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

Although corticosteroid treatment is clearly beneficial to patients with temporal arteritis, its exact risk/benefit ratio in these old and side effects-prone patients is unknown. We have thus surveyed that available French and English literature, in order to pool the published series and to evaluate the iatrogenic potential of corticosteroids in this situation. We selected 11 series, yielding a total of 1008 patients. A treatment failure resulted in the death of the patient in five cases. Twenty-seven patients became blind, but only 2 under treatment. The side-effects involved 29% of the patients and are responsible of 29 deaths (2.9%): osteoporosis was the main problem, followed by femoral head necrosis and muscle wasting. Gastroduodenal ulcers were uncommon and generally benign; sigmoid colon diverticulitis was infrequent but dangerous; some infectious complications were noted (herpes zoster, tuberculosis, etc...); high blood pressure and diabetes were common problems. Psychiatric side-effects were rare. Thus, the unwanted effects of corticosteroids in the treatment of temporal arteritis are relatively infrequent and generally not severe, except osteoporosis. They should be systematically prevented by appropriate diet and treatments (e.g., calcium, potassium, and vitamin D supplements).
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PMID:[Benefits of corticosteroids in the treatment of Horton's disease and rhizomelic pseudopolyarthritis: advantages and inconveniences. A meta-analysis]. 134 39

The active form of vitamin D, 1,25(OH)2D3, can prevent various forms of experimentally induced autoimmune disorders. The aim of this study was to confirm these findings in NOD mice that spontaneously develop an autoimmune type of diabetes mellitus. Therefore, the effect of a long-term 1,25(OH)2D3 treatment on the incidence of insulitis, the histological lesion preceding diabetes, was studied. Forty-three NOD mice were treated with 1,25(OH)2D3 (5 micrograms/kg) i.p. every other day from age 21 days on, when no insulitis was present yet. At day 100, 16 control mice receiving the treatment vehicle (arachis oil) had an incidence of insulitis of 75%, whereas only 41% of the 1,25(OH)2D3-treated animals developed insulitis (P < 0.025). Calcemia, determined 24 h after the last 1,25(OH)2D3 injection was 2.5 +/- 0.1 mM, which was higher than in control animals (2.3 +/- 0.1 mM), but was well tolerated. Cellular immunity, as assessed with the mixed lymphocyte reaction performed at day 100, was not impaired significantly. This study demonstrates that long-term treatment with high doses of 1,25(OH)2D3 is able to decrease the incidence of insulitis in spontaneous autoimmune diabetes without major side effects.
Diabetes 1992 Nov
PMID:1,25-Dihydroxyvitamin D3 prevents insulitis in NOD mice. 139 23

The influence of insulin on plasma and bone mineral homeostasis was studied in the BB rat model, which develops an autoimmune form of diabetes at the age of about 100 days. Untreated diabetes of short duration resulted in hypercalciuria and intestinal calcium malabsorption despite increased free concentrations of serum 1,25-dihydroxyvitamin D. The concentrations of two vitamin D-dependent calcium-binding proteins were also decreased: a low duodenal calbindin-D 9K concentration corresponding to the low intestinal active calcium absorption and a low serum osteocalcin concentration, corresponding to a low bone formation and highly correlated with serum IGF-I concentration. Indeed, on bone histology a very low number of osteoblasts and low osteoblast activity (osteoid formation and mineral apposition rate) were observed. Similar abnormalities persisted in rats with long-standing diabetes resulting in markedly decreased bone mass and increased brittleness of bone. Diabetes therefore resulted in low-turnover osteoporosis. Several hormones (testosterone, growth hormone and 1,25-dihydroxyvitamin D) and growth factors (IGF-I and its binding proteins) with known effects on bone were markedly decreased in diabetic rats. A continuous infusion of testosterone, GH or 1,25-(OH)2D3 for 14 d by miniosmotic pumps could not improve the biochemical or histomorphometric abnormalities. Insulin infusion for 2 weeks, however, rapidly increased and overcorrected the number of osteoblasts, normalized serum osteocalcin and IGF-I concentrations but could not yet normalize bone mineralization. Continuous infusion of IGF-I alone did not improve the osteoblast number of osteocalcin but markedly stimulated bone mineralization. From these data we can conclude that both insulin and IGF-I are potent bone growth factors but with different mode of action. In human type 1 diabetes, a similar decrease in serum osteocalcin and IGF-I was observed. A reduction of regional bone mass, both in long and trabecular bones, is frequently observed in human diabetes. Cumulative data from case control studies indicate that the life-time fracture risk is increased in diabetes.
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PMID:Diabetic bone disease. Low turnover osteoporosis related to decreased IGF-I production. 146 60

Untreated diabetic (BB) rats exhibited compensatory intestinal growth which was associated with hyperplasia and was accompanied by an increase in unoccupied vitamin D receptors. Although vitamin D receptors were increased, low circulating 1,25-dihydroxy-vitamin D3 [1,25(OH)2D3] prevented amplification of the action of 1,25(OH)2D3, as evidenced by reductions in calbindin D-9K and alkaline phosphatase activity in the BB rat intestine compared to control. In the kidney, a lesser degree of compensatory growth was observed which was not associated with hyperplasia, and no significant effect of diabetes on vitamin D receptors or calbindin D-28K was observed. These studies suggest tissue-specific changes in 1,25(OH)2D3 metabolism during spontaneous diabetes which may be related to the hyperplasia which occurs during compensatory tissue growth.
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PMID:Vitamin D receptors and compensatory tissue growth in spontaneously diabetic BB rats. 165 63

A role for vitamin D in the defense against falling serum calcium (Ca) concentrations following cord clamping has been suggested. Since race and season are known to affect vitamin D status, we theorized that black race and birth in winter are additional risk factors for neonatal hypocalcemia (NHC). We retrospectively studied 13,462 infants born at University Hospital (Cincinnati, OH) between January 1, 1984 and December 31, 1987. Serum Ca was measured at 24 hours of age routinely in infants with low birth weight (less than 2500 g), preterm delivery (less than 2500 g), preterm delivery (less than 37 weeks), neonatal asphyxia, and diabetic mothers. After exclusion of infants of diabetic mothers (to remove maternal diabetes as a major confounder) and infants with major congenital anomalies, 714 infants remained. In multiple regression analysis, low serum Ca values were significantly associated with low gestational age (p less than 0.01), low Apgar score (p less than 0.01), and white race (p less than 0.01) (R2 = 0.457). Season or month of birth was not significant. In pair-matched analysis controlling for factors other than season, season of birth did not affect serum Ca. In pair-matched analysis controlling for factors other than race, white race was once again a risk factor for hypocalcemia. Thus, low gestational age, low Apgar score, and white race, but not black race and delivery in winter, are risk factors for NHC. We speculate that in our climate and with the prevailing diet in pregnancy, vitamin D deficiency does not appear to play a role in NHC.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A case-control study of hypocalcemia in high-risk neonates: racial, but no seasonal differences. 189 77

Sarcoidosis is a multisystem disorder of unknown etiology that frequently involves the lymph nodes, lungs, eyes, and skin. The disease can involve any organ system, and noncaseating granulomas are characteristically present. Synthesis of 1,25-dihydroxyvitamin D, the most biologically active form of vitamin D, occurs in granulomatous tissue and may give rise to increases in its concentration in the peripheral circulation and to hypercalcemia and hypercalciuria. Infiltration of endocrine organs also occurs. Involvement of the hypothalamus and pituitary can cause primary polydipsia and disordered regulation of thirst; diabetes insipidus, impaired secretion of anterior pituitary hormones (with clinically apparent hypothyroidism, hypogonadism, hypoadrenalism, or impaired growth), and increases in serum prolactin may also result. Galactorrhea, however, seldom occurs. Involvement of the thyroid and adrenal glands rarely leads to hypofunction. Involvement of the pancreas rarely occurs but does not produce diabetes mellitus. Involvement of the male reproductive system results in epididymitis and hypogonadism, and involvement of the uterus causes abnormalities in menstrual function.
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PMID:Endocrine complications of sarcoidosis. 193 22

Our data confirms previous reports of intestinal and kidney compensatory growth, low plasma 1,25(OH)2D3 and up regulation of intestinal VDRs during untreated diabetes. All of these parameters were normalized in diabetic rats treated with exogenous insulin. There were no alterations in VDR numbers in kidneys or thymus of untreated diabetic animals, indicating that up-regulation of VDRs during untreated diabetes did not occur in all vitamin D target tissues. Compensatory growth of the intestine during untreated diabetes was associated with both hypertrophy and hyperplasia, whereas diabetic kidney growth appeared to be associated with hypertrophy without hyperplasia. Diabetes did not affect somatic index of thymus. The data suggests that the up regulation of VDRs during untreated diabetes may be unique to the intestine and further that VDR up regulation may be related to hyperplasia. Calbindin D-9K was significantly lower in diabetic intestine, suggesting that low circulating 1,25(OH)2D3 prevented amplification of 1,25(OH)2D3's action despite up regulation of intestinal VDRs.
Diabetes Res 1990 Dec
PMID:Vitamin D receptors in intestine, kidney and thymus of streptozotocin diabetic rats. 196 37

In diabetic animals, there is a decrease in serum 1,25-dihydroxyvitamin D [1,25(OH)2D] and in renal production of 1,25(OH)2D. In nondiabetic animals, renal 1,25(OH)2D production is markedly stimulated by parathyroid hormone (PTH) and calcitonin (CT). There is evidence that diabetes impairs the responsiveness of the kidney to PTH. The effect of diabetes on responsiveness to CT is unknown. The studies reported here determined the effect of streptozotocin-induced diabetes on renal responsiveness to PTH and CT. Experiments were performed in 7- to 8-week-old rats that were fed a diet sufficient in calcium and vitamin D and were thyroparathyroidectomized (TPTX) 5 days before hormone treatment. PTH (0.33 U/g body weight at 24, 12, and 2 hours before death) significantly increased renal 1,25(OH)2D production by threefold in nondiabetic rats. This effect was markedly attenuated by diabetes. On the other hand, CT (20 U/100 g body weight at 12 and 2 hours before death) produced a maximal response in both groups of animals. In diabetic rats, CT stimulated renal 1,25(OH)2D production fivefold, whereas PTH stimulated production only 1.5-fold. Diabetes did not affect the capacity of PTH to increase serum calcium or decrease renal tubular reabsorption of phosphorus (TRP). These findings suggest that the decrease in renal 1,25(OH)2D production seen in experimental diabetes may be due to decreased renal responsiveness to PTH, but not to decreased responsiveness to CT.
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PMID:Calcitonin stimulates 1,25-dihydroxyvitamin D production in diabetic rat kidney. 198 64

Because insulin-dependent diabetes mellitus is associated with altered electrolyte metabolism and a derangement of the parathyroid hormone (PTH)-vitamin D endocrine system, we studied 23 children with diabetes (age 9.4 +/- 2.5 years) and found lower serum values for total and ionized calcium, magnesium, intact PTH, calcitriol, and osteocalcin than in age- and sex-matched control subjects. All patients were given magnesium orally (6 mg/kg daily of elemental magnesium) for up to 60 days. During treatment, serum magnesium, total and ionized calcium, intact PTH, calcitriol, and osteocalcin concentrations significantly increased, reaching control values. After a 3-day low-calcium diet, the patients had a significantly reduced delta-increment of PTH and calcitriol in comparison with values obtained during hypomagnesemia. After magnesium repletion, the delta-increments of both PTH and calcitriol, in response to the low-calcium diet, were not significantly different from control values. These data suggest that magnesium deficiency plays a pivotal role in altering mineral homeostasis in insulin-dependent diabetes mellitus.
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PMID:Hypomagnesemia and the parathyroid hormone-vitamin D endocrine system in children with insulin-dependent diabetes mellitus: effects of magnesium administration. 191 9

The basic prerequisite of treatment of diabetic osteopenias is perfect metabolic compensation of diabetes. Insulin administration is an advantage in this respect, as it enhances calcium absorption from the gut and reduces its urinary excretion. Conversely, oral antidiabetics interfere in a negative way with vitamin D metabolism and thus also calcium metabolism and mineralization of bone. The combination of calcium, small doses of vitamin D, NaF and exercise used in the treatment of diabetic osteoporoses leads in general to a significant rise of the calcium serum level, an insignificant rise of the phosphorus level and it reduces alkaline phosphatase activity. A certain disadvantage is the elevated urinary calcium excretion. The main drug in diabetic osteomalacia are usually large doses of vitamin D. The rise of the serum calcium level improves the metabolic compensation of diabetes in a linear fashion. Thiazide diuretics used to reduce excessive calciuria cause slight deterioration of the glucose tolerance but the compensation does not cause major difficulties.
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PMID:[Diabetic osteopathies. 6. Treatment and its pitfalls]. 213 68


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