Vitamin A toxicity in a physical culturist patient: a case report and review of the literature

Excessive intake of vitamin A may produce acute or chronic toxicity. Vitamin A can be consumed in foods, fortified products and supplements. We present a case of a young physical culturist man who was referred to our Unit because of chronic liver disease of unknown origin. The patient had a history of increased vitamin A intake from natural source with the addition of high dose of vitamin A supplements with the purpose of improving his muscular development. Our patient showed chronic liver disease with severe fibrosis, signs of portal hypertension and marked hyperplasia of Ito cells. In conclusion, chronic vitamin A toxicity may produce severe liver damage and should be recognized in the differential diagnosis of chronic liver diseases.     

Systemic sarcocystosis in a patient with acquired immune deficiency syndrome

Sarcocystis sp is a tissue coccidian parasite in humans that causes intestinal and muscular sarcocystosis in immunocompetent patients. Intestinal sarcocystosis can be diagnosed at the tissue level in the lamina propria of the small bowel and by fecal examination. Muscular sarcocystosis is diagnosed by microscopic examination of muscle biopsies. This report describes a case of systemic sarcocystosis in an HIV-infected patient. We studied a 31-year-old patient with AIDS, chronic diarrhea, cholestatic hepatitis, and musculoskeletal pain by stool analysis and endoscopy with duodenal and liver biopsy specimens that were processed for routine histology. The microgamete and macrogamete stages of Sarcocystis sp were present in the lamina propria, with sporulated oocysts in feces. Schizont stages of the protozoa were found in liver biopsy. In summary, sarcocystosis should be considered another opportunistic infection in HIV-infected patients.     

Entry sites for oral vaccines and drugs: A role for M cells,enterocytes and dendritic cells?

M cells have long been considered as the unique entry site of macromolecules and pathogens in the intestine, allowing delivery to antigen-presenting cells in the Peyer's patches. Therefore, antigen formulation for the development of oral vaccines has been based on administration of antigens in the form of live replicating pathogens or soluble antigen vectorized into biodegradable microspheres. However, progress in the understanding of the biology of dendritic cells, as well as identification of their localization at different sites of the intestine, suggest that they may capture antigen directly from the lumen of mucosal tissues or from epithelial cells of the intestine. Besides, a role for the absorptive epithelium in antigen presentation through both classical or non-classical MHC elements suggests that PP may not be the exclusive inductive site of the immune response in the gut. Thus, depending on the nature of the antigen (soluble or infectious) there may be different sites of antigen entry through the intestine, and each site may have distinct efficiency to promote a protective immune response, depending on the presence and function of dendritic cells. Cross talk between M cells, epithelial cells and dendritic cells may play an important role in determining the outcome of tolerance versus immunity.     

Cyclospora cayetanensis in patients with AIDS and chronic diarrhea

Cyclospora spp. is a protozoan parasite responsible for significant gastrointestinal disease in patients infected with the human immunodeficiency virus. We report the clinical features of two patients with chronic diarrhea and intestinal cyclosporosis caused by Cyclospora cayetanensis. The average value for CD4 count in these patients was lower than or equal to 100 cells/mm3. The oocysts were detected in smears from stool samples stained with modified acid-fast or safranin technique. Light microscopy revealed parasites in the enterocytes and these parasites were associated with villous atrophy. Cyclospora cayetanensis infection might be an important cause of diarrhea in patients with AIDS in Argentina.     

Evidence that acute taurine treatment alters extracellular AMP hydrolysis and adenosine deaminase activity in zebrafish brain membranes

Taurine is one of the most abundant free amino acids in excitable tissues. In the brain, extracellular taurine may act as an inhibitory neurotransmitter, neuromodulator, and neuroprotector. Nucleotides are ubiquitous signaling molecules that play crucial roles for brain function. The inactivation of nucleotide-mediated signaling is controlled by ectonucleotidases, which include the nucleoside triphosphate diphosphohydrolase (NTPDase) family and ecto-5′-nucleotidase. These enzymes hydrolyze ATP/GTP to adenosine/guanosine, which exert a modulatory role controlling several neurotransmitter systems. The nucleoside adenosine can be inactivated in extracellular or intracellular milieu by adenosine deaminase (ADA). In this report, we tested whether acute taurine treatment at supra-physiological concentrations alters NTPDase, ecto-5′-nucleotidase, and ADA activities in zebrafish brain. Fish were treated with 42, 150, and 400 mg L⁻¹ taurine for 1 h, the brains were dissected and the enzyme assays were performed. Although the NTPDase activities were not altered, 150 and 400 mg L⁻¹ taurine increased AMP hydrolysis (128 and 153%, respectively) in zebrafish brain membranes and significantly decreased ecto-ADA activity (29 and 38%, respectively). In vitro assays demonstrated that taurine did not change AMP hydrolysis, whereas it promoted a significant decrease in ecto-ADA activity at 150 and 400 mg L⁻¹ (24 and 26%, respectively). Altogether, our data provide the first evidence that taurine exposure modulates the ecto-enzymes responsible for controlling extracellular adenosine levels in zebrafish brain. These findings could be relevant to evaluate potential beneficial effects promoted by acute taurine treatment in the central nervous system (CNS) of this species.     

Cross-priming of CD8+ T cells stimulated by virus-induced type I interferon

CD8+ T cell responses can be generated against antigens that are not expressed directly within antigen-presenting cells (APCs), through a process known as cross-priming. To initiate cross-priming, APCs must both capture extracellular antigen and receive specific activation signals. We have investigated the nature of APC activation signals associated with virus infection that stimulate cross-priming. We show that infection with lymphocytic choriomeningitis virus induces cross-priming by a mechanism dependent on type I interferon (IFN-alpha/beta). Activation of cross-priming by IFN-alpha/beta was independent of CD4+ T cell help or interaction of CD40 and CD40 ligand, and involved direct stimulation of dendritic cells. These data identify expression of IFN-alpha/beta as a mechanism for the induction of cross-priming during virus infections.