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Aims: To establish the prevalence of cyclooxygenase-2 (COX-2) expression in a large series of resected Barrett's adenocarcinoma and associated preneoplastic lesions and to correlate this expression with clinicopathological data and prognosis. Methods: COX-2 expression was assessed by immunohistochemistry in resected surgical specimens of 66 Barrett's adenocarcinomas and 32 cases of Barrett's mucosa (with dysplasia in 17 cases). Results: Epithelial expression of COX-2 protein was increased in Barrett's mucosa compared with normal oesophagus. Epithelial expression of COX-2 was found in 91% of Barrett's specialized mucosa negative for dysplasia, 94% of Barrett's mucosa with dysplasia, and 97% of Barrett's adenocarcinoma. COX-2 expression was significantly higher in the well-differentiated adenocarcinomas when compared with the poorly differentiated tumours. There was no significant correlation between COX-2 expression and the other pathological features of the tumours. Survival analysis showed no significant prognostic value for COX-2. Conclusion: Our results confirm up-regulation of COX-2 in Barrett's oesophagus—metaplastic and dysplastic—and in Barrett's adenocarcinoma. Increased COX-2 expression did not differ during the progression from Barrett's oesophagus negative for dysplasia to Barrett's adenocarcinoma and is related to adenocarcinoma whose histology is well differentiated. This suggests that enhanced expression of COX-2 may occur early during Barrett's-associated neoplastic transformation. [ABSTRACT FROM AUTHOR]

MLH1 and MSH2 protein immunohistochemistry is useful for detection of hereditary non-polyposis colorectal cancer in young patients Aims: Hereditary non-polyposis colorectal cancer is related to germline mutations of DNA mismatch repair genes MLH1 and MSH2 , which result in microsatellite instability and loss of protein expression of the corresponding mutated gene in the tumour tissue. Methods and results: MLH1 and MSH2 protein expression was studied by immunohistochemistry in paraffin-embedded surgical samples of 100 colorectal adenocarcinomas occurring before 50 years of age. Absence of tumour cell nuclear staining with positive internal control (normal mucosa, lymphoid follicles) was considered negative. Loss of MLH1 or MSH2 expression was found in 20 cases with microsatellite instability in 15 cases. Twelve of these patients had a family history of colorectal cancer. Compared with MLH1- and MSH2-positive cases, MLH1- or MSH2-deficient colorectal adenocarcinomas were significantly associated on multivariate analysis with a younger age (38 vs. 43 years, P; 0.0224), a larger tumour size (60 ± 6 vs. 46 ± 2 mm, P =0.0291), an expanding margin (85% vs. 51%, P =0.0159), a higher number of tumour-infiltrating lymphocytes assessed by CD3 immunostaining (202 ± 48 vs. 33 ± 4 CD3+ lymphocytes/10 high-power fields, P =0.0039), and a grade 2 Crohn's like lymphoid reaction (70% vs. 9%, P =0.0037). The two groups were not different for tumour site, differentiation, pTNM stage, vascular and perineural invasion, peripheral adenomatous residue, and 5-year survival rates. Conclusions: MLH1- or MSH2-deficient colorectal carcinomas of young patients exhibit pathological and molecular features similar to hereditary non-polyposis colorectal cancer. This suggests that MLH1 and MSH2 immunohistochemistry is valuable for detecting hereditary non-polyposis colorectal cancer in young patients. [ABSTRACT FROM AUTHOR]

SUMMARY Glomerulonephritis with organized microtubular monoclonal immunoglobulin deposits (GOMMID) and glomerulonephritis related to type I cryoglobulin are well-known but rare complications of B cell derived chronic lymphocytic leukaemia. In these disorders, monoclonal Ig have never been studied at the molecular level. We conducted a pathological and molecular analysis in a patient with chronic lymphocytic leukaemia, glomerulonephritis and a single circulating monoclonal Ig. Unusual IgG1κ kidney deposits were observed. The heavy and light chain variable region sequences of that cryoprecipitating monoclonal Ig were characterized. Light microscopy revealed glomerulonephritis typical of cryoglobulinaemia, with neutrophil and macrophage infiltration, endocapillary hyperplasia and few protein thrombi. Electron microscopic study clearly evidenced numerous subepithelial mixed granular and organized deposits with a unique microtubular organization, reminiscent of the GOMMID. The Ig molecule sequence revealed alterations of charge and hydrophobicity potentially promoting a crystal-like aggregation and the aggregation of microtubules.This description suggests that common mechanisms are involved in various forms of precipitation and/or deposition of complete Ig molecules, with a variable extent of organization and with a possible overlap between pathological patterns of either glomerulonephritis with microtubular deposits or type I cryoglobulinic glomerulonephritis. [ABSTRACT FROM AUTHOR]

Clin Microbiol Infect 2012; 18: E531-E532 Abstract Lyme borreliosis is a common tick-borne disease with a wide variety of clinical manifestations. Cardiac involvement has been reported during both the acute phase (atrioventricular block, pericarditis) and the chronic stage (dilated cardiomyopathy), but is rare (<5%). Here we describe the first case of Borrelia afzelii Lyme endocarditis, in a 61-year-old man living in an endemic area of France. The diagnosis was confirmed by detection of B. afzelii DNA in the mitral valve by specific real-time PCR. He was treated empirically with amoxicillin for 6 weeks and remains well 12 months later. [ABSTRACT FROM AUTHOR]

Focuses on acute renal failure and hematuria in marathon runners, examining the role of glomerular bleeding in tublar injury in the risk of renal failure in runners and referencing the case report of a 46-year-old male marathon runner. Details on the symptoms the runner presented; Factors which contributed to the onset of renal failure; Information on the tests conducted on the patient; Treatment administered to the patient.

Objectifs L’hémochromatose néonatale (HN) est caractérisée par une insuffisance hépatocellulaire aiguë avec cirrhose et surcharge ferrique diffuse liée à une allo-immunisation maternofoetale avec activation du complément. La destruction hépatocytaire massive, à l’origine d’une carence en hepcidine foetale entraînant un afflux transplacentaire de fer. Le SHU est une microangiopathie thrombotique (MAT). Sa survenue en période néonatale doit faire évoquer une forme atypique (SHUa) généralement liée à une activation incontrôlée de la voie alterne du complément. Sujet Nous rapportons les observations de deux nouveau-nés décédés précocement ayant présenté un tableau évocateur de SHUa avec insuffisance rénale aigue (IRA), anémie hémolytique mécanique et thrombopénie. Les autopsies ont permis de poser le diagnostic d’HN. L’histologie rénale n’a pas retrouvé de lésions de MAT ni de dysgénésie tubulaire rénale mais de rares dépôts ferriques. Discussion L’HN est une cause classique d’insuffisance hépatocellulaire à transaminases normales. La particularité de nos observations est la présence de stigmates de MAT non décrits dans l’ HN. Conclusion Le diagnostic d’HN devra être évoqué chez un nouveau-né présentant des signes de SHU, a fortiori si des troubles de l’hémostase sont présents. [ABSTRACT FROM AUTHOR]