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

Low serum ionized calcium concentrations were observed in twenty-five insulin dependent diabetic outpatients compared with twenty-three age-matched normal subjects: mean 1.16 mmol/l (SEM 0.01) versus 1.20 mmol/l (0.01), P less than 0.002. Despite this, there was no compensatory increase in serum concentrations of immunoreactive parathyroid hormone, nor was serum total calcium decreased in the diabetic patients. Serum magnesium was significantly decreased in the diabetics compared with normals: mean 0.75 mmol/l versus 0.83 mmol/l, P less than 0.001. No significant correlation could be demonstrated between serum magnesium and serum ionized calcium or parathyroid hormone in the diabetic patients. Since no significant correlations were observable between serum ionized calcium and indices of diabetes control, the etiology and pathogenesis of decreased serum calcium ion in insulin-dependent human diabetes mellitus remain unknown.
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PMID:Decreased serum concentration of ionized calcium in insulin-dependent human diabetes mellitus. 640 51

In a retrospectively analyzed series of 441 patients operated for primary hyperparathyroidism (HPT), the prevalence of diabetes mellitus was 8.2%, which was three times higher than in the unselected age-matched population. Following parathyroid surgery, the need for antidiabetic treatment was unchanged. The insulin response to an intravenous glucose load was enhanced preoperatively [95 mU/1 +/- 41 (SD)] in twenty-six prospectively studied patients compared to postoperative (65 +/- 41 mU/1) investigations (P less than 0.01). This response was inversely correlated (r = 2, P less than 0.01) to the serum phosphate concentrations but not related to calcium or parathyroid hormone levels. Postoperatively, most HPT patients experienced a deterioration of their glucose tolerance (t 1/2 for i.v. glucose 54 +/- 12 and 64 +/- 21 min, respectively, P less than 0.05), and one-third of them had pathological values at follow-up. Despite this, neither the fasting blood glucose levels nor the values for haemoglobin A1c were significantly affected.
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PMID:Diabetes mellitus, glucose tolerance and insulin response to glucose in patients with primary hyperparathyroidism before and after parathyroidectomy. 641 50

Diabetes mellitus was induced in Lewis rats by streptozotocin, and these animals and control rats fed ad lib were studied after 7 weeks. At the time of sacrifice, nondecalcified histological sections of bone were prepared and subsequently quantitated by micromorphometric techniques. In addition, tibial alkaline phosphatase and mineral ash content were determined. The bones obtained from the diabetic animals are characterized by significant decrements in the quantities of osteoid and osteoclasts and by failure to acquire a tetracycline label. These histological features are attended by reduced quantities of urinary hydroxyproline and tibial alkaline phosphatase. As compared with control animals fed ad lib, diabetic rats are hyperphosphatemic and markedly hypercalciuric. Circulating alkaline phosphatase is also elevated and associated with a parallel increase in intestinal content of this enzyme. Although serum corticosterone levels are increased, diabetes is associated with decrements in both circulating immunoreactive parathyroid hormone and 1,25(OH)2D. We conclude that prolonged streptozotocin-induced diabetes mellitus in the rat results in reduced bone turnover. The relative roles that functional caloric deprivation, low circulating levels of 1,25(OH)2D, hypercalciuria, hypercortisolemia, and decreased blood parathyroid hormone levels play in the genesis of these skeletal abnormalities remain to be determined.
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PMID:The effect of streptozotocin-induced chronic diabetes mellitus on bone and mineral homeostasis in the rat. 645 Feb 54

Calcium metabolism was studied in hemodialyzed patients with diabetes mellitus nephropathy (HD/DM) and in hemodialyzed nondiabetic patients with chronic glomerulonephritis (HD/non-DM). Incidence of bone changes visible in X-ray films, assessed by changes in the lamina dura and trabecular patterns of mandibulae, was less in HD/DM than in HD/non-DM patients. Serum c-terminal parathyroid hormone was significantly lower in HD/DM than that in HD/non-DM. Serum calcitonin was higher in HD/DM than that in HD/non-DM. The lower level of c-terminal parathyroid hormone would be a reason that bone changes were less in HD/DM than in HD/non-DM patients.
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PMID:Abnormal calcium metabolism in hemodialyzed patients with diabetic nephropathy. 647 29

Lipoadenoma is the accepted diagnosis of a single enlarged parathyroid gland that contains large quantities of mature fat cells and focal myxoid stroma, all widely separating small parenchymal cell nests in patients with hyperparathyroidism. Here we are reporting, for the first time, on five cases of hyperparathyroidism in which all four parathyroid glands are enlarged and each gland is noted to have an admixture of fat and parenchymal cells. We will introduce the descriptive diagnosis of lipohyperplasia to name this condition and keep it in perspective with other forms of parathyroid disease. All five patients were women between the ages of 36 and 62 years who underwent neck exploration, at which time four enlarged light-tan parathyroid glands were observed. Three and one half gland resections were performed, and all patients returned to a normocalcemic state except one who had borderline serum hypercalcemia after operation. Most of the resected parathyroid glands weighed in the range of 100 to 200 mg. The largest measured gland weighed 820 mg. Parathyroid histology showed an admixture of mature fat cells with parathyroid parenchymal cells often in a 1:1 ratio. One patient who had renal failure exhibited a lower ratio of fat cells. Two patients had chronic lymphocytic thyroiditis that was severe enough to require synthetic thyroid hormone therapy. Two patients had a history of urinary tract infections. Three patients had hypertensive cardiovascular disease, and several patients had arteriosclerotic cardiovascular disease. One patient had diabetes mellitus, one had a history of pituitary adenoma, and one had polydipsia. All of these patients were first seen with parathyroid glands measuring an average of five times normal size, yet they showed the usual 50% fat/50% parenchyma pattern of normal mature parathyroid glands. This means that the enlarged glands contain a 500% increase in parathyroid tissue, justifying the diagnostic term "lipohyperplasia." This easily represents enough parathyroid tissue to generate excessive parathyroid hormone production. At this time, there is no explanation of the pathogenesis of lipohyperplasia or how it varies from other previously described forms of parathyroid hyperplasia.
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PMID:Five cases of parathyroid lipohyperplasia. 664 2

Serum immunoreactive parathyroid hormone in patients with juvenile-onset diabetes mellitus and end-stage renal failure on chronic haemodialysis treatment is significantly lower than the values obtained from patients with adult-onset diabetes mellitus and non-diabetic patients with end-stage renal disease being similarly dialysed. The major determinants of parathyroid hormone secretion, such as calcium and magnesium, do not seem to be the factors responsible for this difference. The histology of the parathyroid glands in juvenile-onset patients shows fibrosis and collagen infiltration which reduce the functional mass of the glands.
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PMID:Parathyroid hormone in patients with diabetes mellitus and end-stage renal disease on chronic haemodialysis. 687 35

To determine the relationships among bone mass, bone growth and serum glucose control in young, insulin-dependent diabetics, we performed photon absorptiometry and radiogrammetry on a clinically well-characterized group of 78 diabetics (mean age 15.2 yr, mean duration of diabetes 6.7 yr). Total and ionized calcium (TCa, ICa), magnesium (Mg), immunoreactive parathyroid hormone (iPTH) and phosphorus (P) were measured in fasting serum. Bone age was calculated from hand x-rays; and bone measurements, heights, and weights were standardized against normal groups of corresponding age, sex, and race. Mean deviation of bone mass measurement score was 1.24 SD below the normal mean (p less than .001); mean cortical area score was .22 SD and percent cortical area .25 SD below the normal means (both p less than .05). Radical width and metacarpal width for the diabetics were not less than normal. Mean percentiles for height and weight were 52.3 and 57.1 respectively, the latter significantly elevated (p less than .02). Bone mass and cortical area were inversely related to duration of disease (r = -.228, p less than .05; r = -.216, p less than .05). They were not correlated with serum parameters of mineral metabolism or of glucose control. Bone age was not significantly different from chronological age in those who had not achieved maturity (14.4 versus 14.5 yr). Mean age of menarche was 12.9 yr. When compared to normals the diabetic sample had diminished serum ICa (p less than .001), and Mg (p less than .001), though P and iPTH were not significantly different. We have demonstrated: (1) bone mass in this sample of juvenile diabetics is depressed, without evidence of impaired overall growth or delayed maturation, (2) this reduced bone mass probably results from a failure to gain the normal component of endosteal bone expected at this age, (3) this abnormality in bone growth progresses with disease but does not appear to vary with serum glucose control, and (4) in this population of diabetics there is a minimal but significant reduction in serum total and ionized calcium and serum magnesium without compensatory elevation of parathyroid hormone. The relationship of this metabolic abnormality of impaired bone growth in unknown.
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PMID:Evaluation of bone mass and growth in young diabetics. 698 Mar 56

There has been doubt as to whether elevated levels of parathyroid hormone, reported previously by radioimmunoassay, reflect increased concentrations of the biologically active hormone. The application of a recently developed, highly sensitive bioassay has shown considerable disparity between bioactivity and immunoreactivity in 5 rheumatic conditions and in normal subjects. Six patients with chondrocalcinosis had elevated levels; 3 of these did not have hypercalcaemia or any obvious cause other than possible subclinical hyperparathyroidism. One patient, assayed during an acute episode, had an elevated concentration of the hormone which reverted to normal when she was asymptomatic. Most patients with osteoarthrosis (13 our of 15) had low normal levels; 2 showed unexplained slightly elevated concentrations. Of 6 patients with haemochromatosis 3 had elevated levels, though this may have been related to the associated presence of diabetes mellitus. A third of patients with ankylosing spondylitis (10 out of 30) showed elevated parathyroid hormone levels but without hypercalcaemia. A number of spondylitic patients also showed anomalous results in this assay, possibly due to the presence of an antagonist. This would be consistent with the absence of clinical or biochemical evidence of hyperparathyroidism.
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PMID:Circulating levels of biologically active parathyroid hormone in rheumatic diseases. 698 29

Biochemical and bone scintigraphic studies were performed in nondiabetic and diabetic patients receiving hemodialysis at the time of kidney transplantation to assess the degree of secondary hyperparathyroidism. Despite lower serum calcium concentrations, diabetic patients had significantly lower parathyroid hormone (PTH) levels than nondiabetic patients. In addition, diabetic patients had lower graded total-skeletal scintigraphic scores than nondiabetic patients. The PTH levels showed positive correlations with bone scan scores and with alkaline phosphatase in nondiabetic patients but not in diabetic patients. Avascular necrosis occurred in 17% of nondiabetic patients and in only 2% of diabetic patients. Patients with avascular necrosis had significantly higher PTH levels than patients without avascular necrosis. Diabetes mellitus seems to confer a protective effect from the skeletal manifestations of secondary hyperparathyroidism, including avascular necrosis.
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PMID:Decreased secondary hyperparathyroidism in diabetic patients receiving hemodialysis. 700 80

Plasma and urine phosphate concentrations were improved in 21 patients with diabetes mellitus during "optimal" metabolic control as compared with "suboptimal" control. During the "suboptimal" control phase the daily insulin dosage averaged 38 +/- 22 (SD) U/day and the mean plasma glucose levels averaged 17.1 +/- 1.8 mmol/l, while during the "optimal" control phase the daily insulin dosage averaged 84 +/- 59 U/day and the mean plasma glucose level was 6.2 +/- 1.4 mmol/l. The institution of rigid diabetic control over 4-10 days significantly raised serum phosphorus from 1.12 +/- 0.16 to 1.26 +/- 0.19 mmol/l (p less than 0.001), and decreased urinary phosphorus excretion from 686 +/- 125 to 588 +/- 88 mg/day (p less than 0.001). These changes were associated with significant reductions in urinary calcium, urinary glucose, plasma immunoreactive glucagon and serum parathyroid hormone. This diminution in urinary phosphorus loss may have been due to diminished glycosuria but equally could have been influenced by a direct action of insulin on the renal tubule or suppression of glucagon and parathyroid hormone secretion. Under the conditions of this study, reduced urinary phosphorus may have been sufficient to cause a rise in serum phosphorus despite the known effects of insulin on the cellular influx of phosphorus.
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PMID:The effect of chronic insulin therapy on phosphate metabolism in diabetes mellitus. 702 29


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