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 48 year old male patient presented with xanthomatosis, hyperbeta lipoproteinemia and hyper-IgA globulinemia; these two serum components occurred as a "complex." The patient has subsequently been studied for 22 years (1952 to 1974). His serum cholesterol and triglyceride levels have been consistently and excessively high despite efforts to regulate them by means of diet or diet and drugs. Serum immunoglobulin A (IgA) concentration ranged from 1,400 to 3,400 mg/dl compared with a normal value of 156 plus or minus 92 mg/dl. The metabolism of lipoproteins, judged by vitamin A turnover studies was slow. Peripheral atherosclerosis became evident 15 years after beginning the study whereas cinecoronary arteriography concurrently demonstrated only minimum changes. Xanthomas exhibited marked regression only during the last 6 years, after 16 years of diet and the addition of clofibrate for 7 years. Beta lipoprotein and IgA globulin determined by immunofluorescent and immunoelectrophoretic technics were demonstrated in the atherosclerotic material obtained from the patient's arterial wall. They were also found in the plasma cells of the bone marrow. The IgA globulin-beta lipoprotein complex in the serum was broken with difficulty. The patient's isolated IgA globulin, free of lipoprotein, formed a firm complex when mixed with beta lipoprotein prepared from normal human serum. Initially, IgA globulin studies showed presence of both kappa and lambda light chains in normal proportion. But after 18 years, the IgA globulin has become monoclonal, type lambda. The plasma cells of the bone marrow have become progressively more atypical and immature. No clinical indications of multiple myeloma have been found. It is concluded that association of lipoproteins with IgA globulin in the serum of this patient with hyperlipidemia, hyper-IgA globulinemia did not prevent the development of atherosclerotic lesions and the deposition of lipids and lipoproteins in the plaques. It is possible that the lipoprotein-immunoglobulin association may have retarded the process, since it became manifest only after many years of known hyperlipidemia.
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PMID:Autoimmune hyperlipidemia in a patient. Atherosclerotic course and chaning immunoglobulin pattern during 21 years of study. 16 71

A case of plane xanthomatosis associated with multiple myeloma and hyperlipoproteinaemia in a 62-year-old woman is reported. The patient had IgG type lambda paraproteinaemia and type II A hyperlipoproteinaemia. The IgG paraprotein showed binding activity against high-density lipoprotein. It could not be demonstrated that these paraprotein-lipoprotein complexes were responsible for the hyperlipidaemia. Microchemical analysis of pathological skin demonstrated a high content of triglycerides, similar to that in eruptive xanthomata. No correlation was found between the lipid composition of the xanthomatous skin and the serum lipid composition. The results obtained with an in vitro culture method showed that the paraprotein present in the patient's serum was synthesized in the bone marrow but not in the normal or pathological skin.
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PMID:Plane xanthomata associated with multiple myeloma and hyperlipoproteinaemia. 17 8

Human LDL were bound and internalized by cultured human fibroblasts. When an antilipoprotein IgA kappa from a case of myeloma with hyperlipidemia and xanthomatosis was introduced into the system, LDL uptake dropped by 50% but LDL binding to fibroblasts was unchanged. In the same system, IgG and IgA controls were inactive.
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PMID:In vitro interaction of LDL, anti-lipoprotein IgA and human fibroblasts. 21 34

LDL interact with fibroblasts through specific membrane sites. This reaction is the first step of a mechanism which leads to the regulation of intracellular cholesterol synthesis. When LDL form a complex with an IgA from a myeloma serum with mixed hyperlipidemia and xanthomatosis, they no longer function as a regulator, and the result is excess production of free intracellular cholesterol. No excess cholesterol production is observed when myeloma IgA is replaced by control IgG and IgA.
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PMID:Cholesterol synthesis by human fibroblasts in the presence of LDL and anti-LDL IgA. 22 98

Clinicopathologic findings are reported of a woman with generalized plane xanthoma, multiple myeloma (IgG type K), and hyperlipemia with very high levels of serum cholesterol and triglyceride. Complexing of the serum lipoproteins and immunoglobulins had cryoglobulin properties and was separable by ultracentrifugation. Immunofluorescent studies of skin and bone marrow demonstrated deposits of IgG with low density lipoprotein apoprotein and IgG with beta-lipoprotein, respectively. Although immunosuppressive therapy resulted in return of serum IgG, lipid, and lipoprotein levels to normal, the patient died from the myeloma. Serum lipoprotein-paraprotein complexes have been demonstrated in at least 20 other cases of cutaneous xanthomatosis and myeloma. This interaction may result in an autoimmune hyperlipemia.
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PMID:Plane xanthoma and multiple myeloma with lipoprotein--paraprotein complexing. 34 19

Investigations performed in a patient with myeloma, hyperlipidemia, and xanthomatosis demonstrated the antilipoprotein activity of the monoclonal IgA directed against an antigenic site--called Ra.--different from those previously described. A complex IgA beta-lipoprotein has been firstly characterized. After isolation and purification of the IgA, it has been shown that the association between IgA and lipoprotein was immunologically mediated. The antibody is an IgA lambda bound via its Fab portion and in fixed combining ratio to an antigenic determinant shared only by LDL and VLDL of humans and some other mammalians to the exclusion of any other serum proteins. The results obtained with passive hemagglutination and inhibition of hemagglutination suggest that the antigenic site Ra. is not located on apoprotein B (major proteic moiety of LDL and VLDL), since the antigenic determinants of apolipoproteins are different in humans and in animals and since IgA Ra. fails to react with apolipoprotein B obtained by delipidation of LDL. On the other hand, the lack of reaction between IgA Ra. and HDL suggests that the antigenic determinant is not only present on the lipid hapten such as in the case of PG and AS determinants which are located on VLDL, LDL, and HDL from humans and animals. So the antigenic determinant revealed by IgA Ra. seems to be different from those previously described.
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PMID:[Monoclonal myelomatous IgA with antilipoprotein antibody activity of Ra specificity (author's transl)]. 51 6

Studies were carried out in two patients with multiple myeloma (immunoglobulin G, [IgG], K light chain), cryoglobulinemia and xanthomatosis with clinical features and lipid transport abnormalities which were quite different. One patient had nodular xanthomatosis and lipemia with delayed triglyceride and apolipoprotein removal. In vivo heparin resistance was present and heparin-paraprotein interaction was shown in vitro. The lipoprotein removal defect may have been due to impaired uptake of the "remnants" of glyceride-rich lipoproteins. Abnormalities were found both in primary platelet aggregation and in the platelet release reaction. The second patient had diffuse plane xanthomatosis with normal lipids. An orange cryoprecipitate contained IgG, beta- and prebeta lipoproteins, albumin, carotenoids and about half of the serumcholesterol. Triglyceride turnover was normal. These observations show that M-proteins may interfere with lipid transport by at least two mechanisms and illustrate the clinical diversity of xanthomatous myeloma.
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PMID:Multiple myeloma, cryoglobulinemia and xanthomatosis. Distinct clinical and biochemical syndromes in two patients. 120 39

The Authors describe the case of a woman affected by generalized plane xanthoma and IgG multiple myeloma with k type immunoglobulins. The association between the two affections is well known. The antilipoprotein activity of the paraprotein has been proved in some cases, associated or not to hyperlipemia. The pathogenetic mechanism of plane xanthoma formation is described briefly. The possible occurrence of plane xanthoma with multiple myeloma is stressed, along with the possible association with other systemic diseases.
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PMID:[Normolipemic plane xanthomas and IgG-k multiple myeloma. Description of a clinical case]. 212 22

We studied a 58-year-old woman with severe therapy-refractory hyperlipidemia, xanthomatosis, and multiple myeloma (immunoglobulin A, lambda light chain). The lipid disorder became evident about half a year prior to the expression of myelomatosis. Clinical symptoms were similar to those found in classical type III hyperlipoproteinemia but the underlying metabolic defect was different from the one described in this primary dyslipoproteinemia. The patient has the heterozygous apolipoprotein E3/2 phenotype and her VLDL-cholesterol/serum-triglyceride ratio is unusually low at 0.05. Evidence is given that the hyperlipoproteinemia is due to an impaired catabolism of intermediate density lipoproteins probably because of a reduced hepatic triglyceride lipase activity.
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PMID:Atypical type III hyperlipoproteinemia in a patient with Ig A myelomatosis. 237 70

Automated methods, with and without cyanide (+CN and -CN), for whole blood hemoglobin (Hb) determination were evaluated on the Technicon H*1TM System. Both automated Hb methods were linear over the range 0-250 g/L (0-25 g/dL) and correlated well with the International Committee for Standardization of Hematology (ICSH) reference method and with the Coulter S+II. Both methods quantitatively converted whole blood containing up to 100% carboxyhemoglobin in less than 24 seconds to their respective end products. With respect to abnormal samples (sickle cell anemia, multiple myeloma, and hyperlipemia), both H*1 methods gave Hb results that were equivalent to the (postfiltration) ICSH method. For samples with white blood cell (WBC) counts less than 36 X 10(9)/L, the +CN method was equivalent to the (postfiltration) ICSH method, whereas for WBC counts greater than 20 X 10(9)/L, the -CN method showed acceptable recovery of the mean but unacceptable imprecision. For WBC counts of 36-164 X 10(9)/L, the +CN method yielded acceptable Hb recovery with unacceptable imprecision. Hyperlipemia, resulting from addition of Intralipid directly to the blood samples, caused large errors in both H*1 methods.
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PMID:Evaluation of 24-second cyanide-containing and cyanide-free methods for whole blood hemoglobin on the Technicon H*1TM analyzer with normal and abnormal blood samples. 277 49


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