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)

Two patients, one with myeloma (Patient 1) and the other with probable chronic lymphocytic leukemia (Patient 2), had reduced renal tubular phosphate reabsorption in the absence of hyperparathyroidism together with other features of the Fanconi syndrome, as consequences of the nephropathy associated with light-chain proteinuria. Both patients had hypophosphatemic osteomalacia, demonstrated for the first time in this condition by iliac bone histomorphometry after in vivo double tetracycline labeling, despite absence of bone pain or Looser zones. Neither patient was vitamin D-depleted, but plasma calcitriol level was normal in Patient 1 and low in Patient 2; only the latter patient had severe muscle weakness. Complete histologic correction of osteomalacia was achieved by treatment in accordance with the biochemical defects--oral phosphate therapy alone in Patient 1 and combined with calcitriol in Patient 2. Both patients are now symptom-free, five and three years after the initial diagnosis of bone disease and hematogenous malignancy. Thirteen previous instances of the same form of osteomalacia were reviewed; in most cases, the Fanconi syndrome developed before its probable cause became apparent. The Fanconi syndrome has also been reported in two cases of osteomalacia due to mesenchymal tumor, but not in osteomalacia associated with prostatic carcinoma. Light-chain nephropathy and consequent renal tubular dysfunction appears to be a third form of oncogenous osteomalacia.
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PMID:Hypophosphatemic osteomalacia and adult Fanconi syndrome due to light-chain nephropathy. Another form of oncogenous osteomalacia. 310 97

The case of 65 year old woman with progressive enlargement and "wooden" induration of the pelvic girdle and thigh muscles due to an amyloid infiltration is reported. Muscle changes appeared two years after a diagnosis of myeloma with free lambda light chains. The patient complained of muscle pain, lassitude and weakness. Macroglossia was present. Skeletal muscle (vastus lateralis) contained large amounts of amyloid substance and showed type 2B atrophy. There was no fiber type grouping. Some amyloid deposits abutted on the muscle fiber, destroyed the basal lamina and sarcolemma, but never infiltrated it. Besides the amyloid phagocytosis by macrophages, a relationship between amyloid filaments and fibroblasts was present. Another non-congophilic substance was revealed using the Avidin-Biotin peroxidase complex to localize lambda light chains by light microscopy and corresponded to a granular substance in electron microscopy. Clinicopathological results are discussed with a review of thirteen similar cases previously reported.
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PMID:[Pseudo-hypertrophic pelvi-crural amyloid myopathy in lambda light-chain myeloma. Clinical, morphological and immunocytochemical study]. 311 Sep 2

Generalized muscle weakness culminating in ventilatory failure developed in a 59-year-old man with kappa light chain multiple myeloma. Physical examination demonstrated skeletal muscle enlargement, severe proximal muscle weakness, and macroglossia, consistent with amyloid-associated muscle pseudohypertrophy. Pulmonary function studies revealed a severe restrictive abnormality with a low maximal inspiratory pressure and maximal voluntary ventilation. Arterial blood gas values and chest radiographic results were normal. There was no clinical evidence of cardiac or central nervous system disease. At autopsy, skeletal muscles and diaphragm were diffusely infiltrated by amyloid. There was also multifocal deposition of amyloid in alveolar septae, esophagus, and subendocardium. This report suggests that ventilatory failure may occur as a complication of myeloma-associated (AL) amyloidosis involving the respiratory muscles.
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PMID:Respiratory muscle weakness and ventilatory failure in AL amyloidosis with muscular pseudohypertrophy. 311 Dec 59

Amyloid deposition in the quadriceps femoris muscle was investigated in 12 cases of systemic amyloidosis including 6 of AL-(primary or myeloma-associated) type, 2 of AA- (secondary) type, and 4 of prealbumin- (familial or sporadic) types. Clinically, muscle weakness was found in 7 patients. Among the 7 patients, one of the AL-type suffered from systemic myopathy showing progressive muscular stiffness, pseudohypertrophy, and weakness. The other 6 presented with polyneuropathy. Pathologically, no amyloid was found to be deposited in the AA-type. In all of the AL- and prealbumin-types, amyloid deposition was found in the blood vessels and peri- and endomysium. The degrees of amyloid deposition were marked in one case of the AL-type, which was considered to be suffering from amyloid myopathy, moderate in one of the AL-type, and slight in the rest of the AL-type and all of the prealbumin-type. Our observations and descriptions in the literature indicate that the presence and degrees of amyloid deposition in the skeletal muscles would be related to the types of amyloid proteins in amyloidosis. It seems likely that the affinity of amyloid to the skeletal muscles is variable in AL-type, probably depending on the molecular heterogeneity of AL protein, is low in prealbumin-type, and is almost absent in AA-type.
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PMID:Skeletal muscle amyloid deposition in AL- (primary or myeloma-associated), AA- (secondary), and prealbumin-type amyloidosis. 338 35

We report a unique case of meningeal involvement of multiple myeloma in a 49-year-old man. The patient developed weakness late in the course of his disease, and a computed tomographic scan revealed intracranial masses. At postmortem examination these tumors were the predominant extramedullary manifestation of the patient's anaplastic myeloma. To our knowledge this is the first case of intracranial myeloma composed of multiple, discrete masses.
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PMID:Multiple myeloma with unusual intracranial manifestations. 375 31

Weakness and stiffness appeared in a 65-year-old man affected by multiple myeloma. Muscle fibre conduction velocity was recorded in situ in the biceps brachii and found to be significantly decreased. Muscle biopsy, performed in the same muscle, showed amyloid deposition and moderate atrophy of muscle fibres, which was not sufficient to explain the reduction in muscle fibre conduction velocity. The results of the study suggest that amyloid interferes with conduction along the sarcolemma and that this plays a pathogenetic role mainly in the early stages of the disease.
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PMID:Early sarcolemmal dysfunction in skeletal muscle amyloidosis. 381 87

Diffuse skeletal muscle enlargement appeared in a 62 years old male without any detectable endocrine disturbance. The patient's weakness contrasted with his athletic appearance. There was no myotonia nor fasciculations. The laboratory investigations were unrevealing until 18 months after the apparent beginning of the disease: free kappa light chains in serum and urine and plasmocytosis in the bone marrow established the diagnosis of multiple myeloma. No amyloid infiltration was observed on the biopsied tissues: skin, muscle and tongue. The diameters of the muscle fibers were at the upper limit of the normal range. There was no fiber type grouping. Kappa light chain deposits surrounding the muscle fibers and numerous coated vesicles beneath the sarcolemmal membrane were found by electron microscopy. The patient's serum was tested on human muscle cell cultures and displayed trophic properties for these cells. This effect was not due to an acceleration of the myoblast proliferation, but to an enhancement of their differentiation. The fusion was more rapid than in presence of control serum and lead to larger and highly branched myotubes. Protein synthesis was increased as demonstrated by the significantly higher 3H-leucine incorporation into the trichloroacetic-acid precipitable material. An identical trophic effect was also found with the kappa light chains purified from the patient's serum but only in the presence of normal human serum.
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PMID:[Effect of the serum of a patient affected by myeloma with diffuse muscular hypertrophy on the growth of human muscle cells in vitro]. 392 91

Neurotoxicity is a well-recognized and commonly observed side effect associated with the use of vincristine sulfate in cancer chemotherapy. The clinical manifestations of vincristine neuropathy cover a wide spectrum of peripheral neurologic dysfunctions that have been described to be reversible and cumulative in most instances (1, 2). Paresthesias, loss of tendon reflexes, and progressive weakness are the most common clinical features (3, 4). Sensory impairment, cranial nerve palsies, gastrointestinal disturbances, and autonomic dysfunctions including atonic bladder, impotence, and orthostatic hypotension may occur (5). Acute CNS complications, usually presenting as generalized seizures, are extremely rare and only a few cases have been reported which were without underlying biochemical or structural abnormalities (1, 5-9). We describe the case of a woman with multiple myeloma, who developed fulminant encephalopathy following 4 days of continuous vincristine, adriamycin, and day 1-4 pulse dexamethasone (VAD) combination therapy.
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PMID:Acute encephalopathy associated with continuous vincristine sulfate combination therapy: case report. 406 27

To investigate individual components of the humoral immune response directed against the acetylcholine receptor in experimental myasthenia, we injected monoclonal antireceptor antibody into normal rats. These antibodies were produced by cloned hybridoma lines formed by fusion of immune spleen cells with the myeloma cell line P3-X63-Ag8. Antibodies from two of seven clones induced acute experimental myasthenia, manifested by clinical weakness, decremental electromyographic response to repetitive nerve stimulation, and diminished mean amplitudes of miniature end-plate potentials (mepps): 0.55 +/- 0.02 mv (SEM) versus 0.71 mv for controls (p less than 0.001). In clinically affected animals, mepp amplitudes from the diaphragm correlated with decremental responses in the gastronemius muscle (r = -0.91, p less than 0.01). The results suggest that binding of a single antibody species to a single determinant on the acetylcholine receptor molecule is sufficient to induce acute experimental myasthenia gravis.
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PMID:Myasthenia induced by monoclonal anti-acetylcholine receptor antibodies: clinical and electrophysiological aspects. 616 99

A 51-year-old, black man presented with severe anemia and weakness. X-ray studies showed diffuse osteosclerosis involving most of his skeleton. He was documented to have similar bone changes on x-ray 5 years previously. Peripheral blood findings were suggestive of a myelophthisic anemia. Open biopsy of the iliac bone showed osteosclerotic myeloma. Secretion of abnormal protein could not be demonstrated through many examination of serum or urine. A unique finding at the autopsy was the presence of extensive erythrophagocytosis by the neoplastic plasma cells and macrophages.
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PMID:Diffuse nonsecretory osteosclerotic myeloma with extensive erythrophagocytosis. 685 68


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