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

Ten patients with primary hyperparathyroidism were placed on a constant 30 mEq of calcium and 120 meq of sodium diet, and alterations in their calcium balance in response to standard oral doses of chlorpropamide were studied over a 4 day control period and a 4 day treatment period. The 10 patients treated with chlorpropamide significantly increased the urinary excretion of calcium and sodium and decreased the excretion of cyclic adenosine monophosphate (AMP). The serum calcium was lowered in six of the patients treated with chlorpropamide, and three of these patients, who had diabetes mellitus and either refused or were too ill for parathyroidectomy, continued to receive chlorpropamide for periods of 9 to 36 months. These three patients experienced prolonged lowering of the serum calcium level and became less confused, lethargic, and fatigued. The interrelationships between the chlorpropamide-induced changes in excretion of calcium, sodium, and cyclic AMP still must be clarified.
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PMID:Chlorpropamide-induced changes in patients with hyperparathyroidism. 41 59

Hypothyroidism in patients with diabetes mellitus is usually primary though rarely secondary hypothyroidism has occurred. An 11 6/12 year old white female developed diabetes mellitus at 8 6/12 years of age. She received treatment up to 40 units NPH daily with adequate control and normal growth. Hypothyroidism was diagnosed after a 3 month history of lethargy, constipation, dryness of skin and decreasing insulin requirement to 10 units NPH per day. Physical examination was entirely normal, except for dry skin. Serum levels of free thyroxine, thyroxine, T3 resin uptake, were low as was 131I uptake. Primary hypothyroidism was ruled out by the absence of goitre, absent antithyroid antibodies, low basal TSH levels and increased 131I uptake after TSH administration. Serum TSH levels rose 4-fold in respone to intravenous TRH administration. The patient was treated with 0.15 mg daily of L-thyroxine with very good response. This report describes a patient with juvenile diabetes mellitus and isolated TSH deficiency with hypothyroidism of probably hypothalamic origin, an association not previously described in children.
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PMID:Isolated thyrotrophin deficiency in diabetes mellitus. 57 89

In a study of 66 children with juvenile diabetes symptoms had often present for over a month before diagnosis. Though polyuria, polydipsia, and weight loss were the commonest features, other important symptoms included tiredness lethargy, and malaise. A gradual onset of diabetes was commoner than is generally realised.
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PMID:Mode of presentation of juvenile diabetes. 97 95

A case of lactic acidosis associated with phenformin therapy for diabetes mellitus is reported, and 34 previously reported cases of lactic acidosis associated with phenformin therapy are reviewed to determine if any predisposing factors to lactic acidosis were apparent. Observations of sex, age, duration of diabetes, pathologic conditions, dosage, duration of phenformin therapy and the onset of symptoms preceding lactic acidosis were made. Renal impairment, urinary tract infections, hepatic impairment, ethanol ingestion and poorly controlled congestive heart failure were found to be predisposing factors to lactic acidosis. The appearance of a syndrome of impending lactic acidosis consisted of anorexia, nausea, vomiting with abdominal pain or lethargy.
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PMID:Phenformin-associated lactic acidosis; a review. 114 21

Eighty-one patients undergoing carotid endarterectomy were divided into two groups based on the degree of stenosis of the carotid artery. Group I, 37 patients, was defined as having severe carotid stenosis (greater than 70%). Group II, 44 patients, was defined as having mild (less than 40%) or moderate (40% to 70%) carotid artery stenosis. Both groups were evaluated for neurologic and psychologic changes in the postoperative period. Prospective analysis demonstrated no significant differences between groups I and II in the areas of cardiac disease, history of preoperative stroke, preoperative and postoperative hypertension, diabetes, or postoperative computed tomography changes. Group II had a significantly higher percentage of carotid artery ulceration (p less than 0.01). Postoperative analysis revealed 34 group I patients had 6 to 8 weeks of lethargy versus two group II patients (p less than 0.01). Eleven group I patients had headaches for the first week postoperatively versus three patients in group II (p less than 0.05). Four group I patients had paranoid ideation, and another four patients had clinical depression, but not one patient in group II (p less than 0.01) had these psychiatric disturbances. These data suggest that significant, reversible neurologic and psychologic changes can occur because of reperfusion after relief of severe stenosis of the carotid artery.
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PMID:Postoperative somnolence in patients after carotid endarterectomy. 235 8

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

Zygomycosis of the basal ganglia should be recognized as a syndrome in intravenous drug users associated with a culture-negative cellular CSF, fever, lethargy, and lesions apparent on contrast-enhanced CT scans of the head. The infection is most likely the result of intravenous inoculation of fungal spores. This entity is different from the rhinocerebral zygomycosis seen with diabetes mellitus and other diseases. In the rhinocerebral form, there are external signs of the disease with involvement of the orbit, paranasal sinuses, and palate. In these drug users, infection was directed to areas deep within the brain.
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PMID:Zygomycosis of the basal ganglia in intravenous drug users. 264 54

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

Ten Kenyan patients with visceral leishmaniasis unresponsive to sodium stibogluconate, at a dose of 16 to 20 mg Sb/kg body-weight/day given for 30 to 98 days, were treated with 20 mg Sb/kg bw given every eight hours. This regimen was modified or abandoned in six patients because of suspected toxicity, although toxicity was difficult to assess because of intercurrent illness. Toxic effects included lethargy, anorexia, vomiting, electrocardiographic changes, fall in haemoglobin and rise in liver enzymes. One patient died, probably from a cardiac arrhythmia. Two patients were cured, four responded partially and four showed no response. Pentamidine, at a dose of 4 mg/kg body-weight given one to 3 times per week for 5 to 39 weeks, was given as initial treatment in one patient and after failure of sodium stibogluconate in seven. Toxic effects included nephritis, hepatitis, transient diabetes and subcutaneous abscesses. Two patients were cured, two responded partially, three showed no response and one, after apparent cure, relapsed and was unresponsive to additional pentamidine treatment. Low-frequency, long-duration pentamidine was often useful in maintaining any improvement made during treatment with the less well tolerated high-dose, high frequency sodium stibogluconate. We observed the step-wise development of resistance to both sodium stibogluconate and pentamidine. The problems of managing patients with visceral leishmaniasis which is unresponsive to conventional doses of pentavalent antimonials are discussed and some tentative suggestions put forward.
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PMID:Visceral leishmaniasis unresponsive to antimonial drugs. II. Response to high dosage sodium stibogluconate or prolonged treatment with pentamidine. 300 95

Symptomatic hypoglycemia developed 5 to 45 months after transplantation in nine children who had renal transplants before 6 years of age. During hypoglycemia, serum glucose levels ranged from 14 to 39 mg/dl (0.8 to 2.1 mmol/L). Hypoglycemic episodes occurred between 1.7 and 7.5 years of age. Six patients had generalized seizures; the remaining three had diaphoresis with stupor or lethargy. None of the children had serious infections, diabetes, congenital defects of glucose metabolism, or a history of treatment with insulin or oral hypoglycemic agents. Six patients had hypoglycemic symptoms after a prolonged fast, and at least four had ketosis. Eight of the nine patients were receiving propranolol when hypoglycemia occurred. No differences in the daily prednisone dose, the number of transplant rejection episodes, or the frequency of treatment with medications other than propranolol were noted between hypoglycemic patients and 56 normoglycemic age-matched renal transplant recipients. All hypoglycemic patients were subsequently treated with frequent feedings and discontinuation of propranolol. No further hypoglycemic episodes have occurred in eight of nine patients. Symptomatic hypoglycemia should be recognized as a potentially devastating complication of pediatric renal transplantation.
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PMID:Hypoglycemia in pediatric renal allograft recipients. 305 55


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