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)

An autopsy case of a very rare form of generalized aspergillosis with a prominent granulomatous pattern simulating sarcoidosis was presented. The patient was a forty-year-old Japanese female with a four years' clinical course. Kveim's test was positive. Multiple epithelioid cell granulomata as well as necrotizing and suppurative lesions were recognized in generalized lymph nodes, liver, epicardium, gall bladder, adrenals, kidneys and duodenal mucosa. Fungal elements in the epithelioid cell granulomata and necrotizing lesions were identified as Aspergillus by fluorescent antibody technique (indirect method). Predisposing factors for the generalized fungal infection could not be clarified in this case. There was neither underlying disease nor evident immunodeficiency state, so far as examined.
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PMID:Generalized aspergillosis showing a granulomatous pattern. 38 9

The discovery of the antifungal activity of azole compounds represented an important therapeutic advance. Miconazole, ketoconazole, and fluconazole are currently commercially available, and itraconazole has undergone extensive clinical evaluation. Because of its limited activity and toxicity, miconazole has been replaced by newer agents. Ketoconazole has proven useful in therapy for superficial infections and invasive infections caused by the pathogenic fungi. Among its disadvantages are limited absorption in the absence of gastric acid and its potential for drug-drug interactions. Fluconazole is the only azole available as oral and intravenous preparations. Unlike other azoles, it is only minimally metabolized in the liver and largely excreted in the urine as active drug. It is more effective than ketoconazole against superficial candidal infections and is the drug of choice for maintenance therapy for cryptococcal meningitis in patients infected with human immunodeficiency virus. An advantage of itraconazole is its activity against aspergillosis. It is also active against many infections caused by pathogenic fungi. Other azole compounds are at varying stages of preclinical and clinical investigation.
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PMID:Azole antifungal agents. 131 5

Itraconazole has emerged as an important new oral agent in the treatment of systemic fungal infections. This paper summarizes the data available on its use in aspergillosis, cryptococcosis and histoplasmosis, compiled in the United States with particular attention to the immunocompromised host. Data have been accrued in open-label studies including 57 patients with cryptococcal disease where the overall response rate among patients with meningitis was 86%, and in 28 patients (8 with acquired immune deficiency syndrome (AIDS) or human immunodeficiency virus (HIV) infection) with invasive aspergillosis where the overall response rates were 80% in patients without AIDS and 86% in patients with AIDS. Data are summarized on 6 patients with allergic bronchopulmonary aspergillosis, 5 of whom demonstrated marked improvement on therapy, and 12 patients with histoplasmosis including 8 with AIDS, 11 of whom responded and 1 recrudesced on therapy. In summary, itraconazole showed activity in human studies of aspergillosis, cryptococcosis and histoplasmosis with minimal toxicity. Itraconazole offers a new oral alternative to conventional amphotericin B therapy in these infections. Comparative studies are needed to clarify its role.
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PMID:US experience with itraconazole in Aspergillus, Cryptococcus and Histoplasma infections in the immunocompromised host. 131 10

Aspergillosis, cryptococcosis and zygomycosis (mucormycosis) are overall the most common systemic mycoses but histoplasmosis is particularly endemic in parts of central USA and other areas worldwide. Orofacial lesions caused by systemic mycoses have rarely been reported in the past though they have been recorded particularly in outdoor workers from geographic areas with a high prevalence of infection and occasionally in immunocompromised individuals. Increasing world-wide travel, and the dramatic increase in numbers of immunocompromised persons, especially those with human immunodeficiency virus (HIV) disease, have been responsible for an increase in reports and other studies of orofacial disease in systemic mycoses and new opportunists are now being recognized. Those in Oral Medicine and Pathology must now be aware of the possibility of a systemic mycosis as the cause of chronic oral ulceration, chronic maxillary sinus infection, or bizarre mouth lesions, especially in patients with HIV disease, lymphoproliferative disorders, or diabetes mellitus, or in those who have been in endemic areas. Diagnosis and management should be undertaken in consultation with a physician with appropriate expertise, as pulmonary and other systemic infection may well be present. This paper reviews the eight main systemic mycoses.
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PMID:Orofacial manifestations of the systemic mycoses. 152 29

Evidence of an acquired T cell-specific deficiency distinct from acquired immunodeficiency syndrome (AIDS) in a 63-yr-old Japanese female is provided. Recently, this patients suffered from primary invasive pulmonary aspergillosis. Skin tests to purified protein derivative of tuberculin (PPD) and Aspergillus antigens were negative. Upon admission to our hospital, her lymphocytes were exclusively unresponsive to T cell mitogens (concanavalin A, phytohemagglutinin, and OKT 3). The level of cells defined by monoclonal antibodies (CD1, CD2, CD3, CD4, WT31, and CD5) was less than 3%. In contrast, no decrease in the number of red blood cells, platelets, neutrophils or B cells was apparent. Five years ago, the patient had a normal white blood cell and lymphocyte count. However, over the following 4 yr, she developed lymphopenia. With medication, her pulmonary disease recovered, while lymphopenia still continued. The levels of immunoglobulins, complements and enzyme activities (adenosine deaminase and purine nucleoside phosphorylase) were normal. Moreover, several tests for HIV (ELISA and Western bolt) were negative suggesting that the T cell-specific deficiency was not a congenital immunodeficiency or AIDS but rather a new type of acquired immunodeficiency.
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PMID:Acquired T cell specific deficiency other than acquired immunodeficiency syndrome (AIDS). 156 29

Since January 1985 more than 100 patients with deep fungal infections have been treated with itraconazole (200 to 400 mg/day) in Northern Italy. Evaluation of the drug efficacy and tolerance was possible in one patient with sporotrichosis, in 34 with aspergillosis, and in 36 with cryptococcosis (mainly patients positive for human immunodeficiency virus). Response to itraconazole alone was obtained in the case of sporotrichosis and in 24 of 34 patients with different forms of aspergillosis (of the 18 patients with invasive pulmonary aspergillosis, 15 were cured). Patients with cryptococcosis received itraconazole for active infection and/or for prevention of relapse. Active infection was treated successfully with itraconazole alone in nine of twelve patients and with itraconazole plus flucytosine in eight of ten patients. Of the 31 patients who received itraconazole maintenance therapy for up to 27 months, four (13%) had relapses; 14 (45%) did not have relapses, and decline of serum antigen was detected in twelve of them; and 13 (42%) were completely cured (serum antigen titer dropped to zero). With the exception of hypokalemia in one patient, itraconazole was well tolerated even in patients who received the drug for several months or years.
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PMID:[Mycoses as opportunistic infections in AIDS patients]. 166 2

Invasive aspergillosis (IA) is a rare infection in patients with the Acquired Immune Deficiency Syndrome (AIDS). We report the first Australian cases of histologically and microbiologically proven IA diagnosed antemortem in AIDS patients. We also describe the first case of laryngeal involvement and the unusual case of a pneumothorax due to IA. These three cases illustrate the varied clinical and pathological features of IA in AIDS and highlight some of the difficulties in diagnosis and treatment. The infections occurred in the setting of advanced immunodeficiency and multiple opportunistic infections and responded poorly to treatment.
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PMID:Invasive aspergillosis in AIDS. 175 26

Chronic necrotizing pulmonary aspergillosis (CNPA), also known as semi-invasive pulmonary aspergillosis , is a recently defined entity. CNPA is characterized by a pulmonary infiltration with cavitation of chronic evolution in patients with chronic pulmonary disease, slight immunodeficiency or healthy patients. Good evolution is obtained with antimicotic treatment. The isolation of Aspergillus niger as a cause of CNPA is infrequent and may bear worse prognosis. A patient who presented CNPA by Aspergillus niger is described. The patient had received radiotherapy for epidermal carcinoma of the esophagus. Three other cases have been reported in the literature. The diagnostic aspects, treatment and prognostic factors of CNPA are commented upon.
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PMID:[Chronic necrotizing pulmonary aspergillosis caused by Aspergillus niger]. 176 84

Oral lesions have rarely been reported in systemic mycoses, though over the past few years they have been recorded particularly in immunocompromised individuals. The dramatic increase in numbers of immunocompromised persons, especially those infected with human immunodeficiency virus, has almost certainly been responsible for the increase in reports of oral disease caused by systemic mycoses, particularly aspergillosis, cryptococcosis, and histoplasmosis. However, reports of coccidioidomycosis, blastomycosis, and paracoccidioidomycosis have, as yet, increased little in this population. Dentists, when they observe chronic oral ulceration, chronic maxillary sinus infection, or bizarre mouth lesions (particularly in immunocompromised patients) should be aware of the possibility of a systemic mycosis. Amphotericin remains the standard therapy for most deep mycoses, while the newer azoles are the first-line agents for superficial mycoses, such as candidiasis, and are increasingly used in the deep mycoses.
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PMID:Oral lesions in the systemic mycoses. 180 2

Adherent cells from human immunodeficiency virus (HIV)-infected subjects but not from normal blood donors, patients with Gram-positive or -negative bacteremia, active tuberculosis, toxoplasmosis, pulmonary aspergillosis, and cytomegalovirus infection produce spontaneously an activity which inhibits alpha chain of interleukin-2 (Tac) expression and interleukin 2 (IL-2) production by normal activated T cells and IL-2 production by these cells. A similar biologic activity was detected in culture supernatants of in vitro HIV-I-infected normal adherent and leukemic U937 cells. Tac-inhibitory activity is not cytotoxic and it could be detected in serum-free conditioned media. Recombinant granulocyte/macrophage colony-stimulating factor and phorbol myristate acetate stimulation of patients' and normal adherent cells did not enhance specifically the production of the Tac inhibitor. Biologically active conditioned media did not contain infectious virus as well as secreted p24, gp120 viral proteins; the biologic activity could not be abolished by anti-p24, anti-gp120, and anti-nef monoclonal antibodies or human purified polyclonal anti-HIV IgG. Gel filtration of conditioned media followed by anion exchange chromatography resulted in a 1,200-fold degree of purification and revealed that the biologically active molecule was cationic. Sodium dodecyl sulfate polyacrylamide gel electrophoresis of this fraction and gel elution of the proteins showed that the biologic activity was associated with a 29-kD protein which was distinct from alpha- or gamma-interferon, tumor necrosis factor-alpha, and prostaglandin E2. The above findings demonstrate the production of inhibitory factor(s) during HIV infection, which might be involved in the pathogenesis of the patients' immune defect.
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PMID:Biological and biochemical characterization of a factor produced spontaneously by adherent cells of human immunodeficiency virus-infected patients inhibiting interleukin-2 receptor alpha chain (Tac) expression on normal T cells. 190 71


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