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

Of 37 adult patients with ureteroceles, 13 also had calculous disease (35 per cent). Of these 13 cases 7 had single ureters and 6 had duplicated ones. None had a metabolic or urinary abnormality such as hypercalcemia, gout, hypercalciuria or hyperuricuria. Two of the patients were a mother and daugher--the first reported familial incidence of ureterocele with calculous disease. A surgical technique is described for removal of the calculus, excision of the ureterocele and reimplantation of the ureter. The procedure was used in 4 of the 7 patients with single ureters, while the stone passed spontaneously in 2 patients and was treated by ureterolithotomy in 1. A modification of the technique was used in 2 of the 6 patients with duplicated ureters but other surgical procedures were used in the remaining 4. Of 10 stones that were analyzed 2 were struvite and none contained cystine or uric acid. Long-term followup is a requisite to assure control of this clinical entity.
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PMID:Management of urinary calculous disease in patients with ureterocele. 83 Sep 66

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

Calculus formation in the renal transplanted patient is uncommon and usually represents a late complication of secondary hyperparathyroidism. A case report of a gouty patient with a transplanted cadaveric kidney is presented. The patient presented without hypercalcemia, or urinary infection, or renal tubular acidosis, or ureteral obstruction, or ingestion of antacids, or metabolic disease, or previous graft lithiasis. Five months after transplantation, a large stone within the renal pelvis was observed on an x-ray film. The radiotransparent nucleus, the patient's past history and the acute gouty arthritis he presented in the immediate postoperative period suggested that the nucleus of the calculus might be mainly composed of uric acid. These facts have drawn our attention to the control of the purine metabolism in the renal transplanted patients who have a past history consistent with gout.
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PMID:Staghorn renal stone in a transplanted kidney. 234 62

Significant alterations in the structure and functions of the kidney are caused by a number of metabolic disturbances and deficiencies of physiological substances. These include intercapillary glomerulosclerosis, gout, hypercalcemia, hereditary cystinuria, potassium depletion, pyrophosphates deficiency, vitamin D deficiency and liver disorders. Some of these metabolic disorders are secondary to drug ingestion.
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PMID:Renal disease secondary to metabolic disorders or physiological deficiency states. 604 89

A series of 38 cases of primary hyperparathyroidism seen at a single hospital within a four a half year period is reported. The importance of hypercalcemia in the diagnosis of this syndrome and its screening in cases of arterial hypertension, gout, osteoporosis, and families with type I multiple endocrine neoplasia are underlined. The patients in the present series had a florid clinical history with a mean duration of 14 years. Main symptoms were urolithiasis (52%), arterial hypertension (28.9%), bone involvement and pain (23.7%), and peptic ulcer (18.4%). There were a high proportion of patients with hyperuricemia (26.3%), some with classical symptoms of gout. One patient presented simultaneous pituitary and pancreatic involvement. Surgical therapy was undertaken in 25 patients, of whom 24 (96%) were cured, one of them after reoperation. There were no cases of relapse, hypoparathyroidism, or postoperative death. Surgery is the only rational and definitive form of treatment of hyperparathyroidism; both experienced surgeons and pathologists are necessary to deal with the anatomic and histologic subtleties of this interesting endocrine disorder.
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PMID:[Comments on a series of 38 cases of primary hyperparathyroidism (author's transl)]. 724 69

The mechanism of crystal deposition in joints varies with the chemical nature of the crystal. Crystallisation of monosodium urate, characteristic of gout, requires a neutral pH and supersatured tissues, which is the basis for the clinical definition of the upper limit of normal blood uric acid level. The appearance of crystals also is dependent on time since crystallisation of monosodium urate is very slow. Inhibitory or promoting factors could intervene and explain rare cases of gout without hyperuricemia or the rapid crystallisation which seems to characterise some types of drug-induced gout. Crystal deposits of calcium pyrophosphate dihydrate form mainly in the cartilage where they seem favoured by ageing or by trauma, which could deplete cartilage of crystallisation inhibitors, notably proteoglycans. High pyrophosphate levels within cartilage also play an important role. The appearance of these pyrophosphates in the interstitial cartilagenous medium would be in large part due to the activity of an ectoenzyme, nucleoside triphosphate pyrophosphatase; increased activity of this ectoenzyme could be responsible for some chondrocalcinosis. Chronic hypercalcaemia can also be involved in the pathogenesis of cartilage deposition of calcium pyrophosphate dihydrate by raising the calcium-pyrophosphate product, or by decreasing the activity of alkaline phosphatase, an enzyme responsible for breakdown of extracellular pyrophosphates. The pathophysiology of calcium phosphate deposits is poorly understood. For some authors, these deposits occur within matrix vesicles, but for others, within collagen fibres. Increase in the calcium-phosphate product can also be a cause, for example, during renal osteodystrophy or vitamin D intoxication.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Mechanism of crystal deposition in the joints]. 817 67

The clinical features and laboratory findings of 91 Thai patients (33 males and 58 females) with CPPD crystal deposition disease were studied. Their average age was 71.54 years. Acute monoarthritis and oligoarthritis were the two most common forms of presentation and were seen in 89 per cent of cases. The knee, wrist and ankle were the three most common joints involved. Associated diseases were common and included hypertension (30 cases), renal insufficiency (23 cases), chronic obstructive pulmonary disease (17 cases), coronary heart disease (13 cases) and diabetes mellitus (12 cases). Eleven patients had malignancies. Five patients had concomitant gout and CPPD crystal deposition disease. The knee and the wrist were the two most common sites of chondrocalcinosis. Of 67 patients who had thyroid function tested, 2 had hyperthyroidism and 5 had hypothyroidism. Hypomagnesemia was seen in 19 per cent. None had hypercalcemia, hypophosphatasia, hemochromatosis or hyperparathyroidism. In contrast to the western series, acute arthritis in our series responded well to oral colchicine alone.
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PMID:Calcium pyrophosphate dihydrate crystal deposition: a clinical and laboratory analysis of 91 Thai patients. 1044 78

3 patients, 2 women aged 71 and 76 and a 55-year-old man, were originally diagnosed with rheumatoid arthritis (RA) and treated with disease-modifying antirheumatic drugs (DMARDs); two of these patients fulfilled the American College of Rheumatology criteria for RA. Because the symptoms persisted, the diagnosis was reconsidered. It turned out that they had pseudogout, which is an arthropathy caused by the deposition of calcium pyrophosphate crystals; the younger woman had no obvious metabolic disorder, the older woman had underlying hyperparathyroidism, and in the man the arthropathy was probably due to benign hypercalcaemia. DMARDs were replaced by NSAIDs. Varying degrees ofarthropathy persisted in the women, but in the man they were clearly decreased. In addition to resembling gout, the clinical manifestations of pseudogout can also mimic RA. It is important to distinguish pseudogout from RA because their treatment is completely different. Furthermore, pseudogout can be the first or sole symptom of a metabolic disorder.
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PMID:[Pseudogout in 3 patients with presumed therapy-resistant rheumatoid arthritis]. 1603 67

Arthritis is inflammation in a joint often with joint damage, usually accompanied by pain, swelling and stiffness, resulting from infection, trauma, degenerative changes, metabolic disturbances, autoimmune or other causes. It occurs in various forms, including rheumatoid arthritis, osteoarthritis, bacterial arthritis and gout. Gallium III can inhibit the production of inflammatory cytokines, such as IL-1beta, produced by macrophage-like cells in vitro. A dose-dependent inhibition of IL-1beta and TPA stimulated MMP activity by gallium nitrate at increasing concentrations occurs, demonstrating that gallium nitrate can be a useful modulator of inflammation in arthritis. Gallium III is an inhibitor of bone resorption and is an effective treatment for hypercalcemia. Gallium III has been reported to be effective in the treatment of mycobacterium butycicum-induced arthritis in rats by antagonism of iron III. Long-term elimination of pain from arthritis by gallium III was first observed in horses primarily being treated for navicular disease. Several people treating their horses with gallium nitrate coincidentally found that arthritis pain in their fingers ended and did not return after soaking their hands in 14% gallium nitrate solution. Therefore, the severely arthritic hands of a 60-year-old woman were topically treated with a 14% aqueous solution of gallium nitrate for 90 min. Pain and inflammation from rheumatoid arthritis diminished rapidly, and neither pain nor inflammation returned during the following 2 years from that single treatment. A 61-year-old woman who had osteoarthritis in her left knee, shoulders and wrists was treated orally with 50 ml of a 1% gallium nitrate solution (120 mg elemental gallium) daily using a two week on and two week off protocol, resulting in almost total elimination of pain while on gallium nitrate, while pain partially returned during the two week off periods. Treatment of frozen shoulder with topical 40% gallium nitrate for 120 min resulted in greatly reduced pain and crepitus almost immediately with complete restoration of range of motion, with pain remaining essentially absent for over 1 year. Mechanisms of action are hypothesized to include anti-inflammatory, bone density improvements, antibacterial, anti-iron III and anti-aluminum III effects. Proper use of gallium III may be effective in terminating pain and inflammation of arthritis for years, often with a single treatment.
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PMID:Elimination of arthritis pain and inflammation for over 2 years with a single 90 min, topical 14% gallium nitrate treatment: case reports and review of actions of gallium III. 1612 80

We report a 66-year-old Chinese man with chronic renal insufficiency (creatinine 1.7 mg/dL) and gout suffering from slurred speech and right hemiplegia for 3 days. Acute cerebral infarction was confirmed by computed tomography. Conscious disturbance occurred on the tenth hospital day without significant changes on imaging study when compared with a previous scan. Hypercalcemia (total calcium 14.1 mg/dL) and acute exacerbation of chronic renal failure (serum creatinine 2.5 mg/dL) were noticed. Hypercalciuria (FECa 3.2%), and low serum levels of intact parathyroid hormone and 1,25(OH)2D3 suggested nonparathyroidal hypercalcemia. An extensive workup failed to identify any etiology of hypercalcemia. Hypercalcemia and renal failure were temporarily ameliorated after aggressive volume expansion and loop diuretic treatment but recurred 2 weeks later. Immobilization hypercalcemia was considered after the exclusion of other discernible causes and was successfully treated with rehabilitative exercises and bisphosphonates without further recurrence during a 2-year follow-up. Clinical alertness to immobilization as a possible cause of hypercalcemia may avoid unnecessary and invasive examinations, life-threatening complications and annoying recurrences.
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PMID:An unrecognized cause of recurrent hypercalcemia: immobilization. 1663 46


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