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Biomedical subjects

S Obałek

Publications and source records attributed to S Obałek.

At least 19 recordsLinked to original sources
PubMed1989

[Coexistence of multifocal bowen disease of the vulva and cervix carcinoma].

The authors described a case of a young woman with vulva carcinoma with features of multifocal pigmentary Bowen disease coexisting with atypical flat condylomas in the uterine cervix with focuses of carcinoma in situ. Both within the vulva and the uterine cervix there were histological features of carcinoma in situ, virological examination revealed the presence of virus HPV 16 genome. Sparing vulvectomy, the removal of pigmentary changes and electrocoagulation were performed. The authors discussed this rare case and presented therapeutic procedures.

Adult↗
PubMed1988

Human papillomavirus type 2-associated basal cell carcinoma in two immunosuppressed patients.

Human papillomavirus-2 genomes were detected by molecular hybridization in two cases of basal cell carcinomas that developed in immunosuppressed individuals. This form of human papillomavirus is usually responsible for common warts in the general population. Although it does not appear to have oncogenic potential, it may be, in some cases, associated with cutaneous malignancy.

Adult↗
PubMed1985

Identification of HLA antigens in familial and non-familial epidermodysplasia verruciformis.

The distribution of HLA specificities was studied in 7 non-familial cases of epidermodysplasia verruciformis (EV) and in 5 cases from one family. In the non-familial cases, six antigens of locus A (2, 3, 9, 10, 24, 26) and eight antigens of locus B (7, 15, 27, 35, 37, 38, 40, 41) were found. All 5 cases of familial EV possessed 26,5 haplotype, however, 6 of the remaining 12 healthy family members inherited the same haplotype. There is no association of EV with HLA-A and B antigens. However, the defect of cell-mediated immunity, present in all EV cases, may indicate the association of the disease with other major histocompatibility products (i.e. loci on immune response genes).

Animals↗
PubMed1981

T cell defect in patients with epidermodysplasia verruciformis due to human papillomavirus type 3 and 5.

Most of the patients with epidermodysplasia verruciformis (EV) were anergic to sensitization to dinitrochlorobenzene (DNCB) and were shown to have a decreased number of T lymphocytes and reduced lymphocyte PHA responsiveness. Preserved cell-mediated immunity (CMI) was found only in the abortive cases of EV infected with human papillomavirus type 3 (HPV-3). CMI was impaired to the same extent in patients with EV induced by HPV-3 and HPV-5, and in EV cases with combined infection with both viruses. In contrast to this, malignant transformation, i.e. of Bowen's carcinoma type, was observed only in the 7 patients infected with HPV-5. This could indicate that malignancy in EV is related rather to the oncogenic potential of HPV-5 type than to the extent of T cell defect that was similar in both EV varieties due to HPV-3 and HPV-5.

Animals↗
PubMed1980

Immune reactions in epidermodysplasia verruciformis.

Serum antibodies against human papilloma virus have been measured using immunodiffusion and enzyme linked immunosorbent assay in twelve patients with epidermodysplasia verruciformis (EV). The results were compared with those from sixty-six patients with other types of human papilloma virus diseases. Antibody prevalences were slightly lower in patients with EV than in the control patients. More remarkable was the difference between EV patiens and control subjects in tests of non-specific cell-mediated immunity, which was markedly depressed in the majority of patients with EV, but in the main preserved in patients with common warts. No specific immunological parameter was shown to be associated with malignant conversion of EV lesions, but malignancy was linked to the character of the inducing virus, and particularly to HPV type 5.

Adolescent↗
PubMed1980

Comparative studies on cell-mediated immunity in patients with different warts.

The distribution of peripheral blood T and B lymphocytes, the in vitro lymphocyte response to PHA, and in vivo experimental DNCB sensitization were studied in patients with different clinical forms of warts (common, 84; flat, 88; plantar, 22; genital, 14) and in 15 cases of epidermodysplasia verruciformis (EV). The percentage of T lymphocytes forming E rosettes was significantly decreased in patients with common (54.8%), flat (47.5%) and plantar (58.3%) warts, and those with EV (47.6%) in comparison with normal controls (68.4%). The DNCB sensitivity developed less frequently and it was less intensive in patients with common and flat warts than in the normal population. 60% of EV cases were anergic to challenging doses of DNCB. The lymphocyte response to PHA was reduced in all groups of patients studied as compared to normals. T cell function was found to be most defective in patients with EV and those with flat warts. Only a slight but statistically significant defect was demonstrated in the common wart group. CMI in patients with both plantar and genital warts was shown to be almost normal; except minor alterations of PHA-induced lymphocyte transformation and E rosetting T lymphocyte counts. These data have shown the divergency of CMI defect in the patients with different clinical forms of warts caused by various HPV types. This could indicate that distinct HPV types varied in their infectiveness and host cell-mediated resistance is a fundamental factor preventing viral infection.

Humans↗
PubMed1979

Epidermodysplasia verruciformis versus disseminated verrucae planae: is epidermodysplasia verruciformis a generalized infection with wart virus?

Recently it has been shown that epidermodysplasia verruciformis is induced by human papilloma/virus different from the papilloma/virus of warts, and that 2 distinct viruses-designated HPV-3 and HP-4--are responsible for it. Ten cases of epidermodysplasia verruciformis were found to have been caused by HPV-3. Clinically and histologically, as well as in the often depressed cell-mediated immunity they closely resembled long-standing verrucae planae, also caused by HPV-3. Contrariwise, in epidermodysplasia verruciformis caused by HPV-4 there are characteristic red, red-brown, and depigmented, pityriasis versicolor-like plaques, and malignant transformation seems almost inevitable. Cases due to HPV-3 may be abortive or even regressive, or stationary, and hard to distinguish from flat warts. No malignant conversion was seen in patients infected only with HPV-3, whereas it occurred in 2 patients infected with both viruses: HPV-3 and HPV-4. Pigmented plaques are the most important adverse prognostic sign in EV induced by HPV-3.

Animals↗
PubMed1979

Twenty-one years of follow-up studies of familial epidermodysplasia verruciformis.

21 years of follow-up study of a family with epidermodysplasia verruciformis (e.v.) have shown that members of one family can be infected with different human papillomaviruses (HPVs), either HPV 3 or HPV 4, and sometimes with both. The clinical picture resembled disseminated flat warts in cases induced by HPV 3, whereas in those caused by HPV 4 there were flat red or red-brownish plaques and depigmented pityriasis versicolor-like lesions. Malignancies developed only in family members infected with HPV 4, whereas the cases due to HPV 3 ran a more benign and slowly progressive or stationary course. There were also abortive and regressive cases, and the 3 children in whom the wart-like lesions did not recur after removal had an unimpaired cell-mediated immunity (CMI). In all cases of e.v., irrespective of the inducing virus, CMI was low, which seems to be an important factor in the pathogenesis of the disease. Humoral antibodies directed specifically against HPV 3 were present in the majority of the cases, mainly those infected with HPV 3.

Adolescent↗
PubMed1978

Defective function of T lymphocytes in psoriasis.

The distribution of thymus-derived (T) and bone marrow-derived (B) lymphocytes in 100 patients with psoriasis were studied by the rosetting techniques. Depression of the number of T lymphocytes forming spontaneous rosettes with sheep erythrocytes (E rosettes) occurred in 66% of patients, whereas no difference in B lymphocytes bearing C3 receptor (EAC rosettes) was observed between psoriatics and normals. The decrease in E rosettes was associated with the active phase of the disease. This disappeared 4-6 wk after onset of remission, which suggested that the abnormality in T-cell marker distribution is transitional. Lymphocytes forming neither E nor EAC rosettes, which were found to be significantly increased in active psoriasis, were identified as T lymphocytes since they reacquired normal E rosette function during short-term preincubation with concanavalin A (Con A). A serum factor was also demonstrated which inhibited E rosette formation by normal peripheral blood lymphocytes. Its activity increased linearly within 2 mo from the onset of skin lesions. The data suggest that in active psoriasis serum factors may be coated on the lymphocyte surface membrane which may be responsible for blocking of specific receptor for sheep erythrocytes and/or interfere with T lymphocyte function.

Animals↗
PubMed1978

Cell-mediated immunity (CMI) in psoriasis.

Patients with psoriasis were found to have less intensive experimental DNCB sensitization and decreased lymphocyte response to nonspecific mitogens, PHA, Con A, and PWM. E rosette formation was defective only in active psoriasis, in contrast to normal T and B cell counts. A reduction in DNCB hypersensitivity development and the percentage of E rosette forming lymphocytes were related to disease activity, but not to extention of skin lesions. The defect of E rosette function appeared to be transitional and completely disappeared in the remission. Abnormalities in CMI in psoriasis were found to be related at least partially to the existence in patients sera of a factor inhibiting normal T lymphocyte function. The study provides no evidence for the presence of primary CMI defect in psoriasis.

B-Lymphocytes↗
PubMed1978

Immunologic abnormalities in psoriasis: the inhibition of leucocyte migration by stratum corneum antigens.

The migration inhibition of peripheral blood leucocytes by stratum corneum (SC) antigens extracted from psoriatic scales and normal skin was studied in 25 patients with psoriasis and 12 normal controls. In 44% of patients, the radius of the area of spontaneous migration in the absence of antigen was significantly reduced. 9 out of 25 psoriatic cases showed inhibition of leucocyte migration after the addition of both SC antigens. Migration inhibition with SC antigens was observed only in patients in whom the radius of spontaneous migration area appeared to be normal. The data did not confirm the evidence of delayed hypersensitivity to epidermal SC antigens in patients with psoriasis. The decrease of spontaneous leucocyte migration in psoriasis might be dependent on the influence of antibodies against stratum corneum and/or immune complexes coated on lymphocyte or leucocyte surface membrane.

Adolescent↗