Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020438 (hypercalciuria)
 2,502 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Abuse of alcohol is considered to be an important risk factor for fractures and osteoporosis. Alcohol abuse is associated with deleterious changes in bone structure detected by histomorphometry, and with a decrease in bone mineral density. These changes may also be produced by factors commonly associated with alcohol abuse, e.g., nutritional deficiencies, liver damage, and hypogonadism. Thus the etiology of alcohol-associated bone disease is multifactorial. Alcohol has, however, clear-cut direct effects on bone and mineral metabolism. Acute alcohol intoxication causes transitory hypoparathyroidism with resultant hypocalcemia and hypercalciuria. Prolonged moderate drinking elevates serum parathyroid hormone (PTH) levels, whereas chronic alcoholics are characterized by low serum levels of vitamin D metabolites with resultant malabsorption of calcium, hypocalcemia, and hypocalciuria. Independently of whether alcohol consumption is of short duration, social, or heavy and chronic, it seems to suppress the function of osteoblasts, as evidenced by low serum levels of osteocalcin. It has recently been reported, however, that alcohol can also have a beneficial effect on bone. Among postmenopausal women, moderate alcohol consumption correlates positively with central and peripheral bone mineral density, and with serum estradiol levels.
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PMID:Alcohol and bone. 193 4

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

In order to analyse the clinical characteristics and the principal causes of osteoporosis in men, 81 osteoporotic males from an out-patient rheumatology department were studied. Bone mass assessment, automated biochemical profile and biochemical markers of bone turnover were performed in all patients, and hormonal measurements were taken when a specific aetiology was not readily apparent. Sixty-three men (78%) had secondary osteoporosis and 18 (22%) primary osteoporosis. Secondary causes of osteoporosis included hypogonadism (12 patients), corticosteroid therapy (10 patients) and alcoholism (10 patients); the remaining patients had various causes of osteoporosis. Eighteen patients had primary osteoporosis, eight of them with associated hypercalciuria. Normocalciuric patients showed lower 25-hydroxyvitamin D and 1-25-hydroxyvitamin D levels than the control group, whereas hypercalciuric patients had lower parathyroid hormone and renal threshold for phosphate excretion. In 69 patients (85%), back pain was the chief complaint. Forty-five of these 69 patients (65%) had chronic back pain and 24 (35%) had subacute episodes. Fifty per cent of the patients with chronic back pain had vertebral fractures. Both patients with and without chronic back pain were found to have a similar number of vertebral fractures. In conclusion, male osteoporosis is frequently associated with major risk factors. Patients with primary osteoporosis may have associated hypercalciuria or decreased vitamin D levels. However, not all the patients for whom back pain was the chief complaint were found to have vertebral fractures.
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PMID:Aetiology and presenting symptoms in male osteoporosis. 758 99

In order to clarify the risk-factors for men with vertebral fractures due to osteoporosis, we carried out a study of 51 cases. Twenty-five percent of patients had an endocrine disorder (hyperparathyroidism, hypogonadism, hyperthyroidism) or had received corticosteroids. These patients were compared with 26 age-matched controls. Eleven patients compared with 2 of the 26 control subjects had arteriopathy of the lower limbs; 11 patients had hypercalciuria or hyperphosphaturia compared with 3 of the control subjects. Arteriopathy appears to be associated with osteoporosis in older patients (mean age 71 years), whereas renal tubular disorders were found in younger patients (mean age 45 years).
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PMID:Renal tubular disorders and arteriopathy of the lower limbs: risk factors for osteoporosis in men? 769 23

Although primary osteoporosis is much more frequent than other diseases associated with osteopenia, the diagnosis of idiopathic osteoporosis should be made only after the causes of secondary osteoporosis have been excluded. Indeed, therapeutic efficiency in secondary osteoporosis depends mainly on the concomitant treatment of the actual cause of osteopenia. Glucocorticoid-induced osteoporosis is the commonest form of secondary osteoporosis, mainly for doses of prednisone of 0.1 mg/kg/day or greater. Hypogonadism in men and women, idiopathic hypercalciuria and chronic alcoholism in men are other frequent causes of osteopenia. The diagnosis of secondary osteoporosis is based on careful examination as well as biochemical and hormonal investigations. Together with the treatment of the associated disease, correction of other risk factors, calcium supplementation, and a regular program of weight-bearing physical activity may be of benefit to reduce bone loss. As fluoride is able to stimulate bone formation, it is an effective agent in the treatment of glucocorticoid or alcohol-induced osteoporosis.
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PMID:[Secondary osteoporosis]. 779 36

Careful examination as well as biochemical and hormonal investigations should be performed in men suffering from vertebral crush fractures, in order to detect a destructive skeletal process (multiple myeloma, bone metastatic lesions, lympho and myeloproliferative disorders), a mineralization defect (osteomalacia) or a secondary osteoporosis: primary hyperparathyroidism, hypogonadism, hyperthyroidism, renal hypercalciuria, alcoholism and tobacco smoking. The diagnosis of idiopathic osteoporosis should be made only after these causes have been excluded; the pathogenesis of the disease is unclear but risk factors have been identified: family history of osteoporosis, low dietary calcium intake, delayed puberty, ethanol use, tobacco smoking, inactive lifestyle and lean body build. Correction of risk factors, calcium supplementation, regular program of weight bearing physical activity, in some instances correction of testosterone deficiency may be of benefit to reduce bone loss. Severe osteopenia or osteoporosis may require sodium fluoride therapy.
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PMID:[Male osteoporosis]. 793 30

In a prospective study, 321 consecutive male patients, aged between 16 and 86 years, referred to the Department of Medicine of the Medical Centre at Leverkusen from many parts of Germany over a three-year period with the diagnosis of osteoporosis, underwent a standardized programme of clinical investigation: 254 (79%) were found to have the condition. The programme consisted of a detailed history, physical examination, a battery of laboratory tests, X-ray examination of the skeleton and osteodensitometry. Where, as a result, underlying disease or risk factors were suspected, further tests were performed. 98 patients (39%) were found by densitometric criteria to have preclinical, 156 (61%) manifest osteoporosis with one or more vertebral body fractures. There was no significant difference regarding bone density between the preclinical and manifest cases. 76 of the 254 (30%) patients had no detectable pathogenetic factors, i. e. their osteoporosis was classified as idiopathic (mean age 51 years), while as senile osteoporosis in 16 elderly patients (mean age 78 years). The remaining 162 patients had 286 risk factors within 24 different categories. Depending on duration, intensity and combination of these risk factors, the osteoporosis was classified as primary with few risk factors or as secondary osteoporosis of single or multiple aetiology (mean age of these three groups was 51, 56 and 52 years, respectively). The most important demonstrable risk factors were (in decreasing order of frequency) glucocorticoid treatment, alcohol consumption, smoking, hypogonadism, hypercalciuria, liver disease, Crohn's disease, low calcium nutrition, hyperthyroidism, physical inactivity, stomach operation and plasmacytoma.--This study indicates that if there is evidence of significant risk factors detailed bone densitometry should be performed so that any necessary treatment can be initiated early. If there is known osteoporosis, staging and exact analysis of risk factors is a precondition for any cause-oriented treatment.
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PMID:[Osteoporosis in men. Pathogenesis and clinical classification of 254 cases]. 802 7

Coffee drinking, smoking and especially alcohol abuse are considered to be risk factors for fractures and osteoporosis. Caffeine causes acute increase in urinary calcium excretion, but epidemiological evidence for the effects of coffee consumption on the risk of fractures is contradictory. Many, (but not all) studies point to decreased bone mass or increased fracture risk in smokers. Alcohol abuse is associated with deleterious changes in bone structure detected by histomorphometry, and with a decrease in bone mineral density (BMD). These changes may also be produced by factors commonly associated with alcohol abuse, e.g. nutritional deficiencies, liver damage and hypogonadism. Alcohol, however, has clear-cut direct effects on bone and mineral metabolism. Acute alcohol intoxication causes transitory hypoparathyroidism with resultant hypocalcaemia and hypercalciuria. As assessed by serum osteocalcin levels, prolonged moderate drinking decreases the function of osteoblasts, the bone-forming cells. In addition, chronic alcoholics are characterized by low serum levels of vitamin D metabolites. Thus, alcohol seems to have a direct toxic effect on bone and mineral metabolism. In contrast, it has recently been reported that moderate alcohol consumption by postmenopausal women may have a beneficial effect on bone.
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PMID:Bone and the 'comforts of life'. 821 8

Eight patients (6 women and 2 men) with osteoporosis caused or aggravated by renal acidification defects are presented. Three of the female patients were premenopausal; the others were 9, 20 and 22 years postmenopausal, and two of them were on hormonal replacement therapy. Two patients had nephrolithiasis: one male with recurrent calcium phosphate stones and a left sided staghorn calculus, and one female with nephrocalcinosis due to medullary sponge kidney and hypercalciuria (patients No. 1 and 2, respectively, Table 1). In the remaining subjects, clinical suspicion was based on: a) Hip fracture in a 44-yr-old premenopausal female without any risk factor (No. 3, Table 2). b) Several vertebral compression fractures in a 45-yr-old male without hypogonadism or other predisposing factors (No. 7, Table 2). c) Lack of response to antiosteoporotic therapy in 3 women (patients No. 4, 6 and 8, Table 2). Serum bicarbonate levels and urine acidification capacity were studied in all patients. Three had low serum bicarbonate (two of whom showed high fractional excretion of bicarbonate), four had a distal defect, and one had a mixed form. Serum creatinine and potassium, and venous blood pH were normal in all cases, suggesting incomplete renal tubular acidosis. Bone mineral density in Z-score (means +/- s.e.m.) was - 1.75 +/- 0.08 in the lumbar spine (n = 8), and - 1.57 +/- 0.09 in the femoral neck (n = 4) [Tables 1 and 2; Figs 1 and 2]. Following one year treatment with oral sodium bicarbonate and potassium citrate, total skeletal calcium increased by 3-10% in five of the patients. Whereas the high prevalence of renal acidification defects among renal stone formers with or without hypercalciuria is well acknowledged, renal tubular acidosis is not included in the list of entities causing secondary osteoporosis. As shown in 6 patients of this series, incomplete RTA should be considered as another disease capable of causing osteoporosis or worsening involutional bone loss.
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PMID:[Renal acidification mechanism disorders in patients with osteoporosis]. 854 15

Osteoporosis is one of the most serious adverse effects experienced by patients receiving long term corticosteroid therapy. Bone loss occurs soon after corticosteroid therapy is initiated and results from a complex mechanism involving osteoblastic suppression and increased bone resorption. There are a number of factors that may increase the risk of corticosteroid-induced osteoporosis [smoking, excessive alcohol (ethanol) consumption, amenorrhoea, relative immobilisation, chronic obstructive pulmonary disease, inflammatory bowel disease, hypogonadism in men, organ transplantation]. The initial assessment of patients about to start taking corticosteroids should include measurement of spinal bone density, urinary calcium level and plasma calcifediol (25-hydroxycholecalciferol) level; serum testosterone levels should also be measured when hypogonadism is suspected. Many different drugs have been used to prevent osteoporosis in patients receiving long-term corticosteroid therapy, including thiazide diuretics, cholecalciferol (vitamin D) metabolites, bisphosphonates, calcitonin, fluoride, estrogens, anabolic steroids and progesterone. At present, however, published studies have failed to demonstrate a reduction in the rate of fracture using different preventive pharmacological therapies in patients being treated with corticosteroids on a continuous basis. Among the drugs studied, bisphosphonates (pamidronic acid and etidronic acid) and calcitonin appear to be effective in increasing bone density. Cholecalciferol preparations have been reported to be effective in some, but not all, studies. Limited data have shown positive results with thiazide diuretics, estrogen, progesterone and nandrolone. When treating patients with corticosteroids, the lowest effective dose should be used, with topical corticosteroids used whenever possible. Auranofin may be considered in patients with corticosteroid-dependent asthma. Patients should take as much physical activity as possible, maintain an adequate daily intake of calcium (1000 mg/day0 and cholecalciferol (400 to 800 U/day), stop smoking and avoid excessive alcohol intake. It is important to detect and treat hypogonadism in men, if present, and to replace gonadal hormones in postmenopausal women or amenorrhoeic premenopausal women, and to detect and correct cholecalciferol deficiency. A thiazide diuretic should be considered if hypercalciuria is present (urinary calcium excretion in excess of 4 mg/kg/day). High-risk patients and those with established osteoporosis should be treated with bisphosphonates (cyclical etidronic acid or intravenous pamidronic acid), nasal calcitonin, or calcifediol or calcitriol. Patients receiving cholecalciferol preparations should be carefully monitored for hypercalciuria and hypecalcaemia.
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PMID:Corticosteroid-induced bone loss. Prevention and management. 894 96


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