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)

During August 1989-August 1994 at the referral-based obstetric practice of MacKay Memorial Hospital in Taipei, Taiwan, obstetricians saw 8 pregnant women with acute pancreatitis. All but 1 patient had gallstones and/or hyperlipidemia. None had ever been diagnosed with pancreatitis or gallstones in the past. None suffered from alcoholism. One woman was lost to follow-up at 33 weeks gestation. No pregnant woman died. Magnesium sulfate and nifedipine controlled preterm labor in 2 patients. Two women underwent cesarean section (fetal distress and elective). Pancreatitis struck all but 1 during the 3rd trimester of pregnancy. One woman presented at 23 weeks gestation with loss of consciousness, abnormally low volume of circulating plasma in the body, upper gastrointestinal bleeding, and a dead fetus. She also had diabetes mellitus which had gone untreated for 2 years. After spontaneous delivery of the dead fetus, she developed metabolic encephalopathy, sepsis, respiratory distress, and acute renal failure. She completely recovered and left the hospital 62 days after arriving. Physicians instituted conservative treatment for pancreatitis and a fat-restricted diet for hyperlipidemia. Labor was induced in 3 women after determining fetal lung maturity. Pancreatitis symptoms diminished after delivery. At 2 weeks postpartum, they underwent cholecystectomy. In fact, all but 3 women underwent cholecystectomy. Five patients had a fever greater than 38 degrees Celsius upon admission. Three patients were jaundiced. All 8 patients experienced nausea and/or vomiting and abdominal pain. Six women had low serum calcium levels. Only 1 had a serum lactic dehydrogenase level above 350 IU/L. Primiparous women were just as likely to develop pancreatitis during pregnancy as multiparous women. These findings suggest that early diagnosis and prompt treatment of acute pancreatitis are essential to a favorable outcome.
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PMID:Acute pancreatitis in pregnancy. 766 Jul 65

A primipara affected by late-onset diabetes and sensory deafness because of mitochondrial myopathy was hospitalized for threatened preterm delivery. Magnesium sulfate was started for tocolysis, resulting in general muscle damage, although the mitochondrial myopathy did not deteriorate during pregnancy. Magnesium sulfate may be contraindicated in pregnancy with mitochondrial myopathy.
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PMID:Contraindication of magnesium sulfate in a pregnancy complicated with late-onset diabetes mellitus and sensory deafness due to mitochondrial myopathy. 1173 May 1

Magnesium deficiency has recently been proposed as a novel factor implicated in the pathogenesis of diabetes complications. Previous studies have shown that magnesium decreases basal tone in normal isolated aortic rings and reduces phenylephrine-induced contraction. The mechanism of this magnesium action is not very well known. The present study was designed to determine the role of endothelium and nitric oxide in magnesium sulfate-induced vasorelaxation in diabetic rat vessels. Diabetes was induced by a single tail injection of streptozotocin. Eight weeks later, superior mesenteric arteries of control and diabetic animals were isolated and perfused according to the McGregor method. Prepared vascular beds were constricted with phenylephrine to induce 70-75% of maximal constriction. Magnesium sulfate at concentrations of 0.001 M to 0.1 M was added into the medium and perfusion pressure was then recorded. Mesenteric bed baseline perfusion pressure in intact and denuded endothelium of diabetic groups was higher than controls. In all groups, relaxant response to magnesium in mesenteric bed was attenuated after endothelium removal, but a relaxatory effect appears at high concentration. In the presence of N (omega)-nitro-L-arginine methyl ester (L-NAME), magnesium-induced relaxation was significantly suppressed in intact mesenteric bed of control animals but in diabetics, the relaxant response was slightly inhibited. From the results of this study, it can be concluded that magnesium-induced endothelium dependent and endothelium independent vasorelaxation are mediated by nitric oxide in control rats while in diabetic animals other mechanisms may be involved.
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PMID:Relaxatory effect of magnesium on mesenteric vascular beds differs from normal and streptozotocin induced diabetic rats. 1568 Feb 69

Vascular disease is one of the complicating features of diabetes mellitus. Magnesium deficiency has recently been proposed as a novel factor implicated in the pathogenesis of diabetes complications. Several studies have indicated that hypertension in diabetic patients is an independent altered reaction of blood vessels to neurotransmitters and circulating hormones. Since magnesium has been proposed to decrease vascular sensitivity to vasoconstrictor agents, the present study was designed to determine whether chronic magnesium sulfate administration could prevent vascular complications of STZ-induced diabetes in rats. The animals were divided into six groups: two groups served as controls and received tap water for 8 weeks, while in the other four groups, made diabetic with a single IV injection of 40 mg/kg STZ, two groups treated with magnesium sulfate (10 g/L) added to the drinking water, and the other two groups received tap water only. After 8 weeks, in 3 groups (control, diabetic and Mg-treated), left common carotid artery was cannulated for continuous recording of blood pressure. All animals in these groups were decapitated and blood samples were drawn for glucose, Ca and Mg measurements. In the 3 remaining groups (again divided into control, diabetic and Mg-treated), the mesenteric vascular bed was perfused according to the McGregor method, and descending thoracic aortas were used for measurement of elasticity. In diabetic rats, plasma glucose was significantly increased and plasma magnesium was significantly decreased compared to controls and Mg-treated animals. Although plasma magnesium of Mg-treated animals increased significantly, it failed to reach to the magnesium level of the control group. Ca/Mg ratio was also increased compared to the control and Mg-treated animals. Mean arterial blood pressure in diabetics was significantly higher than control and Mg-treated rats. Similarly, there was a significant difference in mean arterial blood pressure of Mg-treated rats compared to control animals. Baseline perfusion pressure of diabetic group was significantly higher than control and Mg-treated groups with intact and denuded endothelium. Magnesium sulfate treatment decreased mean perfusion pressure of mesenteric vascular bed in intact and denuded endothelium in comparison with non-treated diabetic rats. There was a significant increase in passive tension in the aorta of diabetic rats compared to control and Mg-treated rats. However, there was no significant difference between Mg-treated and control rats. From the results of this study it may be concluded that magnesium could control STZ-induced diabetes and prevent its vascular complications.
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PMID:Oral magnesium administration prevents vascular complications in STZ-diabetic rats. 1568 Mar 10

Preeclampsia is defined as the association of pregnancy-induced hypertension and proteinuria of 300 mg/24h or more after 20 weeks gestation. It complicates 0.5 to 7% of pregnancies. It is a severe complication of pregnancy, which leads to persisting fetal morbidity and mortality. It is also responsible for maternal morbidity as placental abruption, HELLP syndrome (hemolysis, elevated liver enzymes, low platelets) and eclampsia. Without treatment, maternal risks are high. Once the disease is confirmed, the treatment consists of ending the pregnancy. Corticosteroids for lung maturity have to be prioritized depending on the term. Antihypertensive drugs are used to limit maternal complications, in particular, in neurological form. Calcium pump inhibitors are increasingly used as a first line choice. Magnesium sulfate, which is probably not used enough in France, needs to be administered with care and strict monitoring. It can be used to prevent a recurrence of eclamptic fits or in the context of early severe preeclampsia with neurological irritability where an eclamptic fit seems imminent. Preventive treatment of preeclampsia consists essentially of low dose aspirin. The efficacy of this treatment is real but moderate. It decreases the risk of recurrence of preeclampsia by 10 to 15%, of prematurity by 8% and of perinatal mortality by 14%. These figures were recently corrected to 10% for the risk of recurrence of preeclampsia: RR=0.95; 90% CI; (0.84-0.97) and prematurity: RR=0.95; 90%CI; (0.83-0.98). It seems that it has no significant effect on intra-uterine growth restriction (IUGR) and perinatal death prevention. For the main outcome of preeclampsia, there was no evidence that women in any of subgroups as preexisting renal disease, preexisting diabetes or hypertension benefited more or less from the use of antiplatelet agents than those in any other subgroup.
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PMID:[Latest developments: management and treatment of preeclampsia]. 1805 75