Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A number of hemodynamic, pharmacologic and metabolic interventions were found to change the extent of acute ischemic injury of the myocardium and subsequent necrosis following experimental coronary artery occlusion. Reduction in myocardial damage occurred by decreasing myocardial oxygen demands (beta-adrenergic blocking agents, intra-aortic balloon counterpulsation, external counterpulsation, nitroglycerin, decreasing afterload in hypertensive patients, inhibition of lipolysis, and digitalis in the failing heart); by increasing myocardial oxygen supply either directly (coronary artery reperfusion or elevating arterial pO2), or through collateral vessels (elevation of coronary perfusion pressure by alpha-adrenergic agonists, intra-aortic balloon counterpulsation); or by increasing plasma osmolality (mannitol, hypertonic glucose); presumably by augmenting anaerobic metabolism (glucose-insulin-potassium, hypertonic glucose); by enhancing transport to the ischemic zone of substrates utilized in energy production (hyaluronidase); by protecting against autolytic and heterolytic damage (hydrocortisone, cobra venom factor, aprotinin). Augmentation of myocardial ischemic damage occurred as a consequence of increasing myocardial oxygen requirements (isoproterenol, glucagon, ouabain, bretylium tosylate, tachycardia); by decreasing myocardial oxygen supply either directly (hypoxia, anemia) or through reduction of collateral flow (hemorrhagic hypotension, minoxidil) or by decreasing substrate availability glycemia). Pilot studies have been carried out in patients with hyaluronidase, nitroglycerin, intra-aortic balloon counterpulsation, beta-blocking agents and Arfonad and have shown that these interventions may also reduce myocardial damage, suggesting that the concept of reduction in infarct size following coronary occlusion is applicable clinically.
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PMID:Effects of metabolic and pharmacologic interventions on myocardial infarct size following coronary occlusion. 0 95

Described here is a patient who had an islet cell carcinoma containing both glucagon (glucagonoma) and insulin (insulinoma). Complete removal of the tumor was possible. Immunoreactive glucagon (IRG) could be extracted from all parts of the tumor (approximately 50 mug./gm.) and was shown to be fully bioactive. Immunoreactive insulin (IRI) could be extracted only from one section of the tumor (approximately 30 mug./gm.). The clinical and biochemical manifestations of the disease were dermatitis, diabetes, weight loss, anemia, hypoaminoacidemia, and hyperketonemia. The diabetes was characterized by low or normal fasting blood glucose concentrations and by impaired glucose tolerance (Kg = 0.4). After complete removal of the tumor, the dermatitis cleared, the catabolic state changed into an anabolic state, blood amino acid concentrations increased, and blood ketone-body concentrations decreased. Fasting blood glucose concentrations, however, rose above 200 mg./dl., and glucose tolerance declined further (Kg = 0.15). Hourly blood sampling for 24 hours, intravenous and oral glucose tolerance tests, intravenous arginine and tolbutamide tolerance tests with serial determinations of IRG, IRI, and blood glucose were performed preoperatively and again two weeks and two months postoperatively. The results of these studies demonstrated marked abnormalities in the stimulation and suppression of glucagon and insulin release. In addition, they failed to demonstrate a glycemic effect on the chronically elevated glucagon concentrations in this patient, while identifying insulin as the dominant factor determining blood glucose homeostasis.
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PMID:An islet cell carcinoma containing glucagon and insulin. Chronic glucagon excess and glucose homeostasis. 19 71

A case of glucagonoma syndrome with necrolytic migratory erythema, glossitis, anemia, hyperglucagonemia and a malignant, pancreatic A-cell tumour in a 68-year-old male is described. Gel filtration of the highly elevated circulating glucagon immunoreactivity (2200 pg/ml) demonstrated 60% pancreatic glucagon and 30% "proglucagon". Metabolic studies before operation demonstrated suppression of the total plasma glucagon concentration on oral glucose tolerance test, unchanged total plasma glucagon concentration during intravenous glucose tolerance test and insulin-induced hypoglycemia. Administration of arginine was followed by a rise in both the pancreatic glucagon and the "proglucagon", whereas alanine increased only the pancreatic glucagon. The plasma somatostatin level was immeasurable preoperatively. Somatostatin infusion completely suppressed the release of the pancreatic glucagon but did not significantly affect the "proglucagon". After removal of the tumour the skin lesions disappeared and the total plasma glucagon values fell to normal levels (120 pg/ml). Also, other abnormal laboratory findings returned to normal, including the preoperatively observed renal glucosuria.
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PMID:Metabolic studies and glucagon gel filtration pattern before and after surgery in a case of glucagonoma syndrome. 21 26

A 66-year-old male patient with non-insulin-dependent diabetes of probably 20 years' duration presented with necrolytic migratory erythema, stomatitis, anemia and weight loss. Plasma-glucagon concentration measured with Unger's antibody 30-K was 8500 pg/ml, representing a hundredfold elevation. Two thirds consisted of high molecular glucagon fractions (10 000--40 000 Dalton). This may be an important index for detection of glucagonoma with endocrine activity. After excision of the glucagonoma the clinical syndrome was reversed and the patient recovered completely. Histological and histochemical investigation confirmed that the tumor was a glucagonoma. Despite complete removal of the tumor and a normal plasma glucagon concentration, the diabetes remained unchanged. Excessive hyperglucagonemia does not appear to play a primary role in the pathogenesis of this patient's diabetes.
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PMID:[The course of diabetes and clinical findings in glucagonoma]. 52 94

Fourteen adults in whom diabetes mellitus and coeliac disease coexist, are described. In no patient was coeliac disease diagnosed (biopsy proven) before the age of 28 years. Diabetes was recognized before coeliac disease in all except one. Diabetic control was very unstable and hypoglycaemia particularly troublesome before treatment with a gluten free diet. Following gluten restriction, insulin requirement increased in six patients, and diabetic control became more stable. Diarrhoea due to coeliac disease in a patient with coexisting diabetes, may be mistakenly diagnosed as 'diabetic diarrhoea'. However, certain clinical and laboratory features should arouse suspicion that the diarrhoea is not of diabetic origin. These included a history of gastrointestinal symptoms preceding the diagnosis of diabetes, the occurrence of repeated hypoglycaemia, absence of neuropathy, anaemia, low serum folate, low serum albumin and a malabsorption pattern on small bowel radiography. A definitive diagnosis of coeliac disease can be made only jejunal biopsy. The opportunity to diagnose coeliac disease in adult diabetics will usually fall to the diabetologist and wider use of jejunal biopsy in diabetics with chronic or recurrent diarrhoea is suggested.
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PMID:Diabetes mellitus and coeliac disease: a clinical study. 67 52

A case of a 27 year old man who developed anemia after fracture of the sella turcica is reported. The diagnosis of anterior pituitary insufficiency was made by a combined provocative test with TRH, LHRH, and insulin. The anemia was characterized by a hypocellular bone marrow which appeared to be functioning only in the thoracic-lumbar vertebrae, an absence of measurable erythropoietic activity, and by the return to normal of the hematological findings after hormonal replacement therapy. This patient had the highly unusual combination of proven panhypopituitarism and significant anemia resulting from a distinct fracture of the sella turcica.
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PMID:Panhypopituitarism and anemia secondary to traumatic fracture of the sella turcica. 75 77

A number of hemodynamic, pharmacologic, and metabolic interventions were found to change the extent of acute ischemic injury of the myocardium and subsequent necrosis following experimental coronary artery occlusion. Reduction in myocardial damage occurred by decreasing myocardial oxygen demands (beta-adrenergic blocking agents, intra-aortic balloon counterpulsation, nitroglycerin, decreasing afterload in hypertensive patients, inhibition of lipolysis, and digitalis in the failing heart); by increasing myocardial oxygen supply either directly (coronary artery reperfusion or elevating arterial pO2), or through collateral vessels (evevation of coronary perfusion pressure by alpha adrenergic agonists, intra-aortic balloon counterpulsation); or by increasing plasma osmolality (manitol, hypertonic glucose); presumably by augmenting anaerobi metabolism (glucose-insulin-potassium, hypertonic glucoxe insulin potassium, hypertonic glucose); by enhancing transport to the ischemic zone of substrates utilized in energy production (hyaluronidase); by protecting against autolytic and heterolytic damage (hydrocortisone, cobra venom factor, aprotinin). Augmentation of myocardial ischemic damage occurred as a consequence of increasing myocardial oxygen requirements (isoproterenol, glucagon, ouabain, bretylium tosylate, tachycardia); by decreasing myocardial oxygen supply either directly (hypoxia, anemia), through reduction of collateral flow (hemorrhagic hypotension, minoxidil), or by decreasing substrate availability (hypoglycemia). Pilot studies have been carried out in patients with hyaluronidase, nitroglycerin intra-aortic balloon counterpulsation, beta-blocking agents and Arfonad and have shown that these interventions may also reduce myocardial damage, which suggests that the concept of reduction in infarct size following coronary occlusion is applicable clinically.
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PMID:Effects of metabolic and pharmacologic interventions on myocardial infarct size following coronary occlusion. 76 15

A summary of the effects of contraceptive pills on vitamins in the b lood is presented. The significant increase of Vitamin-A in the plasma of contraceptive users is believed to be a result of the increase of bet alipoprotein, which binds chiefly to Vitamin-A. Although high concentrations of Vitamin-A have caused teratogenicity in test animals, the increase found in humans using contraceptive pills is not high enough to cause risk. A lowering of Vitamin-B6 (pyridoxin) levels has occurred with the use of contraceptive pills. This can cause alteration in the metabolism of tryptophan, which could cause depression in pill users. The lack of pyridoxine can also increase the production of xanthuric acid which binds with insulin, resulting in a decreased glucose tolerance. A decrease in folic acid in pill users has also been observed, caused by some effect of the pill on the folate deconjugate. The Vitamin-B12 level is also lowered for unascertainable reasons related to the decrease in folic acid. No anemia occurs in spite of the lowered Vitamin-B complex levels in the blood. A lack in Vitamin-C in users of pills containing estrogens is possibly effected by a corresponding increase between estrogens and ceruloplasmin, a protein active in the oxidation of ascorbic acid. This lack of Vitamin-C has had no clinical significance thus far.
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PMID:[P-pills and vitamins]. 114 66

A patient with idiopathic marrow hypoplasia associated with short stature and other anomalies (Fanconi's anaemia) is described: treatment with human growth hormone for one year did not accelerate his growth rate or significantly affect his anaemia: androgen treatment considerably improved both features. Endocrine studies suggest that though he had poor and insufficient production of endogenous growth hormone to insulin-induced hypoglycaemia, the major defect in this syndrome is determined more at the end-organ than at the pituitary or gonadal level.
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PMID:Fanconi's aplastic anaemia with short stature. Absence of response to human growth hormone. 114 71

Sixty-three patients with duodenal ulcer were operated upon with selective proximal vagotomy (SPV). In 34 patients the vagotomy was combined with a pyloroplasty (PP). Before and after operation the acid secretion was investigated after Histalog (50 mg) stimulation. Insulin tests were performed 4-6 weeks, 1 year, and 3 years after operation. One and 3 years after operation ESR, Hb, SeFe, Protein, Albumin, Calcium, and Alkaline phosphatases were determined. One patient developed gastric retention and 3 got relapses during the first year. At reoperation, overlooked vagal branches in the region of the cardia were found. Five patients developed a minor anemia and 2 sideropenia, which is less than after truncal vagotomy and PP. The operation caused a highly significant reduction in acid output after Histalog stimulation. The postoperative insulin test was graded according to Bachrach: 49 were complete, 12 extensive but incomplete, and 2 incomplete. During the second hour after stimulation a probably significant increase was noted in the acid output between the postoperative and the one-year investigation. Between the one- and the three-years tests a significant increase was found during the first hour after insulin stimulation and a probably significant increase during the second hour. The gastric emptying of a composite fluid test meal was significantly faster after operation than before in patients where the insulin stimulation did not give rise to any acid production.
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PMID:Clinical, secretory and motor effects of selective proximal vagotomy. A three-year follow-up. 116 44


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