Zinc deficiency due to low intake or unavailability by bioactive compounds may lead to morphological changes in the intestines resulting in disruptions in gut function. This study aims to assess effects of phytic acid on gut morphology of rats.
Diets supplemented with sweet potato phytate extract were fed to Wistar rats in zinc-deficient and zinc-sufficient states for 4 weeks. Similar test animals also had diets supplemented with the commercially available sodium phytate salt (IP6) for comparison. At the end of the feeding period, body weights, feed intake and markers of intestinal function were assessed.
Acute zinc deficiency adversely affected the glycocalyx, goblet and Paneth cells within the small intestine. This may eventually lead to compromisation of the gut's immune system and further reductions in its metabolic and absorptive capacity. This was further aggravated by sweet potato phytate extract consumption. IP6 supplementation on the other hand, increased surface amplification in the jejunum resulting in increased gut transit time and more efficient absorption of nutrients.
To minimize compromisation of the gut's immune, absorptive and metabolic functions, adequate zinc supplementation is necessary especially if foods rich in phytates are included in the diet. Supplementation of the diet with IP6 seems to offset some of these effects with maximum benefits observed if the diet is properly supplemented with essential minerals.
The biologic behavior of gastrointestinal stromal tumors (GIST) is a topic of continuing controversy. The assessment of accurate mitotic figures is known to be one of the major indicators for patients with GIST. However, it is not always easy to search for mitotic figures (MFs) and count them accurately on hematoxylin and eosin stained (H&E) slides.
In this study, phopho-histone H3 (PHH3), which is a recently described specific mitosis marker, was immunohistochemically examined and compared to the mitotic count on H&E sections (H&E-MI) and Ki-67 expression (Ki-67 PI). A hundred cases of histologically confirmed GISTs were reviewed based on counting MF on H&E slides. PHH3 positive MFs (PHH3-MI) were counted in the same way, and the Ki-67 PI was calculated for each case.
A strong correlation was found between PHH3-MI and H&E-MI. Recurrence-free survival was correlated with risk category by National Institutes of Health (NIH) consensus criteria (P = 0.017), mucosal invasion (P = 0.005), H&E-MI (P = 0.002), Ki-67 PI (P = 0.005), and PHH3-MI (P = 0.000). None of these factors was an independent prognostic factor.
Among GISTs, PHH3 staining was primarily found to support grading by facilitating mitotic counting, and it might have a prognostic value in GISTs.
Primary adrenal lymphoma is rare, but clinically important. We report a unique case of adrenal lymphoma which showed extensive cystic change mimicking a pseudocyst. Seventy-three-year-old man visited our hospital for healthcare check-up, and was found to have a large adrenal cystic mass. He was received adrenalectomy on the impression of an adrenal pseudocyst. On gross examination, the mass was a unilocular cyst with no solid mass formation. Microscopically, the cyst wall had no epithelial lining, but was infiltrated by some atypical large lymphoid tumor cells. The cystic space was filled with coagulative necrotic material with the tumor cell shadow. The most of the tumor cells expressed leukocyte common antigen, CD20, PAX5, Ki-67, and Epstein-Barr virus (EBV)-encoded RNA, which was consistent with EBV-positive diffuse large B-cell lymphoma of the elderly. No extra-adrenal involvement was observed in imaging studies. We concluded that primary adrenal lymphoma should be considered as a rare but important cause of adrenal cysts.
Anti-glomerular basement membrane antibody-mediated glomerulonephritis (anti-GBM Ab-mediated GN) is a rare autoimmune disease, characterized by crescentic glomeruli and linear GBM staining with immunoglobulin G (IgG). Exposure to viruses can trigger the formation of autoantibodies to the GBM. We report the first case of anti-GBM Ab-mediated GN associated with hepatitis A virus (HAV) infection. Although the pathogenesis of HAV-related anti-GBM Ab-mediated GN has not been documented, we suggest that the immune complexes produced by HAV infection might be deposited in the glomerular capillary walls and lead to immune complex-mediated glomerular damage, resulting in exposure of the sequestered GBM antigens and the formation of anti-GBM antibodies. Under immunosuppressive and intravenous cyclophosphamide therapy, his renal function has been improving without development of pulmonary symptoms.