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Biomedical subjects

M Duvic

Publications and source records attributed to M Duvic.

At least 163 records · Page 9Linked to original sources
PubMed1989

Eruptive dysplastic nevi associated with human immunodeficiency virus infection.

The cutaneous manifestations of the acquired immunodeficiency syndrome include infections and neoplasms resulting from the immunodeficient state. Seven patients presenting with the symptom of new eruptive nevi with dysplastic histologic findings are described. These patients noted multiple new moles, which occurred in crops and in individuals without the dysplastic nevus syndrome (familial melanomas). This symptom occurred as the patients became symptomatic from their human immunodeficiency virus infection, developing acquired immunodeficiency syndrome or its related complex. Further confirmation and study of this phenomenon could lead to a better understanding of the pathogenesis of melanocytic dysplasia and its relationship to the immune system.

AIDS-Related Complex↗
PubMed1988

Major histocompatibility complex genes in systemic lupus erythematosus, Sjögren's syndrome, and polymyositis.

Current concepts about the roles of human leukocyte antigen (HLA) and complement genes in predisposing to connective tissue diseases are reviewed. Precise localization of disease conferring alleles and epitopes is confounded by two major phenomena: (1) clinical and serologic heterogeneity of the diseases and associations of several different HLA alleles with different and often overlapping autoantibody responses; and (2) linkage disequilibrium of many potentially relevant gene loci located on the disease-associated HLA haplotypes. Using molecular genetic tools in serologically homogeneous patient populations, and across racial lines, the Ro (SS-A) and la (SS-B) autoantibody responses in systemic lupus erythematosus and Sjögren's syndrome appear to associate most strongly with HLA-DQ alleles, whereas the anti-Jo-1 autoantibody in myositis correlates best with HLA-DRw52. A gene deletion of C4A within HLA predisposes to systemic lupus erythematosus in both white and black patients.

Alleles↗
PubMed1988

Molecular heterogeneity of complement component C4-null and 21-hydroxylase genes in systemic lupus erythematosus.

C4A-null alleles (C4A*Q0) and hereditary complete C4 deficiency (homozygous C4A*Q0,C4B*Q0) are associated with systemic lupus erythematosus (SLE). Using Southern blot analysis with C4 and 21-hydroxylase (21-OH) DNA probes, we studied SLE patients and normal control subjects with or without C4A*Q0, and 2 C4-deficient SLE patients. A previously reported large C4A,21-OHA gene deletion associated in normal subjects with the HLA-A1;B8;DR3;C4AQ0 haplotype was detected by the appearance of a new C4 Hind III 8.5-kb fragment and disappearance of a 3.2-kb 21-OH Taq I fragment. In 3 SLE patients with homozygous C4A*Q0 and 15 with heterozygous C4A*Q0, this deletion pattern occurred almost exclusively in association with the HLA-B8;DR3;C4A*Q0 phenotype; the one exception was a black SLE patient. Other C4A*Q0-bearing HLA phenotypes in white patients and black patients with SLE, and the 2 completely C4-deficient SLE patients, had normal DNA hybridization to both C4 and 21-OH probes. The genetic basis for C4-null alleles in SLE is heterogeneous. A large C4A,21-OHA deletion occurs mainly on the HLA-B8;DR3;C4AQ0 haplotype in SLE and controls. Other HLA haplotypes bearing C4A*Q0 have normal C4 and 21-OH genes, as demonstrated by Southern blot analysis.

Alleles↗
PubMed1988

Use of monospecific antisera and cRNA probes to localize the major changes in keratin expression during normal and abnormal epidermal differentiation.

We report here the isolation and characterization of three antisera, each of which is specific for a single keratin from one of the three different pairs (K1/K10, K14/K5, K16/K6) that are differentially expressed in normal human epidermis and in epidermal diseases of hyperproliferation. We have used these antisera in conjunction with monospecific cRNA probes for epidermal keratin mRNAs to investigate pathways of differentiation in human epidermis and epidermal diseases in vivo and in epidermal cells cultured from normal skin and from squamous cell carcinomas in vitro. Specifically, our results suggest that: (a) the basal-specific keratin mRNAs are down-regulated upon commitment to terminal differentiation, but their encoded proteins are stable, and can be detected throughout the spinous layers; (b) the hyperproliferation-associated keratin mRNAs are expressed at a low level throughout normal epidermis when their encoded proteins are not expressed, but are synthesized at high levels in the suprabasal layers of hyperproliferating epidermis, coincident with the induced expression of the hyperproliferation-associated keratins in these cells; and (c) concomitantly with the induction of the hyperproliferation-associated keratins in the suprabasal layers of the epidermis is the down-regulation of the expression of the terminal differentiation-specific keratins. These data have important implications for our understanding of normal epidermal differentiation and the deviations from this process in the course of epidermal diseases of hyperproliferation.

Amino Acid Sequence↗
PubMed1988

Expression of pemphigus vulgaris antigen in cultured human keratinocytes: effect of inhibitors, tunicamycin, and lectins.

We have investigated expression of pemphigus vulgaris antigen(s) in cultured human keratinocytes induced by the addition of extracellular calcium. Cycloheximide (10(-4) M) inhibited pemphigus antigen expression and stratification but actinomycin D (2 micrograms/ml) had no effect. Tunicamycin, which inhibits dolichol pyrophosphate-mediated glycosylation of asparaginyl residues specifically, was used to study the role of glycosylation. When calcium switching was carried out in the presence of tunicamycin, human keratinocytes did not stratify, and the expression of pemphigus antigen was partially inhibited and limited to cell-cell contact areas. Analysis of biosynthetically labeled proteins showed that the synthesis of high-molecular-weight proteins was markedly reduced in the tunicamycin-treated cells. A reciprocal blocking test demonstrated that concanavalin A and wheat germ agglutinin receptor share an epitope with pemphigus vulgaris antigen(s). These results suggest that Ca++, newly synthesized protein, and N-asparaginyl glycosylation are required for normal pemphigus antigen expression and epidermal stratification in vitro. Pemphigus vulgaris antigen may have a highly glycosylated, high-molecular-weight protein chain with carbohydrates playing an important role in epidermal cell morphology, adhesion, and stability of cell surface antigens.

Anti-Bacterial Agents↗
PubMed1987

Inflammation of actinic keratoses from systemic chemotherapy.

Seven patients receiving systemic chemotherapy for solid tumors developed an erythematous papulosquamous eruption resembling a drug eruption in sun-exposed areas. Careful examination revealed that the lesions were actually inflamed actinic keratoses. Biopsies of typical lesions in three of the patients confirmed this clinical impression. While one patient was receiving systemic 5-fluorouracil alone, and three were receiving 5-fluorouracil and cisplatin, three others developed inflammatory flares of actinic keratoses while receiving other chemotherapeutic drugs. One patient received doxorubicin and vincristine, one received doxorubicin alone, and one received the combination of dactinomycin, vincristine, and decarbazine. Since this phenomenon appears to be due to the effect of chemotherapy on the atypical keratinocytes present in actinic keratoses, discontinuation of the chemotherapy is not indicated in this situation.

Adult↗
PubMed1987

Human immunodeficiency virus-associated vitiligo: expression of autoimmunity with immunodeficiency?

Persistent viral infections have been postulated to be trigger factors for the development of autoimmune disease. We report the development of vitiligo in four patients with human immunodeficiency virus (HIV)-related conditions and in one patient with hepatitis who later developed both psoriasis and acquired immunodeficiency syndrome (AIDS). Other common features were hepatitis and multiple other viral infections. Ribavirin was associated with repigmentation in one patient. Vitiligo may be an example of an autoimmune disease triggered by viral infection in a genetically predisposed host.

AIDS-Related Complex↗
PubMed1987

Glucan-induced keratoderma in acquired immunodeficiency syndrome.

Six of 20 patients with acquired immunodeficiency syndrome (AIDS) or AIDS-related complex receiving intravenous infusions of soluble glucan (beta-1-3 polyglucose) developed a keratoderma of the palms and soles. The eruption began during the first two weeks of therapy and resolved two to four weeks after its discontinuation. The eruption was different in appearance from our previously reported keratoderma blennorrhagica in AIDS-associated psoriasis. None of the other 735 patients with AIDS or AIDS-related complex not treated with soluble glucan developed a similar keratoderma. The correlation between receiving glucan and the hyperkeratosis is highly significant. Since glucan is a naturally occurring component of the cell walls of yeast, fungus, and some bacterial organisms, recognition of its ability to induce such a striking reaction pattern may be of general significance and interest, although the reaction itself may be limited to patients with AIDS.

AIDS-Related Complex↗
PubMed1987

Acquired immunodeficiency syndrome-associated psoriasis and Reiter's syndrome.

Human immunodeficiency virus (HIV) causes a spectrum of immunodysfunction, the most severe of which is the acquired immunodeficiency syndrome (AIDS). We have followed the course of psoriasis in 13 patients over 2 1/2 years in a population of more than 1000 HIV-positive individuals. Four patients had a history of mild psoriasis that became severe and uncontrollable as symptoms of immunodeficiency developed. Psoriasis and HIV positivity, AIDS-related complex, or AIDS simultaneously developed in nine patients. In addition to psoriasis, Reiter's syndrome (arthritis, urethritis, and conjunctivitis) developed in one patient in the first group and three patients in the second group. Opportunistic infections, especially candidiasis and Staphylococcus, drugs, and an altered immune system may contribute to the development or flare of psoriasis in these patients. The appearance of severe psoriasis (especially in a patient with other risk factors for HIV) should prompt evaluation for HIV, and may be a poor prognostic indicator in HIV-positive patients, since nine of our 13 patients have died. Immunosuppressive therapy with methotrexate is contraindicated in this group of patients. Newer forms of drug therapy including etretinate show promising results for the management of AIDS-associated psoriasis.

AIDS-Related Complex↗
PubMed1986

Oral acyclovir for the prevention of herpes-associated erythema multiforme.

Herpes simplex virus is the single most common precipitator of erythema multiforme. Typically, erythema multiforme lesions appear 10 to 14 days after a recurrent herpes simplex virus infection and attacks can be disabling when they occur at frequent intervals. Prior to the introduction of acyclovir (Zovirax), there was no effective therapy to prevent herpes-associated erythema multiforme. Four patients were treated with a maintenance dose of acyclovir for periods ranging from 10 to 26 months; there were no significant side effects from the drug and only one recurrence of erythema multiforme. Oral acyclovir may become the treatment of choice for herpes-associated erythema multiforme.

Acyclovir↗
PubMed1986

Lupus panniculitis.

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Electromyography↗