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

To assess the relationship between the decreased bone mass observed in young insulin-requiring diabetic patients and vitamin D metabolism, we measured serum 25-hydroxyvitamin D, 24,25-dihydroxyvitamin D, and 1,25-dihydroxyvitamin D concentration in 45 white, insulin-dependent diabetic subjects, 7-18 yr of age. Metacarpal cortical thickness in 87% of these diabetics was below the mean for their respective ages, while 16% had a cortical thickness value greater than 2 sDs below the mean. Serum calcium and phosphate concentrations were normal, immunoreactive parathyroid hormone was in the low normal range, and total serum alkaline phosphatase was elevated compared to age- and sex-matched controls. Circulating 24,25-dihydroxyvitamin D concentrations were significantly elevated, and 1,25-dihydroxyvitamin D was significantly decreased. The increase in 24,25-dihydroxyvitamin D was greater in the diabetics with the most severe bone loss and was maximally increased during the first 5 yr of clinical diabetes. No apparent correlation was seen between metabolic control, as measured by hemoglobin A1C and urine and plasma glucose, and the circulating levels of the vitamin D metabolites. Despite appropriate insulin replacement, alterations in vitamin D metabolism occur in the young insulin-dependent diabetic and could relate to the decrease in cortical bone mass observed in these patients.
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PMID:Alterations in circulating vitamin D metabolites in the young insulin-dependent diabetic. 702 72

In a university-affiliated community hospital, medical records of 58 patients on whom the intact parathyroid hormone immunoassay (I-PTH) and 29 patients on whom both the carboxyl terminal PTH(C-PTH) and I-PTH ordered by physicians were reviewed to determine the reasons for requesting these tests. Reasons for ordering the PTH tests include (1) the evaluation of hypercalcemic patients (25/58 I-PTH); (2) the evaluation of hypocalcemic patients (2/58 I-PTH); (3) to rule out primary hyperparathyroidism in normocalcemic stone formers (4/58 I-PTH, 4/29 C-PTH) and in those with abnormal skeletal x-ray (3/48 I-PTH 1/29 C-PTH); (4) to follow patients with chronic renal failure on dialysis (11/58 I-PTH, 9/29 C-PTH); (5) to rule out ectopic hyperparathyroidism in patients with cancer (2/58 I-PTH, 3/29 C-PTH); (6) to satisfy physicians' intellectual curiosity of patients with diabetes mellitus (3/58 I-PTH, 3/29 C-PTH) and obesity (5/58 I-PTH; 6/29 C-PTH); (7) to evaluate acute renal failure (1/29 C-PTH). In 3/58 patients on whom I-PTH tests were ordered, reason(s) could not be determined. The C-PTH was elevated in 9/9 patients with chronic renal failure, 4/6 obese patients, 2/3 patients with cancer, 1/3 diabetic patients, 1/4 stone formers, 2/2 patients with primary hyperparathyroidism. Patients with chronic renal failure had the highest C-PTH. Based on well established indications for ordering the PTH immunoassays, 25 out of 58 (43%) of I-PTH and 9 out of 29 (31%) of C-PTH ordered are inappropriate.
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PMID:Diagnostic utility of carboxyl-terminal and intact parathyroid hormone immunoassays in hospitalized patients. 709 Oct 50

A 32-year-old man with insulin-dependent diabetes secondary to chronic calcifying pancreatitis of alcoholic origin in whom hypocalciuria (22 to 88 mg/24 hours) was discovered by chance, renal function being normal. Plasma phosphate levels were between 25 and 35 mg/l and the level of parathyroid hormone was at the upper limit of normal. Cervicotomy led to the discovery of three parathyroid glands which were removed. Their weight was increased and their histological appearance normal. The fourth parathyroid was not seen. Hypercalcaemia and hypocalciuria were found during the operation and persis 3 years after, with none of the usual causes being found. This patient has a certain number of characteristics reminiscent of familial hypercalcaemia-hypocalciuria syndrome: high plasma calcium levels associated with low calciuria despite normal renal function and a plasma parathyroid level normal in most cases. The physiopathology of this syndrome remains unknown. Its course is benign, without renal complications. Partial parathyroidectomy is ineffective.
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PMID:[An unrecognised cause of hypercalcaemia: hypercalcaemia-hyocalcluria syndrome]. 736 69

Serum immunoreactive parathyroid hormone (iPTH) and indices of mineral and glucose metabolism were determined in 58 insulin treated diabetic patients (duration of disease 1-11 years). The mean serum iPTH level in all diabetic patients, measured simultaneously with sera from normal subjects, was 55% of normal mean (P < 0.01). The diabetic patients had hypomagnesaemia (P < 0.001), hypercalciuria (P < 0.001) and a 9.6% decrease in bone mass (P < 0.001). Low serum iPTH values were correlated with high glycosuria (R = -0.28, P < 0.05) and with long duration of diabetes (R = -0.31, P < 0.02). Patients with both high glycosuria and long diabetes duration had especially low iPTH values (mean 16 ng/l, n = 16) compared with patients with both low glycosuria and short diabetes duration (mean 32 ng/l, n = 15, P < 0.005) and with normal subjects (mean 37 ng/l, n = 28, P < 0.001). The 16 patients with low serum iPTH values also had higher urinary calcium excretion rate (P < 0.05) than the 15 patients with low glycosuria and short duration of diabetes. The diabetic hypoparathyroidism may be secondary to a primary disturbance of bone metabolism, with a negative net calcium balance.
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PMID:Hypoparathyroidism in diabetes mellitus. 745 85

An elderly man with diabetes mellitus and end-stage renal disease managed with continuous ambulatory peritoneal dialysis (CAPD) was hospitalized with peripheral vascular insufficiency; he developed hypercalcemia and became mentally obtunded. Lowering dialysate Ca from 3.5 mEq/L to 2.5 mEq/L, stopping calcium acetate, and ultimately hemodialysis with calcium-free dialysate did not lead to reversal of the hypercalcemia or improvement of his symptoms. The intact parathyroid hormone PTH level was 187 pg/mL, a value rarely associated with significant osteitis fibrosa. A search for other causes of hypercalcemia was unrevealing, and a iliac crest bone biopsy was done. The latter showed osteitis fibrosa, and the patient underwent parathyroidectomy. The hypercalcemia reversed quickly, and his mental symptoms slowly improved. The discussion reviews the probable causes of hypercalcemia in diabetic patient undergoing CAPD with 3.5 mEq/L dialysate calcium and using calcium-containing phosphate binders, with hyperparathyroidism certainly not the usual cause. The reason for the occurrence of significant hyperparathyroidism in the face of only modest elevation of PTH is considered. The value of bone biopsy in resolution of this problem is apparent.
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PMID:Symptomatic hypercalcemia in a diabetic patient undergoing continuous ambulatory peritoneal dialysis: value of bone biopsy in the diagnosis and management. 748 41

To clarify the incidence and contributing factors of hypoparathyroidism in a hemodialysis (HD) population, 224 patients undergoing maintenance HD were investigated. They were divided into 4 groups according to their high-sensitive parathyroid hormone levels: extra-high (EH) group > 420,000 pg/ml; high (H) group 20,000-420,000 pg/ml; moderate (M) group 4,500-20,000 pg/ml; low (L) group, < 4,500 pg/ml. In group L, a 25-mg/kg deferoxamine (DFO) infusion test was undertaken to estimate aluminum (Al) accumulation. The distribution in each group was 42, 35, 12, and 11% for groups L, M, H and EH, respectively. Group-L patients were relatively older than those of the other groups. Diabetes was seen in 20% of group-L patients, as opposed to no diabetes in groups H and EH. Among the 22 diabetics, 82% were in group L. 70% of group-L patients showed a less than 50-micrograms/l Al increment after the DFO infusion test. Bone mineral density (BMD) did not differ between the groups with relative hypoparathyroidism (RHP=L) and background-matched non-RHP, either at the initiation of HD or the recent period, and the changes in BMD were comparable between the 2 groups. These results suggest that a considerable number of HD patients show RHP. Diabetes, but not Al accumulation, was considered to be one of the predisposing factors of RHP. Though the outcome of RHP will be aplastic bone disease (ABD) in HD patients, the clinical significance of ABD has not been fully evaluated. Further studies are required to clarify the precise mechanisms of RHP and the significance of ABD.
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PMID:Relative hypoparathyroidism in hemodialysis patients. 756 27

Renal osteodystrophy in diabetic patients on maintenance hemodialysis is characterized by a higher prevalence of low bone turnover and is associated with a relative deficiency of parathyroid hormone (PTH) as compared with non-diabetic hemodialysis patients. The goal of the study was to evaluate how diabetes affected the development of secondary hyperparathyroidism (2 degrees HPT) and bone disease in azotemic rats. Three groups of 5/6 nephrectomized, pair-fed male Wistar rats maintained on a high phosphorus (1.2%) diet were studied: (1) the control group, non-diabetic azotemic rats (NDR); and two streptozotocin-induced diabetic azotemic groups, (2) poorly-controlled diabetic rats (PCDR) which received only enough NPH insulin to maintain the blood glucose between 300 and 400 mg/dl, and (3) well-controlled insulin-treated diabetic rats (IDR) which received a continuous insulin infusion for 14 days via a subcutaneously implanted miniosmotic pump. Serum calcium, phosphorus and creatinine levels were similar among the three groups. Blood glucose levels were greater in the PCDR group than the IDR and NDR groups (358 +/- 11 vs. 83 +/- 9 and 87 +/- 8 mg/dl, respectively; P < 0.001). Rats in the PCDR group weighed less at sacrifice as compared with the IDR and NDR groups (P < 0.05). Serum PTH levels (normal 47 +/- 2 pg/ml) were elevated, but not different among the three groups (136 +/- 34, 147 +/- 21 and 98 +/- 8 pg/ml in the PDCR, IDR and NDR groups, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Development of secondary hyperparathyroidism and bone disease in diabetic rats with renal failure. 764 45

The present study was undertaken to determine whether improvement of hyperglycemia alters calcium and phosphorus handling, parathyroid hormone (PTH) secretion and bone turnover in patients with non-insulin-dependent diabetes mellitus (NIDDM). We measured serum and urinary mineral levels, serum intact PTH and osteocalcin on admission and at discharge (38 +/- 3 days later, Means +/- SEM) in 28 patients with poorly-controlled NIDDM (63 +/- 2 years old, 13 males and 15 females). During the hospitalization period, glycemic control was markedly improved. Serum calcium levels remained unchanged, but serum phosphorus increased. Urinary calcium and phosphorus excretion decreased. Serum intact PTH decreased from mid-normal (30.0 +/- 2.2 ng/l) to low normal values (24.0 +/- 1.3 ng/l) (P < 0.01, normal values: 10-65 ng/l). Serum osteocalcin increased from 4.14 +/- 0.35 to 4.92 +/- 0.40 micrograms/l (P < 0.01, normal values: 2.5-13 micrograms/l). On admission, urinary calcium and phosphorus excretion showed a positive correlation with urinary glucose excretion. Serum calcium levels showed a negative correlation with serum intact PTH (r = -0.46, P < 0.05). Moreover, the change in serum calcium during the hospitalization was negatively correlated to the change in serum intact-PTH (r = -0.45, P < 0.05). Serum phosphorus concentrations showed a positive correlation with the renal threshold for phosphorus excretion on admission (r = 0.86, P < 0.01). These results indicate that hyperglycemia causes excess urinary calcium and phosphorus excretion in patients with NIDDM. In response to urinary calcium loss, PTH secretion is mildly stimulated. Bone formation seems to be suppressed in the hyperglycemic state in spite of increased PTH secretion.
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PMID:Effect of glycemic control on calcium and phosphorus handling and parathyroid hormone level in patients with non-insulin-dependent diabetes mellitus. 767 May 67

To assess the risk factors associated with renal osteodystrophy, we examined the database of 256 patients who were prospectively studied in three Toronto dialysis centers between October of 1987 and 1989. The potential risk factors examined included age, sex, type and duration of dialysis, type and dose of phosphate binders, vitamin D treatment, and history of diabetes mellitus, renal allograft failure, parathyroidectomy, and bilateral nephrectomy. All patients had undergone a bone biopsy and were categorized into one of four disease groupings: (1) osteitis fibrosa and mixed bone disease, (2) aluminum bone disease, (3) mild bone disorder, and (4) aplastic bone disorder. The mean (+/- SD) age of the patients at bone biopsy was 57 +/- 15 years, and 62% were men. Forty-five percent of patients were treated by hemodialysis and 55% by peritoneal dialysis. The mean duration of dialysis was 4 +/- 4 years. Twenty-five percent were also diabetic. The most common disorder was the aplastic (or "adynamic") bone disorder, found in 34% of patients. Aluminum bone disease was found in 27%, osteitis fibrosa or mixed bone disease in 27%, and mild bone disorder in 12% of patients. Cumulative intake of aluminum gels was associated with aluminum bone disease, whereas peritoneal dialysis with supraphysiologic calcium concentrations, ingestion of calcium carbonate, and diabetes mellitus were associated with both mild bone disorder and aplastic bone disorder. These three latter risk factors may be important in predisposing patients to a low bone turnover state through modulation of parathyroid hormone secretion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Risk factors for renal osteodystrophy: a multivariant analysis. 774 22

Amylin is normally secreted in a regulated fashion by the pancreatic beta-cells in parallel with insulin and has been reported to have bone-conserving properties. Type I diabetes mellitus results in a low-turnover osteopenia in the presence of decreased amylin, which is in contrast to type II diabetes where less bone loss, in the presence of high amylin levels, occurs. We investigated the effects of amylin on bone mineral metabolism in normal and diabetic (streptozotocin-induced) rats, in order to ascertain whether amylin would modify the streptozotocin-induced diabetic osteopenia. Ten-week-old male Sprague-Dawley rats were randomized as follows: group A (n = 18) received normal saline; group B (n = 18) received amylin; group C, diabetic rats (n = 23), received normal saline; and group D, diabetic rats (n = 23), received amylin. Amylin (100 pmol/100 g b.w.) was administered by a daily subcutaneous injection. Double calcein-labeled tibiae were removed for histomorphometric analysis followed sacrifice on day 19. Results showed no difference in blood ionized calcium between groups. Blood glucose remained above 600 mg/dl in the diabetic animals and was not affected by the administration of amylin. Serum osteocalcin, insulin-like growth factor-1 (IGF-1), parathyroid hormone (PTH), and 1,25 dihydroxyvitamin D [1,25(OH)2D] were significantly lower in the diabetic rats compared with control group A by day 19. Amylin produced higher levels of serum osteocalcin in group B on day 9 (P < 0.05) compared with controls but returned to control values (group A) by day 19; no such change occurred in the diabetic group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Amylin increases bone volume but cannot ameliorate diabetic osteopenia. 779 48


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