American journal of clinical pathology
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Am. J. Clin. Pathol. · Mar 2010
Clinicopathologic features of agranulocytosis in the setting of levamisole-tainted cocaine.
Levamisole is a known contaminant of cocaine and, via this route, has been associated with otherwise unexplained agranulocytosis. Levamisole is currently present in the majority of cocaine samples seized by the US Drug Enforcement Agency. We identified 20 cases of unexplained agranulocytosis in our practice locations of Albuquerque, NM, and Vancouver, Canada. ⋯ Of 5 patients tested, 3 (60%) were HLA-B27+ and showed antineutrophil antibodies, consistent with known associations of levamisole-induced agranulocytosis. One patient, who was positive for cocaine and levamisole by toxicology testing, died of infectious complications. Inadvertent consumption of levamisole via cocaine is a severely under-appreciated risk factor for agranulocytosis, and specific laboratory features are suggestive of this etiology.
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Am. J. Clin. Pathol. · Nov 2009
Case ReportsEmbolization of hydrophilic catheter coating to the lungs: report of a case mimicking granulomatous vasculitis.
Hydrophilic coatings are used on intravascular devices to facilitate ease of manipulation and to minimize complications such as thrombosis during a procedure and vasospasm after a procedure. We report a case of embolization of hydrophilic coating of a central venous catheter to the lung that resulted in cavitary lung nodules in a 34-year-old woman. The microscopic features of this unusual complication warrant emphasis so that pathologists will not overlook the embolic foreign material and make a faulty diagnosis of noniatrogenic granulomatous vasculitis.
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Am. J. Clin. Pathol. · Oct 2009
In situ evidence of KRAS amplification and association with increased p21 levels in non-small cell lung carcinoma.
Recent advances in the characterization of the lung cancer genome have suggested that KRAS may frequently be amplified, although little is known regarding the significance of this finding. This is in contrast with activating mutations of KRAS, which occur in approximately 20% of non-small cell lung carcinomas (NSCLCs). We used fluorescence in situ hybridization to provide direct evidence of KRAS amplification for the first time in clinical specimens. ⋯ KRAS amplification was associated with greater expression of p21 as assessed by quantitative immunohistochemical analysis (P = .015). Our data indicate that a sizable subgroup of NSCLCs harbor KRAS amplification, some of which also contain point mutations, and suggest that an increased KRAS copy number may drive p21 overexpression. KRAS amplification may define a unique clinicopathologic subset of NSCLCs with potentially altered responsiveness to targeted therapies.
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Am. J. Clin. Pathol. · Sep 2009
Implementation of a rapid whole blood D-dimer test in the emergency department of an urban academic medical center: impact on ED length of stay and ancillary test utilization.
Overcrowding and prolonged patient length-of-stay (LOS) in emergency departments (EDs) are growing problems. We evaluated the impact of implementing a rapid whole blood quantitative D-dimer test (Biosite Triage, Biosite Diagnostics, San Diego, CA) in our ED satellite laboratory on 252 patients before vs 211 patients after implementation. All patients also underwent testing with the existing central laboratory method (VIDAS D-dimer, bioMérieux, Durham, NC). ⋯ No difference in the utilization of radiologic studies was observed (P = .86). At 3 months' follow-up, none of the after-implementation patients with negative D-dimer results were admitted for subsequent venous thromboembolic disease. The rapid D-dimer test was associated with a shorter ED LOS and fewer hospital admissions.
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Am. J. Clin. Pathol. · Sep 2009
Exertional dysnatremia in collapsed marathon runners: a critical role for point-of-care testing to guide appropriate therapy.
Dysnatremia may cause life-threatening encephalopathy in marathon runners. Hypernatremia and exercise-associated hyponatremia (EAH) may manifest with mental status changes and, if untreated, progress to coma and death. We reviewed the on-site blood sodium testing and treatment in collapsed runners at the finish-line medical tent at the Boston marathons from 2001 through 2008. ⋯ Sixteen runners with EAH able to drink a concentrated oral hypertonic solution recovered within 30 minutes. Based on on-site sodium testing, dysnatremic runners were treated with appropriate intravenous fluids according to validated standards of care. Hyponatremic runners able to drink an oral hypertonic solution recovered promptly.