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

Diabetic ketoacidosis is an acute medical emergency that requires immediate diagnosis and treatment. Diagnosis may be established rapidly by measurement of urinary glucose and ketones, arterial blood pH and blood gases, and serum ketones. Rapid infusion of large volumes of fluids and electrolytes, together with continuous infusion of low doses of insulin, provides effective restoration of fluid and electrolyte balance and correction of metabolic derangements. Hyperosmolar nonketotic coma is characterized by marked hyperglycemia in the absence of ketoacidosis and occurs usually in patients with mild adult-onset diabetes. Symptoms develop more slowly than in diabetic ketoacidosis. Treatment is the same for both conditions. In alcoholic ketoacidosis, hyperketonemia is present without hyperglycemia. The syndrome differs from diabetic ketoacidosis in that blood glucose levels are lower and glycosuria is absent. Treatment consists of intravenous administration of dextrose in water and, if necessary, of sodium bicarbonate. Insulin administration usually is not necessary.
 ...
PMID:Combating diabetic ketoacidosis and other hyperglycemic-ketoacidotic syndromes. 0 17

The relation between serum and red blood cell (RBC) inorganic phosphate levels, RBC 2,3-diphosphoglycerate (2,3-DPG) levels, RBC nucleotide phosphate (Pn), and RBC total phosphate (Pt) levels were studied during the early phases of treatment and recovery from diabetic ketoacidosis (DKA). A steady drop in serum inorganic phosphate was found during the first 24 hours of insulin treatment and was most profound at 24 hours. No statistically significant changes (P less than 0.05) were found in red cell inorganic phosphate or nucleotide phosphate levels during the 24-hour study period. The levels of total red cell phosphate were lower in this group of patients than in nonacidotic diabetic subjects and decreased slightly after 24 hours of treatment. The red cell 2,3-DPG levels were low at the initiation of therapy and remained low during the 24-hour study period. Glucose, bicarbonate, lactate, and ketone levels fell in linear patterns with treatment. In view of the current evidence for the effects of low 2,3-DPG on oxygen delivery and the relation of low serum phosphate levels to RBC glycolysis and 2,3-DPG formation, this study reemphasizes the need for phosphate replacement during the early phases of treatment of DKA.
Diabetes 1977 May
PMID:2,3-diphosphoglycerate, nucleotide phosophate, and organic and inorganic phosphate levels during the early phases of diabetic ketoacidosis. 1 18

Three children presented as acute surgical emergencies due to undiagnosed diabetes mellitus. Where diabetic ketoacidosis mimicks the acute abdomen three clinical features are important in reaching the right diagnosis-namely, a history of polydipsia, polyuria, and anorexia preceding the abdominal pain, the deep sighing and rapid respirations, and severe dehydration.
 ...
PMID:Acute diabetic abdomen in childhood. 5 84

The pituitary-thyroid axis was investigated in nineteen euthyroid patients with severe diabetic ketoacidosis. A 'low T3 syndrome' was found, with the following characteristics: lowered serum concentrations of triiodothyronine (T3), increased reverse triiodothyronine (rT3), slightly low thyroxine (T4), normal thyrotrophin (TSH), slightly increased triiodothyronine uptake (RT3U) values, and a blunted TSH response to thyrotrophin-releasing hormone (TRH). These disturbances in thyroid-function tests required several days good control of the diabetes to be corrected, at least partially. The data suggest the presence of an abnormal extrathyroidal T4 metabolism as well as a pituitary defect. Caution is recommended in the interpretation of thyroid-function tests during and several days after the treatment of diabetic ketoacidosis.
 ...
PMID:A low T3 syndrome in diabetic ketoacidosis. 9 34

Cell-mediated immunity was evaluated in 11 children with diabetes mellitus; six children were evaluated during ketoacidosis and five were evaluated with ketonuria in the absence of acidosis. Five of the six ketoacidotic children had at least one positive delayed-hypersensitivity skin test. Lymphocytes from two ketoacidotic patients were unresponsive to phytohemagglutinin and pokeweed mitogen, and lymphocytes from these two patients plus a third patient were unresponsive to concanavalin A. Lymphocytes from all six patients responded to these three mitogens after one week of therapy. In the five diabetic children without ketoacidosis, lymphocyte responses were normal to all three mitogens. Similarly, the addition of glucose to normal plasma did not alter the lymphocyte transformations of three healthy nondiabetic controls. These data suggest that cell-mediated immunity may be transiently defective in children with acute diabetic ketoacidosis.
 ...
PMID:Abnormalities of in vitro lymphocyte response to mitogens in diabetic children during acute ketoacidosis. 10 85

Changes in glucagon, growth hormone (GH), cortisol, renin and aldosterone accompanying the metabolic disturbances and dehydration of severe diabetic ketoacidosis were studied over a 24 h period in eight patients treated with a constant intravenous insulin infusion. Mean steady state plasma-free insulin levels achieved were 28.6--49 mu/1 in patients receiving 2 u/h but a satisfactory rate of fall of glucose was not always obtained until the infusion dose was increased to 4 u/h or more. The total insulin dose administered was positively correlated with the level of plasma glucagon and cortisol on admission. During insulin infusion, both glucagon and cortisol fell but the rate of fall was not related to dose or plasma level of free insulin achieved. In six of eight patients studied increments in plasma GH above admission levels were observed during insulin treatment. Admission values of both plasma renin activity and plasma aldosterone were raised. The renin levels were highest in newly diagnosed diabetics, and two patients with long-established diabetes showed only small increments despite profound dehydration. Plasma renin activity, but not plasma aldosterone correlated with the fluid and sodium retention over the initial 24 h treatment period, but not with potassium requirements. The urinary excretion rates of the small molecular weight proteins GH and insulin, were considerably elevated over the treatment and convalescent periods.
 ...
PMID:Hormonal responses during treatment of acute diabetic ketoacidosis with constant insulin infusions. 10 71

This study investigates the effects of insulin antibody binding on free insulin levels measured in patients with acute diabetic ketoacidosis receiving insulin by constant infusion. In spite of antibody binding ranging from 10 to 90 per cent of the total circulating insulin, the steady state concentrations of free insulin were similar to those observed in individuals on identical infusion rates but without insulin-binding antibodies. However, the levels of free insulin in two patients were substantially lower than expected for the rate of insulin infusion, even though levels of bound insulin were not greatly elevated. An infusion rate of at least 4 U. per hour produced satisfactory rate of fall of plasma glucose, whereas lower dose regimens (2 U. per hour)--producing steady state free insulin concentrations ranging from 28 to 49 mU. per liter in different subjects--were unreliable in controlling the metabolic abnormalities of diabetic ketoacidosis.
Diabetes 1978 Dec
PMID:Antibody binding of insulin in diabetic ketoacidosis. 10 56

The prolactin response to 200 microgram thyrotropin-releasing hormone (TRH) IV was studied in seven patients with diabetic ketoacidosis, at the start of the treatment, and again, in the same patients, five days after recovery, when the diabetes was well controlled. Normal basal prolactin concentrations and prolactin responses to TRH were found in both situations. There was no correlation between basal prolactin concentrations, or magnitude of prolactin responses to TRH, and any of the metabolic variables measured. These findings do no suggest a role for prolactin in the development of diabetic ketoacidosis.
 ...
PMID:Prolactin response to TRH in diabetic ketoacidosis. 11 89

Eight years ago, in caring for persons with diabetes at Grady Memorial Hospital, Atlanta, priority was given to the use of oral hypoglycemic agents and insulin, with only minimal attention to nutrition. In 1971, an "expanded nutritional care program" was instituted, with emphasis on nutritional education and follow-up. Use of oral agents was discontinued, and, since 1972, less insulin has been used. The new dietary program, with dietitians playing a key role, includes a one-week total fast, stringent low-calorie diets, individualized dietary planning and instruction, and careful follow-up monitoring. Comparative pre-1971 and current data show: a 50 per cent reduction in lower extremity amputations, less diabetic ketoacidosis, fewer hospitalizations, weight reduction of 40 per cent with no increase in plasma glucose (in a 127-patient cohort with complete follow-up), and a savings to the hospital of more than $96,000 in the cost of medications and $3,700,000 in hospitalizations in eight years.
 ...
PMID:Spin-off cost/benefits of expanded nutritional care. 11 38

The effects of intravenous administration of potassium phosphate in the treatment of diabetic ketoacidosis were studied in nine children, ages 9 9/12 to 17 10/12 yr. During phosphate infusion (20--40 meq/L of fluid), all children maintained normal serum concentrations of phosphorus. Transient hypocalcemia occurred in six and transient hypomagnesemia in five patients. One child developed carpopedal spasms refractory to intravenous infusion of calcium gluconate but responsive to intramuscular injection of magnesium sulfate. In three patients, serum levels of intact parathyroid hormone were low at the time of hypocalcemia, an observation that suggests transient hypoparathyroidism. This study indicates that the use of potassium phosphate as the sole source of potassium replacement might potentiate ketoacidosis-induced hypocalcemia through multiple mechanisms.
Diabetes Care
PMID:Hypocalcemia, hypomagnesemia, and transient hypoparathyroidism during therapy with potassium phosphate in diabetic ketoacidosis. 11 30


1 2 3 4 5 6 7 8 9 10 Next >>