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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical results of truncal vagotomy and drainage for duodenal ulcer in 500 patients are evaluated by a personal 6-8 year follow up. Pyloroplasty was used unless pyloric stenosis made a gastrojejunostomy necessary. Forty-three patients had recurrence (39 were reoperated) and gastric ulcer was seen in five. The rate of dumping was 24% (severe in 3%) and rate of daily-monthly diarrhoea 40% (severe in 8%). Neither dumping nor diarrhoea was related to histamine-activated gastric acid secretion ten days after vagotomy and insulin-activated acid secretion 3 to 4 years later. Dumping was related to epigastric fullness and diarrhoea. Recurrence was related to histamine-activated secretion before and 10 days after vagotomy and to insulin-activated secretion 10 days and 3-4 days after vagotomy. Minor changes were seen in weight- and laboratory-measurements. Anemia was not related to prophylactic intake of iron. Satisfactory results (Visick I-III) were seen in 80% of the patients. The figure may be increased to 86%, including results of operations for recurrence, gastric ulcer and other diseases occurring after the original vagotomy and drainage; even then, the results seem less satisfactory than those after other operations for duodenal ulcer.
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PMID:Clinical results 6 to 8 years after truncal vagotomy and drainage for duodenal ulcer in 500 patients. 121 Oct 38

Anaemia is a feature almost invariably complicating chronic renal failure. Its pathophysiology is multifactorial but the most important cause is erythropoietin (Epo) deficiency. However, either no relation or even a weakly positive relation generally exists between serum immunoreactive (i) Epo and haematocrit values in uraemic anaemia, whereas in anaemias of non-renal origin the correlation is most often strongly negative. Recent evidence indicates that growth hormone also stimulates erythropoiesis. Moreover, late erythroid progenitor cells (CFU-E) require insulin and/or insulin-like growth factor I (IGF-I) for development in vitro. IGF-I has been shown to have a synergistic action with Epo. We have measured serum iEpo and IGF-I levels in 17 haemodialysis patients with severe hyperparathyroidism (mean +/- SEM serum iPTH, 988 +/- 88 pg/ml). Mean age and duration of dialysis treatment were 46.1 +/- 3.4 and 8.8 +/- 1.0 years respectively. Mean haematocrit and haemoglobin values wer 28.1 +/- 1.7% and 9.39 +/- 0.54 g/dl respectively. Mean serum iEpo and IGF-I levels were 20.3 +/- 4.7 mU/ml and 320 +/- 20 ng/ml respectively (normal values for serum iEpo and IGF-I, 17.9 +/- 6 mU/ml and 91 +/- 23 ng/ml respectively). We found that serum IGF-I concentrations were well correlated with haematocrit values (r = 0.68, n = 15, P less than 0.004) whereas serum iEpo values were not (r = 0.41, n = 12, P = 0.18). IGF-I could therefore be an important factor regulating erythropoiesis in uraemic patients, at least when associated with severe hyperparathyroidism.
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PMID:Insulin-like growth factor I: a modulator of erythropoiesis in uraemic patients? 131 79

Several studies have demonstrated the efficacy of cyclosporin A in modifying the initial course of Type 1 (insulin-dependent) diabetes mellitus in older children and adults but none have reported the effects in very young children. We treated 14 newly-diagnosed Type 1 diabetic patients aged 22 months to 95 months with cyclosporin A. Mean insulin dose at entry was 0.7 +/- 0.07 IU.kg-1.day-1. Initial cyclosporin A dose was 10 mg.kg-1.day-1. Insulin dose reached a nadir of 0.13 IU.kg-1.day-1 by 180 days. Mean glucagon-stimulated connecting peptide levels were maximal at 6 months (0.75 nmol/l) and were maintained while on cyclosporin A. Insulin was discontinued in four patients for 4, 12, 15 and 30 months respectively. In five other patients the insulin dose was less than 0.15 IU.kg-1.day-1 for at least 3 months. Glycated haemoglobin levels for all patients were within the normal range. Side effects included anorexia, stomach pains, poor weight gain, hypertrichosis, gum hyperplasia, mild anaemia and elevated creatinine. All patients have now discontinued cyclosporin A and all but one have been followed for 5 years after discontinuation. Reasons for discontinuing cyclosporin A included exposure to chicken pox (varicella), non-resolving otitis media, incomplete or no response and relapse. All side effects have resolved since the treatment was discontinued. Following discontinuation of cyclosporin A insulin requirements and glycated hemoglobin levels increased while glucagon-stimulated connecting peptide levels declined dramatically.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cyclosporin A treatment of young children with newly-diagnosed type 1 (insulin-dependent) diabetes mellitus. London Diabetes Study Group. 139 85

In lambs with a very restricted intake of nutrients and an increase of the body mass of less than 60 g per day (group A) and in those with an increase of more than 220 g/day (group B), analyses of components of the blood and the plasma were performed at certain intervals. In the lambs of group A an anemia developed in the course of 77 days. The concentrations of alpha-amino-N, non-protein-N, urea, glucose and insulin as well as the activity of the alkaline phosphatase of the plasma of the lambs of group A were always lower than those of group B. The beta-hydroxybutyrate concentration of the lambs of group A on the 7th and 21st day of the experiment was higher than that of group B. The concentrations of inorganic phosphate and iron in the plasma of group A at most points during the study were lower than that in group B.
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PMID:[The content of Hb in the blood and of different constituents in the plasma of lambs with low and normal increase in body mass]. 148 Dec 12

Ischemic hepatitis is not an uncommon complication of reversible severe hypotension or cardiac failure. The prognosis usually is determined by the cause of the initial hypotension or cardiac failure, rather than the subsequent hepatic dysfunction. We report a retrospective analysis of nine patients with ischemic hepatitis in which previously unreported clinical and biochemical abnormalities are noted. The clinical and biochemical course of the patients were reviewed until recovery or death from ischemic hepatitis. All the patients had a rapid striking elevation of aspartate aminotransferase, and lactic dehydrogenase, with an equally rapid resolution of these parameters. Abnormal serum glucose levels occurred in six patients (none of whom had a prior carbohydrate intolerance). Insulin therapy was given to three patients for a limited period. Renal impairment was manifest in all nine patients, and it resolved spontaneously within 10 days. Altered mental status was detected in six patients; the changes reverted to normal within 7 days of their onset. A preexisting anemia (hemoglobin less than 11.0 g/dl) was noted on admission in four patients, and it did not appear to potentiate the manifestations of the hepatic ischemia. We conclude that ischemic hepatitis should be anticipated in all patients with a recent history of systemic hypotension. It should be considered in the differential diagnosis of patients with unexplained hepatitis; the early massive rise in lactic dehydrogenase, the rapid fall in transaminases, and the early mild/moderate renal failure strongly suggest ischemic hepatitis. Patients with ischemic hepatitis can manifest reversible renal failure, mental confusion, and hyperglycemia which may require insulin for its control.
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PMID:Ischemic hepatitis: widening horizons. 848 Jul 56

Attempts have been made to determine the reason for the depletion of glycogen reserves in tumour-bearing rats. The possible roles of anorexia, competition for glucose by the tumour, and lack of hormonal control of glycogen biosynthesis have been investigated. The glycogen content of the liver, skeletal muscle, and brain, and the levels of glucose and the hormones corticosterone, insulin, and glucagon were determined in healthy rats which had been starved for various periods and in tumour-bearing rats carrying the fast-growing Zajdela ascites hepatoma or the slow-growing solid hepatoma 27. It was found that towards the terminal stages of tumour development there was an increase in the content of corticosterone and glucagon in the blood serum and also an increase in the glycogen reserves in skeletal muscle and brain despite the presence of hypoglycaemia and hypo-insulinaemia. There was at this time a sharp fall in the level of liver glycogen. It is shown that neither anorexia nor excessive competition for glucose by the tumour were the main reasons for liver glycogen depletion and hypoglycaemia. A strong correlation was observed, however, between the occurrence of anaemia and the loss of liver glycogen, which suggests that the former may be an important factor in the changes in host tissue observed in response to tumour growth.
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PMID:Factors within the body determining the glycogen reserves in the tissues of rats with transplantable tumours. 177 67

Prematurity in Indian births is modeled, based on the hypothesis that reduced protein and glucose and aminoacids and maternal anemia and preeclampsia lead to placental dysfunction which is also affected by metabolic disturbance and fetal circulation related to cellular growth and questions about genetics. There may be an ethnic propensity for early maturation of the fetus which affects the higher stillbirth rates and perinatal mortality. It was observed that among, for instance, black and Indian racial groups there may be meconium release and fetal distress. The significance is that physicians should increase antenatal surveillance before 40 weeks. Maternal nutrition should be advanced and hyperalimentation by cordocentesis. Other interventions such as glucose, oxygen, and aspirin administration are still very experimental. The evidence that velocity of growth is different and low birth weight is due to abnormal growth and shortened gestation is currently being researched among different ethnic groups. The discussion is concerned with reports of ethnic variation among Indian and Malay babies in Singapore and babies of French or African ancestry in France. In these studies findings were that the Indians and Malays in Singapore vs. the Chinese had higher mortality, and black African ancestry in mixed ancestry babies was related to higher infant mortality. Another study on neonatal mortality in India led to the recommendation that 2000 gm be established as the limit for defining low birth weight. In the 1501- 2000 gm birth weight groups, 30-45% are preterm, and the remainder are term or postterm. Low birth weight may transcend generations in India even with emigration. Experimental studies show that intrauterine weight is related to placental volume. Reduced growth and lower fetal insulin/glucose ratio with elevated fetal glycine/valine ratio was found to be related to reduced glucose supply among fetuses with fetal hypertriglyceridemia. Fat seems to be lacking among low birth weight fetuses. Studies of somatomedin and somatostatin in metabolism are helping to provide greater understanding of fetal growth processes.
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PMID:The prematurity paradox of the small Indian baby. 180 Mar 24

The non-obese diabetic mouse (NOD mouse) is widely used as a model of organ-specific autoimmunity because it develops specific autoimmune destruction of pancreatic beta cells mediated by T cells and culminating in insulin-dependent diabetes mellitus. Here, we report that the NOD mouse also develops Coombs'-positive hemolytic anemia, a B cell-mediated autoimmune disease. Aged NOD mice were found to have splenomegaly and jaundice predominantly due to raised unconjugated serum bilirubin. Their hematocrits were markedly lowered, and there was a reciprocal increase in the reticulocyte count. Red blood cells (RBC) from anemic mice showed a normal lytic response to hypotonicity. RBC from non-anemic mice had normal half lives in non-anemic, non-diabetic NOD mice by 51Cr labeling but, dramatically shortened half lives in anemic mice. Similar results were obtained with RBC from anemic mice. Hemolysis could be transferred with serum from anemic mice resulting in reticulocytosis. The antibody-mediated nature of the anemia was confirmed with the direct Coombs' test. Anemia was found only in mice aged greater than 200 days and was more common in diabetic (4/8) than non-diabetic (1/16) mice at 300 days. However, by 550 days, 14/17 non-diabetic mice were affected.
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PMID:Hemolytic anemia in non-obese diabetic mice. 188 56

Fulminant malaria infections are characterised by hypoglycaemia and potentially lethal lactic acidosis. In young adult Wistar rats (n = 26) infected with Plasmodium berghei (ANKA strain), hyperparasitaemia (greater than 50%), anaemia (PCV 19.6 +/- 5.3%; mean +/- SD) hypoglycaemia (1.04 +/- 0.74 mmol/litre), hyperlactataemia (13.2 +/- 2.20 mmol/litre), hyperpyruvicaemia (0.51 +/- 0.12 mmol/litre) and metabolic acidosis (arterial pH 6.96 +/- 0.11) developed after approximately 14 days of infection. Hypoglycaemia was associated with appropriate suppression of plasma insulin concentrations. In a second series of experiments the metabolic effects of treatment with glucose (500 mg/kg/hr), quinine (5 mg/kg bolus followed by 10 mg/kg over 1 hr) and a potent activator of pyruvate dehydrogenase, dichloroacetate (300 mg/kg) were studied over a 1-hr period. In control animals quinine had no measurable effects, but dichloroacetate significantly reduced arterial blood lactate (74%) and pyruvate (80%). In infected animals, glucose infusion attenuated the rise in lactate (38% compared with 82%; P less than 0.01) but quinine had no additional metabolic effects. Dichloroacetate further attenuated the rise in lactate (14%; P less than 0.01).
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PMID:Plasmodium berghei: lactic acidosis and hypoglycaemia in a rodent model of severe malaria; effects of glucose, quinine, and dichloroacetate. 190 Dec 69

A case of isovaleric acidemia appearing as diabetic ketoacidosis with acute encephalopathy and pancytopenia was reported. A three-year-old male patient, with mild psychomotor retardation, had recurrent bouts of acute encephalopathy and pancytopenia after episodes of upper respiratory infection. At admission, he had vomiting associated with dehydration, acidosis, ketonuria, coma and a pungent, rather unpleasant odor. Laboratory features included hyperglycemia, hyperammonemia, hyperamylasemia, hypocalcemia, neutropenia, thrombocytopenia and subsequent anemia. Urine organic acid profiles showed profuse amount of 3-beta-hydroxyisovaleric acid (295 mg/ml) and isovalerylglycine (616 mg/ml) by gas chromatography-mass spectrometry. Levels of amino acids in the serum and urine were normal. The patient received treatment with rehydration and insulin, with rapid improvement. After the acute illness, blood glucose levels returned to normal. The patient was doing well on a low-protein diet in recent 3 months.
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PMID:Isovaleric acidemia: report of one case. 212 76


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