Diagnoses of brown recluse spider bites (loxoscelism) greatly outnumber actual verifications of the spider in four western American states.

We attempt to demonstrate that physicians overdiagnose loxoscelism (colloquially known as 'brown recluse spider bites') by comparing the numbers of such diagnoses to the historically known numbers of Loxosceles spiders from the same areas in four western American states. The medical community from non-endemic Loxosceles areas often makes loxoscelism diagnoses solely on the basis of dermonecrotic lesions where Loxosceles spiders are rare or non-existent. If these diagnoses were correct then Loxosceles populations should be evident, specimens should readily be collected over the years and there should be a reasonable correlation between diagnoses and spider specimens. In 41 months of data collection, we were informed of 216 loxoscelism diagnoses from California, Oregon, Washington and Colorado. In contrast, from these four states, we can only find historical evidence of 35 brown recluse or Mediterranean recluse spiders. There is no consistency between localities of known Loxosceles populations and loxoscelism diagnoses. There are many conditions of diverse etiology that manifest in dermonecrosis. In the western United States, physician familiarity with these conditions will lead to more accurate diagnoses and subsequent proper remedy.     

Use of molecular tumor characteristics to prioritize mismatch repair gene testing in early-onset colorectal cancer.

PURPOSE: The relationships between mismatch repair (MMR) protein expression, microsatellite instability (MSI), family history, and germline MMR gene mutation status have not been studied on a population basis. METHODS: We studied 131 unselected patients with colorectal cancer diagnosed younger than age 45 years. For the 105 available tumors, MLH1, MSH2, MSH6, and PMS2 protein expression using immunohistochemistry (IHC) and MSI were measured. Germline DNA was screened for hMLH1, hMSH2, hMSH6, and hPMS2 mutations for the following patients: all from families fulfilling the Amsterdam Criteria for hereditary nonpolyposis colorectal cancer (HNPCC); all with tumors that were high MSI, low MSI, or that lacked expression of any MMR protein; and a random sample of 23 with MS-stable tumors expressing all MMR proteins. RESULTS: Germline mutations were found in 18 patients (nine hMLH1, four hMSH2, four hMSH6, and one hPMS2); all tumors exhibited loss of MMR protein expression, all but one were high MSI or low MSI, and nine were from a family fulfilling Amsterdam Criteria. Sensitivities of IHC testing, MSI (high or low), and Amsterdam Criteria for MMR gene mutation were 100%, 94%, and 50%, respectively. Corresponding positive predictive values were 69%, 50%, and 75%. CONCLUSIONS: Tumor IHC analysis of four MMR proteins and MSI testing provide a highly sensitive strategy for identifying MMR gene mutation-carrying, early-onset colorectal cancer patients, half of whom would have been missed using Amsterdam Criteria alone. Tumor-based approaches for triaging early-onset colorectal cancer patients for MMR gene mutation testing, irrespective of family history, appear to be an efficient screening strategy for HNPCC.     

Bed‐sharing among six‐month‐old infants in western Sweden

Aim: In spite of several reports of an increased risk of sudden infant death syndrome (SIDS) in connection with bed‐sharing, it is not an uncommon practice. The aim of this study was to examine bed‐sharing at 6 months of age and the factors that are associated with bed‐sharing. Methods: Our cohort comprised 8176 randomly chosen families. At 6 month of age, the families received an invitation to the study, with a questionnaire, which was completed by 5605 families (response rate 68.5%). Results: Of the families, 19.8% bed‐shared. In the multivariate analysis, we found a correlation between breast‐feeding and bed‐sharing (breast‐feeding at 6 months: OR 1.94; 95% CI 1.56, 2.41). Moreover, we found an association with 3+ nightly awakenings at 6 months (2.70; 2.20, 3.32). It was more common to share a bed if the parent was single (2.04; 1.19, 3.51) and less common if the infant was bottle‐fed in the first week (0.70; 0.54, 0.90). Never using a pacifier was associated with a higher frequency of bed‐sharing. Conclusion: We found a correlation between breast‐feeding and bed‐sharing as well as between sleeping problems and a single parent. A lower percentage of infants sleeping in the parental bed were seen in association with formula feeding in the first week after birth.     

Decreased expression of phospholipase C-beta 2 isozyme in human platelets with impaired function

Platelets from a patient with a mild inherited bleeding disorder and abnormal platelet aggregation and secretion show reduced generation of inositol 1,4,5-trisphosphate, mobilization of intracellular Ca2+, and phosphorylation of pleckstrin in response to several G protein mediated agonists, suggesting a possible defect at the level of phospholipase C (PLC) activation (see accompanying report). A procedure was developed that allows quantitation of platelet PLC isozymes. After fractionation of platelet extracts by high-performance liquid chromatography, 7 out of 10 known PLC isoforms were detected by immunoblot analysis. The amount of these isoforms in normal platelets decreased in the order PLC- gamma 2 > PLC-beta 2 > PLC-beta 3 > PLC-beta 1 > PLC-gamma 1 > PLC- delta 1 > PLC-beta 4. Compared with normal platelets, platelets from the patient contained approximately one-third the amount of PLC-beta 2, whereas PLC-beta 4 was increased threefold. These results suggest that the impaired platelet function in the patient in response to multiple G protein mediated agonists is attributable to a deficiency of PLC-beta 2. They document for the first time a specific PLC isozyme deficiency in human platelets and provide an unique opportunity to understand the role of different PLC isozymes in normal platelet function.