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)

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

MRL-lpr/lpr mice spontaneously develop an autoimmune disease resembling systemic lupus erythematosus and rheumatoid arthritis. One of the unique serological abnormalities in this strain is remarkably high concentrations of cryoglobulins. Analysis of immunoglobulin components in their cryoglobulins has shown selective enrichment of a particular IgG subclass, IgG3. As IgG3 enrichment is also found in two other cryoglobulins, which are induced after injection with bacterial lipopolysaccharides or infection with malaria, IgG3 apparently represents a major source of murine cryoglobulins. Studies on murine IgG3 monoclonal antibodies (mAbs) have clearly shown that murine IgG3 have the unique physiochemical property to self associate through non-specific IgG3 Fc-Fc interaction, and that most of them can generate monoclonal cryoglobulins. Most strikingly, IgG3 monoclonal cryoglobulins with rheumatoid factor (RF) activity induce extensive pathological manifestations: skin vascular purpura and glomerulonephritis with 'wire loop' lesions. Although the cryoglobulin activity of IgG3 RF mAb is solely responsible for the generation of glomerular lesions (both RF and cryoglobulin activities are necessary for skin vascular lesions), the absence of nephritogenic activity by some IgG3 cryoglobulins supports the idea that qualitative features of cryoglobulins are critical to determine their pathogenic activity. The demonstration of a positive correlation between the production of IgG3 cryoglobulins and the development of lupus nephritis in MRL-lpr/lpr mice further substantiates the pathological importance of cryogenic autoantibodies. On the other hand, it should be emphasised that non-cryogenerating IgG3 autoantibodies may not be harmful, but even protective, as a result of their interaction with pathogenic IgG3 cryoglobulins. Finally, the development of an experimental model of cryoglobulinaemia associated with vascular and glomerular disease certainly represents an invaluable opportunity to study the molecular mechanisms responsible for the generation of cryoglobulins and their associated tissue lesions, and also to assess various therapeutic approaches. Our demonstration that anti-idiotypic mAb can prevent the pathogenic effects of the cryoprecipitable IgG3 RF mAb suggests strongly that such a therapeutic approach might be successful in similar diseases in man.
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PMID:IgG3 cryoglobulins in autoimmune MRL-lpr/lpr mice: immunopathogenesis, therapeutic approaches and relevance to similar human diseases. 848 Oct 59

The binding capacity to cardiolipin and the functional affinity of affinity-purified anticardiolipin (aCL) IgG of patients with autoimmune disease have been compared with those of individuals with malaria and acquired immunodeficiency syndrome (AIDS). The binding of autoimmune IgG aCL was enhanced gradually by the incorporation of increasing amounts of beta 2-glycoprotein I (beta 2GPI) into the assay, in contrast to that of patients with infectious diseases. In addition, there were significant reductions of functional affinity in autoimmune disease, but not in malaria or in AIDS. These results indicate that beta 2GPI requirement for binding to the target antigen varies inversely with functional affinity in autoimmune disease when beta 2GPI was present, and suggest that IgG aCL are more heterogeneous in this type of disorder than in patients with infectious disease.
Lupus 1995 Dec
PMID:Role of beta 2-glycoprotein I in the anticardiolipin antibody affinity for phospholipid in autoimmune disease. 874 71

Systemic lupus erythematosus and sarcoidosis, both diseases in which immune responses are aberrant, are not found in Africans in West Africa, but their prevalence in people of West African descent in the USA and UK is higher than that for white people. It is argued here that malaria both prevents these diseases in West Africa by its effects on macrophage function, and has also selected for a predisposition to them.
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PMID:Malaria and macrophage function in Africans: a possible link with autoimmune disease? 886 23

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

During a four-year period, 86 children with fever lasting for at least 6 days without diagnosis at admission after initial physical examination and preliminary laboratory tests were included in a retrospective analysis. Their ages ranged from 2 months to 16 years, and there were 55 males and 31 females. Bacterial infections occurred in 19 patients (22%), viral infections in 17 (20%), mycoplasmal infections in 3 and malaria in 1. Collagen vascular diseases were diagnosed in 13 children (15%), including 7 juvenile rheumatoid arthritis and 5 systemic lupus erythematosus. Thirteen children (15%) had neoplastic or hematological diseases, including leukemia, lymphoma, myelodysplastic syndrome, and neuroblastoma. The fevers of the other 14 patients (16%) were attributed to central fever. The overall diagnostic rate was 98%. Twenty-two children had a poor outcome, including 6 children with collagen vascular diseases and 12 with neoplasms. Diagnoses were made mainly through a complete medical history, meticulous physical examination, regular laboratory tests, and an observation of clinical course. Invasive tissue studies can be fruitful when used appropriately and should be considered for specific indication only.
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PMID:Prolonged fever in children. 893 8

Chloroquine is commonly used in the chemotherapy of malaria fever, and as an antiinflammatory disease-modifying agent in patients with rheumatoid arthritis or systemic lupus erythematosus. Administration of chloroquine (20.0 mg/kg IP) significantly (p < 0.05) increased the frequency of body scratching in rats to 29.5+/-9 in 30 min, compared to saline control animals (6.5+/-2/30 min). Morphine, a mu-opiate receptor agonist (1.0 mg/kg IP), potentiated the chloroquine-induced rat body scratching to 40+/-6.6, while the mu-opiate receptor antagonist, naltrexone (0.25 mg/kg, IP, given 15 min prior) blocked the chloroquine induced body scratching to 4.5+/-2 (p < 0.05 ANOVA). In addition, the frequency of chloroquine (20.0 mg/kg IP)-induced body scratching was significantly reduced to 9.1+/-3 in 30 min in rats rendered tolerant to morphine (p < 0.05 ANOVA) compared to the scratching frequency of 40+/-6.6 in morphine-naive rats. These suggests an involvement of mu-opioid receptors and/or endogenous opioid peptides in chloroquine induced body scratching in rats. Promethazine, a histamine-receptor antagonist (1.0 mg/kg IP, given 15 min prior to chloroquine) and the corticosteroid, dexamethasone (1.0 mg/kg, IP, given 15 min prior) separately and significantly (p < 0.01) inhibited the chloroquine-induced scratching in rats, in a similar manner to clinical studies in malaria. Collectively, the novel results implicate opioidergic mechanisms, and confirm the efficacy of antihistamine and corticosteroids in chloroquine body scratching in rats. It also strongly suggests that the chloroquine-induced body-scratching behavior in the rat may be a useful experimental model for chloroquine-induced pruritus in humans.
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PMID:Mechanisms of chloroquine-induced body-scratching behavior in rats: evidence of involvement of endogenous opioid peptides. 1067 87

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

Recently it was reported that 19.8% of the patients with rheumatoid factor, who had no previous history of malaria and had not visited endemic regions for at least the past five years, generated false-positive results in two rapid malaria tests that capture two different plasmodium antigens. This intriguing finding supports the hypothesis presented, suggesting systemic lupus erythematosus and possibly several other autoimmune diseases are caused by a scanty amount of persistent plasmodium parasites in the internal tissues, which provokes diverse autoantibodies production, and can be transmitted congenitally. This hypothesis suggests a comprehensive explanation for the predominance of autoimmune diseases in African populations in the West yet their infrequency in tropical Africa, and for the studies reporting that several of these diseases benefit from antimalarials. The implication of this hypothesis is that these autoimmune diseases are actually infectious, and may infect individuals who contracted malaria in the past or whose female ancestors had contracted it, and possibly blood transfusion recipients.
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PMID:Scanty congenital plasmodium parasites as a possible cause for several autoimmune diseases. 1135 56

A new 4-month long study is testing the combination of hydroxychloroquine and AZT in HIV-positive people. Hydroxychloroquine has been used for treating malaria, rheumatoid arthritis, and lupus. Participants must be 18 years old or older with a T4 cell count between 200 and 500. Two groups will be studied, one using both drugs, and the other using AZT only.
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PMID:Treatment for HIV-related inflammation. 1136 90


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