Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024530 (malaria)
44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Membranous nephropathy (MN) accounts for about 20 percent of cases of the nephrotic syndrome. The importance of renal biopsy in establishing the diagnosis is emphasized. In the great majority of MN patients, no etiologic factor can be discerned. In a significant minority, MN appears to be a manifestation of sarcoidosis, diabetes, lupus, syphilis, malaria, or toxicity from heavy metals or drugs. In some cases the "cause" is neoplasia (including lymphoma) or a viral infection. Massive proteinuria, hypoproteinemia and edema are the principal manifestations of MN, finally resulting in renal failure. Treatment consists chiefly of diet and diuretic drugs. In the more pronounced cases, corticosteroids may have a favorable effect and in very resistant cases, cyclophosphamide is indicated. Judicious use of these modalities if often associated with the diminution or disappearance of the clinical signs of MN.
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PMID:Membranous nephropathy: an overview. 120 87

In a study of connective tissue and infectious disease sera, we have demonstrated IgM and IgG anti-cardiolipin activity, in a solid phase radioimmunoassay, in systemic lupus erythematosus (SLE), rheumatoid arthritis, syphilis and in acute malaria caused by four different species of Plasmodium. The highest values were noted in SLE (IgM anti-cardiolipin P less than 0.005, IgG anti-cardiolipin P less than 0.01), but there was no correlation with anti-dsDNA, rheumatoid factor or VDRL titres in any disease group. Anti-cardiolipin binding was significantly associated with the lupus anticoagulant, thrombocytopenia, spontaneous abortions and thromboses in the SLE patients. Ten SLE sera from this thrombotic subset and 10 syphilitic sera with similar anti-cardiolipin activity, were tested against four phospholipid antigens and showed significantly different anti-phosphatidyl ethanolamine/anti-phosphatidyl serine binding ratios (P less than 0.001). These differences in phospholipid epitope specificity could explain the specificity of the VDRL antigen in syphilis serology, and we discuss a putative role for anti-phosphatidyl serine in the thrombotic diathesis of SLE.
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PMID:Anti-phospholipid antibodies in syphilis and a thrombotic subset of SLE: distinct profiles of epitope specificity. 257 56

Sera from 16 patients with falciparum malaria, 16 patients with vivax malaria and 31 patients with leprosy were tested for autoantibodies to intracellular proteins and nucleic acids. Precipitating antibodies to soluble protein extracts were not detected in any serum. Sera from malaria patients showed prominent immunofluorescence staining of the HEP2 nuclear membrane as well as frequent 75% (24/32) and intense Western blot reactivity. In contrast, only 20% and 36% of patients with leprosy had positive immunofluorescence or positive immunoblots respectively, and reactivity was weak in most cases. Neither the malaria nor leprosy sera contained autoantibodies with specificities similar to the characteristic lupus autoantibodies such as double stranded DNA (dsDNA), Ro/SSA, La/SSB, Sm, RNP and P proteins. Low levels of antibodies to single stranded (ssDNA) were however found in 11 (34%) malaria sera and in seven (23%) leprosy sera. Thirteen percent of patients with leprosy had anti-histone antibodies. These findings demonstrate considerable differences in the capacity of infectious agents to induce autoantibodies and also the infrequency with which autoantibodies characteristic of idiopathic systemic lupus erythematosus are induced.
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PMID:Comparison between autoantibodies in malaria and leprosy with lupus. 332 2

Chloroquine is a drug used mainly as an anti-malaria agent with many other pharmacological properties. It was given to a patient with chorea and disseminated lupus erytematosus seeking the anti-inflammatory effect of the drug. The unexpected result on chorea hastened its use in 7 other patients with the same success. Chloroquine seems to be an effective drug for the relief of chorea. The mechanism of action is unknown.
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PMID:[Chorea and chloroquine. A new treatment for an ancient malady]. 732 46

Dapsone is used to treat several systemic inflammatory diseases, many of which have head and neck manifestations, such as leprosy, systemic lupus erythematosus, rhinosporidiosis, relapsing polychondritis, dermatitis herpetiformis, pemphigus vulgaris and bullous pemphigoid. It has also been recently used prophylactically alone or in combination against malaria and in AIDS patients against Pneumocystis carinii infections. This is significant to the otolaryngologist-head and neck surgeon since approximately 40% of AIDS patients will have head and neck manifestations. Thus, the likelihood that otolaryngologists will be treating patients who are taking dapsone regularly is significant. We present a case of a 16-year-old female who presented with a presumptive diagnosis of discoid lupus for biopsy confirmation of her disease. Induction of general anesthesia was complicated by methemoglobinemia, an uncommon side effect of dapsone. We will discuss recognition and prevention of this side effect, its potential anesthetic implications, complications and treatment.
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PMID:Dapsone-induced methemoglobinemia: an anesthetic risk. 755 44

The epidemiology of SLE in people of African origin clearly varies from one geographical setting to another. It appears to be very rare in West Africa, increasing in frequency in Central and Southern Africa, and of high frequency in America, the Caribbean and Europe. Whether this is predominantly genetic or environmental may be difficult to unravel. Most African-Americans and Caribbeans came from West Africa, where SLE is now rare. This might suggest that environmental factors are more important. However, in the generations since the first Africans arrived in the Americas there has been considerable genetic admixture and this may have lead to increased susceptibility to lupus. Conversely, the increase in SLE may be explained by a reduction in exposure to malaria in most parts of the world except West Africa.
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PMID:Frequency of lupus in people of African origin. 765 86

Malaria infection is accompanied by the production of a number of autoantibodies, including some that react with DNA. Epidemiological evidence implicates these in the nephritides that arise in human quartan malaria and in experimental malaria infections in mice. Through parallels with the involvement of DNA-reactive antibodies in the autoimmune syndrome systemic lupus erythematosus, a role for DNA-reactive antibodies in forming phlogistic immune deposits in the kidneys is implied. To more fully understand the relationship between antibodies of this specificity made in malaria and systemic lupus erythematosus, we prepared monoclonal DNA-reactive antibodies from BALB/c mice infected with Plasmodium berghei (clone RC) and compared their properties with those of other antibodies previously isolated from lupous MRL/Mp lpr/lpr and (NZB x NZW)F1 mice. Antibodies from malarial mice were all immunoglobulin M class and bound to single-stranded but not double-stranded DNA in an enzyme-linked immunosorbent assay. They also reacted with synthetic polyribonucleotides in the enzyme-linked immunosorbent assay and with parasitized erythrocytes and parasite pigment in kidney sections. None of the antibodies from lupous mice had identical specificities. The potential involvement of the DNA-reactive antibodies in malarial nephritis was demonstrated, by use of immunocytochemical methods, on the basis of their binding to existing immune deposits in kidney sections from malarial mice, a similar property having been previously demonstrated for antibodies from lupous mice. Furthermore, antibodies from malarial mice expressed public idiotypes, notably Id.V-88, which is a member of the Id.16/6 family, commonly found on DNA-reactive antibodies in lupus and other infectious and connective tissue diseases. This study indicates that DNA-reactive antibodies in malaria have immunochemical properties similar but not identical to those of such antibodies in systemic lupus erythematosus and that they have the potential to participate in the formation of immune deposits in nephritic malarial kidneys.
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PMID:Characterization and pathological significance of monoclonal DNA-binding antibodies from mice with experimental malaria infection. 816 66

What were first called simply false-positive Wassermann reactions and then lupus anticoagulant are now known as antiphospholipid or anticardiolipin antibodies (ACA). These are known to cause a tendency to thrombosis and are frequently present in many neurological conditions and infections. The pathological significance of these antibodies in acute infections, if any, is unknown. We investigated the presence of these antibodies in Plasmodium falciparum malaria in an endemic area in Natal/KwaZulu, and attempted to correlate the presence of this antibody with cerebral manifestations. Immunoglobulin G-anticardiolipin antibodies measured by enzyme-linked immunosorbent assay occurred significantly more frequently in 62 patients with acute Plasmodium falciparum malaria (33.9%) than in 37 control subjects (2.7%) (P < 0.0001). There was no significant difference in the mean parasite loads in those patients who were positive for ACA (1.75%) and those who were negative (1.59%) (P = 0.83). No correlation was found between parasite load and ACA levels in the patient group, or between the number of cerebral manifestations in patients with and without the antibody. The frequency of splenomegaly was not significantly different in patients with and without ACA (P = 0.06). We conclude that there is a high prevalence of ACA in acute falciparum malaria. The pathological significance of this antibody and its relationship to complications, especially cerebral ones, warrant greater attention and may improve the understanding of cerebral malaria and its management.
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PMID:Are anticardiolipin antibodies responsible for some of the complications of severe acute Plasmodium falciparum malaria? 831 Mar 60

B cell deficient animals obtained by various strategies of gene targeting were used to study the B cell development and examine the role of different immune compartments in the immune response to microbes. Study of muMT, JHD, lambda 5T and JHT models of B cell deficiency, was essential in order to understand the role of pre-B cell receptor in B cell development, allelic exclusion and variable gene rearrangement regulation. In the immune response to influenza virus, a protective role of T cells in a total absence of B cell compartment, was revealed by studying the JHD -/- model. Further, it was established that a T cell compartment is sufficient to mediate the recovery from influenza infection. Examination of immune response in muMT and JHD models of definitive B cell deficiency to various blood stage Plasmodia species, showed that whereas B cells are not required for recovery from infection with P. chabaudi adami, P. vinckei petteri and P. chabaudi chabaudi (CB), B cell compartment is important in the later stages of infection with P. chabaudi chabaudi (AS). Studies carried out in muMT model suggested a possible role for T gamma delta subpopulation in the immune response to blood stage malaria parasite. B cell deficiency models are valuable for understanding the normal and pathological immune response. Studies carried out in muMT model indicated that T cell responses are not significantly affected in the absence of B cells. These data can neither rule out a role for B cells in T cell priming, nor in triggering an effective T cell help for humoral response. Study of double homozygous mice deficient for B cells and FAS or IL-2 gene, pinpointed the role of B cells in pathogenesis of lupus-like nephritis and vasculitis from lpr mouse and in hemolytic anemia from IL-2 -/- mouse model, respectively.
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PMID:Immunoglobulin deficient mice generated by gene targeting as models for studying the immune response. 888 29

Vibrio vulnificus infection with septicemia is a life threatening disease in the immunocompromised hosts. Renal involvement has not been documented. We reported herein 8 patients with V. vulnificus septicemia. All were immunocompromised hosts. Four patients had cirrhosis of the liver, 3 were heavy alcohol drinkers and one had systemic lupus erythematosis. Presenting symptomatology included fever, chills, leg pain and skin rash. Renal failure was observed in 6 patients. Four patients died shortly after admission. Two survived with clinical course of tubular necrosis. Renal failure is therefore common in V. vulnificus infection. This should be brought to attention, and vigorous antibiotic treatment is required. The disease may be confused with leptospirosis, scrub typhus, malaria and other forms of sepsis which also present with renal failure.
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PMID:Renal failure in vibrio vulnificus infection. 1084 44


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