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Query: UMLS:C0005940 (bone disease)
 7,459 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

The relationship between bone disease and alcohol abuse is well established. A large percentage of individuals whose drinking habits have caused them to seek medical help can be diagnosed, with routine X-rays, as having bone disease. The degree to which bone disease is present in the overall drinking population remains uncertain. The predominant form of bone disease is osteoporosis, and it seems likely that most osteoporosis in the middle-aged man can be attributed to alcohol abuse. The reason alcohol abuse leads to osteoporosis remains unclear. Vitamin D deficiency, hyperparathyroidism, and decreased intestinal calcium absorption may play a role, but a direct inhibitory effect of alcohol on bone remodeling seems a more likely explanation. No effective form of treatment has yet been established. Bone lost may not be regained. The best approach is to stop the alcohol abuse before the bone disease becomes manifest.
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PMID:Effects of alcohol abuse on bone. 327 34

Mseleni Joint Disease (MJD), a polyarticular osteoarthritis of uncertain etiology is endemic among the Tonga-Zulu tribe. The traditional diet is deficient in calcium, and palm wine (2-4% alcohol) is drunk widely. Patients with MJD are reported to be more osteopenic than those without. Iliac bone biopsies of 19 arthritic patients were examined by routine histomorphometry and revealed decreased trabecular bone volume (p less than 0.0005), increased resorption surfaces (p less than 0.01), decreased bone formation rate at the BMU (p less than 0.01) level and increased mineralization lag time (p less than 0.01). Six of the 19 patients (31.6%) had features of osteomalacia and six (31.6%) signs of osteoblast failure. The most likely cause of the bone disorder is calcium deficiency, but inanition, inactivity and alcohol abuse may have contributed. Although the joint disorder may have contributed to the bone disorder, the converse is unlikely the case.
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PMID:Histomorphometric analysis of osteopenia associated with endemic osteoarthritis (Mseleni joint disease). 337 19

This paper aims to examine the relative contributions made by alcohol and iron overload and hypovitaminosis C to the osteoporosis associated with African hemosiderosis. To characterize this bone disorder, we examined double-tetracycline-labeled iliac crest bone biopsies and serum biochemistry in 53 black male drinkers, 38 with (Fe+) and 15 without (Fe-) iron overload, and in controls. We reasoned that abnormalities found in both patient groups were likely to be caused by alcohol abuse and those found only in the Fe+ group to be caused by iron overload and hypovitaminosis C (iron/C-). The patient groups differed only with respect to greater erosion depth (p < 0.05) and abnormal markers of iron overload in the Fe+ group. Ascorbic acid levels were lower in the Fe+ group than in controls (p < 0.001). Bone volume and trabecular thickness were significantly lower in both patient groups compared with controls and therefore likely caused by alcohol. There were no positive correlations between formation and erosion variables in either patient group, which suggests uncoupling of formation from erosion, possibly as a result of alcohol abuse. Prolonged mineralization lag time associated with thin osteoid seams was found in 32% of patients, affecting both groups. This rules out osteomalacia and suggests osteoblast dysfunction, probably caused by alcohol. The number of iron granules in the marrow correlated with erosion depth (r = 0.373, p < 0.01), trabecular number (r = -0.295, p < 0.05), and trabecular separation (r = 0.347, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Osteoporosis in African hemosiderosis: role of alcohol and iron. 787 51

Alcohol abuse can induce osteopenia in some subjects. In order to study the effect of a single dose of alcohol on mineral metabolism and osteoblastic function, we have measured calcium, phosphate, parathyroid hormone midmolecule (PTHm), parathyroid hormone intact molecule (PTHi) and bone-gla-protein (BGP) in serum of 8 healthy men after the ingestion of a single dose of alcohol (0.6 g/kg body weight). Urinary calcium and magnesium were also measured. After alcohol intake, both serum PTHm and PTHi were decreased, as well as serum BGP. Serum phosphate and urinary calcium and magnesium were increased. An inverse significant correlation was found between PTHi and serum phosphate (r = 0.42; p < 0.02). Our data show that acute alcohol ingestion lowers serum PTH and BGP in humans, suggesting an inhibitory effect on parathyroid and osteoblastic function. These changes and the alcohol-induced transient hypercalciuria could contribute to the development of bone disease associated with chronic alcohol abuse.
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PMID:Effect of acute alcohol ingestion on mineral metabolism and osteoblastic function. 854 Sep 12

Generalized osteoporosis currently represents a heterogeneous group of conditions with many different causes and pathogenetic mechanisms, that often are variably associated. The term "secondary" is applied to all patients with osteoporosis in whom the identifiable causal factors are other than menopause and aging. In this heterogeneous group of conditions, produced by many different pathogenetic mechanisms, a negative bone balance may be variably associated with low, normal or increased bone remodeling states. A consistent group of secondary osteoporosis is related to endocrinological or iatrogenic causes. Exogenous hypercortisolism may be considered an important risk factor for secondary osteoporosis in the community, and probably glucocorticoid-induced osteoporosis is the most common type of secondary osteoporosis. Supraphysiological doses of corticosteroids cause two abnormalities in bone metabolism: a relative increase in bone resorption, and a relative reduction in bone formation. Bone loss, mostly of trabecular bone, with its resultant fractures is the most incapacitating consequence of osteoporosis. The estimated incidence of fractures in patients prescribed corticosteroid is 30% to 50%. Osteoporosis is considered one of the potentially serious side effects of heparin therapy. The occurrence of heparin-induced osteoporosis appeared to be strictly related to the length of treatment (over 4-5 months), and the dosage (15,000 U or more daily), but the pathogenesis is poorly understood. It has been suggested that heparin could cause an increase in bone resorption by increasing the number of differentiated osteoclasts, and by enhancing the activity of individual osteoclasts. Hyperthyroidism is frequently associated with loss of trabecular and cortical bone; the enhanced bone turnover that develops in thyrotoxicosis is characterized by an increase in the number of osteoclasts and resorption sites, and an increase in the ratio of resorptive to formative bone surfaces, with the net result of bone loss. Despite these findings, the occurrence of pathological fractures in patients with hyperthyroidism is relatively low, and probably due to the fact that deficiencies in bone mass may be reversed by treatment of the thyroid disease. Most, but not all, studies on insulin-dependent diabetes mellitus (IDDM) report an association with osteopenia. In IDDM, the extent of bone loss is usually slight, which helps explain the discrepancy between the frequency of decreased bone mineral density, and the frequency of osteoporotic fractures in long-standing diabetes. Contradictory results have been obtained in non-insulin-dependent diabetes mellitus (NIDDM) patients. Increased rates of bone loss at the radius and lumbar spine were demonstrated either in patients with two-thirds gastric resection and Billroth II reconstruction, or in those with one-third resection and Billroth I anastomosis, and the metabolic bone disease following gastrectomy may consist also of osteomalacia or mixed pattern of osteoporosis-osteomalacia, with secondary hyperparathyroidism. Miscellaneous causes of secondary osteoporosis are also immobilization, pregnancy and lactation, and alcohol abuse.
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PMID:Secondary osteoporosis. 980 31

Although best characterized in chronic cholestatic liver disease, osteopenic bone disease and fracturing are well-recognized complications of cirrhosis, particularly after liver transplantation. We sought to compare the prevalence of osteopenia and osteoporosis, to assess the effect of orthotopic liver transplantation (OLT) on bone density, and to determine fracture rates before and after OLT in three groups of patients with advanced cirrhosis: patients with cirrhosis from hepatitis C virus (HCV) alone, from alcohol abuse (ALD), and from HCV in conjunction with alcohol abuse (HCV+ALD). Between 1991 and 2001, 207 consecutive patients who underwent OLT for HCV (68 patients), ALD (66), and HCV+ALD (73) were assessed clinically, biochemically, radiologically, and by bone densitometry. The baseline mean T score was lower in the HCV group than in the ALD group (-1.43 versus -0.87, P =.048) despite ALD patients having more advanced liver disease; patients with HCV+ALD had intermediate T scores. The pattern of significant bone loss at 4 months and 12 months was similar for all three groups. The baseline fracture rate was lowest in the HCV group and highest in the ALD group, despite the latter having the highest bone density. Fractures occurred in 17% of patients in the first year after transplantation, the majority being vertebral compression fractures. Patients with cirrhosis caused by HCV, ALD, or a combination of both should be screened for osteopenia, especially before OLT.
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PMID:Osteopenia and osteoporosis in patients with end-stage liver disease caused by hepatitis C and alcoholic liver disease: not just a cholestatic problem. 1458 77

Considering the aging dialysis population of today, increasing our knowledge about the nature, diagnosis and the treatment of bone mineral density (BMD) problems in end-stage renal disease (ESRD) patients deserves more attention. Osteoporosis is basicly defined as a decrease in bone mass. Large epidemiological studies in general population have identified several risk factors for osteoporosis including advancing age, female gender, white race, decreased calcium intake, gastric acid suppression therapy, sedentary lifestyle, premature loss of gonadal function, decreased estrogen secretion, thin body habitus, decreased physical activity, cigarette smoking, alcohol abuse, excess glucocorticoid exposure, and possibly some genetic factors. Osteoporosis in ESRD patients is only a part of a wider spectrum of metabolic bone problems, namely uremic osteodystrophy. Therefore, its diagnosis, management and follow-up may differ from the general population and an individualization of diagnosis and definition for dialysis population may be necessary. However, standard diagnostic tools such as dual energy X-ray absorptiometry (DEXA) have been widely used for the assessment of bone mineral deficiency status in ESRD patients. Regardless of the methods, most of the studies are in concordance with a reduced BMD in HD and PD patients. Dialysis patients are known to be at increased risk for low-trauma fractures. Thinning of cortical bone, which is responsible for the largest contribution toward reduced bone mineral content in chronic renal failure results in increased fracture risk. In either normal population and dialysis patients, fracture risk is increased with age. But in dialysis patients, besides age, several other factors may also affect the degree of bone mineral deficiency, and age-BMD relationship may be blunted. Female sex, in hemodialysis patients is negatively associated with total hip BMD. While several studies have been unable to demonstrate any association between BMD and PTH levels, larger body size has been shown to have a significant positive effect on BMD in both hemodialysis and peritoneal dialysis patients. Although they have been used in small groups of chronic kidney disease (CKD) and ESRD patients, because of their potential nephrotoxicity and hypocalcemic effects, use of biphosphonates in renal patients is questionable. Currently, bone biopsy, in order to exclude adynamic bone disease is recommended before beginning treatment with bisphosphonates in chronic kidney disease and dialysis patients.
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PMID:Osteoporosis in the elderly with chronic kidney disease. 1710 30

Osteoporosis in men has not received much attention compared to that directed at the skeletal morbidity of postmenopausal osteoporosis. The available literature and an evaluation of 47 men referred to our metabolic bone disease clinic present arguments that causes for secondary osteoporosis can be identified in most instances, Major causes include hypogo-nadism, hyperglucocorticoidism, and alcohol abuse. Primary osteoporosis in men is idiopathic and has heterogeneous features. At present, no controlled, randomized therapeutic trials have been reported in men with osteoporosis. Improved screening for early detection and prevention of bone loss is needed in men with disorders, lifestyles, and/or medications that cause bone loss. Further investigations of primary osteoporosis should lead to identification of mechanisms of bone loss that can be prevented.
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PMID:Osteoporosis in men. 1907 46

Osteoporosis is a frequent complication in patients with chronic liver disease, especially in end-stages and in cases with chronic cholestasis, hemochromatosis and alcohol abuse. The problem is more critical in transplant patients when bone loss is accelerated during the period immediately after transplantation, leading to a greater incidence of fractures. Advanced age, low body mass index and severity of the liver disease are the main risk factors for bone disease in patients with cholestasis. Mechanisms underlying osteoporosis in chronic liver disease are complex and poorly understood, but osteoporosis mainly results from low bone formation, related to the effects of retained substances of cholestasis, such as bilirubin and bile acids, or to the effects of alcohol on osteoblastic cells. Increased bone resorption has also been described in cholestatic women with advanced disease. Although there is no specific treatment, bisphosphonates associated with supplements of calcium and vitamin D are effective for increasing bone mass in patients with chronic cholestasis and after liver transplantation. The outcome in reducing the incidence of fractures has not been adequately demonstrated essentially because of the low number of patients included in the therapeutic trials. Randomized studies assessing bisphosphonates in larger series of patients, the development of new drugs for osteoporosis and the improvement in the management of liver transplant recipients may change the future.
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PMID:Liver and bone. 2053 77


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