Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A mixed metabolic alkalosis and metabolic acidosis, resulting in an alkalemic state, occurred in a hyperlipemic patient with previously diagnosed non insulin dependent diabetes. The metabolic alkalosis, due to large loss of gastric HCl, was more severe than the diabetic acidosis and resulted in an alkaline blood pH. Initially the metabolic acidosis was due to ketoacidosis and coexistent lactic acidosis. During the improvement of the alkalemic and hyperglycemic state, lactic acidosis disappeared but a paradoxical rise of plasma NEFA and ketone body concentrations supervened so that the high anion gap metabolic acidosis was virtually unchanged. The rise of plasma NEFA was probably related to the marked removal of plasma triglycerides, by insulin activation of lipoprotein lipase, and consequent saturation of the pathways of fatty acid incorporation into adipose tissue.
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PMID:Metabolic alkalosis in diabetic ketosis: a case report. 643 80

A 67 year old woman was admitted with a three week history of vomiting, having become increasingly confused for three days. Investigations revealed deranged serum biochemistry consistent with a combination of a diabetic non-ketotic hyperosmolar state and a metabolic alkalosis consistent with gastric outflow obstruction. She was treated with intravenous saline, intravenous insulin, and subcutaneous heparin, but did not improve clinically and had an asystolic cardiac arrest the following day; she was transferred to the intensive care unit and despite treatment with inotropes she died 40 hours after admission. Necropsy revealed that the stomach was massively dilated with gas and stomach contents, and contained many small black faceted gall stones. In addition a large nonfaceted brown-yellow gall stone was wedged in the pyloric antrum causing total obstruction. The patient had died from a complex metabolic derangement including non-ketotic hyperosmotic diabetic coma and metabolic alkalosis precipitated by the acute gastric outflow obstruction complicated by previously undiagnosed type II diabetes mellitus.
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PMID:Gastric outflow obstruction caused by gall stones and leading to death by complex metabolic derangement. 946 52

We report a rare case of Bartter's syndrome in a 35-year-old woman with type 2 diabetes mellitus. The patient presented with leg weakness, fatigue, polyuria and polydipsia. Hypokalemia, metabolic alkalosis, and high renin and aldosterone concentrations were present, but the patient was normotensive. Gitelman's syndrome was excluded because of the presence of hypercalciuria, secondary hyperparathyroidism and bilateral nephrocalcinosis. The patients condition improved upon administration of a prostaglandin synthetase inhibitor (acemetacin), oral potassium chloride and potassium-sparing diuretics. Five months later, the patient discontinued acemetacin because of epigastric discomfort; at the same time, severe hypokalemia and hyperglycemia developed. Glucagon stimulation and water deprivation tests were performed. Type 2 diabetes mellitus with nephrogenic diabetes insipidus was diagnosed. To avoid further gastrointestinal complications, the patient was treated with celecoxib, a selective cyclooxygenase 2 inhibitor. This case serves as a reminder that Bartter's syndrome is associated with various metabolic derangements including nephrogenic diabetes insipidus, nephrocalcinosis and diabetes mellitus. When treating Bartter's syndrome, it is also prudent to remember that the long-term use of nonsteroidal anti-inflammatory drugs and potassium-sparing diuretics may result in serious adverse reactions.
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PMID:Bartter's syndrome with type 2 diabetes mellitus. 1925 37