Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.16.2 (PCP)
 3,761 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The acquired immune deficiency syndrome (AIDS) was recognized as a distinct entity in 1981. It began as a medical curiosity affecting only several dozen individuals in a restricted segment of the U.S. population. In the 12 years since its description, AIDS has become a pandemic affecting tens of millions with cases reported from all major countries. The illness is caused by a retrovirus, termed human immunodeficiency virus (HIV). It is a blood-borne disease with sexual, parenteral, and perinatal modes of transmission. Infection with the virus can be determined by a number of serologic techniques as well as viral culture. The pathophysiology of illness is incompletely understood, but is in large part related to destruction of helper, CD4 lymphocytes. This results in immune dysfunction and the development of a variety of opportunistic infections and malignancies. A great deal has been learned over the last decade, with important advances in treatment. Zidovudine (AZT) remains the most important agent in slowing progression of the disease and has resulted in prolonging survival. All organ systems can be affected by HIV, and many clinical manifestations are protein. Fever, weight loss, and diarrhea are often encountered general symptoms. The skin is frequently involved, with Kaposi's Sarcoma the most common malignancy and a variety of fungi and viruses the most frequent cause of infection. The lung is involved in the majority of patients, with Pneumocystis Carinii (PCP) and mycobacteria emerging as the most important pathogens. A variety of treatments have demonstrated efficacy for PCP. The risk of PCP is related to the decay in CD4 lymphocytes so that prophylactic treatment is recommended when CD4 counts fall below 200. Mycobacterial infection with multiresistant organisms has complicated the management of these infections and poses new risks to health care workers. Part 1 of this two-part series on AIDS discusses the pathophysiology and clinical expression, epidemiology, laboratory testing, and the general clinical manifestations of AIDS, as well as dermatologic, pulmonary, and cardiac symptoms. Part 2 will discuss the gastrointestinal, neurologic, and ocular symptoms, as well as the treatment and management of the AIDS patient.
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PMID:The acquired immune deficiency syndrome: an overview for the emergency physician, Part 1. 804 May 96

Pneumocystis jiroveci (formerly carinii) pneumonia (PCP) is a serious opportunistic infection in children and adolescents with cancer. It was the most common cause of death among children receiving chemotherapy prior to the inclusion of PCP prophylaxis as part of standard care for children with leukemia. The incidence of PCP has decreased significantly since initiation of prophylaxis; however, breakthrough cases continue to occur. Hematologic malignancies, brain tumors necessitating prolonged corticosteroid therapy, hematopoietic stem cell transplantation, prolonged neutropenia, and lymphopenia are the most important risk factors for PCP in children not infected with HIV. Of children with leukemia, 15-20% may develop PCP in the absence of prophylaxis. Infection with P. jiroveci occurs early in life in most individuals. However, clinically apparent disease occurs almost exclusively in immunocompromised persons. Dyspnea, cough, hypoxia, and fever are the most common presenting symptoms of PCP. Chest radiography and high-resolution CT scans of the chest demonstrate a characteristic ground-glass pattern. Induced sputum analysis and bronchoalveolar lavage are the diagnostic procedures of choice. Gomori's methenamine-silver stain, Geimsa or Wright's stain, and monoclonal immunofluorescent antibody stains are most commonly used to make a diagnosis. However, identification of P. jiroveci DNA using polymerase chain reaction assays in bronchoalveolar lavage fluid is more sensitive. Trimethoprim-sulfamethoxazole (TMP-SMZ; cotrimoxazole) is the recommended drug for the treatment of PCP. Patients who are intolerant of TMP-SMZ or who have not responded to treatment after 5-7 days of therapy with TMP-SMZ should be treated with pentamidine. A short course of corticosteroids is recommended for moderate to severe cases of PCP within the first 72 hours after diagnosis. Mutations in the dihydropteroate synthetase gene may confer resistance to TMP-SMZ; however, the clinical relevance of these mutations is not well established. TMP-SMZ is the most commonly used agent for prophylaxis. Myelosuppression is the most important adverse effect of TMP-SMZ and the most frequent cause for choosing alternative prophylactic agents in children undergoing chemotherapy. Alternative agents for chemoprophylaxis include dapsone, aerosolized pentamidine, and atovaquone. Alternative prophylactic agents must be used in patients developing myelosuppression secondary to TMP-SMZ or dapsone.
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PMID:Management of Pneumocystis jiroveci pneumonia in children receiving chemotherapy. 1792 2

Infection with Candida species remains a major problem in HIV infected patients. The analysis of over 15,000 hospitalisations (1985-2007) in the AVK cohort shows an increasing incidence of non-albicans species in candida esophagitis. Although our analysis shows a decreasing incidence of opportunistic infections like PCP, cerebral toxoplasmosis and others since the introduction of highly active antiretroviral therapy the incidence of candida esophagitis remains as high as in the years before the HAART era. This observation might reflect the development of resistance against fluconazole and the selection of non-albicans species as a consequence of a long-term prophylactic treatment of HIV+ patients over years.
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PMID:Candida infection in HIV positive patients 1985-2007. 1872 33

Infection with the opportunistic fungal pathogen, Pneumocystis jirovecii causes life-threatening pneumonia in immunocompromised individuals. In addition to HIV-1 infected patients, individuals at risk of Pneumocystis infection include those receiving immunosuppressive therapies due to transplantation, cancer or autoimmune disease. Antibiotic treatment is not always successful, and it does not prevent obstructive lung disease after clearance of the pathogen. Therefore, it is essential to develop therapeutic alternatives that are more effective against PCP. We reported that Pneumocystis recombinant protein KEX1 induces protective immunity against the development of PCP in a non-human primate model of HIV-induced immunosuppression. In this study, we tested the immunogenicity KEX1 immunization of healthy rhesus macaques and the durability of these responses during drug-induced immunosuppression using tacrolimus (FK506) and methylprednisolone. We observed that vaccination with KEX1 prior to the start of the immunosuppressive regimen generated a robust and long-lasting antibody response that was maintained throughout the immunosuppressive treatment. Furthermore, boosting with KEX1 during immunosuppression induced recall of memory responses against recombinant KEX1. The durability of the anti-KEX1 response and the ability to induce a recall response during immunosuppressive therapy provide a proof-of-concept data supporting further investigation of the KEX1 as a prophylactic vaccine to prevent PCP in drug-induced immunosuppression. This approach provides fundamental knowledge for the elaboration of therapeutic and prophylactic alternatives for PCP in patients undergoing severe immunosuppressive therapy.
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PMID:Immunization with Pneumocystis recombinant KEX1 induces robust and durable humoral responses in immunocompromised non-human primates. 3284 Apr 16