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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The natural history of human immunodeficiency virus (HIV) infection is marked by a progressive deterioration of the host immune system and a concomitant increase in host viral burden. The rationale for major HIV disease staging systems is discussed in light of this natural history. The need for early diagnosis and treatment of HIV-infected patients is underscored by the prolonged phase during which patients are simultaneously asymptomatic and infectious. Clinical, immunologic, and virologic markers of disease stage, progression, and response to therapy will require continuing refinement as we better understand the pathobiology of HIV disease.
Dermatol Clin 1991 Jul
PMID:Natural history of human immunodeficiency virus infection. 187 24

HIV-1 disease has been recognized as a distinct clinical entity for fewer than 10 years. Yet during that time, the virus has spread around the world and affects people of virtually all ages, genders, sexual behaviors, and geographic regions. In the United States, there have been more than 140,000 individuals diagnosed with AIDS, the clinical end stage of HIV-1 disease, and it is projected that AIDS incidence will accelerate through at least 1993. In the early years of the infection epidemic in the United States, the virus spread rapidly and insidiously, predominantly among homosexual men, intravenous drug users, people with hemophilia, and recipients of infected blood products. Since then, the epidemic has been propagated concurrently with epidemics of drug use (intravenous and noninjectable) and sexually transmitted diseases such as syphilis. Since its beginning, HIV-1 has disproportionately affected members of racial and ethnic minorities, particularly in large cities, where transmission takes place sexually, parenterally, and perinatally. The epidemic of HIV-1 has spread outside of traditional urban epicenters and is more significantly affecting adolescents, women, and heterosexuals. There is a great need for renewed and refocused infection-prevention efforts. Projections of resource and medical service needs should be based on up-to-date and accurate assessments of infection epidemic parameters, including infection prevalence, incidence, and acceleration (changes in epidemic velocity over time) rates.
Dermatol Clin 1991 Jul
PMID:Epidemiology of HIV infection and AIDS in the United States. 187 25

Infectious complications are the most common cutaneous manifestations of HIV infection. In this article, the bacterial, viral, fungal, and parasitic infections seen in HIV-infected patients are described and illustrated. The relation of these infections to the overall health of the patient and current therapies that have been found beneficial are outlined.
Dermatol Clin 1991 Jul
PMID:Bacterial, viral, fungal, and parasitic infections in HIV disease and AIDS. 187 26

The management of an HIV-infected patient with syphilis is an evolving and difficult area of clinical medicine. Many such patients initially present with dermatologic problems, and the practicing dermatologist must be alert to the variety of presentations syphilis may take in these patients. The role of biopsy with immunofluorescent or Warthin-Starry silver staining is often crucial in correctly diagnosing confusing cases. The treatment of early syphilis in HIV-infected patients may need to be more intensive than has previously been recommended, because the immunosuppression induced by HIV can accelerate the pace of the infection and increase the risk of progression to neurosyphilis. After treatment, careful and frequent follow-up is essential so that the often irreversible consequences of late syphilis can be avoided.
Dermatol Clin 1991 Jul
PMID:Syphilis and HIV infection. 187 27

Oral lesions are frequently seen in association with all stages of infection with the human immunodeficiency virus (HIV). Many of these lesions occur as the first clinical sign of HIV infection. These lesions include candidiasis, hairy leukoplakia, warts, ulcers, and an aggressive form of periodontal disease. Careful oral examination may reveal lesions that alter Centers for Disease Control staging.
Dermatol Clin 1991 Jul
PMID:Oral manifestations of HIV infection. 187 29

Papulosquamous eruptions are the most frequently seen cutaneous manifestations of human immunodeficiency virus (HIV) infection. Especially common and useful in making a diagnosis of HIV infection are seborrheic dermatitis, xerosis or ichthyosis, and a pruritic or papular eruption. There is some evidence from transgenic mice studies that the transactivating gene TAT and the HIV provirus may produce epidermal hyperplasia, either directly or through cytokine production, without associated immunodeficiency. The association of certain papulosquamous diseases, especially psoriasis, with HIV has opened up new avenues of research on pathogenesis of hyperproliferative skin disease.
Dermatol Clin 1991 Jul
PMID:Papulosquamous disorders associated with human immunodeficiency virus infection. 187 30

The vast majority of children with infection with the human immunodeficiency virus (HIV) develop some form of mucocutaneous disease during the course of their illness. Candidal, fungal, bacterial, and viral infections of the skin and mucous membranes tend to be more severe and less responsive to therapy than in the healthy child. Children with HIV infection are also at risk for drug eruptions, seborrheic dermatitis, and several other inflammatory disorders of the skin. An understanding of the cutaneous manifestations of HIV infection may aid in the early diagnosis and appropriate treatment of this disease.
Dermatol Clin 1991 Jul
PMID:Cutaneous manifestations of HIV infection in children. 187 31

In summary, the AIDS epidemic has created many new questions for the dermatologist, with no clear answers. As dermatologic surgery is increasing in most dermatology practices, the dermatologic surgeon must take a careful look at his office techniques and educate his personnel on the proper handling of blood and body fluids. The medical and ethical issues raised by the AIDS epidemic are complex, with new issues being raised as more is learned about the disease. The adage "do no harm" should be kept in mind in the counseling, diagnosis, and treatment of HIV-infected individuals.
Dermatol Clin 1991 Jul
PMID:AIDS and infection control in dermatologic surgery. 187 33

The prevalence of dermatologic problems during the course of human immunodeficiency virus infection makes knowledge of these skin manifestations imperative to all practicing dermatologists. Detection of early infection is encouraged as effective therapy now exists both to delay the progression of human immunodeficiency virus-induced immunodeficiency and to prevent opportunistic infections. Skin manifestations of human immunodeficiency virus infection discussed in this article include the following groups: neoplastic, ie, Kaposi's sarcoma, lymphoma, and squamous cell carcinoma; infectious, ie, viral, bacterial, fungal, protozoal, and arthropod infestations; and a miscellaneous group including papulosquamous, papular, vascular, autoimmune, oral, and drug-related skin disorders.
Arch Dermatol 1991 Sep
PMID:Cutaneous manifestations of human immunodeficiency virus infection. Part I. 189 8

Because the beneficial effects of zidovudine in human immunodeficiency virus infection-associated psoriasis have recently been observed, this study focused on the drug's action on the rapidly proliferating human HaCaT keratinocyte line as an in vitro model for epidermal hyperproliferation. Cultures in log growth phase were exposed to zidovudine for 2 days. Zidovudine slowed proliferation in a dose-dependent fashion as evidenced by 50% inhibition concentrations of 33 mumol/L (cell number), 30 mumol/L (protein content), 0.9 mumol/L (protein synthesis), and 0.7 mumol/L (DNA synthesis). Significant (p less than 0.01) reduction of cell viability to 94.6% and 87.2%, as well as morphologic manifestations of cytotoxicity, were first evident after 2 days' exposure to maximal drug concentrations of 10 and 100 mumol/L, respectively. Control viability, assayed by trypan blue exclusion, was 98.0%. Direct cytotoxic plasma membrane injury could be ruled out by the absence of any increase in cytoplasmic lactate dehydrogenase release into supernatants at least during the 1 day of maximal dosage exposure. The drug-induced inhibition of proliferation was reversible within 7 days after a 2-day exposure to 100 mumol/L zidovudine. Two days of treatment with a 10 mumol/L dose did not alter the pattern and synthesis of keratins in vitro. Thus the known antipsoriatic efficacy of zidovudine might be explained, at least partly, by the drug's cytostatic potency.
J Am Acad Dermatol 1991 Sep
PMID:Antiproliferative potential of zidovudine in human keratinocyte cultures. 191 88


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