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Query: UMLS:C0005940 (bone disease)
 7,459 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Polya partial gastrectomy was performed for peptic ulcer in a previously healthy woman aged 28 years. She complained afterwards of a variety of non-specific symptoms including weakness, tiredness, debility, slowness of walking, poor appetite and constipation. Within ten years her back became bent. She was treated for intercurrent hypertension and epilepsy. Bone fractures on low-impact trauma occurred in her fifties. At 57 years, she was unable to care for herself and had to be admitted to a nursing home. She could still walk slowly with the aid of a stick. For three months at the age of 65 years, she was unable to rise from her chair. Investigations disclosed severe post-gastrectomy bone disease. At no time had she complained of bone pains.
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PMID:Post-gastrectomy bone disease undiagnosed for forty years. 1049 25

Recent realizations have begun to change how 'osteoporoses' are diagnosed, managed and studied. This article explains the nature and basis of some resulting controversies, chiefly for clinicians who manage such patients but do not participate in resolving those controversies. Currently the size of a bone 'mass' deficit serves to diagnose 'osteoporosis', but recently clarified physiology suggests at least three different kinds of osteoporosis could occur in people with identical bone 'mass' deficits. Indeed, they do occur. (a) In one kind, people have less bone than 'normal' but no bone problems unless they sustain injuries. Most of their resulting fractures, usually from falls, affect extremity bones. This condition can affect children, men and women. (b) In a second kind an osteopenia exists in which voluntary physical activities (not injuries) cause spontaneous fractures and/or bone pain, mainly in the spine, more often in women than men and seldom in children (osteogenesis imperfecta excepted). (c) A third kind combines features of the first two. As for the physiology involved in those affections, bone modeling can increase bone strength and 'mass', while BMU (Bone Multicellular Unit)-based bone remodeling can reduce them. Mainly bone strains control those two activities and muscles cause the largest strains, so muscle strength should strongly influence bone modeling, remodeling, strength and 'mass'. If so chronic muscle weakness should usually cause an osteopenia and weakened bones. Excessive amounts of fatigue damage or microdamage can also weaken bones. From that physiology one could argue that chiefly chronic muscle weakness instead of an intrinsic bone disorder would cause (a), while intrinsic but still enigmatic modeling and remodeling disorders would cause (b), and (c) could combine features of both conditions. If so, these ideas could have significant effects on the future criteria used to diagnose osteoporoses and osteopenias, on how they are studied in the clinic and laboratory, and on how they are prevented or, if they occur, are managed.
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PMID:Changing views about 'Osteoporoses' (a 1998 overview). 1059 31

Stress fractures can occur if normal bone is exposed to repeated abnormal stress (fatigue fractures) or if normal stress is placed on bones with compromised elastic resistance (insufficiency fractures). This article describes two patients without a history of excessive stressful activity or apparent metabolic bone disease who developed bilateral distal tibial stress fractures. Different etiologies, clinical presentation, differential diagnosis, and diagnostic imaging modalities of stress fractures are discussed.
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PMID:Evaluation of suspected stress fractures. 1151 7

Pruritus, fatigue and metabolic bone disease represent three major extrahepatic manifestations of chronic cholestatic liver disease that considerably affect the patient's quality of life. The present article reviews pathogenetic aspects of and current therapeutic approaches to extrahepatic manifestations of cholestatic liver disease. Pathogenesis of pruritus of cholestasis remains poorly understood. The involvement of putative peripherally acting pruritogens, such as bile acids or endogenous opioids, is being discussed. More recently, central mechanisms, including an increased central opioidergic tone and pertubations in the serotonergic system have been proposed. Treatment of the underlying disease is beneficial also for the control of cholestasis-associated pruritus. Current therapeutic recommendations include ursodeoxycholic acid, cholestyramine, rifampicin and opioid antagonists. Liver transplantation may be indicated when severe pruritus is refractory to medical treatment. Fatigue is being recognized as the most frequent and one of the most disabling complaints in chronic cholestasis. Fatigue is presumably of central origin and its association with other neuropsychiatric disorders (e.g. depression, obsessive-compulsive disorders) is consistent with defective central neurotransmission. No specific therapies are currently available and a healthy lifestyle, regular sleep and avoidance of unnecessary stress and other precipiting factors are recommended. Antidepressant therapy may be warranted in selected patients. Osteopenia and osteoporosis are common in chronic cholestatic liver disease, whereas osteomalacia is rare. The pathophysiology of cholestasis-associated metabolic bone disease is regarded as multifactorial. Therapeutic recommendations include regular exercise, calcium and vitamin D supplementation in late stage disease, hormone replacement therapy in postmenopausal women and bisphosphonates.
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PMID:Extrahepatic manifestations of cholestasis. 1216 13

We describe a case of multiple pathologic fractures in a woman with Cushing's syndrome during pregnancy. Pathologic fractures were seen in the pubic and ischial bones and in T12 and L1 of the vertebral body. These findings, accompanied by easy fatigue, amenorrhea without nursing, psychological disorder, and premature birth, were retrospectively compatible with those of Cushing's syndrome, not pregnancy-associated osteoporosis. After adrenalectomy, the pain in her groin and back ceased. Plain radiographs showed healing of the fractures and increased mineralization. This case demonstrates the need to be alert to the possible presence of metabolic bone disease, including Cushing's syndrome, when we encounter multiple pathologic fractures with osteoporosis in young patients, even if the patient is pregnant.
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PMID:Case report of a Cushing's syndrome patient with multiple pathologic fractures during pregnancy. 1218 67

An 80-year-old white woman who presented with fatigue, weakness, weight loss, constipation and polydipsia is reported. The patient was given a diagnosis of severe hypercalcemia and was subsequently found to have clinical, roentgenographic and pathological evidence of hepatocellular carcinoma. Further studies revealed a low parathyroid hormone level, excluding the possibility of primary hyperparathyroidism, and a negative bone survey, precluding metastatic bone disease. The patient's hypercalcemia was believed to emanate from the humoral secretion of a parathyroid hormone-related peptide, which was found to be elevated, and was abated with conservative management while her cancer was being treated with chemotherapy. The details of this rarely documented presentation, which can easily be mistaken for hepatic encephalopathy, are provided.
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PMID:Severe hypercalcemia as an initial presenting manifestation of hepatocellular carcinoma. 1236 13

Primary biliary cirrhosis is a chronic cholestatic liver disease of adults. This disorder is characterised histologically by chronic non-suppurative destruction of interlobular bile ducts leading to advanced fibrosis, cirrhosis, and liver failure. The precise aetiopathogenesis of primary biliary cirrhosis remains unknown, although dysregulation of the immune system and genetic susceptibility both seem to be important. Affected patients are typically middle-aged women with abnormal serum concentrations of alkaline phosphatase. Presence of antimitochondrial antibody in serum is almost diagnostic of the disorder. Identification of primary biliary cirrhosis is important, because effective treatment with ursodeoxycholic acid has been shown to halt disease progression and improve survival without need for liver transplantation. However, therapeutic options for disease-related complications-including fatigue and metabolic bone disease-remain unavailable. Mathematical models have been developed that accurately predict the natural history of primary biliary cirrhosis in individuals. Despite advances in understanding of the disease, it remains one of the major indications for liver transplantation worldwide.
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PMID:Primary biliary cirrhosis. 1285 1

A 72-yr-old white female who had previously enjoyed excellent health presented with global bone and muscle pain, and chronic fatigue. Her evaluation revealed an increased sedimentation rate and mild anemia, and a diagnosis of polymyalgia rheumatica was made. Prednisone therapy was of little benefit. A laboratory evaluation revealed mild hypocalcemia, marked hypophosphatemia, elevated alkaline phosphatase, normal 25- hydroxyvitamin D, and undectable 1,25-dihydroxyvitamin D. A diagnosis of oncogenic osteomalacia was made and the patient received calcitriol and neutraphos therapy. The patient's initial bone density by dual energy X-ray absorptiometry of the lumbar spine was 0.847 g/cm2 (T score -1.96) and of the femoral neck was 0.669 gm/cm2 (T score -2.89). After 40 mo of treatment with calcitriol and neutraphos, the bone mineral density of the lumbar spine and hip rose dramatically by 47.8 and 59.1%, respectively. Although oncogenic osteomalacia is a very rare metabolic bone disease, its recognition and appropriate treatment can have a dramatic effect not only on the bone mineral density of the patient, but also on the patient's general health and feeling of well-being.
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PMID:Oncogenic osteomalacia: clinical presentation, densitometric findings, and response to therapy. 1530 16

A clear relationship between vitamin D status and the clinical indices of primary hyperparathyroidism (pHPT) severity has not been convincingly established. We proposed that such a relationship might exist, in so far as vitamin D deficiency could contribute to the severity of metabolic bone disease and promote the growth of the parathyroid tumor. Accordingly, we undertook a retrospective study and analyzed the clinical, biochemical, radiological and histopathological findings in a group of 49 patients who underwent parathyroidectomy at our center. Patients who had skeletal X-rays were grouped, according to their X-ray findings, in group A (19 patients; 45%) if they had severe bone changes, or group B (23 patients; 55%) if they had mild or no bone changes. Patients were also stratified according to their 25-hydroxyvitamin D (25-OHD) levels in tertiles. The 2 groups were compared using Fisher's exact test or analysis of variance as appropriate. Group A patients were younger (p=0.001), had more musculoskeletal symptoms (p=0.0003), and complained more frequently of fatigue (p=0.02). They had higher alkaline phosphatase (AP; p=0.0002), PTH index (p=0.0007), and serum Ca level (p=0.006). There were more patients from the lower and middle vitamin D tertiles and fewer patients from the upper vitamin D tertile in group A (p=0.02). Post-operative severe hypo-calcemia was more prevalent in group A patients (p<0.0001). Resected parathyroid tumors were larger in size in group A patients (p=0.01), and weighed more (p=0.01). There was a positive correlation between the weight of the parathyroid tumor and the PTH index (p=0.002), and AP level (p=0.0007). We concluded that vitamin D deficiency is a contributing factor to both the severity of bone disease and the high activity of parathyroid tumors seen in many patients with pHPT in vitamin D deficient regions.
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PMID:The effect of vitamin D status on the severity of bone disease and on the other features of primary hyperparathyroidism (pHPT) in a vitamin D deficient region. 1564 43

Pruritus, fatigue, and metabolic bone disease are frequent complications of cholestatic liver diseases, which can be quite distressing for the patient and can considerably reduce the quality of life. The molecular pathogenesis of these extrahepatic manifestations of cholestasis is poorly understood, and hypotheses to explain these symptoms are being discussed. This article provides treatment recommendations for the complications of cholestasis based on putative pathomechanisms and summarizes recent experimental and clinical data involving management options.
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PMID:Extrahepatic manifestations of cholestatic liver diseases: pathogenesis and therapy. 1587 20


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