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Query: UMLS:C0018099 (gout)
 5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renal transplantation is associated with several abnormalities of function and structure of the musculoskeletal system. Some of these skeletal problems result from incomplete resolution of abnormalities of bone and mineral metabolism present at the time of transplantation. In this regard, persistent hyperparathyroidism, diabetes mellitus type 1, and accumulation of beta 2-microglobulin may lead to residual skeletal effects despite excellent function of the allograft. Persistent hyperparathyroidism may accelerate bone loss and increase the risk for osteonecrosis, as well as cause hypercalcemia and hypophosphatemia; some patients with severe hyperparathyroidism require parathyroid surgery. Osteonecrosis is the most debilitating skeletal complication after transplantation and frequently requires surgical therapy. Although osteomalacia associated with aluminum overload generally resolves after transplantation, bone complications due to dialysis amyloidosis and diabetes mellitus type 1 often fail to improve. Alternatively, skeletal abnormalities can be acquired after transplantation. Most of the new derangements of bone and mineral metabolism are due to the immunosuppressive medications. Toxic effects of glucocorticoids on bone contribute to the pathogenesis of osteonecrosis, increase the risk for fractures by decreasing cancellous bone mass and synthesis of bone matrix, and dampen the linear growth response in pediatric recipients. Whether cyclosporine independently causes appreciable toxic effects on bone metabolism is not yet clear, but use of this drug increases the prevalence of gout and dental problems. Osteonecrosis, osteopenia, and short stature remain important skeletal complications in recipients of renal allografts. Therapeutic efforts should be directed toward alleviating pretransplant bone disease and attenuating bone loss after transplantation.
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PMID:Musculoskeletal complications after renal transplantation: pathogenesis and treatment. 129 May 51

We measured lead and calcium in multiple bone biopsies from 11 cadavers without known excessive past exposure to lead. Paired iliac crest, transiliac and tibial bone biopsies from these cadavers indicated that in bone biopsy specimens the lead/calcium ratio is more reproducible than the absolute lead concentration. There were no significant differences between the lead/calcium ratios from the iliac crest, transiliac, or tibial specimens. Transiliac bone biopsies from 35 patients (13 patients showing symptoms of slight or moderate degree of renal failure, medical history of gout and/or arterial hypertension and 22 lead workers with chelatable lead in excess of 1000 micrograms) indicated that the lead and the lead/calcium ratio in bone biopsies reflect body lead stores as estimated by the EDT A test (r = 0.87 and 0.83, respectively). Chemical and histological studies of transiliac biopsies previously obtained from 153 dialysis patients (from 8 dialysis centers from Belgium, France and Germany) for studies of aluminum-induced bone disease showed that chronic renal failure and dialysis do not cause accumulation of lead in bone and elevated bone lead does not appear to alter trabecular bone histomorphometry. We found that in 5% of the hemodialysis population studied, bone lead concentrations approximated levels found in active lead workers.
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PMID:Bone lead in dialysis patients. 312 11

We report an asymptomatic man found to have simultaneous renal transport defects for magnesium and phosphate. Associated findings include gout, high frequency hearing loss, chronic elevations of SGOT and SGPT, metabolic bone disease, and hyperparathyroidism. The clinical expression of hyperparathyroidism was masked for 5 years by hypomagnesemia, and the patient became hypercalcemic only when magnesium levels were normalized by intravenous infusion. Both the phosphate and magnesium transport abnormalities persisted after parathyroidectomy. The many unique features of this case distinguish it from previously described disorders of magnesium or phosphate wasting.
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PMID:Renal wasting of magnesium and phosphate. 344 Nov 43

A frequent manifestation of severe primary hyperparathyroidism was the bone disease osteitis fibrosa cystica. Rarely, excess parathyroid hormone (PTH) was associated with gout and calcium pyrophosphate crystal deposition disease. Surgical cure of primary hyperparathyroidism was occasionally associated with pseudogout. Today, primary hyperparathyroidism is generally asymptomatic. Clinically overt rheumatologic and skeletal effects are mainly of historical interest. Skeletal disease is still detectable by more sensitive techniques. In certain circumstances, PTH may be protective and anabolic for the skeleton.
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PMID:Rheumatic manifestations of primary hyperparathyroidism and parathyroid hormone therapy. 1189 Aug 84

Patients with parathyroid disease can have important musculoskeletal problems.Hypoparathyroidism can cause subcutaneous calcifications, tetany, muscle cramps,and paresthesias, but also myopathies and an ankylosing spondylitis-like back disease. Hypoparathyroidism can occur in SLE caused by antiparathyroid antibodies.Patients with hyperparathyroidism can develop bone disease with cysts, erosions,and deformities. They can also develop pseudogout, gout, myopathies, and tendon ruptures.
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PMID:Parathyroid disease. 2109 44

Acute monoarthritis can be the initial manifestation of many joint disorders. The most common diagnoses in the primary care setting are osteoarthritis, gout, and trauma. It is important to understand the prevalence of specific etiologies and to use the appropriate diagnostic modalities. A delay in diagnosis and treatment, particularly in septic arthritis, can have catastrophic results including sepsis, bacteremia, joint destruction, or death. The history and physical examination can help guide the use of laboratory and imaging studies. The presence of focal bone pain or recent trauma requires radiography of the affected joint to rule out metabolic bone disease, tumor, or fracture. If there is a joint effusion in the absence of trauma or recent surgery, and signs of infection (e.g., fever, erythema, warmth) are present, subsequent arthrocentesis should be performed. Inflammatory synovial fluid containing monosodium urate crystals indicates a high probability of gout. Noninflammatory synovial fluid suggests osteoarthritis or internal derangement. Pitfalls in the diagnosis and early treatment of acute monoarthritis include failure to perform arthrocentesis, administering antibiotics before aspirating the joint when septic arthritis is suspected (or failing to start antibiotics after aspiration), and starting treatment based solely on laboratory data, such as an elevated uric acid level.
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PMID:Acute Monoarthritis: Diagnosis in Adults. 2792 77

p62, a protein capable of binding both ubiquitin and autophagy substrates, is well established as a key regulator in cancer and neurodegenerative diseases. Recently, there has been accumulating evidence that p62 is also a pivotal regulator in metabolic diseases, such as obesity, T2DM, NAFLD, metabolic bone disease, gout and thyroid disease. This review summarizes the emerging role of p62 on these diseases by considering its functional domains, phenotypes in genetically modified animals, clinically observed alterations, and its effects on downstream metabolic signaling pathways. At the same time, we highlight the need to explore the roles played by p62 in the gastrointestinal environment and immune system, and the extent to which its elevated expression may confer protection against metabolic disorders.
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PMID:Multifunctional p62 Effects Underlie Diverse Metabolic Diseases. 2896 79

Chronic kidney disease (CKD) is common. People with CKD have a wide range of comorbidities and, therefore, the majority of non-nephrologists will care for people with CKD. This paper aims to provide a brief overview of the diagnosis and management of CKD for the non-nephrologist. Identifying those with CKD and optimising treatment is essential as CKD has a direct association with adverse patient outcomes. There are modifiable factors where interventions may delay progression of CKD, including: smoking cessation, dietary advice, hypertension management, renin-angiotensin system blockade, glycaemic control and relieving urinary outflow obstruction. Complications, such as renal anaemia, metabolic acidosis, CKD-related mineral bone disease, hyperkalaemia and gout, are best managed in conjunction with nephrology input. The progression of CKD is often variable and nonlinear, but person-centred intervention can delay progression of CKD, reduce morbidity and mortality, and allow time for preparation for renal replacement therapy, ultimately providing the best possible personalised care.
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PMID:A practical guide to diagnosis and assessment of chronic kidney disease for the non-nephrologist. 3253 44