Hyponatraemia is a common electrolyte disturbance, with moderate (serum sodium: 125–129 mmol/L) to severe (serum sodium: ≤125 mmol/L) forms of the disease occurring in 4–15% of hospitalised patients. While it is relatively common, determining the underlying cause of this condition can be challenging and may require extensive laboratory investigations. To this end, it is important to ascertain the efficacy of laboratory tests in determining the cause of hyponatraemia. Up to 10% of patients with hypothyroidism also have hyponatraemia. Routine evaluation of thyroid function is often advocated in cases of low serum sodium. A review and discussion of the available literature is presented here to examine this recommendation.

Pelger-Huët anomaly (PHA) is a rare benign autosomal-dominant anomaly with an incidence of ∼1 in 6000. It does not cause neutrophilia, but it can cause a false increase in band forms. It should be differentiated from acquired or pseudo-Pelger-Huët anomaly (PPHA), which has similar morphology, however; it is associated with different pathological states like Myelodysplastic syndrome, as well as with certain infections and drugs. We report a case of a 67-year-old Caucasian gentleman with past medical history of rheumatoid arthritis, type II diabetes mellitus and hypothyroidism, who presented with 1 day history of fever (101°F) and night sweats. Medications include ibuprofen, methotrexate, hydroxychloroquine and levothyroxine. Patient denied any other symptoms. His work-up showed normal WBC count (8.6) and increase in bands (24%). The patient was admitted for further evaluation. During the next 2 days, the patient did not have any fever or any new symptoms. Peripheral blood smear was done as part of his work-up for bandemia, showed findings suggestive of PHA. Ibuprofen was discontinued. Follow-up few weeks later showed normal blood smear. Diagnosis of PPHA was made. The presented case showed that we should think of PHA\PPHA in any case with normal total WBC count and significant shift to the lift with no apparent explanation. Looking at smears directly under the microscopes is crucial to make diagnosis.

Statins reduce inflammation in end-stage renal disease patients and improve endothelial function beyond cholesterol lowering. Despite this, statins do not improve the maturation rate, primary patency rate, and the cumulative survival of arteriovenous fistulas (AVFs). It is unknown if statins decrease the number of stenoses developing in AVFs or prolong the intervals between angioplasties needed to treat recurring stenoses. We conducted a retrospective chart review of our 265 active dialysis patients. The statin group was significantly more likely to be diabetic (64% vs. 43.6%) and treated with aspirin (64% vs. 40%) when compared to those not treated with statins (P=0.04 and 0.01). The mean time to first intervention (primary patency) was 16.5months in statin users and 15.8months in the nonstatin group (P=0.49) with standard deviations of +/- 18.5 and 16.6months, respectively. Statin use was not associated with a significant decrease in the number of stenoses diagnosed (P=0.28). The mean time between recurrent stenoses' angioplasties was 8.9months in statin users and 7.3months in the nonstatin patients (P=0.25). Aspirin users were more likely to have a decreased primary patency (rate ratio=1.65, P=0.03) compared with nonaspirin users. Patients who were prescribed aspirin developed 1.6 (P 0.01) times more stenoses than those not treated with aspirin. We report for the first time that statin therapy does not decrease the number of stenotic lesions developing in the AVF or prolong the interval between procedures required to treat recurrent stenoses.

SESSION TITLE: Cancer Student/Resident Case Report Posters II

Vascular access dysfunction is a major contributor to end stage renal disease patient morbidity, and the cost of maintaining it is staggering. Any intervention able to improve the vascular access maturation rate and/or patency would be significant progress. Based on the anti-inflammatory and vascular beneficial effects demonstrated in non-end stage renal disease patients, we were hoping that statin use might provide the much needed improvement in the hemodialysis vascular access outcome. The reality proved disappointing. The statins failed to improve every aspect of hemodialysis vascular access studied. The present editorial discusses the current data regarding the effect of statins on vascular access and attempts to explain their lack of success.

BACKGROUND:1,5-Anhydroglucitol (1,5-AG) is a glucose analogue, which is decreased in hyperglycemic individuals. We report the technical performance of an assay (GlycoMark) on a chemistry analyzer, evaluation of analyte stability and determination of reference intervals for 1,5-AG in a non-diabetic US population. METHODS:NCCLS protocols were followed to evaluate the reagent on a Hitachi 917 chemistry analyzer. RESULTS:Intra- and interassay imprecision ranged from 1.3% to 3.8% and 0.79% to 3.7%, respectively. The assay was linear to 110 microg/ml. Interference from triglyceride, hemoglobin and bilirubin was <10% to concentrations of 12.6 mmol/l, 12.1 and 911.4 micromol/l, respectively. Correlation coefficients between lot numbers on the Hitachi 917 and between analyses on the Hitachi 917 and the Hitachi 7170 analyzers were >0.99. The lowest limit of detection was 0.49 microg/ml (mean+/-2 S.D.). 1,5-AG was stable at 4 degrees C for 7 days, at 22 degrees C for 5 days, at -80 degrees C for 14 days and for three freeze-thaw cycles at -80 degrees C. The US reference intervals (nonparametric 2.5th-97.5th percentiles) were 10.2-33.8 microg/ml (males) and 5.9-31.8 microg/ml (females). CONCLUSIONS:The performance of the GlycoMark assay for the measurement of 1,5-AG was acceptable on the Hitachi 917 analyzer.

In myxoid/round cell liposarcoma, the t(12;16)(q13; p11) and its associated fusion transcript, FUS-CHOP , characterize greater than 95% of cases. The variant translocation t(12;22)(q13;q12) and associated EWS-CHOP fusion transcript are rare. A second non-random aberration observed in roughly 20% of Ewing’s sarcomas, and to a lesser extent other select sarcomas, is the unbalanced 1;16 translocation. Recognition of this secondary aberration in the absence of an obvious primary karyotypic abnormality strongly suggests that the use of other genetic approaches will be infor-mative in uncovering a clinically suspected primary anomaly. The following case illustrates the utility of molecular cytogenetic and reverse transcriptase-poly-merase chain reaction techniques in diagnosing an ins(22;12)(q12;q13q14) and associated EWS-CHOP fusion transcript in a myxoid/round cell liposarcoma exhibiting a der(16)t(1;16)(q11;q11). (J Mol Diagn 2003, 5:191–194)

Journal of Pediatric Gastroenterology and NutritionVolume 37, Issue 5 p. 624-626 Case Report Metastatic Hepatocellular Carcinoma in a Patient with Niemann-Pick Disease, Type C Nathan C. Birch, Nathan C. Birch Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NESearch for more papers by this authorStanley Radio, Stanley Radio Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NESearch for more papers by this authorSimon Horslen, Corresponding Author Simon Horslen [email protected] Department of Pediatric Gastroenterology, University of Nebraska Medical Center, Omaha, NE, U.S.A.Address correspondence and reprint requests to Dr. Simon Horslen, 986495 Nebraska Medical Center, Omaha, NE 68198-6495, (E-mail: [email protected]).Search for more papers by this author Nathan C. Birch, Nathan C. Birch Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NESearch for more papers by this authorStanley Radio, Stanley Radio Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NESearch for more papers by this authorSimon Horslen, Corresponding Author Simon Horslen [email protected] Department of Pediatric Gastroenterology, University of Nebraska Medical Center, Omaha, NE, U.S.A.Address correspondence and reprint requests to Dr. Simon Horslen, 986495 Nebraska Medical Center, Omaha, NE 68198-6495, (E-mail: [email protected]).Search for more papers by this author First published: 01 November 2003 https://doi.org/10.1002/j.1536-4801.2003.tb12075.xCitations: 5Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat No abstract is available for this article. REFERENCES 1.Fink JK, Filling-Katz MR, Sokol J, et al. Clinical spectrum of Niemann-Pick disease type C. Neurology 1989; 39(8): 1040–9. 10.1212/WNL.39.8.1040 CASPubMedWeb of Science®Google Scholar 2.Vanier MT. Phenotypic and genetic heterogeneity in Niemann-Pick disease type C: current knowledge and practical implications. Wien Klin Wochenschr 1997; 109(3): 68–73. CASPubMedWeb of Science®Google Scholar 3.Vanier MT, Rodriguez-Lafrasse C, Rousson R, et al. Type C Niemann-Pick disease: biochemical aspects and phenotypic heterogeneity. Dev Neurosci 1991; 13(4-5): 307–14. 10.1159/000112178 CASPubMedWeb of Science®Google Scholar 4.Yerushalmi B, Sokol RJ, Narkewicz MR, et al. Niemann-pick disease type C in neonatal cholestasis at a North American Center. 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The synthesis of a novel spirooxazine (1-benzyl-3,3-dimethylspiro[indoline-2,3′-naphtho [2,1-b] [1,4] oxazine, BSP-SP) was developed as a colorimetric probe for the quantitative analysis of Fe2+ and Pb2+ in water samples. The device is based on a microfluidic paper-based analytical device (μPAD). BSP-SP was characterized by various techniques, e.g. single-crystal X-ray diffraction (SC-XRD) and time-dependent density functional theory (TD-DFT). In addition, the density functional theory (DFT) allowed us to understand better the adsorption of Fe2+ and Pb2+ over other cations adsorption on the BSP-MO structure. The structural isomerization of BSP-SP occurs as an open-form merooxazine (BSP-MO), which acts as a ligand to form Fe2+/BSP-MO and Pb2+/BSP-MO complexes. We observed these complexes under UV irradiation as having a light blue coloration. The μPADs were also proposed as detection platforms to maintain photostability and photochromic efficiency and extend the lifetime of the spirooxazine. Under optimal conditions, the developed μPAD enables rapid and sensitive quantitative analysis of Fe2+ at pH 6 and Pb2+ at pH 11. The limits of detection (LOD) were 0.036 mg L−1 for Fe2+ and 0.152 mg L−1 Pb2+. Overall, the developed sensors, particularly the μPADs, promise the practical analysis of Fe2+ and Pb2+ in water samples.

Detection of Chlamydia trachomatis and/or Neisseria gonorrhoeae infection in urine using molecular amplification assays has permitted institutions with limited medical facilities to offer testing for these sexually transmitted diseases (STDs). The Nebraska Public Health Laboratory (NPHL) investigated the validity of urine samples submitted for C trachomatis and/or N gonorrhoeae amplification after receiving a substantial number of clear specimens. Approximately 75% of all urine specimens submitted for STD testing to the NPHL were from correctional facilities. The falsification of urine specimens submitted for microbiology studies is not evaluated routinely, and this problem was previously undocumented. By using the criteria for specific gravity of 1.001 or less and a creatinine concentration of less than 5 mg/dL (442 mumol/L), approximately 8% of all specimens submitted during the study interval were determined to be inconsistent with urine. The microbiology laboratory should be aware of the possibility for specimen manipulation to identify facilities submitting falsified specimens, to initiate appropriate intervention, and to minimize false-negative reporting.

Cytogenetic analysis has improved our understanding of the histopathogenesis of many benign and malignant bone and soft tissue tumors, as well as served as an important diagnostic adjunct for these pathologic entities. Cytogenetic reports of benign cartilaginous tumors, however, are relatively few. This is unfortunate, as distinguishing benign and malignant cartilaginous neoplasms can often be difficult. In this study, the cytogenetic findings of two enchondromas, two periosteal chondromas, and one soft part chondroma and a review of the literature are reported. Abnormal diploid or near-diploid clones were detected in all specimens analyzed. Although a tumor-specific anomaly did not emerge from these studies, involvement of certain chromosomes/chromosomal regions appears recurrent.