 days to a maximum of 105.2 °F. In the other case, a 63-year-old man being treated for serious complications of elective surgery developed extreme fever (maximum temperature of 107.1 °F) about 4 days after receiving two bolus doses and a continuous infusion of rocuronium. In both cases, the discontinuation of rocuronium therapy was followed by the rapid diminution of fever over 12–36 hours. After consultations with medical staff and consideration of other potential causal and contributory factors (e.g., neurologic injury, antimicrobial-induced fever), rocuronium was deemed the most likely trigger of the severe febrile response experienced by these two patients. Conclusion A 27-year-old man and a 63-year-old man received rocuronium and subsequently developed delayed-onset malignant hyperthermia, which resolved after the rocuronium was discontinued

Rocuronium and Malignant Hyperthermia

Authors response to a comment on: Beggs A, McCann J, Powers J. “Delayed-onset malignant hyperthermia in association with rocuronium use ” Am J Health-Syst Pharm 2012; 69:1128-34

Beers criteria and STOPP/START criteria: medication evaluation with screening tools in elderly outpatients. [abstract 79]

Poster presented at the ACCP Virtual Poster Symposium; May 2012

Simultaneous MLPA-based multiplex point mutation and deletion analysis of the dystrophin gene

The Multiplex Ligation-dependent Probe Amplification assay (MLPA) is the method of choice for the initial mutation screen in the analysis of a large number of genes where partial or total gene deletion is part of the mutation spectrum. Although MLPA dosage probes are usually designed to bind to normal DNA sequence to identify dosage imbalance, point mutation-specific MLPA probes can also be made. Using the dystrophin gene as a model, we have designed two MLPA probe multiplexes that are specific to a number of commonly listed point mutations in the Leiden dystrophin point mutation database (http://www.dmd.nl). The point mutation probes are designed to work simultaneously with two widely used dystrophin MLPA multiplexes, allowing both full dosage analysis and partial point mutation analysis in a single test. This approach may be adapted for other syndromes with well defined common point mutations or polymorphisms