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)

Using the radioactively-labeled alkaline-degraded acid-soluble fraction of amyloid ([ 125I ]DAA), we developed a radioimmunoassay for the previously described amyloid-related component of the human serum (SAA). Screening the sera of 228 normal individuals and of 297 patients with a variety of illnesses, we found that SAA is a component of all human sera, including cord blood (mean 94 plus or minus 57 ng/ml). The concentration of this component increases significantly with the aging process, reaching very high levels in the eighth and nine decades. It is also elevated in all cases of amyloidosis (except for those associated with nephrotic syndrome) as well as in many patients with myeloma, macroglobulinemia, lymphoma, carcinoma, rheumatoid arthritis, and tuberculosis. A marked increase was noted in the early stages of a variety of acute inflammatory and infectious states with a return to normal levels paralleling clinical improvement and faster than the erythrocyte sedimentation rate. The possible implications of this component in the genesis of amyloid and in the immune process are discussed.
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PMID:Variation with age and disease of an amyloid A protein-related serum component. 4 33

In a male patient with pure monoclonal IgG kappa cryoglobulin associated with the nephrotic syndrome, finger print deposits were observed in the subendothelial space and mesangial matrix of the kidney by electron microscopy. The structure was similar to a unique tubular crystal structure of IgGl kappa cryoglobulin which was reported by Bogaars et al. [1973] in the serum of a patient with multiple myeloma. It was therefore supposed that the finger print deposits in the kidney of this patient were the precipitation of the monoclonal IgG kappa cryoglobulin in serum.
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PMID:Finger print deposits of the kidney in pure monoclonal IgG kappa cryoglobulinemia. 11 89

Two patients with multiple myeloma are described in whom an unusual complication developed: pleural effusion containing myeloma cells. There are 7 previously reported cases of myeloma in the English literature with this type of effusion. Pleural effusion in myeloma may be due to plasma cell infiltration of the pleura, congestive heart failure, pulmonary embolism, nephrotic syndrome, and second neoplasms. In view of these multiple etiologies, diagnostic thoracentesis should be performed in order to treat the effusion appropriately.
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PMID:Pleural effusion in multiple myeloma. 38 71

This paper describes the detection of a paraprotein in blood or urine in 12 of 260 patients with 'idiopathic' proteinuria, most of whom presented with the nephrotic syndrome. None had myeloma at presentation and only two have developed it. Initial clinical and biochemical findings did not suggest paraprotein-associated disease, total serum globulins and individual immunoglobulin levels usually being in the normal range. In seven of the 12 cases the paraprotein was detected only after repeated analysis of serum and urine specimens over months or years. Renal histopathology varied from case to case and is described in detail; amyloid deposition did not occur in patients who excreted kappa chain Bence Jones protein and was extensive in only three. One of these eventually developed myeloma. Patients were aged 27--69 years at onset and were observed without specific therapy for up to 56 months. Glomerular filtration rate tended to decline and proteinuria persisted. All patients have now been treated by a chemotherapeutic regimen consisting of 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), cyclophosphamide, melphalan, and prednisolone, in repeated short courses. In some patients, particularly those who had kappa Bence Jones protein, there was striking improvement. Overall survival is good, eight patients being alive 17--90 months after the onset of symptoms. The importance of repeated search for paraprotein in apparently idiopathic renal disease in adults is emphasized.
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PMID:Detection, significance and treatment of paraprotein in patients presenting with 'idiopathic' proteinuria without myeloma. 68 53

The myeloma kidney is characterized by casts in the distal and collecting tubules. The glomeruli are hardly affected unless amyloidosis is present. When the glomeruli are involved, the proteinuria is nonselective and, in some cases, the whole paraprotein is excreted in the urine. Nephrocalcinosis may be present and focal myeloma cell infiltration in the interstitium is a characteristic, but inconstant, finding. The nephrotic syndrome is extremely rare; if it exists, amyloidosis should be suspected. In contrast to multiple myeloma, the glomeruli are frequently involved in macroglobulinemia of Waldenstrom. Hyaline intracapillary deposits consisting of pure IgM are a characteristic finding as is infiltration of the kidney with lymphoid cells. No characteristic lesion of the kidney has been described in the heavy-chain diseases. Mixed cryoglobulinemia associated with an IgM paraprotein can produce glomerulonephritis that is due to the deposition in the glomeruli of an immune complex consisting of IgG, IgM, and complement.
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PMID:Renal pathologic findings associated with monoclonal gammopathies. 80 64

From 1960 through 1972, 236 cases of amyloidosis with histologic proof were found. The amyloidosis was primary (without evidence of preceding or coexisting disease) in 132 cases (group 1) and associated with multiple myeloma in 61 (group 2). Secondary amyloidosis appeared in 19 cases (associated with rheumatoid arthritis or osteomyelitis in two-thirds of them). There were 22 patients with amyloid localized to a single organ (bladder, lung, skin, or larynx in more than half of them). Two patients had familial amyloidosis. In group 1 and group 2, the most common presenting symptoms were fatigue, weight loss, edema, dyspnea, light-headedness or syncope, and paresthesias. Symptoms of the carpal-tunnel syndrome were frequent. The liver was palpable in almost 50% of the series, but splenomegaly was an initial finding in less than 10%. Macroglossia was recorded in 26% of group 2 and in 12% of group 1. Enlargement of submandibular structures was noted in about 10% of cases; and purpura, particularly around the eyes, was a significant feature. Substantial numbers of the patients had carpal-tunnel syndrome, nephrotic syndrome, congestive heart failure, sprue, peripheral neuropathy, or orthostatic hypotension. Approximately 50% of patients had renal insufficiency at the time of diagnosis. Proteinuria was found in more than 90%. A monoclonal protein was found in the serum of 49% of group 1 and in 74% of group 2. Monoclonal proteins were found in the urine of 35% and 81%, respectively. Only 12% of patients in group 1 had no monoclonal protein when both serum and urine were analyzed, and all patients of group 2 had a monoclonal protein in the serum or urine when both were analyzed. Lambda light chains were more common than kappa. None of the patients in group 1 had more than 15% plasma cells in the marrow, whereas more than half of group 2 had more than 15% plasma cells. Roentgenograms showed no evidence of skeletal disease in 94% of group 1, but 50% of group 2 had skeletal abnormalities. Rectal biopsy was positive for amyloid in 84% of cases. Kidney, liver, and carpal-tunnel biopsies were positive in 90% or more. Follow-up of all 193 patients in groups 1 and 2 revealed that 80% of group 1 and 97% of group 2 had died. The median survival was 14.7 months in group 1 and 4 months in group 2. Cardiac failure was the most common cause of death, accounting for 30% of the fatalities. We also reclassified all cases by the method of Isobe and Osserman (105), which is based on clinical patterns: pattern I--principal involvement of tongue, heart, gastrointestinal tract, muscle, nerves, skin, and carpal ligaments; pattern II--principal involvement of liver, spleen, kidneys, and adrenals; and mixed pattern I and II. This analysis failed to reveal predictive value in the clinical pattern classification, and did not discern the survival differences between primary amyloidosis (group 1) and amyloidosis with myeloma (group 2). Consequently, for the present we prefer the classification used in this study.
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PMID:Amyloidosis: review of 236 cases. 115 71

A 45-year-old man developed in 1965 skin lesions on cold exposure and was found to have cryoglobulinemia due to an M-component of IgG class. Glomerular damage was first noted in 1970, and progressed to renal impairment and nephrotic syndrome during the next two years. Reduced serum levels of complement components C3 and C4 were found, indicating in vivo complement activation. Renal biopsy revealed proliferative glomerulonephritis and deposition of IgG and C3 along the glomerular basement membrane. Electron microscopical examination revealed a striking deposition of a 'fibrillar' or microcrystalline material in the glomerular basement membrane. This material had an ultrastructure similar to that found in the cryoprecipitate from serum. There were no tubular changes of myeloma type, neither were there any monoclonal light chains detected in the urine. So far, there are no other signs of myeloma or lymphoma. Immunosuppressive treatment with prednisone and cyclophosphamide resulted in a decrease in the serum M-component as well as a decrease in protein leakage through the glomeruli and a return to normal of glomerular filtration rate. The finding of monoclonal cryoglobulinemia, demonstrable at room temperature, in a patient developing proliferative glomerulonephritis with complement activation is unusual. It is probably that the M-component is causally related to the glomerular lesions.
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PMID:Monoclonal IgG cryoglobulinemia with secondary development of glomerulonephritis and nephrotic syndrome. 117 19

Thirty-four patients with primary generalized amyloidosis (PGA) and 14 with multiple-myeloma-related amyloidosis (MRA) were studied. The commonest clinical manifestations in PGA were nephrotic syndrome, hepatomegaly and congestive heart failure, and in MRA, low back pain, plasmacytoma and rheumatoid-arthritis-like syndrome. Eight patients with PGA had limited clinical expression of the disease, such as involvement of only kidneys, joints, parotid glands or gastrointestinal tract; in one patient amyloidosis was limited to lymph nodes. Low serum concentrations of total protein and albumin were common. M components were detected in the serum of 91% of patients with PGA and 92% of patients with MRA: 70% of the M components in PGA and 25% of those in MRA had lambda light chains. Bence Jones proteinemia was detected in 56% of the patients with PGA and in 77% of those with MRA. The serum concentration of immunoglobulins was decreased substantially in more than two thirds of the patients with PGA. Proteinuria (greater than 250 mg/24 h) was observed in 78% of patients with PGA and in 93% of patients with MRA. Bence Jones proteinuria was noted in 75 and 77% of patients, respectively. Plasmacytic infiltration of the bone marrow was found in 90% of the patients with PGA. The mean survival time of the patients with PGA was 28 months and of those with MRA, 29 months from the time of diagnosis.
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PMID:Clinical and laboratory findings in primary generalized and multiple-myeloma-related amyloidosis. 126 76

A patient with nephrotic syndrome secondary to renal amyloidosis was consistently observed to have serum anion gap levels as low as -1 mEq/L and averaging approximately 2 mEq/L. Neither multiple myeloma nor extreme hypertriglyceridemia was present, and the patient's serum albumin concentrations were not low enough to depress the anion gap to this degree. An increased serum bromide level (below the range expected to produce clinical toxicity) was the apparent cause of the low anion gap. The patient's parents, who live in the same apartment, also manifested low anion gaps and inexplicably elevated serum bromide levels. Despite detailed investigation, no environmental or pharmacologic source of bromide was uncovered. Although the source of the bromide in the present instance remains elusive, this report illustrates the necessity to measure serum bromide when a low anion gap cannot be explained by other factors, even when there is no history to suggest bromide exposure.
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PMID:Low anion gap resulting from unexplained exposure to bromide in a patient with renal amyloidosis. 130 42

A 67-year-old man was hospitalized with a diagnosis of nephrotic syndrome. Physical findings at admission were generalized edema and macroglossia. Urinalysis showed massive proteinuria, + +occult blood, and granular and broad casts. Ig A lambda monoclonal gammopathy was noted in the serum. There was no evidence of myeloma in the bone marrow aspirate, scintigram or X-ray of the bone. A biopsy specimen of the kidney showed massive deposits of structureless material in the glomeruli. Marked cell infiltration was also observed in the interstitium. Multinucleated giant cells were occasionally seen in the Bowman's capsules and the interstitium. There were reactive changes in the Bowman's capsule adjacent to the giant cell. The deposits were proved to be amyloid by positive staining with Congo red and apple-green birefringence by polarized light. In addition, microfibrills seen on electron microscopy displayed deposits. Amyloid depositions were observed in other tissues such as gingiva, skin and tongue. Staining of amyloid with Congo red was resistant to potassium permanganate, and amyloid was positively stained with lambda-light chain of immunoglobulin. These findings indicated that the patient had primary amyloidosis. Infiltration of the multinucleated giant cell has been reported only in patients with familial amyloidosis and secondary amyloidosis associated with rheumatoid arthritis. To our knowledge the present case is a first report of the giant cell infiltration in a Bowman's capsule in primary amyloidosis.
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PMID:[A case of primary amyloidosis associated with giant cell infiltration within a Bowman's capsule]. 147 13


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