Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During the past decades insulin has been given in relatively high doses when treating diabetic coma. Recently low-dose insulin treatment has been proposed by several groups. In the reported investigation insulin was initially given in moderate to high doses (12-200 U/h) with a steady reduction in dose during the course of treatment. Insulin infusion was regulated either manually with an adjustable infusion pump (7 patients) or automatically with an artificial endocrine pancreas (glucose-controlled insulin infusion system; 11 patients). Thus 18 patients with decompensated diabetes mellitus (coma or precoma) were treated. In 14 patients with ketoacidotic decompensation laboratory data on hospital admission were: blood glucose 7.35 +/- 0.61 g/l, serum potassium 4.7 +/- 0.4 mmol/l, pH 7.1 +/- 0.04, base excess - 19,7 +/- 2.2 mmol/l (x +/- SEM). The other patients had hyperglycaemic or hyperosmolar non-ketotic decompensation. In all patients controlled reduction of blood glucose levels was achieved within 2.3 to 18 hours. The amounts of insulin infused during this ranged from 17 to 320 units, but in one instance was 1950 units. There were no complications.
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PMID:[Insulin treatment of decompensated diabetes mellitus with a new artificial endocrine pancreas (author's transl)]. 33 2

We studied the changes in plasma arginine vasopressin in 5 patients with diabetic ketoacidosis and one patient with non-ketotic hyperosmolar coma who had marked hyperglycemia (36.6 +/- 4.6 mmol/l, mean +/- SEM) and dehydration. Plasma osmolality (Posm) was 342.2 +/- 11.4 mOsm/kg H2O, and hematocrit, serum protein, and blood urea nitrogen were also elevated at hospitalization. Circulating blood volume was decreased by approximately 21% as compared with that on day 7. Plasma AVP level was increased to 8.5 +/- 1.6 pmol/l at hospitalization. When hyperglycemia was improved by iv infusion of a small dose of insulin plus fluid administration, plasma AVP level promptly decreased to 2.4 +/- 0.4 pmol/l within six hours. When plasma AVP level had normalized, Posm was still as high as 305 mOsm/kg H2O, but the loss of circulating blood volume was only 4.2% of the control state. Plasma AVP level was positively correlated with change in hematocrit (plasma AVP = 3.58 + 0.45.hematocrit, r = 0.468, p less than 0.01), serum protein (r = 0.487, p less than 0.01), Posm (r = 0.388, p less than 0.01), and blood glucose (r = 0.582, p less than 0.01). Plasma AVP level was negatively correlated with the change in circulating blood volume (plasma AVP = 3.6 - 0.14.change in circulating blood volume, r = -0.469, p less than 0.01). These results indicate that both non-osmotic and osmotic stimuli are involved in the mechanism for AVP release in patients with diabetic coma, and that the non-osmotic control of AVP may contribute to circulating homeostasis, protecting against severe blood volume depletion in diabetic patients suffering from hyperglycemia and dehydration.
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PMID:Prompt recovery of plasma arginine vasopressin in diabetic coma after intravenous infusion of a small dose of insulin and a large amount of fluid. 211 Apr 10

We investigated the causes of death of 98 subjects with diabetes mellitus over the past 10 years at our hospital. As was expected, the cause with the highest incidence (48.0%) was vascular disease including cerebral vascular disease (20.4%), coronary heart disease (15.3%), aortic disease and miscellaneous (3.1%), followed by malignant tumors (39.8%), infectious diseases (4.1%) and other diseases. Only one patient died from diabetic coma. The abnormal ECG findings of these patients were analyzed according to the Minnesota Code and 57%, 31%, 26%, 24%, 19% of them showed arrhythmias, ST-T abnormalities, LVH, VPC, and abnormal Q-wave, respectively. These findings showed no statistical difference between diabetics and non-diabetics. Abnormal p-wave, especially LA-load was found more often in diabetics (35%) than in non-diabetics (21%). Q-T interval corrected by Bazett's formula (Q-Tc) was 430 +/- 3.03 (M +/- SEM) msec in diabetics and it was significantly longer (p less than 0.01) than 417 +/- 3.73 msec in patients with other diseases.
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PMID:Causes of death of diabetic patients in the past 10 years and their ECG findings. 668 May 44

We reviewed diabetic gangrene in 104 American blacks and found that the clinical features were similar to those reported for the general diabetic population. We observed, however, that there was a significant association of hypertension with above-knee and bilateral amputations in our patients (P less than .001 and .01, respectively), and that the mean blood pressure of the bilateral amputees (124.5 +/- 3.8 mm Hg) (SEM) was significantly higher (P less than .005) than that of the unilateral amputees (114.4 +/- 1.7 mm Hg). There results suggest a strong association of hypertension with far-advanced occlusive vascular disease of the lower limbs. Moderately severe anemia (hematocrit 20% to 30%) was associated significantly with primary above-knee amputation and mortality (P less than .02 and .05, respectively). Mortality resulted mostly from mixed causes (cardiopulmonary failure, uremia, sepsis, diabetic coma). The dead patients had significantly increased prevalence of cardiac disease (P less than .02), higher frequency of above-knee amputation (P less than .01), and a duration of diabetes (17.4 +/- 2.8 years) significantly longer (P less than .025) than that of the surviving patients (12.0 +/- 1.0 years).
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PMID:Diabetic gangrene in black patients. 706 2

We studied the changes in serum sodium (Na) and potassium (K) levels in seventeen patients in diabetic ketoacidosis and nine patients in non-ketotic hyperosmolar coma, who had marked hyperglycemia (707.4 +/- 75.6 mg/dl, mean +/- SEM) and dehydration. The disorder characterized two types of alteration. The one group was hyponatremia with hyperkalemia in 17 patients in diabetic ketoacidosis (132.9 +/- 2.0 and 5.7 +/- 0.2 mEq/l), and 4 patients in non-ketotic hyperosmolar coma (125.8 +/- 4.3 and 5.2 +/- 0.5 mEq/l). The other was hypernatremia (162.5 +/- 1.8 mEq/l) with hypokalemia (3.4 +/- 0.2 mEq/l) in 5 patients in non-ketotic hyperosmolar coma. Intensive therapy with insulin and fluid administration improved the diabetic hyperglycemia and associated abnormalities. The vectors showing the normalization of serum Na and K levels was in quite opposite directions between the patients with hyponatremia with hyperkalemia and those with hypernatremia with hypokalemia. The amounts of loss of circulatory blood volume exceeded 20% in three groups of patients, a loss greater in the hypernatremic patients than in the hyponatremic ones. These results indicate that serious body water depletion produces hypernatremia instead of hyponatremia in patients in diabetic coma. The disorder may be caused by the altered distribution of electrolytes between the intra- and extra-cellular spaces.
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PMID:Opposite changes in serum sodium and potassium in patients in diabetic coma. 795 50