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

Several types of vasculitis have been described in patients with human immunodeficiency virus infection. Erythema elevatum diutinum is a rare variant of cutaneous leukocytoclastic vasculitis which, with the exception of the case reported herein, has been described only once in human immunodeficiency virus-infected patients. Our male patient, a longtime intravenous drug abuser, had cutaneous lesions, closely resembling Kaposi's sarcoma, on the extensor surfaces of the lower extremities. Cutaneous biopsy specimens, however, demonstrated leukocytoclastic vasculitis with fibrinoid necrosis of the vessel walls and areas of basophilic degeneration of collagen bundles in early lesions, whereas late lesions showed dense diffuse fibrosis with proliferation of dermal spindle cells and some foci of residual leukocytoclastic vasculitis. Oral therapy with dapsone resulted in marked clearing of the cutaneous lesions within few days. This case raises the necessity of histologic confirmation for all cases of suspected Kaposi's sarcoma in patients with acquired immunodeficiency syndrome. We discuss the possible pathogenesis of leukocytoclastic vasculitis in human immunodeficiency virus-infected patients.
Arch Dermatol 1991 Dec
PMID:Erythema elevatum diutinum in a patient with acquired immunodeficiency syndrome. Another clinical simulator of Kaposi's sarcoma. 184 81

Three males infected with the human immunodeficiency virus (HIV) were noted to have extensive flat warts of the face and/or body. In two there were also pityriasis versicolor-like lesions. Biopsies showed foamy, basophilic, distended cytoplasm in granular layer keratinocytes, characteristic of the human papillomavirus types seen in epidermodysplasia verruciformis. DNA hybridization techniques demonstrated the presence of HPV-type 8 in one patient and HPV 5 and 8 in another. Patients with immune suppression due to HIV infection may demonstrate the clinical features of epidermodysplasia verruciformis with the same potentially oncogenic HPV types.
Br J Dermatol 1991 Jan
PMID:Epidermodysplasia verruciformis-associated papillomavirus infection complicating human immunodeficiency virus disease. 184 68

Cytomegalovirus inclusions have been reported in perineal ulcers from immunosuppressed adults. The importance of this finding is unknown. We report the first pediatric case of cutaneous cytomegalovirus infection in an infant with congenital human immunodeficiency virus infection, presenting as a diaper dermatitis. Cytomegalovirus was cultured from the skin biopsy specimen, and characteristic inclusions were seen on hematoxylin-eosin-stained sections. Results of this biopsy specimen analysis prompted further investigation revealing disseminated cytomegalovirus infection, including retinitis. Aggressive pursuit of a pathogen in common conditions such as diaper dermatitis is strongly recommended in immunosuppressed pediatric patients.
Arch Dermatol 1991 Mar
PMID:Cytomegalovirus diaper dermatitis. 184 93

The human immunodeficiency virus type 1 (HIV-1) has been isolated from a number of body fluids, including semen, tears, cerebrospinal fluid, saliva, breast milk, alveolar fluid, and vaginal fluid, but it has not been isolated from fluid-containing skin lesions. We report the isolation of HIV-1 from cutaneous blister fluid in a patient with concomitant HIV-1 infection and porphyria cutanea tarda. Although transmission of HIV-1 through casual contact has not been reported, appropriate precautions should be taken to avoid direct contact with cutaneous fluid-containing lesions in HIV-1-positive patients.
Arch Dermatol 1991 Aug
PMID:Isolation of human immunodeficiency virus type 1 in cutaneous blister fluid. 186 79

Many cutaneous diseases have been reported in patients with human immunodeficiency virus infection. We report two patients with pityriasis rubra pilaris and human immunodeficiency virus infection. In one patient, the onset of pityriasis rubra pilaris preceded the discovery of human immunodeficiency virus infection. In the second patient, the onset of pityriasis rubra pilaris occurred shortly after the patient tested positive for human immunodeficiency virus infection. Both patients had a severe form of pityriasis rubra pilaris, and both had a minimal therapeutic response to etretinate.
J Am Acad Dermatol 1991 May
PMID:Pityriasis rubra pilaris and HIV infection. 186 40

The cases of three HIV-positive men with generalized psoriasis and staphylococcal sepsis are reported. In each case the skin appeared to be the source of infection. While the patients received antibiotic therapy, the psoriatic plaques resolved despite minimal or no topical treatment.
J Am Acad Dermatol 1991 Jun
PMID:Staphylococcal sepsis in HIV antibody seropositive psoriasis patients. 186 86

AIDS has been a recognized clinical entity now for just 10 years. In that time in the United States alone, it is estimated that 1 to 2 million people may be infected with HIV. Estimates of numbers infected worldwide are as high as 10 million. Over these 10 years, considerable progress has been made. The disease and all its protean manifestations have been accurately described. How HIV spreads and where it is spreading have been accurately recorded. The cause is known and well understood, with more detailed information available about HIV than about any other virus. Drugs that slow down the replication of HIV have been discovered and are in widespread use. A cure or vaccine, however, seems unlikely in the near future. The major hope for the present would appear to be continued education to prevent the spread of AIDS and better antiviral agents that will keep HIV suppressed and, ideally, soon allow infected individuals to lead a close-to-normal lifespan (if treatment is commenced at an early-enough stage in the course of the infection).
Dermatol Clin 1991 Jul
PMID:AIDS: a historical overview. 187 19

HIV is a complex retrovirus. Like some other viruses it infects host cells for life, but unlike other viruses it appears to do so every time. Its elaborate genetic regulation enables it to remain relatively dormant, replicating steadily but slowly. On appropriate stimulation, it is capable of explosive up-regulation, releasing high numbers of new infectious virus. It replicates in an error-prone way, constantly changing its structure to improve its infectivity while presenting the host's immune system with a constantly moving target.
Dermatol Clin 1991 Jul
PMID:The human immunodeficiency virus. 187 21

In summary, the understanding of the pathogenesis of immune dysfunction in HIV infection is incomplete. New mechanisms by which HIV disrupts the immune system through alterations in basic biochemical events in CD4 T cells are continually being discovered. In a positive light, because of the complexity involved in HIV-mediated induction of immune suppression, logic suggests there is potential for reversing some of these processes.
Dermatol Clin 1991 Jul
PMID:The immunopathogenesis of AIDS. 187 22

Cells of the immune system are the target of infection with HIV. CD4 + T cells latently carry much of the viral burden in the blood and ultimately are depleted by infection with HIV. In contrast, infected tissue macrophages are long-lived and may serve as a viral reservoir. They are productive of relatively greater quantities of viral message RNA and its transcriptional product, infectious virions. Viral production by both cell types is modulated by environmental cytokines, the availability of which may be modified by the virus itself or by abnormally functioning HIV-infected immune cells. Not all susceptible cells are equally infected; although this phenomenon is not well understood, it has been related in vitro to maturation or differentiation. Blood DC and LC, antigen-presenting cells bearing many similarities to cells of the monocyte-macrophage lineage, are susceptible to HIV infection in vitro. Some evidence clearly indicates that, in vivo, epidermal LC may be infected with and productive of HIV and may be depleted or phenotypically altered in the HIV-infected individual. We, and others, have been unable to substantiate these findings by routine techniques used in the identification of HIV-infected macrophages in susceptible tissues, such as the brain, lungs, and lymph nodes (in situ hybridization for HIV-specific mRNA, electron microscopy for typical viral particles, recovery of infectious virus onto target cells, immunohistochemical staining of surface proteins in tissue, and polymerase chain reaction amplification of viral DNA). Evidence for the presence of HIV within the dermis of patients is clear; however, dermis contains a great variety of cell types as well as cells from the peripheral blood. We feel strongly that were the epidermis to harbor virus to any significant degree, it would have been identified by at least some of the methods described earlier. Although it is difficult to reconcile these reported differences, it appears that LC must be infected rarely. LC from lesional and apparently normal skin of HIV-infected individuals do not serve as an important reservoir of infectious HIV. Additionally, the diverse cutaneous manifestations seen in this population cannot be attributed directly to viral presence within the lesions but are more likely to result from the multifacted immunologic disregulation occurring systemically.
Dermatol Clin 1991 Jul
PMID:Monocytes, dendritic cells, and Langerhans cells in human immunodeficiency virus infection. 187 23


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