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)

Metastatic pulmonary calcinosis is a rare complication seen in malignancies accompanied by hypercalcemia, or chronic renal failure. We reviewed the clinicopathological findings of 8 cases of metastatic pulmonary calcinosis accompanied malignancy revealed at autopsy. The underlying diseases were malignant lymphoma in 3 cases (adult T cell lymphoma in 2 cases), multiple myeloma in 2, lung cancer in 2, and acute myelocytic leukemia in 1, all cases were complicated by hypercalcemia and renal failure. Chest X-ray revealed almost normal findings in 2 cases, bilateral diffuse infiltrates in 4, bilateral infiltrates in the apex in 1, and right atelectasis in 1. Bone scintigraphy was performed in 4 cases, and revealed warm pulmonary uptake in 1 patient with multiple myeloma and 1 with lung cancer, but normal findings in the 2 other cases. Histopathological examination revealed diffuse alveolar septal edema and fibrosis due to calcium deposition, which were considered to be the cause of respiratory failure. Metastatic pulmonary calcinosis is a rare but a serious complication in malignancies accompanied by hypercalcemia and renal failure, and bone scintigraphy seems to be a useful method for its diagnosis.
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PMID:[Clinicopathological features of metastatic pulmonary calcinosis with malignant neoplasm]. 175 31

A 58-year-old female was admitted to our hospital because of anemia in March 1987. Monoclonal protein (IgA, kappa) was detected and a diagnosis of multiple myeloma was made. Partial remission was obtained after VAD therapy with alpha-interferon. In December 1989, she was readmitted because of a pathological fracture of the left humerus. A white blood cell count was 4400/microliters with 30% myeloma cells and the urine protein (Bence Jones protein) was 26 g/day. Systemic chemotherapy was not effective. She developed pleural and pericardial effusions, bone mass, disturbance of consciousness and died of respiratory failure only 3 months after readmission. The pleural and pericardial fluids contained many myeloma cells. c-myc gene rearrangement was detected in myeloma cells obtained from the pleural fluid using c-myc exon1 and exon2 probes. The levels of interleukin-6 (IL-6) measured by ELISA was 107.4 pg/ml in serum, 56.2 pg/ml in pleural fluid and 780.0 pg/ml in pericardial fluid. Because of the lack of any overt infectious focus, the level of IL-6 appears to have been related to aggressive proliferation of myeloma cells. It was of interest that C-reactive protein, induced by IL-6, was a good marker reflecting disease activity.
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PMID:[A high serum level of interleukin-6 in a patient with aggressive multiple myeloma]. 175 53

A case of multiple myeloma with diffuse metastatic calcinosis of the lung is presented. The patient was a 60-year-old male with IgA-kappa-myeloma who developed renal failure and hypercalcemia. Multiple small nodular shadows were observed both in plain chest films and CT films. The patient died of progressive respiratory failure. Postmortem examinations showed pulmonary infiltrations and massive pulmonary calcifications. Small nodular shadows were due to diffuse calcium deposits which were observed in and around the alveolar basement membranes of both the bronchioles and the blood vessels. It is generally believed that pulmonary calcinosis may not be detected by routine chest films; however, the nodular shadows observed in our patient seem to be pathognomonic and may indicate the severity of calcinosis.
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PMID:[Case report of multiple myeloma associated with diffuse pulmonary calcinosis]. 177 Jun 90

Ten patients with severe hematologic malignancies (four with acute leukemia, three with multiple myeloma, one with prolymphocytic leukemia, one with malignant lymphoma and one with blastic crisis of chronic myelogenous leukemia) developed respiratory failure during the period between April 1986 and May 1990. Clinically, the patients manifested high-fever, dyspnea refractory to oxygen therapy, diffuse pulmonary rales and severe hypoxemia without evidence of cardiogenic pulmonary edema. Chest roentgenograms displayed diffuse alveolar infiltrates. Respiratory failure occurred as early as 48 hours and as late as 66 days after the administration of intensive anti-neoplastic chemotherapy. At that time leukocyte count was between 100/microliters and 54,900/microliters. Marked leukocytosis was observed in two patients with AML and PLL. Respiratory failure was preceded by sepsis in one patient with AML and by pneumonia in nine patients. DIC was diagnosed in four patients. All patients treated with high dose methyl prednisolone (mPSL) within 12 hours after the onset of respiratory failure. Only one patient required assisted ventilation. High dose mPSL had significant effect on seven of ten patients. But three patients died from progressive respiratory failure, sepsis, pneumonia and multi-organ failure.
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PMID:[Clinical investigation on acute respiratory failure in patients with severe hematologic malignancy]. 194 22

A 78-year-old man was admitted because of lumbago and chest pain. A diagnosis of non-secretory primary plasma cell leukemia was made based on the laboratory findings and his history. However, the plaque-forming cells assay of bone marrow cells revealed secretion of monoclonal immunoglobulin from the myeloma cells. Hyperammonemia was detected in the serum. Although the patient was treated with 4 courses of combination chemotherapy (vincristine, adriamycin, cyclophosphamide, methylprednisolone), he died of respiratory failure five months after diagnosis. Autopsy showed widespread multiple myeloma and prominent infiltration of myeloma cell in the sinusoid of the liver. Recently, there have been a few reports which increased the plasma ammonia concentration with multiple myeloma. This report strongly suggested that liver infiltration of myeloma cell caused hyperammonemia.
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PMID:[Non-secretory primary plasma cell leukemia with hyperammonemia]. 206 85

A 63-year-old man was admitted to our hospital with a chief complaint of general malaise in March 1986. A diagnosis of Bence Jones protein (kappa) type of multiple myeloma was made from increased atypical plasma cells in the bone marrow, urinary BJP (kappa) and osteolytic lesions. Urinary BJP (kappa) was decreased by MP and VENP therapies. In April 1987, he visited us again with the complaint of pain on the left shoulder. An examination revealed multiple osteolytic lesions and bilateral pleural effusion containing atypical plasma cells. Jaundice was developed at the end of July 1987. An ultrasound examination revealed a hypoechoic mass in the area of pancreatic head. The effusion was gradually increased without response to the treatment. He died of respiratory failure on July 31, 1987. On autopsy, extramedullary plasmacytoma was found in the head of pancreas. It was a rare case of multiple myeloma in which pleural effusion and multiple plasmacytomas, and finally obstructive jaundice were developed although urinary BJP (kappa) was reduced by treatment.
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PMID:[Multiple myeloma causing obstructive jaundice by extramedullary plasmacytoma after Bence Jones protein loss--an autopsy case report]. 217 1

Hybridoma cells were obtained by fusing spleen cells from mice, immunized against the 15 kDa porcine surfactant apoprotein, with a myeloma cell line. Adult mice were inoculated intraperitoneally with this hybridoma; mice that were not inoculated or were inoculated with myeloma cells served as controls. Lung-thorax compliance was measured at various intervals after inoculation. The animals were then killed for histologic-morphometric evaluation of alveolar air expansion, inflammatory reaction in the pulmonary parenchyma, and intraalveolar edema. In the hybridoma group, the mice developed respiratory failure 9 days after inoculation, with markedly reduced lung-thorax compliance, lung congestion, alveolar collapse, hemorrhagic pulmonary edema, and hyaline membranes. Morphometric data from the same animals showed reduced volume density of alveolar air, and increased volume densities of intraalveolar "fluid" (edema) and tissue components. These lung lesions are similar to those in the adult respiratory distress syndrome.
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PMID:Respiratory failure in mice caused by a hybridoma making antibodies to the 15 kDa surfactant apoprotein. 339 79

Plasmapheresis and irradiation of the tumor were performed in conjunction with prednisolone therapy to a severe case of polyneuropathy associated with a solitary sclerotic secreting myeloma and endocrinological abnormalities. The patient was 27-year-old male with progressive history of polyneuropathy of seven months duration. On admission, he was quadriplegic with cranial nerve involvements. Pitting type of generalized edema, skin pigmentation and sensory impairment were also present. Respiratory failure occurred soon after the admission. Plasmapheresis lowered the level of M protein but failed to improve clinical course in the short term. On the other hand, prompt amelioration of clinical symptoms followed the irradiation of the tumor. It is difficult to prove clinical effects of plasmapheresis upon symptoms of chronic polyneuropathy. It is suggested that some humoral factor of myeloma might attribute to this syndrome and secreted at higher rate than our plasmapheresis but easily suppressed by the irradiation of the tumor. We suppose that radiation therapy could be the treatment of the first choice for such a severe case like ours. However, further experiences of plasmapheresis of this syndrome are necessary to determine the effect of plasmapheresis. Some other etiological aspects are also discussed.
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PMID:[Polyneuropathy associated with plasma cell dyscrasia and endocrinological abnormalities--a trial of plasmapheresis]. 640 62

Pathologic flail chest complicated the initial presentation of multiple myeloma in two patients. Both had severe hypercalcemia and diffuse bone disease. Atelectasis and pulmonary edema preceded the appearance of flail chest in one patient; atelectasis complicated the flail chest in the second patient and increased the severity of the flail. Both were treated with radiotherapy and chemotherapy. However, delay in stabilizing the first patient's chest wall with positive airway pressure was followed by extension of the flail chest and irreversible respiratory failure. On the other hand, prolonged stabilization of the chest wall in the second patient until a chemotherapy-induced remission occurred was associated with resolution of the flail chest.
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PMID:Pathologic flail chest complicating multiple myeloma. 736 61

A 57-year-old male patient with multiple myeloma showed an aggressive course with characteristic clinical features: rapid progression of plasmacytoma in the thoratic cavity, high serum levels of lactate dehydrogenase (LDH), which is usually not elevated in myeloma patients, and neutrophil infiltration in pleural effusion. Despite treatment with vincristine, doxorubicin and dexamethasone, the tumor mass had become non-responsive to chemotherapy and been increasing in size in correlating with the increase of serum levels of LDH. The patient died of respiratory failure 4 months after treatment. Thus the serum level of LDH is thought to be a useful clinical marker to monitor disease activity as well as other markers such as monoclonal immunoglobulin and beta 2-microglobulin. To investigate the cause of neutrophil infiltration into pleural effusion, we cultured plasma cells obtained from the effusion for 3 days in serum-free medium and examined the activity of neutrophil chemotaxis in the culture supernatant. The results showed chemotactic activity in the supernatant as high as in positive controls stimulated with a chemotactic factor, formyl-methionyl leucyl phenyl-alanine, suggesting that tumor cells produced neutrophil chemotactic factor(s).
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PMID:[Drug-resistant multiple myeloma with high serum levels of lactate dehydrogenase and neutrophil infiltration in pleural effusion]. 813 2


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