Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The association between autoimmune atrophic gastritis and thyroid disorders has been observed since the early 1960s and the expression "thyrogastric syndrome" was coined to indicate the presence of thyroid autoantibodies or autoimmune thyroid disease in patients with pernicious anemia, a late clinical stage of autoimmune atrophic gastritis. More recently, it was confirmed that autoimmune thyroid disorders, in particular Hashimoto's thyroiditis, may be frequently associated with other organ-specific, immune-mediated disorders, such as autoimmune atrophic gastritis or celiac disease. The association of Hashimoto's thyroiditis with autoimmune atrophic gastritis or celiac disease in adult patients is currently considered part of the polyglandular autoimmune syndromes which include several autoimmune disorders associated with an autoaggressive impairment of endocrine glands. From a clinical point of view, the thyro-entero-gastric autoimmunity may lead to potentially serious consequences like anemia, micronutrients deficiencies, and drugs malabsorption, as well as to an increased risk for malignancies. These alterations may frequently present in an underhand manner, with consequent diagnostic and treatment delays. Many aspects of the association between thyroid, gastric and intestinal autoimmune diseases still await clarification. The present review focuses on the embryological, genetic and pathophysiological aspects of thyro-entero-gastric autoimmunity. In particular, the current diagnostic criteria of autoimmune thyroid disease, autoimmune atrophic gastritis, and celiac disease are reviewed, along with the evidences for their association in poly-autoimmunity syndromes. The benefits of proactive screening of autoimmune thyroid disorders in patients with autoimmune gastritis or enteropathy and viceversa are also discussed.
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PMID:Thyro-entero-gastric autoimmunity: Pathophysiology and implications for patient management. 3186 9

Vitamin B-12 (cobalamin) deficiency in humans is a worldwide problem emanating from varied causes such as insufficient dietary intake or malabsorption of the micronutrient due to an underlying condition (absence or failure of intrinsic factor, atrophic gastritis, post-operative bariatric surgery, inflammatory bowel disease, cobalt deficiency etc.). As oral supplementation is limited by its bioavailability due to the absorptive property of intrinsic factor, clinicians often prescribe parenteral forms of administration to replenish diminished levels rapidly. The gold standard in parenteral delivery of cobalamin is subcutaneous and/or intramuscular injections. The relatively large molecular size of cobalamin (1355.39 Da) makes passive transdermal patch-based delivery via the stratum corneum quite challenging. Hence, the primary goal of this study is to investigate the feasibility of intradermal (ID) delivery of Vitamin B-12 via an almost painless microneedle injection and subsequent comparison with standard subcutaneous (SC) delivery. This work reports on a custom-made microneedle device built from a commercial insulin needle and it's use to perform ID delivery of Co-57 radiolabeled Vitamin B-12 in-vivo in rabbits. The pharmacokinetic profile and bioavailability were studied and compared with SC delivery. It is the first comprehensive study, to our best knowledge, that compares a micronutrient (eg. Vitamin B-12) delivery via ID and SC routes in-vivo. While the bioavailability for the SC route is found to be slightly higher compared to the ID route (99% vs. 96%), the Tmax for both are almost identical. Thus, ID delivery of Vitamin B-12 using a microneedle injection could be a viable and minimally invasive alternative to existing parenteral options.
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PMID:In-vivo Intradermal Delivery of Co-57 labeled Vitamin B-12, and Subsequent Comparison with Standard Subcutaneous Administration. 3194 17

Autoimmune gastritis (AIG) is an increasingly prevalent, organ-specific, immune-mediated disorder characterized by the destruction of gastric parietal cells, leading to the loss of intrinsic factor and reduced acid output. These alterations result in malabsorption of iron, vitamin B12 (pernicious anaemia) and potentially other micronutrients. For several years, most studies have focused on pernicious anaemia only, generating confusion between the two entities. In AIG, the gastric proton pump, H+/K+ ATPase, is the major autoantigen recognized by autoreactive T cells. The T cell-dependent activation of B cells stimulates the production of anti-parietal cell antibodies, the serological hallmark of AIG. The role of Helicobacter pylori infection in activating or favouring the autoimmune process is still uncertain. Early histopathological alterations allowing a more precise and prompt recognition have recently been described. AIG is burdened by a substantial diagnostic delay as it can present with varied clinical signs including, among others, gastrointestinal symptoms and neuropsychiatric manifestations. In advanced stages, AIG might progress to neuroendocrine tumours and gastric adenocarcinoma. Management includes early detection through a proactive case-finding strategy, micronutrient supplementation and endoscopic surveillance. This Primer comprehensively describes the most important insights regarding the epidemiology, pathophysiology, diagnosis and management of AIG, focusing on the most controversial, outstanding issues and future directions.
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PMID:Autoimmune gastritis. 3264 73


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