![]() ![]() Change in MMSE score from baseline was compared by 2-tailed T-test. Mini Mental Status Examination (MMSE) was used as outcome measure. Double blind pharmacogenetic study: We performed double-blind pharmacogenetic analysis on the effect of AChEI therapy based on CHRFAM7A carrier status in two paradigms: response to drug initiation and DMT effect. ![]() Genome edited human induced pluripotent stem cells (iPSC) were used as a model system with the human context. ![]() doi:10.1016/j.diabres.2009.02.Molecular methods: Function of CHRFAM7A alleles was studied in vitro in two disease relevant phenotypic readouts: electrophysiology and Aβ uptake. Characteristics of the antibodies of two patients who developed daytime hyperglycemia and morning hypoglycemia because of insulin antibodies. Insulin autoimmune syndrome: from diagnosis to clinical management. Lupsa BC, Chong AY, Cochran EK, Soos MA, Semple RK, Gorden P. Evidence for multiple populations of insulin receptor antibodies with different receptor binding and insulin-mimicking activities. Characterization of the serum from a patient with insulin resistance and hypoglycemia. Insulin autoimmunity in a case of spontaneous hypoglycemia. Below both panels is reported a schematic representation of glucose and insulin concentrations over time: the continuous line represents plasma glucose concentrations, dotted line represents total insulin, pointed line represents free unbound insulin. Due to the relatively low affinity for insulin, IAA subsequently release insulin molecules irrespective of plasma glucose concentrations, thus inducing hypoglycemic episodes (phase 2). In the early postprandial phase, inclusion intro macro-complexes prevents insulin to act on its receptors in peripheral tissues, thus inducing hyperglycemia (phase 1). Following glucose intake, pancreatic beta-cells secrete insulin which enters into the blood stream getting included in the insulin-IAA macro-complexes. Panel ( B) schematic overview of the double-phase mechanism of the insulin autoimmune syndrome. Notes: Panel ( A) schematic overview of the physiologic insulin secretion and action: following glucose intake, pancreatic beta-cells secrete insulin which enters into the bloodstream, getting to peripheral tissues when it exerts its physiological functions in order to maintain glucose homeostasis. The insulin autoimmune syndrome pathogenesis. Hirata IAS autoimmunity hypoglycemia insulin autoimmune syndrome. The purpose of this review is to provide a comprehensive analysis of the disease, by describing the burden of knowledge that has been obtained in the 50 years following its first description, took in 1970, and by highlighting the points that are still unclear in its pathogenesis and management. Available therapies may include drugs that reduce pancreatic insulin secretion (somatostatin analogues and diazoxide, for instance) and immunosuppressive agents (glucocorticoids, azathioprine and rituximab). Pharmacological therapies may occasionally be necessary for patients presenting with severe manifestations of IAS. Because IAS is frequently a self-remitting disease, its management mostly consists of supportive measures, such as dietary modifications, aimed at preventing the development of hypoglycemia. The gold standard for the definitive diagnosis is the finding of IAA in a blood sample. The diagnosis of IAS is challenging, requiring a careful workup aimed at excluding other causes of hyperinsulinemic hypoglycemia. IAS pathogenesis involves the formation of insulin-IAA complexes that induce glycemic alterations with a double-phase mechanism: IAA prevent insulin to bind its receptor in the postprandial phase, possibly resulting in mild hyperglycemia thereafter, insulin is released from the complexes irrespective of blood glucose concentrations, thus inducing hypoglycemia. IAS is a form of immune-mediated hypoglycemia, which develops when a triggering factor (ie, a medication or a viral infection) acts on an underlying predisposing genetic background. Insulin autoimmune syndrome (IAS), also named Hirata's disease, is a rare condition characterized by hypoglycemic episodes due to the presence of high titers of insulin autoantibodies (IAA). ![]()
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