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Query: UMLS:C0020438 (
hypercalciuria
)
2,502
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
By use of histomorphometry and photon and physical, calcium homeostasis, bone morphology, bone mass and bone growth were studied in freely fed control, streptozotocin-induced diabetic, long-term and short-term insulin treated diabetic rats 14 weeks after the induction of diabetes. We conclude that untreated chronic streptozotocin-induced diabetic rat could result in abnormal bone and mineral metabolism, which is characterized by
hypercalciuria
, hyperphosphaturia and hyperphosphatemia, significant bone loss and growth arrest. The extent of bone loss correlated with the duration of the disease process. The anatomical basis of bone mass reduction is the diminution of osteoblasts activity which results in reduction of bone formation and insufficient bone calcification and relative increment of osteoclasts activity. Thus, bone resorption overweight bone formation leading to a negative balance of bone remodeling. The effect of PTH and CT on bone changes in diabetic rats can't be affirmed in our experiments. It is probable that metabolic disorder and/or insulin deficiency has a direct effect on bone changes. Insulin therapy started earlier in the course can prevent and somewhat later can completely normalize the altered skeletal morphology of diabetic rats. Whether this result is due to direct effect of insulin on skeletal tissue or through the correction of metabolic disorder remains to be resolved.
Zhonghua
Nei
Ke Za Zhi 1992 Nov
PMID:[Effect of insulin therapy on abnormal bone and mineral metabolism in chronic streptozotocin-induced diabetic rat]. 130 70
52 patients with Cushing syndrome were studied. According to the appearance of X-ray film of bones, they were divided into three groups: (I) Without osteoporosis, 12 cases (23.1%), (II) Mild osteoporosis, 17 cases (32.7%), (III) Severe osteoporosis with fractured ribs and/or wedge-shaped vertebrae, 23 cases (44.2%). It was found that the mean level of serum calcium in the patients was significantly lower than that in 94 normal subjects (mean +/- S 2.3 +/- 0.2 versus 2.4 +/- 0.1 mmol/L P less than 0.001). The mean concentrations of blood alkaline phosphatase and parathyroid hormone in the patients were much higher than those in normal subjects (65.0 +/- 27.6 versus 42.6 +/- 15.6 IU/L P less than 0.001, 44.6 +/- 22.4 versus 20.6 +/- 8.0 pg/ml P less than 0.001 respectively). The mean level of serum 25 (OH)-D in the patients was significantly lower than that in controls (10.9 +/- 5.6 versus 16.2 +/- 4.6 ng/ml P less than 0.001). Urinary calcium excretion increased in the patients as compared with that in controls (P less than 0.01). The urinary calcium excretion correlated well with the blood total cortisol and urinary free cortisol. It is suggested that
hypercalciuria
might cause decrease of serum calcium. Thus the parathyroid glands were stimulated and the parathyroid hormone (PTH) secretion was increased. Excess of PTH stimulates bone resorption. All of these factors are involved in the pathogenesis of osteopenia in Cushing's syndrome.
Zhonghua
Nei
Ke Za Zhi 1989 Sep
PMID:[Metabolism of calcium and phosphorus in Cushing syndrome with osteoporosis]. 262 28
Objective:
To study the clinical characteristics of childhood- and adolescent- onset hypoparathyroidism.
Methods:
The clinical data of 128 hypoparathyroidism patients with onset before the age of 18 years were collected and analyzed retrospectively.
Results:
The predominant features of the hypoparathyroidism were carpopedal spasm (89.3%, 108/121) and seizures (66.1%, 84/127). Intracranial calcification was identified in 89.4%(101/113) of the patients. Duration is an independent predictive factor (
OR
=1.483,
P
=0.011) for intracranial calcification. All the patients were treated with calcium and vitamin D or its metabolites.
Hypercalciuria
was associated with serum calcium (
P
=0.016).
Conclusions:
Carpopedal spasm and seizures were the main manifestations of childhood- and adolescent- onset hypoparathyroidism. Calcium and vitamin D or its metabolites are effective. Monitoring the concentration of serum and urinary calcium is of highly importance for the prevention of
hypercalciuria
.
Zhonghua
Nei
Ke Za Zhi 2016 Oct 01
PMID:[The clinical characteristics of 128 childhood- and adolescent-onset hypoparathyroidism in Peking Union Medical College Hospital: a retrospective analysis]. 2768 37
Objective:
To study the clinical characteristics of primary hypoparathyroidism in adults.
Methods:
The clinical data of 200 cases with adult-onset primary hypoparathyroidism in Peking Union Medical College Hospital during December 1987 to December 2015 were collected and analyzed retrospectively. Among them, 128 cases were followed up for a median period of 3 years.
Results:
The major manifestations at their first visits were tetany and numbness in the distal extremities(81.5%, 163/200 and 62.0%, 124/200). Thirty-two percent of the cases (62 cases) had history of seizures, and 60.9%(98/161) and 74.4%(96/129) of them were with intracerebral calcifications and cataracts, respectively.Most of subjects(155/200)had more than one year delay in diagnosis.
Hypercalciuria
occurred in 67.2%(86/128) of the cases during the follow-up. No significant differences in the clinical characteristics and biochemical markers between the
hypercalciuria
subjects and the non-
hypercalciuria
subjects. Renal nephrocalcinosis or stones were found in 6.5%(5/77) of the cases, and kidney function decreased in 6.6%(6/91) of the patients. Kidney function was negatively associated with age and duration of disease.
Conclusions:
The predominant manifestations of primary hypoparathyroidism in adults included tetany and numbness in the distal extremities and seizures. It is often misdiagnosed. Calcium supplement combined with vitamin D or its metabolites effectively relieve clinical symptoms and signs. The serum and urinary calcium levels should be monitored frequently to reduce renal complications.
Zhonghua
Nei
Ke Za Zhi 2017 Jan 01
PMID:[Clinical characteristics of adult-onset primary hypoparathyroidism: a retrospective analysis of 200 cases]. 2805 18