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 role of T lymphocytes in atopic disease is of considerable importance because animal studies indicate that cells of this lymphoid series may influence reaginic antibody response. T lymphocyte subpopulations were studied in a group of 76 children with allergic respiratory disease. There was no statistical difference between atopic children with asthma and those with allergic rhinitis as compared with an age-matched control population of 20 non-atopic children in terms of levels of active T lymphocytes or total T lymphocytes. The results of this study do not support the concept of a T cell immunodeficiency in children with allergic respiratory disease.
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PMID:T lymphocytes in children with allergic respiratory disease. 30 67

Allergic rhinitis and sinusitis are independently common disorders. Studies document the presence of both disorders in the same patient 25% to 70% of the time. Because this is above the prevalence of allergic rhinitis in the general population, the literature supports that allergy is an important associated factor in sinusitis. Younger children appear to be even more at risk of sinusitis, perhaps because of small anatomic structures, more frequent viral infections, and more exposure to indoor allergens and irritants. Immunodeficiency appears to play an independent role in resistant, severe sinusitis.
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PMID:The role of allergy in sinusitis in children. 152 43

Forty-five homosexual male subjects with human immunodeficiency virus (HIV) infection, who received care during a 4-month period in an ambulatory center for acquired immunodeficiency syndrome (AIDS), were classified according to their principal presentation with characteristic secondary infections (CDC group IV C, N = 28), cancers (IV D, N = 10), or limited or no symptoms (groups II, III, IV A, or IV B, N = 7). The incidence of allergic rhinitis and conjunctivitis increased after HIV seroconversion by approximately twofold in patients of groups IV C and IV D. The mean serum concentration of IgE was significantly higher for group IV C than for the other HIV-seropositive groups and for a control group of 45 HIV-seronegative homosexual male subjects from the same community who were studied concurrently. More patients in groups IV C and IV D had positive RASTs for a panel of environmental antigens than patients in the other HIV-seropositive groups and the HIV-seronegative control group. Patients with AIDS presenting with typical secondary infections thus have a high frequency of some clinical and laboratory manifestations of allergic diseases.
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PMID:Elevated serum concentrations of IgE antibodies to environmental antigens in HIV-seropositive male homosexuals. 226 44

Peripheral blood mononuclear cells of 10 out of 26 patients with human immunodeficiency virus type 1 (HIV-1) released IgE-binding factors, as determined by two independent assays. The formation of the factors by the mononuclear cells was enhanced by incubation of the cells with homologous IgE. In the presence of IgE, peripheral blood mononuclear cells from 15 of the 26 patients formed a detectable amount of IgE-binding factors, whereas those of normal individuals of allergic rhinitis patients failed to do so. The major source of IgE-binding factors was the T cells of the HIV-1-infected patients. The CD8+ T cells from a HIV-1-infected patient formed IgE-binding factors upon incubation with IgE, and type II receptors for Fc epsilon were detected on both CD4+ T cells and CD8+ T cells in one of five patients studied. It was also found that culture supernatants of mononuclear cells from HIV-1-infected patients released soluble factors that induce normal human T cells to form IgE-binding factors. The results suggest that lymphocytes of some HIV-1-infected patients are activated to produce lymphokines regulating formation of IgE-binding factors.
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PMID:Formation of IgE-binding factors by T cells of patients infected with human immunodeficiency virus type 1. 326 70

We report a 20 year old man with short stature, microcephaly, unusual facies, numerous pigmented naevi, hypodontia, immunodeficiency, and a high pitched voice. Tympner et al had assumed that the patient had a new syndrome of "progressive combined immunodeficiency and ectomesodermal dysplasia". We show here that the condition is identical to the Mulvihill-Smith syndrome (McKusick 176690), a progeroid disorder described in four or possibly five sporadic cases to date. We describe his clinical progress up to the age of 20 years. Our patient suffered from severe viral infections, allergic rhinitis and conjunctivitis, delayed puberty, visual loss, modest achievement in high school, and reactive depression. The immunological, facioskeletal, and dental abnormalities are presented in detail.
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PMID:Mulvihill-Smith syndrome: case report and review. 781 40

During an infection with human immunodeficiency virus (HIV) the immune system is deregulated, even before real immunodeficiency, lymphopenia and AIDS occur. The immunologic alterations that have been described are a differentiation of a T-lymphocyte subclass, Th1 to Th0. Immunologic stimulation of these Th0 cells afterwards, makes them mature into Th2 cells. This causes a imbalance between the Th1 and Th2 cells, in favor of the second group. The clinical expression of this imbalance is an elevated risk of HIV-seropositive patients for allergies and for autoimmune disease, specially those autoimmune disease in which the production of autoantibodies prevails. Sometimes of differential diagnosis with systemic lupus erythematosus is difficult. There has been describes a major prevalence of allergic diseases, especially allergic rhinitis, in adult patients infected by HIV. Reports in pediatric patients are still sporadic, and the prevalence of allergies in children infected with HIV-AIDS is unknown. Only after recognizing the allergic nature of some symptoms, the treatment will be complete, reducing morbidity and infectious complications.
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PMID:[Allergic diseases and infection with human immunodeficiency virus (HIV)-AIDS in pediatric patients]. 929 27

Infection with the human immunodeficiency virus (HIV) is increasing in prevalence, and disease patterns are changing as patient survival lengthens. The purpose of this cross-sectional epidemiological study was to assess the prevalence and severity of self-reported symptoms of otolaryngologic disease in a group of patients attending a general HIV outpatient clinic (n = 203), and to compare the prevalence of self-reported symptoms with a sample of patients without HIV infection (n = 100). Of the HIV-infected patients, 65% of patients had AIDS, 35% were HIV-positive, and the median CD4 count was 135. Although only 11% of patients had seen an otolaryngologist in the prior 6 months, the majority of patients (66%) reported the presence of sinonasal disease during that time. Allergic rhinitis (80%) and sinusitis (54%) were the most commonly reported sinonasal symptoms, and 44% regularly used nasal or sinus medications. Sinonasal disease severity was significantly higher than the self-reported severity of mouth/throat disease (p = 0.01), ear disease (p = 0.03), and neck/salivary disease (p = 0.01). Although patients' self-reported overall health status was associated (p = 0.02) with CD4 count, the severity of sinonasal symptoms was not associated (p = 0.93) with CD4 count. Similarly, sinonasal symptom severity did not differ between HIV-positive and AIDS patients (p = 0.45). In other words, sinonasal disease severity did not improve as general health status improved.
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PMID:Prevalence of sinonasal symptoms in patients with HIV infection. 1039 39

Selective IgA deficiency has been reported to be the most common primary immunodeficiency disease in Western countries. A markedly lower frequency of this condition has been reported in the Japanese population. While most of the IgA deficient cases are healthy, some patients develop significant recurrent sinopulmonary infections, allergic disorders and autoimmune diseases. Herein, we report three cases of IgA deficiency among Thai patients, all of whom suffered from chronic sinopulmonary infections. Two of the three patients had absolute IgA deficiency while the third had a partial IgA deficiency. The associated conditions found in these three patients were deficiencies of an IgG subclass, allergic rhinitis and lupus nephritis. The youngest child (5 years old boy with lupus nephritis) expired from Pneumocystis carrinii pneumonia complicated with adult respiratory distress syndrome.
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PMID:IgA deficiency: a report of three cases from Thailand. 1258 45

Two types of allergic rhinitis are differentiated: seasonal rhinitis caused in particular by pollen allergens, and the perennial form caused by such year-round allergens as house dust (mites), moulds and animal hair. The diagnosis is based on a comprehensive history (family/occupation/environment), clinical symptoms, a rhinoscopic examination, and testing for allergens, e.g. conjunctival tests, prick test or nasal provocative test. The treatment of choice is elimination of the allergens as completely as possible. An additional causal therapeutic option is specific immune therapy (SIT) which, however, is contraindicated in the presence of intercurrent infections, use of beta blockers and immunodeficiency. Available medications include mast cell stabilizers, antihistaminic agents and corticosteroids, which are applied in stepped fashion, depending upon severity. In addition, adjuvant surgical measures may improve obstructive symptoms.
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PMID:[Allergic rhinitis to be diagnosed and treated correctly. Tips for a runny nose]. 1268 24

A 15-year-old, unmarried female presented to our dermatology department for an intensely pruritic skin rash that had appeared abruptly 3 days earlier. She had a remarkable medical history for a case of allergic rhinitis and several attacks of asthma in her early childhood. The condition waxed and waned initially but had improved in recent years. Physical examination revealed several erythematous plaques, papules studded with scattered pustules having diameters less than 0.3 mm. Conspicuous scratch marks had caused erythematous wheal-like indurations also studded with pustules in a linear distribution across the waist, forearms (Fig. 1), and back (Fig. 2). Discrete papulopustules were present on the face, nape and neck. The patient was otherwise healthy. There were no other symptoms such as fever, malaise, weakness, or lymphadenopathy Laboratory results were normal for hepatic and renal functions, serum electrolytes, glucose, protein, erythrocyte sedimentation rate (8 mm/h), and C-reactive protein (0.355 mg/l). A human immunodeficiency virus (HIV) antibody screen test was negative. Serum was positive for herpes simplex virus (HSV)-1 and HSV-2 IgG (in low titers), but negative for HSV-1 and HSV-2 IgM. White blood cell count revealed leukocytosis (11.2 x 10(3)/l), with a differential count of 68% neutrophils, 27% lymphocytes, and 8% eosinophils. Serum IgA, IgG, and IgM were within normal limits, but the IgE level was elevated (677 mg/dl). Cultures from peripheral blood and pustules were negative. A Tzank smear performed on the pustules showed no multinucleated giant cells. Fungal testing of skin scrapings from the initial lesion site gave negative results. Routine stool tests, including common pathogen and parasite screens, were negative, and urinalysis results were unremarkable. A biopsy specimen obtained from a skin pustule showed subcorneal eosinophilic and neutrophilic pustules in the follicular infundibulum with marked spongiosis of the follicular epithelium. (Fig. 3). There was a moderately dense superficial and deep perivascular mixed inflammatory cell infiltrate comprising eosinophils, neutrophils and lymphocytes. Migration of eosinophils and neutrophils through the vessel wall with variable luminal intramural fibrin deposition, histologically indicative of vasculopathy, was seen. There was concomitant slight perivascular dermal necrosis. (Fig. 4). Based on the clinical presentation and light microscopic findings on biopsy, a diagnosis of eosinophilic pustular folliculitis with pathergy was made. Systemic prednisolone 30 mg in divided doses was given. After 1 week of systemic corticosteroid therapy, the patient's condition was significantly improved and the patient was subsequently discharged. Two months later she had a relapse, upon which corticosteroid therapy was commenced leading to lesional resolution. The foci of eosinophilic folliculitis healed with areas of hyperpigmentation with variable scarring.
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PMID:Pathergy in atypical eosinophilic pustular folliculitis. 1580 26


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