Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026764 (multiple myeloma)
36,148 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient with primary hyperparathyroidism and multiple myeloma did not have roentgenographic evidence of either disease, yet there was biochemical evidence for both diseases. Hyperparathyroidism was diagnosed by hypercalcemia and increased parathyroid hormone values. Multiple myeloma was diagnosed by serum gamma-globulin component of 2.74 g/dL with a monoclonal spike and bone marrow plasmacytosis of 31%. The serum IgA level was 2.22 g/dL and the IgG and IgM levels were normal. Serum and urine immunoelectrophoresis showed abnormal IgA and lambda arcs. Computed tomography of the neck localized a parathyroid adenoma that was found and removed at surgery.
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PMID:Primary hyperparathyroidism complicated by multiple myeloma. 648 91

A case of multiple myeloma in which hypercalcaemia persisted despite an otherwise good response to conventional treatment is described. The hypercalcaemia was eventually found to be due to a parathyroid adenoma. Despite the frequent association of hypercalcaemia and malignant disease, and the relative frequency of primary hyperparathyroidism as a cause of hypercalcaemia, there are very few reports of multiple myeloma and parathyroid adenoma occurring together. This case emphasizes the need to be aware that there may be more than one cause of hypercalcaemia in a patient with multiple myeloma.
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PMID:Refractory hypercalcaemia. Parathyroid adenoma or multiple myeloma? 669 88

For 2 weeks 27 patients with hypercalcemia received a standard oral treatment with (3-amino-1-hydroxypropylidene)-1,1-bisphosphonate (APD) as the sole agent. Results were grouped according to causes of hypercalcemia and compared with effects of APD in 13 normocalcemic patients with Paget's disease of bone and 7 with osteoporosis. In 12 hypercalcemic patients with osteolytic bone lesions and in the 20 normocalcemic patients, the mean serum calcium decreased to final levels that were subnormal and significantly lower than those obtained after treatment of 8 patients with primary hyperparathyroidism. In 3 patients with myeloma and in 4 tumor patients without bone lesions, serum calcium did not always decrease to the normal range. Implications of these observations for the mechanism of hypercalcemia are discussed.
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PMID:Efficacy of amino-hydroxypropylidene bisphosphonate in hypercalcemia: observations on regulation of serum calcium. 681 19

Association of monoclonal gammopathies of undetermined significance with primary hyperparathyroidism has been reported by several investigators. We reviewed the records of our cases of surgically proven parathyroid adenoma with serum protein electrophoresis within 6 months preceding parathyroidectomy. Among 911 patients who had hyperparathyroidism and were more than 50 years old, immunoelectrophoresis revealed a monoclonal gammopathy of undetermined significance in nine (1.0%). This incidence is similar to those in two studies of a normal population (1.25% and 1.6%). In our nine patients, the monoclonal proteins ranged from 1.0 to 1.9 g/dl. The monoclonal protein was unchanged during follow-up (median 62 months) in eight and increased in one (who probably has evolving multiple myeloma). Nine of the 911 patients with hyperparathyroidism had a malignancy, and this also is similar to previously reported experience.
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PMID:Primary hyperparathyroidism and monoclonal gammopathy of undetermined significance. 708 Nov 54

A 70-year-old woman presented with back pain due to vertebral crush fractures and was found to have hypercalcaemia. Investigation revealed evidence of both primary hyperparathyroidism and Bence Jones myeloma and this was subsequently confirmed at necropsy. This is the first description of a case in which the simultaneous occurrence of both diseases was reliably established. The case illustrates the difficulty in identifying the cause of hypercalcaemia in some patients, and emphasises the need to consider the diagnosis of myeloma in all cases of hypercalcaemia.
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PMID:Hypercalcaemia due to the coexistence of parathyroid adenoma and myelomatosis. 709 95

Milk-alkali syndrome can be caused by ingesting large amounts of calcium carbonate. Coincident with the promotion of calcium carbonate as treatment for both dyspepsia and osteoporosis, milk-alkali syndrome is now a common cause of hypercalcemia severe enough to require admission to the hospital. The syndrome accounted for less than 2% of such admissions before 1990, but from 1990 through 1993, it was the cause of hypercalcemia for over 12% of these patients. Only primary hyperparathyroidism and hypercalcemia of malignancy (excluding multiple myeloma) are more common. The diagnosis of milk-alkali syndrome is made almost entirely based on the patient's history; careful attention to dietary practices and over-the-counter drug use is required, as numerous over-the-counter medications contain calcium carbonate. Modern assays for PTH demonstrate the expected suppression of PTH by hypercalcemia. Nonetheless, measurement of PTH must be performed in a timely manner as treatment with intravenous saline may result in hypocalcemia and elevated PTH soon after admission. Given the pathophysiology of milk-alkali syndrome compared to other causes of hypercalcemia, hypocalcemia with rebound hyperparathyroidism is probably unique to milk-alkali syndrome.
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PMID:Milk-alkali syndrome associated with calcium carbonate consumption. Report of 7 patients with parathyroid hormone levels and an estimate of prevalence among patients hospitalized with hypercalcemia. 789 47

Careful examination as well as biochemical and hormonal investigations should be performed in men suffering from vertebral crush fractures, in order to detect a destructive skeletal process (multiple myeloma, bone metastatic lesions, lympho and myeloproliferative disorders), a mineralization defect (osteomalacia) or a secondary osteoporosis: primary hyperparathyroidism, hypogonadism, hyperthyroidism, renal hypercalciuria, alcoholism and tobacco smoking. The diagnosis of idiopathic osteoporosis should be made only after these causes have been excluded; the pathogenesis of the disease is unclear but risk factors have been identified: family history of osteoporosis, low dietary calcium intake, delayed puberty, ethanol use, tobacco smoking, inactive lifestyle and lean body build. Correction of risk factors, calcium supplementation, regular program of weight bearing physical activity, in some instances correction of testosterone deficiency may be of benefit to reduce bone loss. Severe osteopenia or osteoporosis may require sodium fluoride therapy.
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PMID:[Male osteoporosis]. 793 30

Though vertebral fractures were required to make the diagnosis of osteoporosis prior to the advent of methods for accurate bone measurement, osteopenia is readily defined by a decrease of bone mineral density by 2 to 2.5 SD from the peak bone density. After excluding other metabolic bone diseases such as primary hyperparathyroidism, osteomalacia, renal osteodystrophy, multiple myeloma and tumor metastases by means of X-ray studies and biochemical studies on serum and urine, by far the largest proportion of patients with osteopenia are usually found to have osteoporosis. Primary osteoporosis is found in males and females after middle age, and secondary osteoporosis at any age with definite causes such as corticosteroid excess, immobilization, rheumatoid arthritis or vitamin C deficiency. Estrogen withdrawal in young women is classified as secondary osteoporosis, but postmenopausal osteoporosis with similar cause is usually classified into primary osteoporosis, creating a confusion. Rapid bone loss occurring only during a few years after menopause should be clearly distinguished from the life-long process of bone loss common to males and females and should not be classified as a "type" of osteoporosis.
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PMID:[Osteoporosis--concept, classification and epidemiology]. 796 67

The authors report the case of an 82 year old woman hospitalized for hypercalcemia associated with low serum phosphate. Multiple myeloma was first diagnosed. However, despite chemotherapy, hypercalcemia persisted and she was subsequently diagnosed as primary hyperparathyroidism; eucalcemic state was then obtained after parathyroidectomy. Fifteen similar cases are reported in the literature and the mechanisms and implications of such an association are discussed.
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PMID:Coexisting kappa light chain multiple myeloma and primary hyperparathyroidism. 810 68

The diagnosis of primary hyperparathyroidism most often results from the incidental finding of hypercalcemia. In two recent cases of osteitis fibrosa cystica (OFC), however, patients without adequate access to health care served as graphic reminders that the clinical spectrum of the disease includes bone disease, and that OFC can be the presenting manifestation of long-standing primary hyperparathyroidism. Both patients complained of bone pain and had widespread osteolytic bone lesions in addition to hypercalcemia on a multitest biochemical panel. The presumptive diagnosis of malignancy with bone involvement (metastatic cancer or multiple myeloma) led to random bone marrow trephine biopsies. Examination of the bone marrow biopsy material revealed the characteristic pathology of OFC, leading to appropriate diagnosis and surgical management of large parathyroid adenomas in both patients.
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PMID:Osteitis fibrosa cystica simulating metastatic tumor. An almost-forgotten relationship. 824 19


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