Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The observation of a non-metastatic reactive hepatopathy associated with a hypernephroma in a 39-year-old man who had had fever for 4 months led to a review of the literature and an analysis of basically three aspects of the disorder: a) The various manifestations of carcinoma of the kidney, which include a large number of paraneoplastic clinical symptoms (polycythemia, anemia, prolonged fever, hypercalcemia, hypertension, nefropathy, loss of salt, peripheral neuropathy, and amyloidosis); b) an alteracion of hepatic function known since 1961 which is characterized by an abnormal retention of sulfobromophthalein, increase of alkaline phosphatase, prothrombin decrease, dysproteinemia with hypoalbuminemia, and alpha2-globulin increase. It may or may not be accompanied by enlargement of the liver. c) Criteria of operability of the primary tumor.
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PMID:[Liver disease associated with hypernephroma. A case report (author's transl)]. 45 99

Amyloidosis primarily involving bone is described in a 59-year-old male pateint. Well circumscribed lytic lesions of the skeleton raised the possibility of myelomatosis. The prolonged insidious course of the disease was uncomplicated by hypercalcemia, pathological fracture, or hematologic abnormalities. The clinical course, together with histological findings and strongly positive bone scan, were the distinguishing features. The osseous manifestations without plasma cell tumor appears to be a rare occurrence in amyloidosis.
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PMID:Bone lesions in primary amyloidosis. 50 49

Ninety-seven patients with light chain disease (LCD) were studied. The median survival from diagnosis was 30 mo for 52 patients with kappa-LCD and 10 mo for 45 patients with lambda-LCD (p less than 0.0007). A lower proportion of kappa-LCD patients (15.7%) than lambda-LCD patients (42.2%) died within the first 6 mo after diagnosis. The survival of the remaining patients with kappa-LCD was still much longer than of those with lambda-LCD (p = 0.022). The shorter survival of lambda-LCD patients could not be ascribed to an increased incidence of recognized manifestations indicating a poor prognosis (e.g., anemia, hypercalcemia, azotemia, low albumin, the extent of osteolytic lesions, or proteinuria), the incidence of amyloidosis, the clinical stage of the disease at diagnosis, or the response to treatment, and remains unexplained. A comparison of the clinical manifestations of LCD with those of other myelomas revealed some differences. LCD patients were slightly younger than IgA and IgG patients but older than IgD patients. A 1:1 ratio of males to females was similar to the ratios in IgA and IgG myeloma, but differed from the 3:1 ratio reported for IgD myeloma. Plasma-cell leukemia developed in 7/97 LCD patients, an incidence that was higher than has been reported in other myelomas. The initial BUN was more than or equal to 30 mg/100 ml in 54 of 95 LCD patients, an incidence that was higher than has been reported for IgA and IgG myeloma, but lower than the incidence in IgD myeloma. The incidence of amyloidosis in LCD (23 of 97 patients) was similar to that reported for IgA and IgG myeloma, but less than the incidence in IgD myeloma.
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PMID:Kappa and lambda light chain disease: survival rates and clinical manifestations. 82 Mar 87

Renal cell adenocarcinoma can be one of the great masqueraders in medicine. More common extrarenal manifestations of renal cell carcinoma include fever, anemia and gastrointestinal symptoms. Other rarer systemic symptoms are caused by amyloidosis, neuromyopathy and tumor thrombus. Humoral manifestations include polycythemia, hypercalcemia, galactorrhea and Cushing's syndrome. Metastatic disease commonly presents as the initial symptom.
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PMID:Extrarenal manifestations of renal cell carcinoma. 85 Mar 16

The clinical, haematological and biochemical correlations of 224 consecutive unselected examples of monoclonal gammopathy have been studied. The paraprotein frequency detedted was IgG 62 percent, IgA 15.2 percent, IgM 10.3 percent, Bence Jones protein 8.9 percent and in 3.6 percent the paraproteins were not identified. In half the monoclonal gammopathy was associated with an immunocytoma (myeloma in 82 and lymphoma in 30). In three cases the associated clinical disease was amyloidosis. In 36 cases (16.1 percent) the associated clincial disease was a nonlymphoproliferative malignant tumour. Monoclonal gammopathy may be a significant marker of malignancy in such cases. In 73 cases (32.6 percent) the associated clinical conditions were unrelated to the gammopathy although only 55 of these cases were sufficiently investigated to warrant classification as examples of benign monoclonal gammopathy. There was a strong correlation between Bence Jones proteinuria and malignancy. Sixty-five patients demonstrated Bence Jones proteinuria and in 59 of these a malignancy was detected. The association was strong between hypercalcaemia and malignancy as this was present in all 27 of the cases who had hypercalcaemia. The relationship between Bence Jones proteinuria and hypercalcaemia was also strong and Bence Jones proteinuria was detected in 73 percent of the hypercalcaemic patients as opposed to 36.7 percent in the whole series. Hypercalcaemia and Bence Jones proteinuria, when found in a patient with monoclonal gammopathy have a grave clinical connotation.
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PMID:Immunocytoma, cancer and other associations of monoclonal gammopathy: a review of 224 cases. 105 67

A review of 869 cases of multiple myeloma seen at the Mayo Clinic from 1960 through 1971 revealed that 98% of patients were 40 years of age or older and that 61% of them were males. Inital findings were bone pain in 68% of patients, anemia in 62%, renal insufficiency in 55%, hypercalcemia in 30%, a palpable liver in 21%, and a palpable spleen in 5%. Proteinuria was noted in 88% and Bence Jones proteinuria was identified in 49%. Skeletal roentgenographic abnormalities were seen in 79%. Serum protein electrophoresis showed a spike in 76%, hypogammaglobulinemia in 9%, and minor or no abnormalities in 15%, and a globulin spike was seen 75% of the urinary electrophoretic patterns. Immunoelectrophoresis of the serum revealed a monoclonal heavy chain in 83% and a monoclonal light chain in the serum, in 8% (Bence Jones proteinemia). Three patients had no monoclonal protein in the serum or the urine ("nonsecretory"). Amyloidosis was found in 7% of the patients. Follow-up information was obtained in 99.7% ; 82% of the 869 patients have died. Infection and renal insufficiency were the most common specific causes of death. The median survival was 20 months; 66% of the patients were alive at 1 year and 18% at 5 years.
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PMID:Multiple myeloma: review of 869 cases. 1252 72

This report deals with an unusual case of primary macroglobulinemia with hypercalcemia, chronic renal failure and systemic amyloidosis. In May 1990, a 63-year-old male was transferred to our hospital because of hypercalcemia (13.5 mg/dl) and renal failure. Clinical examinations showed anemia, macroglossia, lymph node swellings and hepatomegaly. Laboratory findings included Bence-Jones (kappa type) proteinuria (0.8 g/day), a monoclonal gammopathy of the IgM-kappa type (2.8 g/dl), a proliferation of lymphoid cells in the peripheral blood (5%) and the bone marrow (59.6%), and lymphomatous involvement of an inguinal lymph node. Serum creatinine concentration was 8.5 mg/dl. The serum levels of parathormone and vitamin D3 metabolites were normal. The roentgenogram of bones showed a compression fracture of the lumbar spine and systemic osteoporosis. The treatment included eel calcitonin, prednisolone and the CHOP regimen, followed by hemodialysis and plasmapheresis. The serum level of IgM increased to 4.6 g/dl. The patient died three months later and postmortem examination demonstrated marked systemic amyloidosis.
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PMID:[Primary macroglobulinemia with hypercalcemia, renal failure and systemic amyloidosis]. 146 88

Bone and joint pathology in patients undergoing long-term dialysis for end-stage renal failure is presented in the light of typical cases and a brief review of the literature. Osteomalacia with bone pain and fractures is caused mainly by aluminium overload due to enteral uptake from aluminium-containing phosphate binders. This is why calcium acetate or calcium carbonate should be used exclusively to lower enteral phosphate reabsorption. If--due to hypercalcemia--aluminium containing phosphate binders--cannot be entirely avoided, they should never be administered together with citrate (citrate-containing medication, fruit juice, etc.), which chelates aluminium and thereby massively increases enteral aluminium uptake. Secondary hyperparathyroidism with overt radiologically demonstrable bone disease develops in many patients on long-term dialysis despite efforts to maintain plasma calcium within or slightly above the upper normal range and concomitant treatment with calcitriol. Intravenous administration of relatively high-dose calcitriol or 1-alpha-OH-D3 (neither readily available at the present time), as well as the newly developed experimental vitamin D analogs such as 22-oxa-(OH)2-D3, which appear to suppress the parathyroid glands without increasing enteral calcium reabsorption, may in future reduce the high incidence of parathyroidectomy in patients on maintenance dialysis. beta 2-microglobulin amyloidosis is a new disease entity which develops in the majority of long-term dialysis patients. Apart from carpal tunnel syndrome, trigger fingers and tendon ruptures, it is associated with acute and chronic painful erosive arthropathy with joint effusions and fractures, particularly around the hip, due to cystic bone lesions where bone is replaced by nodular amyloid deposits.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Bone and joint problems in long-term dialysis]. 159 6

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

Monoclonal immunoglobulin deposition occurs in tissues as Congo Red binding fibrils in light chain amyloidosis, as less structured deposits in light chain deposition disease, and as similar but distinct deposits in light and heavy chain deposition disease. The nonamyloid forms were found in 13 patients who had evidence of plasmacytic dyscrasia by the immunohistochemical detection of immunoglobulin light chains of kappa or lambda class (with or without staining for a single heavy chain isotype) and by the absence of amyloid P component in tissue sections that did not show the birefringence characteristic of amyloid after Congo Red staining. All but two of the patients presented with proteinuria with or without azotemia. Clinical syndromes involving other organ systems were less common but occasionally severe. Four patients had overt multiple myeloma. Three others had hypercalcemia and mild bone marrow plasmacytosis but no lytic lesions. Analyses of immunoglobulin synthesis in bone marrow cells from seven patients showed excess light chains in all and incomplete light chains or heavy chain fragments in six, regardless of whether an intact monoclonal protein or related subunit was in the serum or urine. The fibrillar (amyloidotic) and nonfibrillar forms of monoclonal immunoglobulin deposition occur either in overt multiple myeloma or in the course of less neoplastically aggressive plasmacytic dyscrasias. Bone marrow cells from patients with either type produce immunoglobulin fragments that are related to those deposited in the affected tissues.
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PMID:Monoclonal immunoglobulin deposition disease: light chain and light and heavy chain deposition diseases and their relation to light chain amyloidosis. Clinical features, immunopathology, and molecular analysis. 210 17


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