Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Six hundred and nine male patients suffering from maturity onset diabetes mellitus, comprising 422 Chinese, 66 Malays, and 121 Indians, were investigated to determine the incidence of G6PD deficiency, ABO blood groups, and haemoglobin types, and these were compared with normal healthy controls. A positive association with a higher incidence of G6PD deficiency in diabetics was observed in Chinese and Indian patients. There was no significant difference in the frequencies of ABO blood groups and haemoglobin types between the patients and the controls in any of the ethnic groups studied.
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PMID:Association of glucose-6-phosphate dehydrogenase deficiency with diabetes mellitus in ethnic groups of Singapore. 53 14

Certain uncommon genetic disorders occur relatively frequently in the various population groups of Southern Africa. Prominent among these are porphyria, colonic polyposis and sclerosteosis in the Afrikaner community, Huntington's chorea in the British, Gaucher's and Tay-Sachs diseases in the Jewish population, glucose-6-phosphate dehydrogenase deficiency (G-6-PD deficiency) and thalassaemia in the Greek community, various skeletal dysplasias in the Black group, lipoid proteinosis and cleidocranial dysostosis in the Cape Coloured population, diabetes mellitus in the Indian community and retinitis pigmentosa in the Tristan da Cunha islanders. In addition, 'private' syndromes have been encountered in virtually every group. Awareness of the ethnic distribution of unusual genetic conditions is of considerable practical importance during the differential diagnosis of obscure disease.
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PMID:Genetic disorders in Southern Africa. 95 24

This hospital-based study demonstrates a statistically significant higher prevalence of glucose-6-phosphate dehydrogenase (G6PD) deficiency among the Saudi patients with diabetes mellitus (12.4%) as compared to healthy population controls (2.0%) (p less than 0.008). The nature of this association is difficult to explain. In view of a higher frequency of G6PD deficiency among diabetics, it is suggested that all patients with diabetes be screened for this enzymopathy in order to avoid the use of certain drugs or toxic agents that can produce hemolysis.
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PMID:Glucose-6-phosphate dehydrogenase deficiency and diabetes mellitus. 177 4

The prevalence of glucose-6-phosphate dehydrogenase (G6PD) deficiency was estimated in 318 diabetic patients using Beulter's fluorescent Spot test. A significantly (p less than 0.001) higher prevalence of G6PD deficiency was detected among diabetic patients (19.6%) as compared to controls (10.4%). The distribution of G6PD deficiency varied with age, sex, and duration of diabetes. Among diabetic men, the prevalence of deficiency was significantly higher than controls in both age groups; 40 years and below, and 41 years and above (p less than 0.005 and p less than 0.02, respectively). Among diabetic women, the significantly higher prevalence of deficiency was observed only in the young age group (p less than 0.005), whereas the difference among the older age group was not significant (p greater than 0.1). A significant increase in the prevalence of deficiency with increase in duration of diabetes was detected among men (p less than 0.05), but not in women. The results of the study suggest a positive association between G6PD deficiency and diabetes mellitus.
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PMID:Association of glucose-6-phosphate dehydrogenase deficiency with diabetes mellitus. 295 93

We present a young man with Mediterranean type glucose-6-phosphate dehydrogenase (G6PD) deficiency and insulin-dependent diabetes mellitus whose brittle course was characterized by recurrent bouts of hypoglycemia and diabetic ketoacidosis (DKA). While neither of the episodes of DKA was complicated by hemolysis, hemolytic anemia consistently followed the recurrent attacks of hypoglycemia. Stringent control of the patient's blood glucose levels in the upper limit and slightly above the normal range successfully prevented recurrence of hypoglycemia and recrudescence of hemolytic anemia. Hypoglycemia is proposed as capable of inducing hemolysis in G6PD deficiency.
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PMID:Hypoglycemia-induced hemolysis in glucose-6-phosphate dehydrogenase deficiency. 393 66

From the opening of a new cardiac surgical programme in November 1992, autologous and fresh donor blood (FDB) were used rather than cold stored blood (CSB) wherever possible in patients undergoing operations involving the use of cardiopulmonary bypass (CPB). In the first 250 consecutive patients, autologous blood was used in 168 (67.2%), fresh blood was used in 188 (75.2%). A total of 740 units of fresh blood were obtained on the day of operation (mean 3.9 +/- 1.6 units per patient able to supply donors; 4.9 +/- 1.7 units in the 147 who received fresh blood) and 728 units of stored blood were used (mean 3.08 +/- 1.84 units per patient where fresh blood was used; 6.2 +/- 2.5 units in the 114 where no fresh blood was used). The use of autologous blood significantly reduced FDB and CSB requirements (p < 0.001), was associated with a shorter intensive care and total postoperative stay (p = 0.006 and p = 0.033 respectively), even though there were more urgent and emergency cases in this group (p = 0.009) and no significant difference in chest drainage. Coagulopathy developed in 41 patients (16.4%) and was significantly associated with bypass time (p = 0.0001) and preoperative renal dysfunction (p = 0.005), although not with advanced age, sex, redo operation, diabetes or glucose-6-phosphate dehydrogenase deficiency. Patients with coagulopathy had significantly more transfused blood and blood products (p = 0.0001) and longer intensive care and total postoperative stays (p = 0.0001). In terms of blood conservation, the use of autologous blood was of primary importance.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Re-inventing the wheel; the use of autologous and fresh donor blood in cardiac surgery. 764 82

The glycogen storage disorders (GSD)-I, -III, -VI and -VIII are associated with hypertriglyceridaemia or mixed hyperlipidaemia which poses the question whether these patients have an increased risk for atherosclerosis. The atherogenicity of triglycerides has remained controversial, while increased plasma cholesterol levels are generally accepted as a significant risk factor for coronary heart disease. However, clinical data show that one has to differentiate between metabolic conditions where triglycerides are atherogenic and those which are not significantly related to early onset of atherosclerosis but may cause other disorders such as pancreatitis. Among the disorders of carbohydrate metabolism patients with diabetes mellitus frequently have enhanced plasma triglycerides associated with a higher risk for coronary heart disease, while patients with certain types of glycogen storage disease have high triglyceride levels but do not seem to have an enhanced risk for atherosclerosis. Here we have compared the biochemical abnormalities and the atherogenic risk of three different disorders of glucose metabolism including GSD-I (glucose-6-phosphatase deficiency), favism (glucose-6-phosphate dehydrogenase deficiency), and diabetes mellitus which are related to either hyper- or hypolipidaemia. The available data indicate that glucose-6-phosphate (Glc-6-P) is a central molecule in cellular glucose metabolism which critically influences pentose phosphate cycle activity and, via NADPH2-generation, regulates glutathione peroxidase activity for radical detoxification and also cholesterol and triglyceride synthesis. Radical detoxification is a major protective factor for cell membrane integrity and together with an appropriate renewal of membrane lipids may protect against the development of atherosclerosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Glucose-6-phosphate: a key compound in glycogenosis I and favism leading to hyper- or hypolipidaemia. 831 30

In a 61-year-old man with glucose-6-phosphate dehydrogenase (G6PD) deficiency and poorly controlled non-insulin-dependent diabetes mellitus, an episode of acute haemolysis occurred after the administration of glyburide (glibenclamide). Erythrocyte fragmentation, with haemoglobin condensation zones next to clear zones, was observed on peripheral blood smears. Since autoimmune haemolysis was excluded on the basis of laboratory data, acute haemolysis was ascribed to G6PD deficiency.
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PMID:Glyburide-induced acute haemolysis in a G6PD-deficient patient with NIDDM. 856 90

Exchange transfusion has an important role in the treatment of hyperbilirubinemia of the newborn. It is used in attempts to prevent kernicterus when bilirubin levels are high. We describe our experience in 203 exchange transfusions performed on 143 infants (81 males and 62 females) with hyperbilirubinemia during 1983-1992. In only 30% of cases was there a specific etiological diagnosis of the jaundice based on a positive Coombs test, G6PD deficiency, or the presence of sepsis or maternal diabetes; the rest were idiopathic. 57% of the neonates were premature (26-36 weeks of gestation). Premature neonates underwent more transfusions than full-term infants (1.6 vs 1.2). There was no direct death from exchange transfusion; morbidity was 6.3% (including bradycardia, apnea, thrombocytopenia, hypoglycemia and hyponatremia). Most complications occurred in preterm infants and those severely ill. All complications were treated immediately and there were no sequelae.
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PMID:[Complications of exchange transfusion in term and preterm newborns]. 868 93

If untreated, severe unconjugated hyperbilirubinemia is neurotoxic. Management of the condition therefore includes preventing serum bilirubin from reaching toxic levels. Identifying infants at risk of developing severe hyperbilirubinemia and early intervention have reduced levels of morbidity and mortality associated with bilirubin encephalopathy. The incidence of neonatal jaundice and the etiological factors associated with hyperbilirubinemia vary by locale. All infants born at Al Ain Hospital, United Arab Emirates, between January 1 and June 30, 1995, who developed clinically relevant hyperbilirubinemia defined as jaundice requiring investigation and treatment were prospectively studied. 85 (3.7%) of the 2300 live births developed hyperbilirubinemia. Of those, 22 were premature, 22 had ABO hemolytic disease of the newborn, 8 had G6PD deficiency (Mediterranean), 7 had breast milk jaundice, 5 were born to mothers with diabetes mellitus, and 1 had Rh incompatibility. No specific factor was identified in 20 (24%) infants. Significant differences in the distribution of diagnostic categories were found among the major ethnic groups in the population studied.
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PMID:Epidemiology of clinical hyperbilirubinaemia in Al Ain, United Arab Emirates. 992 69


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