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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We described the course of a young man with SLE who developed hepatitis B virus and human immunodeficiency virus infections through contaminated blood transfusion. He presented with severe SLE, improved on treatment and then developed hepatic failure which responded to conservative treatment. He now has AIDS and the SLE and HBV infection are quiescent.
Lupus 1993 Jun
PMID:Blood transfusion related HBV and HIV infection in a patient with SLE. 836 14

Antibodies reactive with retroviral gag proteins have been detected in patients with systemic lupus erythematosus (SLE). We investigated the immune responses against human immunodeficiency virus (HIV) 1 antigens in the sera of 44 Turkish patients with SLE. Serum samples were tested by using two different commercial enzyme immunoassay (EIA) kits and by Western blotting. EIA studies revealed positive results in 12 patients (27%) for HIV-1 antigens by one of the kits that coated with purified viral antigens. Immunoblot analysis showed antibodies mainly to retroviral gag proteins in 23 patients (52%). The most frequent reactivity was against the p18 gag protein (n = 9). Although antibodies reactive particularly with p24 antigen were described in the previous reports, antibodies to p24 were found in only two patients. These findings might reflect a serologic diversity in different ethnic groups and also suggest the involvement of different triggers in the etiopathogenesis of SLE.
Lupus 1996 Apr
PMID:Antibodies reactive with HIV-1 antigens in systemic lupus erythematosus. 874 24

This report describes a young girl who developed systemic lupus erythematosus at the age of 11. In the years thereafter a conversion took place from hypergammaglobulinemia to hypogammaglobulinemia with the absence of circulating and bone marrow B-cells. Some aspects of the aetiopathogenesis of common variable immunodeficiency are discussed.
Lupus 1996 Jun
PMID:Common variable immunodeficiency in a patient with systemic lupus erythematosus. 880 98

Tuberculosis of the skin is now becoming one of the rare diseases. However, we can still see it in the patients with immunodeficiency or treated with immunosuppressants for a long time. Diagnosis of this disease is made by the characteristic clinical findings and the results of laboratory findings. This disease is divided into two types: true cutaneous tuberculosis and tuberculid. The former is produced by the proliferation of the tuberculous bacilli in the skin. Lupus vulgaris, tuberculosis verrucosa cutis, cutaneous primary tuberculosis, tuberculosis cutis orificialis and cutaneous miliary tuberculosis are included. The latter type is the skin manifestation of allergic reaction against tuberculous bacilli in the tuberculous lesions of other organs. Culture of tuberculous bacilli from the skin lesions shows usually negative. Erythema induratum Bazin, papulonecrotic tuberculid, penis tuberculid and lichen scrofulosorum are included.
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PMID:[Tuberculosis of the skin]. 988 28

Alloimmune antiphospholipid antibodies react with phospholipids and are an epiphenomenon of an infectious disease. Most autoimmune antiphospholipid antibodies recognise phospholipid-protein complexes or proteins, such as beta2 glycoprotein I or prothrombin and are related to the clinical features of the antiphospholipid syndrome. Lupus anticoagulant, anticardiolipin antibodies, antiprothrombin, and anti-beta2 glycoprotein I antibodies were studied in 61 human immunodeficiency virus (HIV) patients, 55 syphilis patients, and 45 selected patients with antiphospholipid syndrome. Lupus anticoagulant was present in 72% of HIV and 81% of antiphospholipid syndrome patients. None of the syphilis patients had lupus anticoagulant. Anticardiolipin antibodies were found at comparable prevalence in the three groups (HIV 67%, syphilis 67%, antiphospholipid syndrome 84%). HIV had more frequently anti-beta2 glycoprotein I (13%) and antiprothrombin (12%) antibodies than syphilis (0 and 4%, respectively), but significantly less than antiphospholipid syndrome (61 and 40%, respectively). Autoimmune antiphospholipid antibodies in HIV without clinical features of antiphospholipid syndrome might be a reflex of the immunological chaos and/or the constant antigenic virus stimulus.
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PMID:Different types of antiphospholipid antibodies in AIDS: a comparison with syphilis and the antiphospholipid syndrome. 1055 81

Systemic lupus erythematosus (SLE) and infection with the human immunodeficiency virus (HIV) are rarely seen in the same patient. Both diseases share clinical and serological features and the differential diagnosis is difficult, with renal manifestations being of special interest. To date, 29 cases of association between the two diseases have been reported, but the diagnosis was simultaneous in just two of these and only 18 fulfilled the ARA criteria for the diagnosis of SLE. Most patients experienced an improvement in their SLE after development of their HIV associated immunosuppression and a reactivation of lupus manifestations has also been noted after immunological recovery secondary to antiretroviral therapy. We present the case of a woman in whom HIV and SLE with renal involvement were diagnosed simultaneously.
Lupus 2002
PMID:Human immunodeficiency virus infection and systemic lupus erythematosus. An unusual case and a review of the literature. 1189 23

Adenosine deaminase (ADA) is an enzyme involved in purine metabolism and has a major role in the development and function of lymphoid cells. Congenital deficiency of ADA results in severe immunodeficiency. Patients with congenital ADA deficiency treated with polyethylene glycol-conjugated bovine ADA develop antibodies to ADA. This leads us to investigate the role of anti-ADA antibodies in patients with systemic rheumatic diseases. Commercially available ADA was used in ELISA and immunoblots for detection of anti-ADA antibodies. Four out of 100 patients examined were positive for anti-ADA antibodies. Two of them had peripheral blood lymphopenia but the antibody levels did not appear to correlate with the lymphocyte counts. Immunoblotting revealed that the antibodies recognized a 40 kDa peptide of ADA, corresponding to ADA1, the major component of ADA. Affinity-purified antibodies were used to locate the distribution of ADA on Hep-2 cells and lymphocytes by indirect immunofluorescence. Anti-ADA antibodies gave a distinct nuclear speckled pattern on acetone-fixed cells. With viable cell immunofluorescence, anti-ADA antibodies also stained the cell surface of HEp-2 cells and lymphocytes, indicating surface expression of ADA. The anti-ADA antibodies failed to gain access into the cytoplasm or nuclei when added to the cultures of HEp-2 cells. In summary, this is the first report of detection of anti-ADA1 autoantibody which is a new type of ANA with discrete, speckled nuclear staining, but which may not be associated with lymphopenia.
Lupus 2002
PMID:Anti-adenosine deaminase antibodies in lupus erythematosus. 1199 81

Infection with human immunodeficiency virus (HIV) may lead to hemostatic imbalances. Forty-nine consecutive patients with acute opportunistic infections were screened for thrombophilic parameters. A follow-up investigation was performed after 10 +/- 8 weeks in 26 patients. In acutely ill patients, the incidence of protein S deficiency was 67% (33/49) and of protein C deficiency 25% (12/49), while at the follow-up visit the incidences were 54% (14/26) and 8% (2/26), respectively. Protein S and protein C levels increased significantly from initial to follow-up visit (p < 0.05). Lupus anticoagulants were not detected and anticardiolipin IgG antibodies were present in 11.4% (5/44). Three patients presented with deep venous thrombosis on admission; in two, protein S or protein C deficiency was observed. In conclusion, an acquired protein S and protein C deficiency often develop in patients with HIV and acute illness; this may be reversible after treatment for opportunistic infections.
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PMID:Acquired protein C and protein S deficiency in HIV-infected patients. 1465 42

Systemic lupus erythematous (SLE) and immunodeficiency are linked in various ways. For example, rare genetic complement deficiencies can pre-dispose to developing SLE, whilst some treatments for SLE can cause secondary immunodeficiencies. Various case reports describe SLE patients who have concomitant or later develop antibody deficiency, possibly related to immunosuppressive treatment, or possibly related to the lupus itself. Other components of the immune system, innate and adaptive may also be affected. Immunosuppressive treatment may also cause infections in the absence of defects on routine immunological testing. It is important for the clinician to be aware of the associations between SLE and immunodeficiency to ensure optimal investigation and management. This review focuses on aspects of humoral and cellular immunity, and their association with SLE.
Lupus 2006
PMID:Immunodeficiency in the lupus clinic. 1663 64

During the budding process, human immunodeficiency virus (HIV) acquires several cellular proteins from the host. Thus, antibodies against self antigens found in sera patients with autoimmune disorders may cross react with host-derived or the HIV-specific proteins gp120 and gp41 on the viral envelope and probably neutralize HIV infection. To verify this hypothesis, 88 sera from HIV negative patients suffering from systemic lupus erythematosus (SLE) and other autoimmune disorders were analysed for cross reacting antibodies against HIV-1 by Western blot and FACS analysis indicating that antibodies cross-react with epitopes expressed on HIV infected or non-infected cells. Virus capture assays revealed that HIV-1(IIIB) was directly recognized by 60% of sera from patients with autoimmune disorders. Sera were also tested in HIV neutralization assays with stimulated T cells. Reduction of the viral load by patient sera correlated with their reactivity in Western blot analysis. Complement further enhanced the reduction of viral titres, although no complement-mediated lysis was observed. These data suggest a possible protective role of auto-antibodies against HIV infection in lupus patients.
Lupus 2006
PMID:Targeting human immunodeficiency virus type 1 with antibodies derived from patients with connective tissue disease. 1721 92


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