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

The diabetic hypersomolar state is defined by a serum glucose greater than 600 mg/dl and a serum osmolarity greater than 320 m Osm/L. Ketoacidosis or lactic acidosis may co-exist with DHS in the same patient. The incidence of this acute complication of diabetes is high enough (17.5 cases per 100,000 person-years) for primary care physicians to encounter a case every year or two. Predisposing factors include older age, female sex, nursing home residence, and infection. A substantial proportion of cases occur in patients with no prior history of diabetes. Common presenting signs include fatigue or weakness, polydipsia, polyuria, nausea, and alteration of consciousness. The mainstay of therapy is intravenous fluid replacement with close monitoring of glucose and electrolytes in a hospital setting. Current mortality figures are high, at 10% to 20%, and the chance of survival is adversely affected by older age, higher osmolarity, and the presence of an associated severe illness. Prevention includes screening for diabetes, educating diabetic patients and their care givers about the symptoms of hyperglycemia, prompt treatment of any infection in a diabetic person, avoidance of drugs that increase carbohydrate intolerance in diabetic people, and encouraging compliance with treatment of diabetes.
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PMID:The diabetic hyperosmolar state. 222 47

Acromegaly was diagnosed in 14 middle-aged to old cats of mixed breeding. Thirteen (93%) of the cats were male and one was female. The earliest clinical signs in the 14 cats included polyuria, polydipsia, polyphagia, all of which were associated with untreated diabetes mellitus. All developed severe insulin resistance within a few months; peak insulin dosages required to control severe hyperglycemia ranged from 20 to 130 U per day. Other clinical findings weeks to months after diagnosis included enlargement of one or more organs (e.g., liver, heart, kidneys, and tongue) (n = 14), cardiomyopathy (n = 13), increase in body size and weight gain (n = 8), nephropathy associated with azotemia and clinical signs of renal failure (n = 7), degenerative arthropathy (n = 6), and central nervous system signs (i.e., circling and seizures) caused by enlargement of the pituitary tumor (n = 2). The diagnosis of acromegaly was confirmed by demonstration of extremely high basal serum growth hormone concentrations (22 to 131 micrograms/l) in all cats. Computerized tomography disclosed a mass in the region of the pituitary gland and hypothalamus in five of the six cats in which it was performed. Two cats were treated by cobalt radiotherapy followed by administration of a somatostatin analogue (octreotide), whereas two cats were treated with octreotide alone. Treatment had little to no effect in decreasing serum GH concentrations in any of the cats. Eleven of the 14 cats were euthanized or died four to 42 months (median survival time, 20.5 months) after the onset of acromegaly because of renal failure (n = 2), congestive heart failure (n = 1), concomitant renal failure and congestive heart failure (n = 3), progressive neurologic signs (n = 2), persistent anorexia and lethargy of unknown cause (n = 1), the owner's unwillingness to treat the diabetes mellitus (n = 1), or unknown causes (n = 1). Results of necropsy examination in ten cats revealed a large pituitary acidophil adenoma (n = 10), marked left ventricular and septal hypertrophy (n = 7), dilated cardiomyopathy (n = 1), arthropathy affecting the shoulder, elbow, or stifle (n = 5), and glomerulopathy characterized by expansion of the mesangial matrix and variable periglomerular fibrosis (n = 10).
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PMID:Acromegaly in 14 cats. 240 66

Ten young adult cystic fibrosis (CF) patients over 16 years of age (average 21.4 years) began nighttime enteral feedings as a method of nutritional rehabilitation to regain and maintain body weight. Patients received nighttime feedings of 1,000 kcal/M2 of a low- (Pulmocare), medium- (Ensure Plus), or high-carbohydrate (Vivonex) formula for at least 2 nights each with pancreatic enzyme therapy. Five of ten young adult CF patients developed nocturnal hyperglycemia (serum glucose greater than 300 mg/dl) and glucosuria (1-3% glucose) with varying degrees of polyuria during enteral feedings. No patient developed ketonuria despite serum glucoses at times greater than 600 mg %. There was no difference between the hyperglycemic and normoglycemic groups in median age, percent of ideal body weight, NIH score, Brasfield scores, pulmonary function tests, or family history of diabetes. All normoglycemic and four of five hyperglycemic patients had normal fasting blood sugars. The percent hemoglobin A1c was greater in the glucose intolerant group than the normoglycemic patients (11.2 +/- 0.8% vs. 6.8 +/- 1.1%, mean +/- SE, p less than 0.005). Twelve to 15 units of NPH insulin prior to initiation of feedings provided adequate therapy in most hyperglycemic patients. There was no apparent difference in the elevation of early morning serum glucoses with the low- medium- and high-carbohydrate formulas. We concluded that hyperglycemia requiring insulin therapy was common in young adult CF patients using nighttime enteral feedings. A hemoglobin A1c appeared to be a useful screening test before initiating such therapy.
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PMID:Glucose intolerance with low-, medium-, and high-carbohydrate formulas during nighttime enteral feedings in cystic fibrosis patients. 249 15

Myogenic satellite cells were isolated from nondiabetic and streptozotocin-diabetic rats and studied in vitro. Streptozotocin (STZ) administration produced both hyperglycemia and glucosuria in adult rats when compared to controls. (P less than 0.01), with 12.5% mortality in untreated animals. Insulin therapy diminished blood glucose levels to those found in nondiabetic animals. Only STZ-diabetic rats displayed symptoms of Type I diabetes, including polydipsia, polyuria, and hyperphagia. STZ-treated rats possessed less leg muscle mass and less subcutaneous, intermuscular, and intramuscular fat. Conversely, nondiabetic rats had a greater mean body weight (P less than 0.01) at the end of the experiment than did diabetic rats. Primary cultures of diabetic-derived satellite cells displayed decreased overall ability (P less than 0.01) to fuse to form multinucleated myotubes in vitro than controls. In addition, secondary cultures of diabetic-derived satellite cells achieved maximal fusion one day later than secondary cultures of control-derived cells. Collectively, these data provide preliminary evidence to suggest that untreated insulin-dependent diabetes results in altered fusion characteristics of myogenic satellite cells. Additional studies utilizing satellite cells from diabetic animals will provide valuable definition of the satellite cell involvement in skeletal muscle autophagy which is a symptom of type I diabetes.
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PMID:Satellite cells derived from streptozotocin-diabetic rats display altered fusion parameters in vitro. 252 36

The effects of streptozotocin-induced diabetes on weight gain, bone growth and GH secretion have been studied in conscious chronically cannulated male rats. In addition to the classic diabetic symptoms (hyperphagia, polydipsia, polyuria, glycosuria and hyperglycaemia), the slow body weight gain (0.95 +/- 0.5 compared with 2.63 +/- 0.5 g/day in non-diabetic controls) was associated with a reduction in bone growth (from 162 +/- 9 to 48 +/- 4 microns/day) and a reduced pituitary GH content (from 1.5 +/- 0.2 to 0.6 +/- 0.06 mg/gland). Serial blood sampling during the day or overnight showed that the normal male episodic GH secretory pattern was obliterated in the diabetic animals. The constant osmotic stimulation of hyperglycaemia and high fluid turnover was reflected in a significant reduction in pituitary oxytocin and arginine vasopressin (AVP) stores. Intravenous insulin infusions (67-1340 pmol/h for 4 or 7 days) caused a large initial weight gain (greater than 20 g in 2 days) followed by a slower increase, and stimulated tibial bone growth (to 100 +/- 16 and 126 +/- 8 microns/day after 4 or 7 days respectively). Insulin infusion for 7 days also increased pituitary GH content (to 1 +/- 0.15 mg/gland), and the normal episodic GH secretory pattern returned. Intravenous infusions of insulin which reduced, but did not completely normalize, blood glucose levels, allowed the resumption of growth and pulsatile GH secretion. Continuous infusion of recombinant human insulin-like growth factor-I (hIGF-I) at 1110 pmol/h for 54 h also caused a large initial rise in body weight in diabetic rats (17.1 +/- 1.6 compared with 7.5 +/- 2.8 g in saline-infused controls) due primarily to increased fluid retention. This effect of hIGF-I occurred without any significant changes in pituitary GH, AVP, oxytocin, blood glucose or bone growth over this short-term infusion, nor was there any obvious effect on spontaneous GH secretion, monitored over the entire infusion period. We conclude that the diabetic rat is not a good model to study growth stimulation by short-term insulin or IGF-I treatments because the insulin-like effects of these peptides obscure their specific growth-promoting activities in this model.
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PMID:Growth hormone and growth in diabetic rats: effects of insulin and insulin-like growth factor-I infusions. 268

We report a rare case of Klebsiella pneumoniae meningitis associated with liver abscess, which was successfully treated with cefotaxime (CTX), one of the third-generation cephalosporins. A 53-year-old man was admitted to Keio University Hospital on June 13, 1988, because of a fever and a headache. On June 3, he suddenly started shivering and his temperature rose to 39 degrees C. He then began to complain of polydipsia, polyuria, and a weight loss of 4 kg a week. On June 11, he developed a severe headache. Four years prior to this incident, he had been diagnosed as having diabetes after a routine medical examination, but had neglected to undergo medical treatment. On admission, laboratory data showed leukocytosis, hyperglycemia (394 mg/dl) and ketonuria (4+). A lumbar puncture yielded cloudy cerebrospinal fluid (CSF) containing 500/3 cells/mm8, of which about 70% were neutrophils. A diagnosis of diabetic ketoacidosis and purulent meningitis was made. A treatment with ampicillin (ABPC) and CTX, (12 g/day, each) was begun. On the third day, cultures of a blood specimen and CSF yielded both K. pneumoniae. The MICs of CTX to K. pneumoniae isolated from blood and CSF were both 0.05 microgram/ml. ABPC was discontinued, gentamicin was administered for 2 days, CTX was continued at the same dosage level and an administration of prednisolone 40 mg daily was begun.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Klebsiella pneumoniae meningitis associated with liver abscess: a case report]. 269 13

The author describes his findings pertaining to spontaneous diabetes mellitus in BB rats and the method and results in juvenile alloxan diabetes in neonatal and adolescent Wistar rats of his own inbreeding F8-10. The author presents also the results of attempts to treat juvenile alloxan diabetes in rats by intrafamilial renal-subscapular allotransplants of 2-5 neonatal collagenase nondigested pancreases. Six of eleven BB females developed latent or manifest insulin dependent diabetes mellitus during the third to fourth month of life. An intraperitoneal injection of alloxan to 2-5-day-old rats causes, after two months of prediabetes, latent or manifest disease, in particular in males. In one-two-month adolescent fasting F6--10 inbred rats (Wistar strain) intravenous injection of 50 mg/kg alloxan causes diabetes mellitus with hyperglycaemia (20-60 mmol/l), glycosuria, polyuria, arrested growth, development of cataract and early death due to pulmonary or intestinal infection. The author tries to prevent these sequelae and complications by insulin therapy or intrafamilial allotransplantations of 2-5 neonatal, collagenase nondigested pancreases beneath the renal capsule, using two-three--week immunosuppression with Cyclosporin A combined with Azathioprine. The author proves permanent cure, histologically and functionally, by repeated allotransplantation which, however, due to the intense thymolymphatic immunological barrier in adolescent rats is less frequent than cure repeatedly achieved by the author in adult diabetic rats.
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PMID:[Spontaneous and experimental models of human juvenile diabetes mellitus]. 275 53

We present a new clinical case of a 25-year-old man with Wolfram's syndrome. Partial central diabetes insipidus was found to cause polyuria, polydipsia and enuresis. The patient had diabetes mellitus for the last 18 years, controlled with diet and/or chlorpropamide during 10 years and showed no typical complications of the disease. The patient was also shown to have a dilated urinary tract and perceptive hypoacusis for high frequencies. The fifth classical component of this syndrome, primary optic atrophy, was not found. Based on the report of this case, Wolfram's syndrome is briefly described.
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PMID:[Description of Wolfram syndrome (DIDMOAD) on the basis of a new case]. 278 Oct 75

During a survey period of 28 years a total of 449 patients suffering respectively from pemphigus, systemic lupus erythematous and chronic nephritis was admitted to the hospital. Of the 286 patients who received glucocorticoid treatment 28 were found to have steroid diabetes (9.8%). The incidences of steroid diabetes in these diseases were as follows: pemphigus 20% (7/35), systemic lupus erythematous 12.5% (14/112), chronic nephritis 5% (7/139). Two thirds of the diabetic subjects appeared asymptomatic, while the remainder showed polydipsia and polyuria. Renal glucosuria was seen in 3 cases and hyperosmolar hyperglycemia in 4. Blood glucose level in 10 out of the 21 remaining cases was 8.9 +/- 1.5 mmol/L and in the other 11 cases 14.8 +/- 2.4 mmol/L. Generally, the treatment of steroid diabetes is not intricate. Satisfactory improvement was seen in about 80% of the patients if a strict line of therapy against primary diabetes was oriented. In this series 18 patients did well under the treatment either with reduction of steroid or with use of oral hypoglycemic agents or insulin or both. Their blood glucose levels returned to normal and urine sugar disappeared rapidly. Four of the 5 deaths were caused by their primary diseases. One died of pemphigus complicated with infection and shock exhibiting an ante mortem blood glucose level as high as 31.7 mmol/L, obviously hyperosmolar status being the predisposing factor. Due to the fact that most of the steroid diabetic patients were clinically asymptomatic, delayed or misbranded diagnosis was not infrequently seen.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Steroid diabetes: an analysis of 28 cases]. 280 46

Hyperadrenocorticism was diagnosed in 7 cats with concurrent diabetes mellitus. Four cats had pituitary adenoma with bilateral adrenocortical hyperplasia, 1 cat had pituitary carcinoma with bilateral adrenocortical hyperplasia, 1 cat had adrenocortical carcinoma, and 1 cat had adrenocortical adenoma of the left adrenal gland. One year later, adrenocortical adenoma involving the right adrenal gland also was diagnosed in this cat. Clinical signs included polyuria and polydipsia (n = 7), development of pot-bellied appearance (n = 5), dermatologic alterations (n = 5), lethargy (n = 3), weight loss (n = 3), dyspnea/panting (n = 2), and recurrent bacterial infections (n = 2). In 6 cats, the diagnosis of hyperadrenocorticism was established before death on the basis of results of the ACTH stimulation test (n = 3) and the dexamethasone screening test (n = 5). Pituitary-dependent hyperadrenocorticism was differentiated from adrenocortical neoplasia on the basis of results of the dexamethasone suppression test (n = 4), endogenous ACTH concentration (n = 3), results of abdominal radiography and ultrasonography (n = 3), and exploratory celiotomy (n = 1). Four cats died or were euthanatized without treatment attempts. Treatment with mitotane followed by 60Co teletherapy was ineffective in one cat with pituitary adenoma. One cat with pituitary carcinoma died one week after bilateral adrenalectomy. Bilateral adrenocortical adenomas were removed surgically in the affected cat.
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PMID:Hyperadrenocorticism in cats: seven cases (1978-1987). 284 Dec 69


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