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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seventeen new cases of diabetes in childhood were given an initial mean dose of insulin of 0-29 unit/kg body weight by intramuscular injection (mean age of patient 7-4 years). This resulted in a fall in blood glucose over the first 2 hours at a mean rate of 88 mg/100 ml per hour. Over the same time the mean total blood ketones fell from 3-23 to 2-3 mmol; and plasma insulin levels rose from a mean of 6 muU/ml to a mean of 65 muU/ml. Thus, with this small initial dose of insulin the 2-hour plasma insulin values were within the range which in adults has been associated with a maximum fall in blood glucose concentration. Three children with established diabetes presenting with ketoacidosis were also treated with a small initial dose of intramuscular insulin, 0-1 unit/kg in 2 of the patients and 0-5 unit/kg in the third. In 2 during a period of rehydration before insulin was given, blood glucose fell at a rate of 100 mg/100 ml per hour. Over the 2 hours after the initial dose of insulin the mean rate of fall of blood glucose for all 3 patients was 73 mg/100 ml per hour. None of these children developed hypoglycaemia nor hypokalaemia during treatment. We conclude that an initial intramuscular injection of soluble insulin in the dose range of 0-1-0-5 units/kg body weight may be more appropriate and possibly safer for the treatment of diabetic ketoacidosis in children than the currently recommended larger doses divided between intravenous and intramuscular routes. Adequate rehydration must, however, remain the first priority in the management of such cases.
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PMID:Immediate metabolic response to a low dose of insulin in children presenting with diabetes. 81 Nov 77

Four cases of cerebral edema associated with therapy for diabetic ketoacidosis are reported. One patient had an inappropriate ADH-like syndrome at the time of onset of clinical symptoms of cerebral edema; he survived. The remaining patients had hyponatremia at or near the time of onset of clinical symptoms of cerebral edema, and they subsequently died. The literature is reviewed and some aspects of therapy, which might be casually related to cerebral edema observed in association with therapy of diabetic ketoacidosis, are discussed.
Diabetes 1976 Feb
PMID:Cerebral edema complicating therapy for diabetic ketoacidosis. 81 23

The diagnosis of diabetic ketoacidosis must be suspected and the initiation of treatment should be prompt to provide a satisfactory outcome in the treatment of diabetic ketoacidosis. Corrections of fluid and electrolyte deficiencies should be made slowly; rapid "push"injections or large infusions of sodium bicarbonate should avoided and ample amounts of potassium should be given early. Precautions should be taken so that blood glucose concentrations do not fall rapidly, and so that blood glucose levels of 250-300 mg/100 ml are maintained by the administration of 5-10% glucose solutions. Bicarbonate therapy is indicated only in severe acidosis (pH less than or equal to 7.1). Physicians who are trained in the care of diabetes mellitus should supervise the treatment. In our hospital the same staff physicians and fellows attend all patients with diabetes. In addition the efforts of our house staff and nurses have contributed significantly to the care of these patients.
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PMID:Pathogenesis, diagnosis and treatment of diabetic ketoacidosis. 81 99

A pharmacokinetic model of the insulin-glucose system was used to examine the effectiveness of insulin administered by a variety of routes and regimens for diabetic ketoacidosis. The blood plasma concentration of glucose was set at 1,000 mg. per dl., and the effects of the following insulin regimens on the glucose plasma level were compared: low dose (90mU. per kg. per hr.) administered by hourly intramuscular injection, constant-rate infusion, hourly intravenous bolus, constant-rate infusion with intravenous loading dose, and high dose (2 U. per kg.) with half given as an intravenous bolus and the remainder administered subcutaneously. Computer simulations showed that the high-dose regimen reduced the plasma glucose concentration rapidly to a hypoglycemic level (less than 34 mg. per dl. at three hours postadministration). The low-dose regimens reduced the plasma glucose level more slowly than did the high-dose regimen. Differences among the low-dose regimens were noted. The initial decline of the plasma glucose level was relatively slow with both the intramuscular and constant-rate infusion regimens. An additional problem with the intramuscular regimen was the accumulation of insulin at sites of administration. This accumulation could make judgment of the appropriate time to discontinue insulin difficult. Both the hourly intravenous bolus and the constant-rate infusion with loading-dose regimens caused a prompt decline in the plasma glucose level. Their potential for causing hypoglycemia was low provided insulin was discontinued when the plasma glucose level reached 180 mg. per dl.
Diabetes 1976 Sep
PMID:Pharmacokinetic evaluation of dosing regimens for insulin in diabetic ketoacidosis. 82 5

The renin-angiotensin-aldosterone system appears to function normally in uncomplicated diabetes mellitus. Alterations in this system, however, have been observed in several of the microvascular and electrolyte complications associated with this disease. Plasma renin activity (PRA) and aldosterone are decreased in diabetic with nephropathy and hypertension, in those with neuropathy including orthostatic hypotension, and in those with hypoaldosteronism. PRA is low in rats with uncontrolled, nonketotic diabetes, and pressor responsiveness to angiotension II is increased in patients with diabetic retinopathy. Potential mechanisms responsible for the decreased PRA include plasma volume expansion, hyalin destruction of the juxtaglomerular cells, defective synthesis of renin, and inadequate catecholamine stimulation of renin, and inadequant cathecholamine stimulation of renin release. In diabetic ketoacidosis, PRA and aldosterone are stimulated secondary to the associated dehydration with hypovolemia. This report reviews the current status of the function of the renin-angiotensin-aldosterone system in diabetes mellitus and proposes a possible role for the altered function of this system in the pathophysiology of several diabetic complications.
Diabetes 1976
PMID:Renin-angiotensin-aldosterone system in diabetes mellitus. 82 63

Unusual increases in the minor hemoglobin components (Hb AIa, b, c) known to be elevated in diabetes mellitus were found in states of relative or absolute insulinopenia: diabetic ketoacidosis, steroid-induced diabetes, insulin-dependent diabetes in cystic-fibrosis patients, and cystic fibrosis occurring in infants who have a marked suppression of insulin secretion. In ketoacidotic diabetics, it required at least a month for high Hb AI levels (16.9 +/- 2.6 per cent) to stabilize at nonacidotic levels (12.8 +/- 0.3 per cent), suggesting that decreases occur only as new red cells form under conditions less favorable to Hb AI synthesis. Abnormal amounts os Hb A and Hb AI resisted removal from diabetic red-cell membranes by low ionic buffers but yielded to hypotonic Tris buffer. Their removal resulted in simultaneous elution of peripheral and integral membrane proteins. It is suggested that Hb so firmly bound could reduce membrane elasticity and cell deformability, characteristics so vital to normal red cell movement through the microvasculature.
Diabetes 1976
PMID:Hemoglobin AIc levels in insulin-dependent and -independent diabetes mellitus. 82 66

Four cases of intravascular coagulation associated with a state of acidosis in diabetics were observed in 57 patients with diabetic acidosis and 19 with lactic acidosis, in a series of 112 cases of consumption coagulopathy admitted to a department of medical resuscitation. In three cases the coagulopathy was found only on investigation; in one there were clinical and anatomic signs. The coagulopathy may be found either during the phase of recovery from ketoacidosis, or during the course of severe lactic acidosis, particularly during a recurrence of this form of acidosis. In spite of the unfavorable outcome in 3 of the 4 cases, the abnormal findings of coagulopathy reverted toward normal along with successful metabolic corrections. The factors responsible for consumption coagulopathy are acidosis, collapse, generalised systemic reactions and alterations of platelet function, of coagulation, of the balance between fibrin deposition and lysis and of lipid levels, all characteristic of diabetes. The clinical effects of this coagulopathy seldom become apparent but provide a possible explanation of some of the complications of diabetic ketoacidosis, particularly certain hemorrhagic or thrombotic events, as well as certain visceral complications, especially those affecting renal, pulmonary and cerebral areas.
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PMID:[Consumption coagulopathy and acidosis in the diabetic patient (author's transl)]. 82 99

To evaluate the effect of physiologic hyperglucagonemia on nitrogen and glucose metabolism and on urinary electrolyte excretion, pancreatic glucagon was administered as a continuous 3-day infusion to three adult-onset non-insulin-dependent diabetics and two insulin-treated juvenile diabetics while on a constant dietary intake. The glucagon infusion resulted in increases in plasma glucagon which were 4-6 fold greater than control values. Despite prolonged hyperglucagonemia, urinary glucose excretion was unchanged. Similarly, urinary urea nitrogen and total nitrogen excretion were not altered by glucagon administration. Urinary sodium tended to rise, albeit not significantly (p less than .01), on the first infusion day, but later declined to control values despite increasing plasma glucagon concentrations. Urinary chloride, potassium, calcium, phosphorus excretion remained unchanged. We conclude that continuous physiologic increments in plasma glucagon do not enhance glycosuria or increase protein catabolism and ureagenesis in diabetes when insulin is available. The augmented protein catabolism and glucogenesis that accompany diabetic ketoacidosis cannot be explained primarily on the basis of hyperglucagonemia.
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PMID:Influence of physiologic hyperglucagonemia on urinary glucose, nitrogen, and electrolyte excretion in diabetes. 83 43

Phycomycetes are ubiquitous saprophytic fungi sharing with other fungi a propensity for invasion and disease production in immunologically compromised hosts. Diabetes mellitus, in particular diabetic ketoacidosis, is a common clinical setting for phycomycosis. A pulmonary phycomycetoma was diagnosed in a diabetic patient from material obtained by bronchial brushing was treated successfully with a combination of surgery and amphotericin B.
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PMID:Pulmonary phycomycetoma in a patient with diabetes mellitus. 90 Jun 36

West, R. J., Lloyd, J. K., and Turner, W. M. L. (1975). Archives of Disease in Childhood, 50, 703. Familial insulin-resistant diabetes, multiple somatic anomalies, and pineal hyperplasia. A syndrome comprising unusual facies, dry skin, acanthosis nigricans, thickened nails, hirsutism, dental precocity and dysplasia, abdominal protuberance, and phallic enlargement is described in 2 sibs. Both have developed diabetic ketoacidosis with insulin resistance. The elder child, a girl, had recurrent septic episodes and died at the age of 7-8 years. At necropsy the pineal gland was hyperplastic, weighing 900 mg. Investigation of the younger sib over a 4-year period has shown decreasing glucose tolerance, and he was frankly diabetic with ketoacidosis by the age of 6-8 years. Serum insulin concentrations have always been grossly raised. Though the mechanism for insulin resistance has not been definitely established, a functional abnormality of the hypothalamus or pituitary is postulated to explain the many endocrine features of the syndrome.
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PMID:Familial insulin-resistant diabetes, multiple somatic anomalies, and pineal hyperplasia. 119 Aug 20


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