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S. Martucci [1,2] F. Biagi [1,2] G.R. Corazza [2] P.J. Ciclitira [1] H.J. Ellis [1] (1.) Gastroenterology Dept, Rayne Institute (KCL), St Thomas' Hospital, London SE1 7EH, UK; (2.) Cattedra [...]

This study provides data on the genetic structuring of the pipefish Syngnathus abaster in the western Mediterranean and Adriatic Seas. A total of 109 specimens were collected in brackish-water biotopes. The control region and three other regions of the mitochondrial genome were analysed. The most relevant result was the high genetic structuring found by Bayesian inference ( BI), maximum likelihood ( ML) and network analyses, which were consistent in showing three well-separated clusters of S. abaster populations. Furthermore, BI and ML did not support the monophyly of the taxon S. abaster. These results suggest the occurrence of a species complex in the study area, whose differentiation may have occurred since the Pleistocene. The results also show a very high genetic variability at the inter-population level, with no shared haplotypes among sites. Evolutionary forces due to the fragmented nature of the brackish-water habitats may account for the high genetic divergence found among the groups and populations. Finally, although dispersal by rafting over long distances may occasionally occur, this study suggests linear stepping-stone model of colonization to be most likely. The complexity of the results obtained suggests that further studies are needed to elucidate the phylogeny of S. abaster. [ABSTRACT FROM AUTHOR]

Background: Whipple disease, which is caused by infection with Tropheryma whipplei, can be treated effectively with antimicrobials. Occasionally, inflammation reappears after initial improvement; this is often interpreted as refractory or recurrent disease. However, polymerase chain reaction for T. whipplei in tissue is sometimes negative during reinflammation, indicating absence of vital bacteria, and this reinflammation does not respond to antimicrobials but does respond to steroids. Objective: To demonstrate that the immune reconstitution inflammatory syndrome (IRIS) occurs in patients treated for Whipple disease. Design: Cohort study. (International Standard Randomised Controlled Trial Number Register registration number: ISRCTN45658456) Setting: 2 academic medical centers in Germany. Methods: 142 patients treated for Whipple disease out of a cohort of 187 were observed for reappearance of inflammatory signs after effective antibiotic therapy. Definitions of IRIS in HIV infection, tuberculosis, and leprosy were adapted for application to Whipple disease. Results: On the basis of study definitions, IRIS was diagnosed in 15 of 142 patients. Symptoms included fever, arthritis, pleurisy, erythema nodosum, inflammatory orbitopathy, small-bowel perforation, and a hypothalamic syndrome. Two patients died. There was a positive correlation with previous immunosuppressive treatment and a negative correlation with previous diarrhea and weight loss. Limitations: The study was observational and thus has inherent weaknesses, such as incomplete and potentially selective data recording. Conclusion: The immune reconstitution inflammatory syndrome was diagnosed in about 10% of patients with Whipple disease in the study cohort; the outcome varied from mild to fatal. Patients who had had previous immunosuppressive therapy were at particular risk. An immune reconstitution syndrome should be considered in patients with Whipple disease in whom inflammatory symptoms recur after effective treatment. Early diagnosis and treatment with steroids may be beneficial; prospective studies are needed. Primary Funding Source: European Commission and Deutsche Forschungsgemeinschaft. [ABSTRACT FROM AUTHOR]

Summary: Background and aim: Microvascular damage of coronary bed has been considered the main pathogenetic factor of cardiac syndrome X (chest pain, exercise-induced ischemic ST-segment changes and angiographically normal coronary arteries). Previous studies have demonstrated that vascular abnormalities are not confined to the heart, suggesting a peripheral vascular dysfunction. On the hypothesis of a generalized microvascular disturbance in cardiac syndrome X, we performed a morphologic and functional study of systemic microcirculation in patients with syndrome X compared to normal subjects. Methods and results: Microvessels were evaluated with intravital videocapillaroscopy (VCP) executed in peripheral and conjunctival observation sites which explore micro and paramicrocirculation; biohumoral study included markers of inflammation and of endothelial function, coagulative–fibrinolytic system and lipid metabolism. Videocapillaroscopy showed several morphologic changes (present in high percent of patients with syndrome X and not in controls) and significant quantitative alterations (capillary density, granular flow score, alterations of vessel profile, length of capillary loop branches and of arteriole/venule diameter) which indicated a severe alteration of whole vessel structure and an important rearrangement of microvascular disposition. In a similar way, the humoral study showed some significant changes of endothelial (vWF, ICAM-1, E-sel, PAI-1), inflammatory (C-reactive protein (CRP), fibrinogen) and metabolic factors (HDL-chol) which are commonly associated with inflammatory response. Conclusions: We conclude that patients with cardiac syndrome X exhibited some structural and functional alterations of systemic microvasculature; the pattern is similar to that detected in systemic inflammatory diseases and suggests a vascular lesion of inflammatory type. The same changes could be operating also in coronary microvessels of patients with syndrome X. [Copyright &y& Elsevier]

Background: Since transglutaminase was shown to be the antigen of endomysial antibodies (EMA), it has become possible to screen for coeliac disease (CD) with an enzyme-linked immunosorbent assay (ELISA) for transglutaminase antibodies (TTA). However, it is possible that sera used to show that TTA are found in CD were obtained from patients diagnosed because they were positive for EMA. So, a comparison between EMA and TTA has not been possible so far. Methods: EMA and TTA were tested in sera from 52 controls and 56 untreated CD patients, who had not undergone serological testing. Samples were tested for TTA with an ELISA kit. Based on the ROC analysis of a pilot study, results were considered as either positive, borderline, or negative. EMA were analysed by indirect immunofluorescence on monkey oesophagus. Results: Forty-nine CD patients were positive for TTA, six borderline, one negative. Forty-four controls were negative, seven borderline, one positive. If we consider borderline results to be positive, sensitivity is 98.2% and specificity 84.6%. EMA were positive in 53 CD patients; the controls were all negative. Performing TTA in all cases and EMA only in the few TTA borderline cases (12.0%) would have a sensitivity of 94.6% and a specificity of 98.1%. Conclusions: This study is the first to compare TTA with EMA. Due to 100% specificity and high sensitivity, EMA seems to be the most accurate coeliac antibody. Conversely, TTA offer advantages in terms of sensitivity and simplicity. A satisfactory strategy is to use TTA first and then EMA to confirm the borderline results. [ABSTRACT FROM AUTHOR]

Focuses on the literature review on the clinical relationship between ulcerative jejunoileitis (UJI), coeliac disease (CD), and enteropathy-associated T-cell lymphoma. Characterization of UJI; Symptoms of intestinal ulceration; Method used in the diagnosis of CD.

Background: Individuals with Down syndrome have an increased prevalence of coeliac disease (CD). The HLA region accounts for only 30% of the heritability of CD, and segregation analyses have suggested the involvement of at least one other non-HLA gene. Distribution of known HLA susceptibility types in Down syndrome and normal populations are similar and do not explain the difference in disease frequency. This study tests the hypothesis that the association between these disorders is due to a susceptibility gene for coeliac disease being present on chromosome 21. Methods: We studied 21 families multiply affected with CD, none of whom had Down syndrome. The typing information of six microsatellite markers across chromosome 21 was used to test linkage. Results: Negative results from lod score and model-free linkage analysis were obtained, providing no support for genetic linkage of coeliac disease to chromosome 21 in this population. Conclusions: The high prevalence of coeliac disease in Down syndrome is not due to an increased copy number of a polymorphic susceptibility gene on chromosome 21. [ABSTRACT FROM AUTHOR]