qr code in excel 2013 ALCOHOL-RELATED HYPOGLYCEMIA 1 Fasting Hypoglycemia after Ethanol in Objective-C

Draw QR in Objective-C ALCOHOL-RELATED HYPOGLYCEMIA 1 Fasting Hypoglycemia after Ethanol

ALCOHOL-RELATED HYPOGLYCEMIA 1 Fasting Hypoglycemia after Ethanol
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During the postabsorptive state, normal plasma glucose is maintained by hepatic glucose output derived from both glycogenolysis and gluconeogenesis With prolonged starvation, glycogen reserves become depleted within 18 24 hours and hepatic glucose output becomes totally dependent on gluconeogenesis Under these circumstances, a blood concentration of ethanol as low as 45 mg/dL can induce profound hypoglycemia by blocking gluconeogenesis Neuroglycopenia in a patient whose breath smells of alcohol may be mistaken for alcoholic stupor Prevention consists of adequate food intake during ethanol ingestion Therapy consists of glucose
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IMMUNOPATHOLOGIC HYPOGLYCEMIA
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This rare cause of hypoglycemia, documented in isolated case reports, may occur as two distinct disorders: one associated with spontaneous development of circulating antiinsulin antibodies and another associated with antibodies to insulin receptors, in which the antibodies apparently have agonist capabilities This latter disorder is extremely rare, having been documented in no more than five cases However, development of anti-insulin antibodies has been reported in over 200 patients most of whom were being treated with methimazole for thyrotoxicosis In Western countries, 23 cases have been reported and include patients with a lupus-like syndrome or with various paraproteinemias The hypoglycemia occurs 3 4 hours after meals
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Diabetes Mellitus & Hypoglycemia
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following an initial postprandial hyperglycemic phase that is due to the antibodies interfering with the exit of insulin from the plasma to reach its target tissues Later, after most of the meal is absorbed, inappropriate high levels of insulin dissociate from this antibody-bound compartment, resulting in hypoglycemia Insulin levels in excess of 1000 pmol/L are observed at time of hypoglycemia, and these persons have high titers of insulin autoantibodies
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Basu A et al Insulin autoimmunity and hypoglycemia in seven white patients Endocr Pract 2005 Mar Apr;11(2):97 103 [PMID: 15901524] Kim CH et al Autoimmune hypoglycemia in a type 2 diabetic patient with anti-insulin and insulin receptor antibodies Diabetes Care 2004 Jan;27(1):288 9 [PMID: 14694017] Sahin M et al Autoimmune hypoglycemia in a type 2 diabetic patient with anti-insulin and insulin receptor antibodies Diabetes Care 2004 May;27(5):1246 7 [PMID: 15111569] Yaturu S et al Severe autoimmune hypoglycemia with insulin antibodies necessitating plasmapheresis Endocr Pract 2004 Jan Feb;10(1):49 54 [PMID: 15251622]
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A number of drugs apart from the sulfonylureas can occasionally cause hypoglycemia, especially when ingested in large amounts These include quinine, quinidine, disopyramide, and salicylates ACE inhibitors, when taken with antidiabetic drugs, can cause hypoglycemia possibly by improving insulin sensitivity Recently, it has been reported that the use of gatifloxacin (an antibiotic that is no longer available in the United States) in diabetic patients is associated with serious hypoglycemic and hyperglycemic reactions Ten to 20 percent of patients receiving pentamidine for Pneumocystis jiroveci pneumonia develop symptomatic hypoglycemia, particularly when the drug is administered intravenously This apparently is due to lytic destruction of pancreatic B cells, causing acute hyperinsulinemia and hypoglycemia It is later followed by insulinopenia and hyperglycemia, which occasionally is persistent Since other drugs have been found to be as effective in treating Pneumocystis pneumonia, pentamidine administration and its hypoglycemic sequelae are less frequently encountered
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For patients with known cardiovascular disease (secondary prevention), cholesterol lowering leads to a consistent reduction in total mortality and recurrent cardiovascular events in men and women and in middle-aged and older patients Among patients without cardiovascular disease (primary prevention), the data are less conclusive, with rates of cardiovascular events, heart disease mortality, and all-cause mortality differing among studies Nonetheless, treatment algorithms have been designed to assist clinicians in selecting patients for cholesterol-lowering therapy based on their lipid levels and their overall risk of developing cardiovascular disease
Lipid Abnormalities
Robert B Baron, MD, MS
LIPOPROTEINS & ATHEROGENESIS
The plaques in the arterial walls of patients with atherosclerosis contain large amounts of cholesterol The higher the level of low-density lipoproteins (LDL) cholesterol, the greater the risk of atherosclerotic heart disease; conversely, the higher the high-density lipoproteins (HDL) cholesterol, the lower the risk of coronary heart disease (CHD) This is true in men and women, in different racial and ethnic groups, and at all ages up to age 75 years Because most cholesterol in serum is LDL, high total cholesterol levels are also associated with an increased risk of CHD Middle-aged men whose serum cholesterol levels are in the highest quintile for age (above about 230 mg/dL) have a risk of coronary death before age 65 years of about 10%; men in the lowest quintile (below about 170 mg/dL) have a 3% risk Death from CHD before age 65 years is less common in women, with equivalent risks one-third those of men In men, each 10-mg/dL increase in cholesterol (or LDL cholesterol) increases the risk of CHD by about 10%; each 5-mg/dL increase in HDL reduces the risk by about 10% The effect of HDL cholesterol is greater in women, whereas the effects of total and LDL cholesterol are smaller All of these relationships diminish with age There are several genetic disorders that provide insight into the pathogenesis of lipid-related diseases Familial hypercholesterolemia, rare in the homozygous state (about one per million) is a condition in which the cell-surface receptors for the LDL molecule are absent or defective, resulting in unregulated synthesis of LDL Patients with two abnormal genes (homozygotes) have extremely high levels up to eight times normal and present with athero-
sclerotic disease in childhood Homozygotes may require liver transplantation to correct their severe lipid abnormalities Those with one defective gene (heterozygotes) have LDL concentrations twice normal; persons with this condition may develop CHD in their 30s or 40s Another rare condition is caused by an abnormality of lipoprotein lipase, the enzyme that enables peripheral tissues to take up triglyceride from chylomicrons and verylow-density lipoproteins (VLDL) particles Patients with this condition, one cause of familial hyperchylomicronemia, have marked hypertriglyceridemia with recurrent pancreatitis and hepatosplenomegaly in childhood Numerous other genetic abnormalities of lipid metabolism are named for the abnormality noted when serum is electrophoresed (eg, dysbetalipoproteinemia) or from combinations of lipid abnormalities in families (eg, familial combined hyperlipidemia) Thus, family members of patients with severe lipid disorders are appropriately studied Other patients have abnormalities in the production of apoproteins, such as increased apoprotein B and its affiliated lipoproteins, LDL and VLDL; reduced apoprotein AII and its affiliated particle; or excess lipoprotein(a) Other mutations occur in lipoprotein lipase and in the gene encoding for cholesterol efflux regulatory protein
Ansell BJ et al High-density lipoprotein function recent advances J Am Coll Cardiol 2005 Nov 15;46(10):1792 8 [PMID: 16286161] Berneis K et al Low-density lipoprotein size and subclasses are markers of clinically apparent and non-apparent atherosclerosis in type 2 diabetes Metabolism 2005 Feb;54(2):227 34 [PMID: 15690318] Drexel H et al Is atherosclerosis in diabetes and impaired fasting glucose driven by elevated LDL cholesterol or by decreased HDL cholesterol Diabetes Care 2005 Jan;28(1):101 7 [PMID: 15616241] Nam BH et al Search for the optimal atherogenic lipid risk profile: from the Framingham study Am J Cardiol 2006 Feb 1;97(3):372 5 [PMID: 16442398]
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