Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 69-year-old female with a fourty-year history of rheumatoid arthritis visited Kobe University hospital with complaints of subcutaneous soft tumor on both hands and arthritic pain of both knees. She has been given 10 mg of predonisolone for several years and had a history of hydronephrosis. Her radiographs revealed periarticular calcification in the hands, shoulder joints and posterior thoracic wall. She had high titer of rheumatoid factor and both erythrocyte sedimentation rate (79 mm/hr) and C-reactive protein (12.79 mg/ml) were elevated. The examination of her serum showed the following values: Ca 7.9 mg/dl, P 5.0 mg/dl, 25 (OH) D3 < 3.6 pg/ml, 1 alpha-. 25 (OH)2 Vit D3 < 6.1 pg/ml, osmolality 974 mOsm/kg, BUN 61 mg/dl, creatinine 1.9 mg/ml, creatinine clearance less than 20 ml/min, indicating chronic renal failure. Intact PTH level was normal, although plasma parathyroid hormone-C (PTH-C) level increased. Together with these findings, it is suggested that metabolic disorders associated with chronic renal failure and tissue damages due to the severe rheumatoid arthritis led to the formation of diffuse soft tissue calcification.
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PMID:[A case report of systemic calcinosis associated with rheumatoid arthritis]. 877 93

Solid cancers metastasize to bone by a multistep process that involves interactions between tumor cells and normal host cells. Some tumors, most notably breast and prostate carcinomas, grow avidly in bone because the bone microenvironment provides a favorable soil. In the case of breast carcinoma, the final step in bone metastasis (namely bone destruction) is mediated by osteoclasts that are stimulated by local production of the tumor peptide parathyroid hormone-related peptide (PTH-rP), whereas prostate carcinomas stimulate osteoblasts to make new bone. Production of PTH-rP by breast carcinoma cells in bone is enhanced by growth factors produced as a consequence of normal bone remodeling, particularly activated transforming growth factor-beta (TGF-beta). Thus, a vicious cycle exists in bone between production by the tumor cells of mediators such as PTH-rP and subsequent production by bone of growth factors such as TGF-beta, which enhance PTH-rP production. The metastatic process can be interrupted either by neutralization of PTH-rP or by rendering the tumor cells unresponsive to TGF-beta, both of which can be accomplished experimentally. The osteoclast is another available site for therapeutic intervention in the bone metastatic process. Osteoclasts can be inhibited by drugs such as the new-generation bisphosphonates; as a consequence of this inhibition, there is a marked reduction in the skeletal events associated with metastatic cancer to bone, such as pain, fracture, and hypercalcemia. However and possibly even more importantly, there is also a reduction of tumor burden in bone. In experimental situations, this has clearly been shown to affect not only morbidity but also survival. The precise mechanism by which bisphosphonates inhibit osteoclasts is still unclear and may represent a combination of inhibition of osteoclast formation as well as increased apoptosis in mature osteoclasts. However, studies with potent bisphosphonates such as ibandronate, pamidronate, and risedronate have clearly documented that reduction of bone turnover and osteoclast activity leads to beneficial effects not only on skeletal complications associated with metastatic cancer, but also on tumor burden in bone.
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PMID:Mechanisms of bone metastasis. 936 21

Bone thinning causing both fractures and severe pain not associated with fractures has been recognized in patients with chronic liver diseases. The patients most commonly affected are those with primary or secondary biliary cirrhosis, but those with alcoholic liver disease and cirrhosis after active chronic hepatitis may also be involved. Chronic liver disease has also been recognized as an important cause of osteoporosis in both sexes, with the mechanism thought to be a combination of calcium and/or vitamin D. The 9.1% patients with chronic active hepatitis accompanied with osteodystrophy. But 50% cirrhotic patients accompanied with osteodystrophy. Bone densitometry was determined by Digital Image Processing Method (Osteodystrophy < mean-2SD: age- and sex-matched normal value). Serum levels of osteocalcin (BGP) and parathyroid hormone (PTH) in patients of hepatic cirrhosis without osteodystrophy were lower than those with osteodystrophy. These results were suggested that hepatic osteodystrophy was rapidly turnover osteodystrophy. To function physiologically, vitamin D must be hydroxylation in liver to 25-(OH)-D and subsequently by the kidney to 1 alfa, 25-(OH)2-D. Osteodystrophy associated with hepatic cirrhosis is due to a defect in the 1 alfa-hydroxylation by the kidney rather than a hepatic hydroxylation defect. 1 alfa OH-D3 is very useful for treatment for hepatic osteodystrophy.
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PMID:[Hepatic osteodystrophy]. 964 89

A 57-year-old female patient presented with painless obstructive jaundice and mild mesogastric pain; she was in good general condition on admission. Abdominal ultrasonography revealed diffuse tumoral invasion of the liver, suggesting diffuse metastases. A liver biopsy showed a tumour with a trabecular growth pattern, composed of uniform relatively small cells, very suggestive of an endocrine carcinoma. Additional immunohistochemical stains, however, did not show any endocrine differentiation, but showed positivity for both hepatocyte-type cytokeratins (cytokeratin 8 and 18) and bile duct-type cytokeratins (cytokeratin 7 and 19). In addition, parathyroid hormone-related peptide, shown to be a good marker for cholangiocarcinoma, was immunoreactive. Electron microscopy revealed tumour cells with an intermediate phenotype: the cells clearly showed hepatocyte features on one hand and bile duct cell features on the other hand. Nine days after admission, the patient died due to liver failure and hepatic encephalopathy. Autopsy excluded another primary tumour site. Overall, this tumour was a primary liver tumour with an intermediate phenotype and with a very rapid clinical course. The intermediate (between hepatocyte and bile duct cell) phenotype suggests an immature progenitor cell origin, which is concordant with a rapid clinical course. This type of tumour has not been described previously and provides additional evidence for the existence of progenitor cells in human liver.
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PMID:Primary liver tumour of intermediate (hepatocyte-bile duct cell) phenotype: a progenitor cell tumour? 976 16

Three patients with extensive, symptomatic tumoral calcinosis (TC) were studied after renal transplantation. Changes in TC-related symptoms, radiological appearances, calcium, phosphate and intact parathyroid hormone concentrations were recorded. All patients noted an immediate reduction in pain and in 2 patients the TC rapidly resolved. Their TC was not palpable by 6 months and radiographs showed near complete resolution at 12 months. Both developed hypercalcemia and in one patient this was associated with polyuria and renal impairment. Bisphosphonates reduced the hypercalcemia but increasing the corticosteroids had no effect. The third patient remained dialysis dependent due to technical problems and rejection but continued on immunosuppression to preserve residual graft function. His TC improved symptomatically but grew radiologically. These cases demonstrate that rapid resolution of TC may occur after successful renal transplantation and that bisphosphonates can ameliorate the associated hypercalcemia. Early symptomatic benefit may occur without graft function and is probably due to the anti-inflammatory action of corticosteroids.
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PMID:Rapid resolution of tumoral calcinosis after renal transplantation. 1087 72

The last decade has been characterized by an emphasis on minimizing interventional techniques, hospital stays, and overall costs of patient care. It is clear that most patients with sporadic HPT do not require a complete neck exploration. We now know that a minimal approach is appropriate for this disease. Importantly, the MIRP technique can be applied to most patients with sporadic HPT and can be performed by surgeons with modest advanced training. The use of a gamma probe as a surgical tool converts the sestamibi to a functional and anatomical scan eliminating the need for any other preoperative localizing study. Quantification of the radioactivity within the removed gland eliminates the need for routine frozen section histologic examination and obviates the need for costly intraoperative parathyroid hormone measurements. This radioguided technique allows the benefit of local anesthesia, dramatically reduces operative times, eliminates postoperative blood tests, provides a smaller scar, requires minimal time spent in the hospital, and almost assures a rapid, near pain-free recovery. This combination is beneficial to the patient whereas helping achieve a reduction in overall costs.
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PMID:Minimally invasive radioguided parathyroidectomy. 1044 97

A 55-year old female patient on long-term hemodialysis began to suffer from pain in her knees and ankles. An ultrasonographic study showed enlargement of all four parathyroid glands. Serum parathyroid hormone and calcium levels were increased. Parathyroidectomy was performed. The right superior gland was enlarged and adherent to surrounding tissues. The other three glands were slightly enlarged. Histologically, the largest gland was a parathyroid carcinoma because capsular and vascular invasion were observed. To our knowledge, there have been only 13 cases of parathyroid carcinomas arising in patients with chronic renal failure reported in the English literature. To evaluate the characteristics of this tumor, we measured nuclear DNA and protein content using stains for HP (hematoporphyrin)/DAPI (4,6-diamidino-2-phenylindole dihydroporphyrin chloride). The nuclear DNA pattern was typically diploid or tetraploid. The cellular protein content was similar to that seen in the controls. The discrepancy between the histology, indicative of malignancy and the cytofluorometrical findings show that it is difficult to determine the prognosis for patients with secondary hyperparathyroidism and parathyroid carcinomas solely from the results of tumor DNA cytometry.
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PMID:DNA cytofluorometric analysis using HP/DAPI double staining of parathyroid carcinoma arising in a patient with chronic renal failure and secondary hyperparathyroidism. 1052 9

This study was performed to determine the prevalence of hypovitaminosis D (HD) and hypovitaminosis D associated with secondary hyperparathyroidism (HD-SHPT) among Indo-Asians attending rheumatology clinics in Wolverhampton. A cross-sectional survey of 98 clinic attenders and 36 normal controls subjects was undertaken. The groups were matched for age, gender, and body mass index. There was a high prevalence of vegetarianism, and milk consumption was low in both groups. Clinical scores for musculoskeletal pain, gait, and muscle strength were all significantly worse in clinic attenders (p < 0.001). Comparing clinic attenders with controls, 25-OH-vitamin D levels were 6.6 +/- 3.9 vs. 8.2 +/- 4.8 microg/L (p < 0.01) and the prevalence of HD (<8 microg/L) was 78% vs. 58% (p < 0.05), but neither parathyroid hormone levels (53 +/- 60 vs. 50 +/- 18 ng/L, n.s.) nor HD-SHPT prevalence (22% vs. 33%, n.s.) were significantly different. Routine biochemical tests were not discriminant, but none of the controls and 10 of 98 (10%) clinic attenders had elevated alkaline phosphatase levels: 6 with HD and 3 with HD-SHPT. Vitamin D deficiency has an extremely high prevalence among Indo-Asians in the U.K., particularly in those attending rheumatology clinics. Detection of HD and HD-SHPT is only possible using measurements of 25-OH-vitamin D and PTH.
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PMID:Prevalence of hypovitaminosis D in Indo-Asian patients attending a rheumatology clinic. 1057 83

A case of tumor-induced phosphaturic osteomalacia in a 54 year old man is reported. The patient was admitted because of progressive muscle spasms with pain and weakness in the bilateral thighs. Laboratory data showed hypophosphatemia, decreased tubular resorption of phosphate (TRP), a low 1,25-dihydroxyvitamin D level, and a high serum alkaline phosphatase level. Radiologic examinations revealed multiple lesions of osteomalacia in the ribs, and a small mass in the lower posterior mediastinum. After removal of the tumor, clinical symptoms disappeared and hypophosphatemia, decreased TRP, and the 1,25-dihydroxyvitamin D level were corrected. Microscopical examination revealed that the tumor was composed of mature adipose tissues, osseous tissues, and primitive stromal zones including osteoclast-like giant cells, non-mineralized woven bone, and various sized blood vessels. Patho-physiologic observations suggested that the tumor secreted some humoral substances inhibiting 25-hydroxyvitamin D-1 alpha-hydroxylase activity, renal phosphate resorption, and parathyroid hormone production.
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PMID:Phosphaturic mesenchymal tumor, mixed connective tissue variant (oncogenic osteomalacia). 1084 77

The treatment of secondary hyperparathyroidism (HPT) in patients with chronic renal disease has improved markedly in recent years. The skeletal pain, disabling fractures, tendon ruptures, and myriad other symptoms associated with HPT can now be avoided, and the quality of life of patients with end-stage renal disease is improved. Control of hyperphosphatemia, maintenance of normocalcemia, and appropriate dosing of vitamin D analogues can prevent HPT in many cases. Palatable, nutritious diets should be followed; serum calcium, phosphorus, alkaline phosphatase, and parathyroid hormone should be monitored; and treatment regimens should be adjusted accordingly. If prevention fails, and even if severe HPT develops, many of these patients can still be controlled medically with correction of hyperphosphatemia and high doses of intravenous calcitriol. In our experience, only a few patients require surgical parathyroidectomy (usually noncompliant patients or patients whose HPT has been poorly managed from early uremia). The essence to medical management is to correct the two most important pathogenetic factors of HPT, hyperphosphatemia, and calcitriol deficiency. We present the current approach to the management of HPT, with highlights of recent advances.
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PMID:Current medical management of secondary hyperparathyroidism. 1098 84


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