Tehran University Medical Journal

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Background: Celiac is one the most common causes of malabsorption and is an autoimmune disorder resulting in damage to intestinal epithelial cells by self T lymphocytes. The main culprit is gluten. The aim of our study was to assess the histopathologic findings of patients suspicious to have celiac disease in their first admission and compare them with serologic findings (endomyosial antibody test: EMA).
Methods: The study is a prospective descriptional type and 95 patients suspicious to have celiac disease were included who went under upper endoscopy and sampling and also serologic studies. Histopathologic findings were grouped by Marsh classification. Specimens in Marsh stage 0 and 1 were also stained for leukocyte common antigen by immunohistochemistry
Results: Ninety five patients, 49 males and 46 females, ranging from 9 months to 17 years (mean: 6.3 ys) were included in the study The most common complaint was abdominal pain. EMA test was positive in 43 patients. Most specimens were categorized as Marsh stage IIIA (51 cases) by histopatholgic examination, which can be seen in many other conditions. Only 16 patients were categorized as Marsh stage IIIB & IIIC, which are seen in established celiac patients No significant correlation was found between histopathologic and serologic findings. No difference was found between H&E staining and immunohistochemical staining in counting of intra- epithelial lymphocytes.
Conclusion: Most of our patients had mild partial villous atrophy which is also seen in many other disorders and also EMA test was negative in this group. It appears that current assessment of celiac disease has many drawbacks and necessity of more specific methods is highly appreciated.

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Background: Immune deficiency is one of the major causes of morbidity and mortality in the modern world. Primary immunodeficiency comprises a wide range of disorders that mainly manifest in early childhood as devastating infections with opportunistic organisms. Thymic aplasia is found on autopsy of some patients afflicted with immune deficiency disorders, such as DiGeorge syndrome and severe combined immunodeficiency (SCID). After a thorough search of the literature, we found little information on the cellular characteristics of these thymuses. Our study aims to elucidate role of apoptosis in the pathogenesis of thymic aplasia and compare various lymphocytic and epithelial markers in normal and aplastic thymuses.

Methods: We selected 12 subjects who died of severe infections with aplastic thymus found on autopsy, and 11 control subjects who died of unrelated causes, such as congenital heart disease. The presence of several markers, including Bcl2, P53, lymphocytic markers, and CD68, was examined using immunohistochemical methods on paraffin-embedded thymus sections. Positively-stained cells were counted per 1000 cells and the results stated as percentage of positive cells.                       

Results: The mean age of the control group was between 7 days to 18 months (mean: 4.5 months). Parental consanguinity was present in 45.5% and 9.1% of the control and case groups, respectively however, this was not statistically significant. We found significantly lower expression of Bcl2 in the case group (p value: 0.038). Furthermore, expression of CD68 was significantly higher in the case group. Epithelial markers were significantly higher in case subjects, although CD8 expression was higher in the control group. The presence of other markers was not significantly different between the two groups.

Conclusions: Increase in apoptosis has a role in aplastic thymuses and prevention of apoptosis may halt this process. Also high CD68 expression denotes increased phagocytic activity in aplastic thymuses.