Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The IgE synthesis is tightly controlled by a complex network of T and B cells. Because human immunodeficiency virus (HIV) disease associates T cell activation and depletion, polyclonal B cell activation, atopic symptoms, drug hypersensitivity, and autoimmune activity, we have evaluated IgE, as well as IgA, IgG, and IgM, in 315 HIV-seropositive individuals with or without acquired immunodeficiency syndrome (AIDS) and compared the results to those of 100 HIV-seronegative subjects. IgE levels were higher in HIV-infected subjects as a whole, compared to levels in seronegative control subjects (p less than 0.05). This difference was particularly marked between patients with AIDS and control subjects (p less than 0.005). A strong relationship appeared between IgE and the immune status as assessed by CD4 cell counts (p less than 0.001 between IgE values in patients with CD4 less than 300 or greater than 300/microliters). In addition, we assessed the predictive value of IgE elevation over disease progression: in subjects with a CD4 count less than 300/microliters, the survival analysis disclosed a 24-month occurrence rate of AIDS of 83% in individuals with IgE greater than 150 KIU/L versus 44% in individuals with IgE less than 150 (p = 0.016). In subjects with an AIDS-related complex, IgE greater than 150 indicated a 100% rate of AIDS versus 9% in individuals with IgE less than 150 (p = 0.003). Thus, IgE levels appear to be a very discriminative marker between patients in late stages of HIV infection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Elevation of IgE in HIV-infected subjects: a marker of poor prognosis. 134 48

Drug hypersensitivity reactions are often observed by clinicians treating patients infected with the human immunodeficiency virus (HIV). For certain drugs, the incidence of these reactions appears to be higher than previously reported in the general population. The best example is trimethoprim-sulfamethoxazole, associated with rash, fever, hematologic disturbances, transaminase elevation, and, less frequently, more severe reactions, including Stevens-Johnson syndrome, toxic epidermal necrolysis, and anaphylactic-like reactions. Other sulfa congeners, pentamidine, antituberculosis regimens containing isoniazid and rifampin, amoxicillin-clavulanate, clindamycin, and thalidomide also have been associated with an increased incidence of adverse reactions, some of which could involve allergic mechanisms. Effective dosage and management strategies are needed to prevent or ameliorate hypersensitivity reactions when they occur.
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PMID:Drug hypersensitivity reactions and human immunodeficiency virus disease. 145 34

Drug allergy is the most common and significant allergic manifestation of HIV3 infection. Initially described in patients treated with SMX-TMP for PCP, allergy is now known to involve a multitude of drugs. The pathogenesis of, and risk factors for, allergy in HIV infection are poorly understood, although there is evidence suggesting that allergy is more common with advancing immunodeficiency. HIV-negative subjects with sulfonamide allergy may have drug-specific antibodies and drug metabolite-induced lymphocyte cytotoxicity, abnormalities that could partly explain the allergic mechanisms and which may have future diagnostic potential; these abnormalities have not been described in HIV-infected subjects. Therapy includes avoidance, suppressive agents such as corticosteroids, and desensitization, although the appropriate role for each is not entirely clear. Serum IgE levels have been shown to rise with progressive disease; those patients with higher levels may have a worse prognosis. The mechanisms of this rise are multifactorial, probably a combination of altered T-lymphocyte regulation of IgE synthesis and of production of specific IgE directed against microbial antigens.
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PMID:Allergic manifestations of human immunodeficiency virus (HIV) infection. 167 34

There is a high incidence of autoimmune disease in patients with primary immunodeficiency. In almost all instances autoantibodies are to antigenic determinants of the formed elements of the blood--erythrocytes, platelets and neutrophils. In some rare cases, autoantibodies to T or B lymphocytes can cause immunodeficiency. IgA is unique in inciting autoantibodies to this serum protein in some patients with IgA deficiency. Organ-specific autoimmune disease is extremely rare in immunodeficiency states. In contrast, drug allergy and allergic contact dermatitis are extremely common in patients with deficiencies of B lymphocytes. Patients with the syndrome of immunodeficiency with elevated IgM (hyper-IgM deficiency) almost invariably develop autoantibodies to formed elements of the blood. Autoantibody production can be suppressed with anti-idiotypic antibodies.
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PMID:Autoimmunity and immunodeficiency disease. 331

Diphenylhydantoin (DFH) treatment for epileptic patients has shown adverse effects such as malignant lymphadenopathy, systemic lupus erithematosus, periarteritis nodosa and recently immunological alterations such as a decreased lymphocytic response to fitohemaglutinin and serum IgA concentration, therefore we thought DFH effect on secretory IgA would be an important finding. This phenomenon might imply a defect in resistance local mechanisms for infection. Two groups of patients were studied: a) 25 children with an established diagnosis of epilepsy, "grand mal" type, that received anticonvulsive treatment with DFH for six months and b) 25 children with a diagnosis of infectious meningoencephalitis that required DFH to control convulsive crisis. Patients with a history of recurrent infections, lymphadenopathies, hepatosplenomegaly, drug allergy, collagenopathies and immunodeficiency were ruled out from this study. In all patients T and B lymphocytes, serum IgA, saliva and duodenal fluid and IgA determinations were made. Results show IgA concentration decrease in saliva and duodenal fluid of epileptic and meningoencephalitic patients (p less than 0.05), as well as lymphocyte T depression in epileptic and non epileptic patients treated with DFH (p less than 0.001).
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PMID:Effect of diphenylhydantoin in serum and secretory IgA concentrations. 677 21

A 47-year-old woman developed pulmonary eosinophilia from the use of maloprim as malaria prophylaxis. The diagnosis was confirmed by bronchoalveolar lavage (BAL) and transbronchial lung biopsy. Her condition improved with drug withdrawal and steroid therapy. With the increased use of pyrimethamine and dapsone in the treatment of human immunodeficiency syndrome (HIV) infection, this form of drug allergy may become more common.
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PMID:Maloprim-induced pulmonary eosinophilia. 841 12

Pneumocystis carinii pneumonia (PCP) is the most common opportunistic human immunodeficiency virus (HIV)-related infection, occurring in 85% of HIV infected patients without prophylaxis. Preventive treatment is required when CD4 cell count falls below 200 cells per cubic millimeter. Cotrimoxazole has been shown to be highly effective but alternative drug regimens are often necessary because of the frequent drug hypersensitivity exhibited by HIV infected patients. The aim of this prospective, open, randomized, one-site study, involving HIV-infected patients with a CD4 cell count below 200/mm3, or a percentage under 20%, randomly assigned to receive either dapsone 50 mg daily or Fansidar one tablet weekly, was to compare the efficacy and safety of these drugs in the primary prophylaxis of PCP. Both dapsone and Fansidar appear to be safe and effective alternative agents for the prevention of PCP. Their role in Toxoplasma gondii prophylaxis requires further evaluation.
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PMID:A controlled trial of dapsone versus pyrimethamine-sulfadoxine for primary prophylaxis of Pneumocystis carinii pneumonia and toxoplasmosis in patients with AIDS. 986 2

CIRCUMSTANCES AND CHARACTERISTICS: The risk of toxiderma is greater in patients infected by the human immunodeficiency virus (HIV). The most common toxidermas are maculopapular exanthema and drug hypersensitivity reactions. These toxidermas are predominantly observed with non-nucleoside reverse transcriptase analogs (nevirapine, efavirenz) and abacavir. Toxiderma has also been observed with other nucleoside reverse transcriptase analogs (zalcitabine) and protease inhibitors. REGARDING SEVERITY: The toxidermas observed are usually benign (maculopapular exanthema) and do not always require suspension of the treatment. However, certain toxidermas (Stevens-Johnson syndrome, Lyell syndrome and drug hypersensitivity syndrome) may be life-threatening and therefore contraindicate the continuation of treatment and also its sudden reintroduction. PREVENTION AND PRACTICAL APPROACH: Several studies have assessed the risk factors for toxiderma induced by nevirapine and hypersensitivity reactions to abacavir. The practical approach varies depending on the drug responsible, the clinical form of the toxiderma and the possible alternatives.
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PMID:[Antiretroviral-induced toxiderma in HIV-infected patients]. 1450 44

There is little data in the literature regarding outpatient consultation in allergy/immunology (A/I). The purpose of this study was to determine the relative frequency of different reasons for A/I outpatient consultation to help guide graduate medical education (GME) and assist with A/I practice management. We retrospectively reviewed the electronic medical records of all outpatient A/I consultations from January 1, 2006 to December 31, 2006. The study was performed at our tertiary care referral center which is a GME training site. There were 1412 A/I consults requested during the 1-year period. The consults per month ranged from a low of 69 to a high of 157. The referrals consisted of 35% pediatric and 65% adult patients. There were 52.8% female and 47.2% male patients. We received 74.3% of referrals from primary care, 19.8% from specialty care, and 5.9% from the emergency department. The most common reasons for consultation included 808 (57.2%) patients for chronic rhinitis, 288 (20.4%) for asthma, 196 (13.9%) for food allergy, 89 (6.3%) for venom allergy, 68 (4.8%) for atopic dermatitis, 66 (4.7%) for drug allergy, 62 (4.4%) for chronic urticaria, 45 (3.2%) for acute urticaria, 34 (2.4%) for immunodeficiency, 31 (2.2%) for anaphylaxis, and 162 (11.5%) for other reasons. More than one reason was given for 27.1% of consults, and there was an average of 1.3 reasons for consultation per patient. Although the allergist/immunologist is consulted for a variety of reasons, the top three reasons make up a majority of outpatient consults, and consults are often requested to address more than one diagnosis.
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PMID:Reasons for outpatient consultation in allergy/immunology. 1933 22

Western blot (WB) is the most widely accepted confirmatory assay for detecting antibodies to the human immunodeficiency virus 1 (HIV-1). We report the case of an HIV-1 patient whose WB was negative for over two years. A 41-year-old Japanese man with Pneumocystis pneumonia (PCP) and pulmonary tuberculosis referred in March 2005 was found to have positive HIV-1 ELISA and HIV RNA PCR, but HIV-1 WB with only two bands, at gp160 and p18, and no WB HIV-2 band. The CD4 count was 37/microL, and total immunoglobulin, IgG, IgM, and IgG subclasses were normal. The man was treated for PCP and pulmonary tuberculosis, then underwent antiretroviral therapy. He had taken short-terms steroids to treat a drug allergy and immune reconstitution syndrome. Six months later, his serological ELISA tests for HIV-1 and HIV DNA PCR were negative and WB showed no positive band. The CD4 count recovered gradually, and exceeded 350/microL two years later, but WB remained negative. Lymphoproliferative assays and interferon y expression against HIV-pl7, p24, and p41 were studied and compared to those of other HIV-1 infected patients. Our patient showed no response to p17 or p24 and only a weak response to p41. Other patients showed a response to HIV-antigens, but patients with antiretroviral therapy or with histories of steroid use responded more weakly than those with neither. These findings show that HIV-specific lymphocytes decline with antiretroviral therapy and steroid treatment within early HIV infection. It is therefore important to interpret negative serological tests carefully in patients such as ours.
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PMID:[A case of HIV-1 infection that showed Western blot analysis for HIV-1 negative after antiretroviral therapy]. 1952 9


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