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Biomedical subjects

M Duvic

Publications and source records attributed to M Duvic.

At least 145 records · Page 8Linked to original sources
PubMed1991

Papulosquamous disorders associated with human immunodeficiency virus infection.

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.

HIV Infections↗
PubMed1991

Psoriasis and psoriatic arthritis associated with human immunodeficiency virus infection.

It has been well established that psoriasis, psoriatic arthritis, and Reiter's syndrome can occur in patients with HIV infection. These arthocutaneous diseases tend to occur in temporal proximity to the development of AIDS and ARC, and their clinical manifestations are unusually severe. The appearance or exacerbation of psoriasis, arthritis, or Reiter's syndrome in a high-risk person should alert the clinician to possible underlying HIV infection. Treatment should be dictated by the severity of the skin and musculoskeletal disease as well as by the status of the immune system. Zidovudine appears to be effective in many diseases, especially psoriasis, and nonsteroidal antiinflammatory drugs are the mainstay for arthritis. Immunosuppressive agents such as methotrexate and azathioprine are contraindicated because they exacerbate immunodeficiency and promote infections. Epidemiologic studies suggest that the prevalence of these diseases, especially Reiter's syndrome, may be higher in HIV-positive populations than previously thought, especially in those patients with AIDS and ARC. Immunogenetic factors like HLA-B27 are important in the predisposition to Reiter's syndrome associated with HIV infection; however, it is not clear what role they play in HIV-associated psoriasis. Mechanisms underlying these observations remain unclear, although potential insights into the pathogeneses of psoriasis and Reiter's syndrome may be gained through future studies. Already it seems likely that CD4-positive helper T-cells, the target of HIV, are not necessary for the expression of psoriasis or Reiter's syndrome, and because of HLA class I associations, a role for CD8 positive cytotoxic T lymphocytes can be suspected. Infections, promoted by the profound immunodeficiency of AIDS, seem to be the most plausible explanations for the cutaneous and articular complications of HIV infection.

Arthritis, Psoriatic↗
PubMed1990

HLA-D region genes associated with autoantibody responses to histidyl-transfer RNA synthetase (Jo-1) and other translation-related factors in myositis.

Myositis has been associated with HLA-B8 and DR3, especially in white patients with polymyositis and serum anti-Jo-1 antibodies. Twenty-eight patients with myositis and serum translation-related autoantibodies anti-Jo-1, anti-PL-7, anti-PL-12, anti-KJ, and anti-SRP were studied for HLA class II specificities by Southern blotting with HLA-DR beta, DQ beta, and DQ alpha probes. The association of HLA-DR3 (DRw17) with anti-Jo-1 antibodies in white myositis patients was confirmed (P = 0.003, relative risk 8.9). However, HLA-DRw52 haplotypes, regardless of subtype, were present in all of the white and black patients with serum anti-Jo-1 and other translation-related autoantibodies. Moreover, one anti-Jo-1 positive patient had HLA-DRw8, an HLA-DRw52 haplotype on which the DR beta 3 gene has been partially deleted. No HLA-DQ specificity or allele was common to all patients. The HLA-DR3, DR5, DRw6, and DRw8 haplotypes, which bear the HLA-DRw52 specificity, share the most homology in the DR beta 1 first hypervariable region at amino acid positions 9-13. Thus, this DR beta 1 region appears to be the most likely candidate "epitope" for translation-related autoimmune responses in inflammatory myositis.

Alleles↗
PubMed1990

Human immunodeficiency virus-associated psoriasis, psoriatic arthritis, and Reiter's syndrome: a disease continuum?

The presence of peripheral arthritis and HLA-A, B, C, DR, and DQ antigens was evaluated prospectively in 18 Caucasian men with human immunodeficiency virus-associated psoriasis. An asymmetric polyarthritis occurred in 32% of the patients and correlated with the presence of HLA-B27. Extensive clinical overlap between psoriatic arthritis, psoriasis, and Reiter's syndrome was noted. No significant excess of the HLA antigens previously found to be associated with psoriasis was seen, which suggests that human immunodeficiency virus-associated psoriasis per se may instead constitute another form of spondylarthropathy that is more closely related to Reiter's syndrome.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Identification of human immunodeficiency virus hybridizing sequences in the peripheral blood of a patient with systemic lupus erythematosus.

Systemic lupus erythematosus, a multisystemic disorder, is considered a prototype of the autoimmune diseases. Although its cause remains unknown, a viral etiology has been proposed. We report that a rapid and sensitive messenger RNA in situ hybridization technique detected hybridizing sequences to the human immunodeficiency virus type in the peripheral blood cells of a woman with systemic lupus erythematosus in whom the presence of acquired immuno-deficiency syndrome was reasonably excluded.

Adult↗
PubMed1990

Myogenin is in an evolutionarily conserved linkage group on human chromosome 1q31-q41 and unlinked to other mapped muscle regulatory factor genes.

Myogenin is a member of a family of muscle-specific regulatory factors which includes MyoD1, Myf-5, and Myf-6 (also called MRF4 and herculin). Extensive regions of sequence homology in genes for these three factors suggest duplication events associated with their evolution. In the present study, the chromosomal location of the myogenin gene in humans (MYOG), mice (Myog), and Chinese hamsters (MYOG) was determined using in situ hybridization to human metaphase chromosomes as well as segregation analysis among interspecific somatic cell hybrid panels and interspecific backcrossed mice. We localize the gene encoding myogenin to human chromosome 1q31-q41 within a linkage group homologous with a region on mouse chromosome 1 and Chinese hamster chromosome 5. The results verify the nonlinkage of MYOG to MYOD1, MYF5, and MYF6 genes and indicate that events associated with the duplication of MYOG with respect to MYOD1, MYF5, or MYF6 loci were not chromosome-wide.

Animals↗
PubMed1990

Placental glutathione-S-transferase-pi mRNA is abundantly expressed in human skin.

Four overlapping cDNA clones were isolated from a lambda gt11 human placenta cDNA library using purified human IgG antibody, from a patient with bullous pemphigoid. The sequence was homologous to human placenta glutathione-S-transferase-pi (GST-pi). Using the placenta clone, epidermal cDNA clones were isolated from a human keratinocyte library. Expression of GST-pi mRNA in human skin, cultured keratinocytes and fibroblasts, and disorders of squamous hyperplasia was demonstrated by Northern blotting and in situ hybridization. Human epidermal and placental cDNA clones hybridized to the same genomic DNA fragments. Hybridization of placental cDNA to interspecific somatic cell hybrids showed retention of chromosome 11, confirming the assignment of GST 3 to the long arm of chromosome 11 by molecular means. Anti-GST-pi antibody did not give a basement membrane zone pattern, although some normal and BP sera contained antibodies to GST-pi. Human skin expresses glutathione-S-transferase-pi, which belongs to an enzyme family important for detoxification and carcinogenesis.

Amino Acid Sequence↗
PubMed1990

Immunology of AIDS related to psoriasis.

The association of severe psoriasis with HIV infection, which dysregulates and destroys the human immune system, supports the hypothesis that psoriasis is an immunologically mediated disease. Psoriasis and Kaposi's sarcoma share angiogenesis as basic early findings and could both be caused by differential cytokine expression or responsiveness. AIDS and research models including transgenic mice offer new models in which to study the role of the immune system and specific gene products in the pathogenesis of psoriasis and other skin diseases.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Connective tissue disease in southeast Georgia. A community based study of immunogenetic markers and autoantibodies.

HLA antigens, C4 allotypes and T cell antigen receptor (TcR)beta DNA polymorphisms were determined in a community based study of connective tissue diseases (CTD). HLA-B8, DR3 and C4A null phenotypes occurred frequently in Caucasian patients with CTD, especially those with systemic lupus erythematosus (SLE), but were also more commonly found among healthy white controls of this southeast Georgia community. TcR beta gene polymorphisms also showed differential segregation patterns between patients with SLE and scleroderma. High frequencies of ANA and anti-ssDNA antibodies occurred among apparently healthy family members and local controls. Genetic factors predisposing to CTD in a community setting appear to be similar to those reported from referral centers.

Alleles↗
PubMed1989

Synergistic enhancement of type I and III collagen production in cultured fibroblasts by transforming growth factor-beta and ascorbate.

Transforming growth factor-beta (TGF-beta) is a prototype of a family of polypeptides that regulates cellular growth and phenotypic differentiation [(1986) Science 233, 532-534; (1987) Cell 49, 437-438]. TGF-beta injection induces angiogenesis and fibrosis locally [(1986) Proc. Natl. Acad. Sci. USA 83, 4167-4171; (1987) Science 237, 1333-1336] and stimulates the synthesis of extracellular matrix proteins, fibronectin, collagens, and proteoglycans in vitro in many cell types [(1986) J. Biol. Chem. 261, 4337-4345; (1987) Biochem J. 247, 597-604]. Ascorbate is also known to induce collagen synthesis and to promote wound healing [(1988) J. Invest. Dermatol. 90, 420-424; (1986) Coll. Rel. Res. 6, 455-466]. We report that in cultured human skin fibroblasts, ascorbate and TGF-beta synergistically enhance the biosynthesis of type I and III collagens and their steady-state mRNAs. TGF-beta alone has no enhancing effect on type III collagen synthesis. The cooperation between ascorbate and TGF-beta may be of significance in wound healing and in disorders of fibrosis.

Ascorbic Acid↗
PubMed1989

C4A gene deletion and HLA associations in black Americans with systemic lupus erythematosus.

In North America and European Caucasoids with systemic lupus erythematosus (SLE) there is an increased frequency of a C4A, CYP21A gene deletion, largely associated with the HLA-B8,DR3,C4A*QO extended haplotype. There have been no consistent HLA associations reported for SLE in blacks, although an increased frequency of serologically determined C4A null alleles has been reported in two studies. We studied 79 black American SLE patients and 68 black controls by restriction fragment length polymorphism analysis to determine if a C4A gene deletion was a genetic risk factor for SLE. Moreover, the nature of the deletion and any HLA phenotypic associations were sought. Nineteen of 79 (24%) patients compared to 5 of 68 (7.4%) controls had a phenotypic C4A,CYP21A gene deletion (P = .005; RR = 4). A homozygous deletion in four patients gave a genotypic frequency of 23/158 (14.5%) SLE patients vs 5/136 (3.7%) controls (P = .001; RR = 4.5). The deletion was associated with HLA-DR2 (P = .03) and HLA-DR3 (P = .03). Moreover, all subjects with the deletion had HLA-DR2 or DR3 (P = 7.7 x 10(-6). HLA-B44 was also associated with the deletion (P = .02), and eight of the nine HLA-B44 positives also carried HLA-DR2. HLA-B8 approached significance (P = .08) and was always accompanied by HLA-DR3. Finally, this black population demonstrated a unique C4B gene size polymorphism with 80% C4B "short" as compared to the 40% C4B "short" frequency reported in whites. We conclude that a large C4A,CYP21A gene deletion, particularly associated with the HLA-B44, -DR2, and -DR3 alleles, is the strongest genetic risk factor thus far identified for SLE susceptibility in black Americans. Furthermore, the unique preponderance of the C4B "short" gene form may be a factor in the actual formation of the deletion.

Black People↗
PubMed1989

Gianotti-Crosti syndrome associated with Epstein-Barr virus infection.

Gianotti-Crosti syndrome, a distinctive eruption occurring after hepatitis B infection, is characterized by symmetric, nonpruritic lichenoid papules usually localized to the face, limbs, and buttocks. In North America, hepatitis B antigenemia is rarely associated with Gianotti-Crosti syndrome in infants. Recent reports indicate there are a variety of infectious agents associated with Gianotti-Crosti syndrome. We report a case of an 11-month-old white female infant with Gianotti-Crosti syndrome and concurrent primary Epstein-Barr virus infection without evidence of hepatitis B infection.

Acrodermatitis↗
PubMed1989

Unusual patterns of keratin expression in the overlying epidermis of patients with dermatofibromas: biochemical alterations in the epidermis as a consequence of dermal tumors.

Dermatofibromas are frequently associated with acanthosis of the overlying epidermis. Using monospecific antisera and cRNA probes, we have examined the pattern of expression of keratin and keratin mRNA in the affected epidermis of patients with these dermal tumors. Our studies reveal several abnormalities in keratin expression within the thickened areas of overlying epidermis. In two of 15 patients, we detected K6 and K16, keratins which are frequently associated with epidermal diseases of hyperproliferation but are not present in normal epidermis. In both cases, K6 and K16 were found in suprabasal layers, similar to that seen for psoriasis and squamous cell carcinomas. Expression of K6 and K16 in skin samples from patients with dermatofibromas seemed to be dependent upon how near was the tumor to the overlying epidermis, and possibly upon the degree of cellularity within the tumor mass. A second aberration in keratin expression, and one which did not appear to be linked to K6/K16 expression, was the altered expression of the basal epidermal keratin K14. Expression of this keratin and its mRNA was variable, often extending into multiple suprabasal layers and including both basal-like and squamous-like cells. In contrast to the expression of K6/K16, aberrant expression of K14 was a relatively frequent event, occurring in greater than 70% of the dermatofibroma skin samples examined. These observations provide the first biochemical evidence in support of previous morphologic studies, indicating that alterations in epidermal differentiation can occur as a consequence of dermal skin tumors.

Fibroma↗
PubMed1989

Kindler syndrome: report of two cases and review of the literature.

We evaluated two patients with hereditary bullous poikiloderma. Both had acral bullae, generalized poikiloderma with prominent atrophy, and acral keratoses. One patient, with sporadic disease, had, in addition, urethral and subglottic stenoses, webbing of digits, and poor dentition. The other patient, whose disease was dominantly inherited, had koilonychia. The results of cutaneous histopathology, electron microscopy, and immunofluorescence mapping studies are presented. It is possible that Kindler syndrome and Weary's hereditary acrokeratotic poikiloderma are variants of the same disease.

Age Factors↗
PubMed1989

Severe perinatal Marfan syndrome.

The cardiovascular manifestations of the Marfan syndrome in older children and adults have been well described. Clinical, radiographic, and echocardiographic data regarding three patients with severe perinatal Marfan syndrome are described. Two of these patients had the syndrome at birth and died in infancy. The syndrome was diagnosed in the third patient at 6 months of age and the child is still alive at 3 years of age. The possible relationship among the Marfan syndrome, Ehlers-Danlos syndrome, and osteogenesis imperfecta is considered. Patients with Marfan syndrome and severe cardiorespiratory problems early in life tend to have a limited life expectancy.

Acute Disease↗