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Medical Dictionary for Regulatory Activities Terminology (MedDRA)
| Id | http://purl.bioontology.org/ontology/MEDDRA/20000041
http://purl.bioontology.org/ontology/MEDDRA/20000041
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| Preferred Name | Hyperglycaemia/new onset diabetes mellitus (SMQ) |
| Definitions |
Diagnosis based on elevated levels of fasting plasma glucose or random plasma glucose plus symptoms. Hyperglycemia in diabetes mellitus (DM) occurs as a result of reduced insulin secretion, decreased glucose usage, or increased glucose production. Type I DM: About 10% of all cases; Insulin deficiency resulting from autoimmune beta cell destruction (type IA) or idiopathic (type IB). Type II DM: About 90% of all cases; Heterogeneous disorder of glucose metabolism characterized by variable degrees of insulin resistance, impaired insulin secretion, and increased hepatic glucose production. Drugs have been associated with hyperglycemia that can progress to new onset DM: Can mimic type I or II; Mechanisms: Diminished insulin production, inhibited insulin secretion, and reduced beta cell volume (e.g., cyclosporine); Autoimmune destruction of beta cells and increased insulin antibody titers (e.g., interleukin-2); Hormone stimulated gluconeogenesis and decreased insulin sensitivity (e.g., glucocorticosteroids); Decreased insulin sensitivity (e.g. protease inhibitors); Often reversible by discontinuation of drug, or can be controlled with oral antidiabetic agents and/or insulin. Common findings/symptoms: polydipsia, polyphagia, polyuria, weight loss, hypercholesterolemia, and hypertriglyceridemia. Acute complications: Diabetic ketoacidosis (DKA) particularly type I; Nonketotic hyperosmolar state (NKHS) particularly type II diabetes; Both can result in neurologic symptoms including coma. Long term complications are microvascular (e.g., retinopathy), macrovascular (e.g., coronary artery disease), neuropathic (e.g., paresthesias).
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| Type | http://www.w3.org/2002/07/owl#Class |
All Properties
| definition | Diagnosis based on elevated levels of fasting plasma glucose or random plasma glucose plus symptoms. Hyperglycemia in diabetes mellitus (DM) occurs as a result of reduced insulin secretion, decreased glucose usage, or increased glucose production. Type I DM: About 10% of all cases; Insulin deficiency resulting from autoimmune beta cell destruction (type IA) or idiopathic (type IB). Type II DM: About 90% of all cases; Heterogeneous disorder of glucose metabolism characterized by variable degrees of insulin resistance, impaired insulin secretion, and increased hepatic glucose production. Drugs have been associated with hyperglycemia that can progress to new onset DM: Can mimic type I or II; Mechanisms: Diminished insulin production, inhibited insulin secretion, and reduced beta cell volume (e.g., cyclosporine); Autoimmune destruction of beta cells and increased insulin antibody titers (e.g., interleukin-2); Hormone stimulated gluconeogenesis and decreased insulin sensitivity (e.g., glucocorticosteroids); Decreased insulin sensitivity (e.g. protease inhibitors); Often reversible by discontinuation of drug, or can be controlled with oral antidiabetic agents and/or insulin. Common findings/symptoms: polydipsia, polyphagia, polyuria, weight loss, hypercholesterolemia, and hypertriglyceridemia. Acute complications: Diabetic ketoacidosis (DKA) particularly type I; Nonketotic hyperosmolar state (NKHS) particularly type II diabetes; Both can result in neurologic symptoms including coma. Long term complications are microvascular (e.g., retinopathy), macrovascular (e.g., coronary artery disease), neuropathic (e.g., paresthesias). |
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| prefLabel | Hyperglycaemia/new onset diabetes mellitus (SMQ)
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| SMQ STATUS | A
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| type | |
| tui | T185
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| notation | 20000041
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| SMQ LEVEL | 1
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| Semantic type UMLS property | |
| SMQ ALGO | N
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| cui | C1869043
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| SMQ SOURCE | 1. Oki JC and Isley WL. Diabetes mellitus. Pharmacotherapy: A Pathophysiologic Approach (5th Ed). DiPiro JT, Talbert RL, Yee GC et al (Eds). McGraw-Hill: New York, 2002. pg. 1335-1358. 2. Powers AC. Diabetes mellitus. Harrison's Principles of Internal Medicine (15th Ed). Braunwald E, Fauci AS, Kasper DL et al (Eds). McGraw-Hill: New York, 2001. pg. 2109-2137. 3. Vanrenterghem YFC. Which calcerineurin inhibitor is preferred in renal transplantation: tacrolimus or cyclosporine? Curr Opin Nephrol Hypertension 1999; 8(6):669-674. 4. Fraenkel PG, Rutkove SB, Matheson JK et al. Induction of myasthenia gravis, myositis, and insulin-dependent diabetes mellitus by high-dose interleukin-2 in a patient with renal cell cancer. J Immunother 2002; 25(4):373-378. 5. Costa J. Corticotrophins and corticosteroids. Meyler's Side Effects of Drugs (14th Ed). Dukes MNG (Ed). Elsevier:Amsterdam, 2000. pg. 1364-1395. 6. Coates P. Miscellaneous hormones. . Meyler's Side Effects of Drugs (14th Ed). Dukes MNG (Ed). Elsevier:Amsterdam, 2000. pg. 1520-1526. 7. Heck AM, Yanovski LA, and Calis KA. Pituitary gland disorders. Pharmacotherapy: A Pathophysiologic Approach (5th Ed). DiPiro JT, Talbert RL, Yee GC et al (Eds). McGraw-Hill: New York, 2002. pg. 1395-1411. 8. Currier J. Management of metabolic complications of therapy. AIDS 2002; 16(Suppl 4):S171-S176. 9. Fantry LE. Protease inhibitor-associated diabetes mellitus: a potential cause of morbidity and mortality. JAIDS 2003; 32: 243-244. 10. Henderson DC. Atypical antipsychotic-induced diabetes mellitus. CNS Drugs 2002; 16(2):77-89. 11. Citrome LL. The increase in risk of diabetes mellitus from exposure to second-generation antipsychotic agents. Drugs of Today 2004; 40(5):445-464. 12. Melkersson K and Dahl M-L. Adverse metabolic effects associated with atypical antipsychotics: literature review and clinical implications. Drugs 2004; 64(7)701-723.
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