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Biomedical subjects

D Metze

Publications and source records attributed to D Metze.

At least 109 records · Page 6Linked to original sources
PubMed1995

[Scarring psoriatic alopecia].

Temporary hair loss is well accepted as a possible result of psoriatic plaques. On the other hand, it is still a controversial issue whether psoriasis can cause scarring alopecia. The following report presents a 38-year-old woman who had been suffering from progressive hair loss from chronic psoriatic plaques of the scalp for some years. Clinical examination revealed an area of scarring alopecia in association with typical features of psoriasis. Histology showed a cord-like fibrosis replacing former hair follicles, a perivascular lymphohistiocytic infiltrate in the upper dermis occasionally invading the follicular epithelium, and characteristic features of psoriasis of the scalp. The clinical course and the lack of evidence for any other causes of scarring alopecia suggest an aetiopathogenetic link between psoriasis and scarring alopecia. Knowledge of this relationship appears to be of practical significance, since efficient antipsoriatic therapy can stop hair loss and thus may be able to prevent scarring.

Adult↗
PubMed1995

Ultraviolet-B-induced apoptosis of keratinocytes: evidence for partial involvement of tumor necrosis factor-alpha in the formation of sunburn cells.

Irradiation with ultraviolet (UV) B radiation results in the formation of apoptotic keratinocytes called sunburn cells. Recently, it was demonstrated that keratinocytes can release tumor necrosis factor-alpha (TNF-alpha), which is known to cause apoptosis in particular cells. In addition, it has been shown that UVB light induces the release of TNF-alpha by keratinocytes and that keratinocytes express the 55-kD receptor for TNF-alpha. Therefore, we investigated whether TNF-alpha is involved in UV-induced apoptosis of keratinocytes. Normal human keratinocytes and HaCaT cells were exposed to UVB light, and apoptosis was examined by nick translation evaluated by fluorescence-activated cell sorter analysis. UVB induced apoptosis in a dose-dependent manner, which was confirmed by electron microscopy. Addition of a polyclonal antibody directed against human TNF-alpha immediately after UVB exposure was able to reduce DNA fragmentation. However, it was not possible to rescue all cells from apoptosis. To prove whether TNF-alpha is also involved in vivo in UVB-induced apoptosis of keratinocytes, Balb/c mice were exposed to UVB on their abdomens, skin biopsies were performed 24 h later, and sunburn cells were counted. A single dose of 2000 J/m2 caused a significant induction of sunburn cells. Subcutaneous injection of a polyclonal antibody directed against murine TNF-alpha immediately after UVB treatment resulted in a significant but incomplete reduction of sunburn cells, whereas injection of a rabbit IgG as a control had no effect. In both the in vitro and in vivo systems, application of recombinant TNF-alpha alone either to untreated keratinocytes or into normal murine skin did not induce sunburn cells. Thus, these data demonstrate that TNF-alpha is involved in UVB-induced apoptosis, but by itself is not able to induce sunburn cells. This further supports the notion that UVB-induced apoptosis of keratinocytes is a multifactorial event.

Animals↗
PubMed1995

Expression of the 27-kDa heat shock protein in human epidermis and in epidermal neoplasms: an immunohistological study.

The 27-kDa heat shock protein (HSP27) is a member of the small heat shock protein (HSP) family. In addition to its putative function in thermotolerance, this protein may play a part in the regulation of cell growth and differentiation. This study was conducted to assess the significance of the expression of HSP27 in human epidermis and in cutaneous neoplasms. Sixty-two biopsy samples from normal human skin and from inflammatory and neoplastic skin diseases were investigated by immunohistochemistry on formalin-fixed paraffin-embedded tissue sections, using a monoclonal antibody specific for HSP27. In normal human epidermis, HSP27 is expressed in the upper epidermal layers with a cytoplasmic staining pattern. The basal cell layer does not express detectable amounts of HSP27. In hair follicles, staining is mainly confined to the outer root sheath and to the infundibular epithelium. Melanocytes, dermal fibroblasts and endothelial cells do not express detectable amounts of HSP27. HSP27 could not be detected in fetal skin until the 20th week of gestation. Tumour cells in basal and squamous cell carcinomas do not express significant amounts of HSP27. In solar keratoses, seborrhoeic keratoses, human papillomavirus (HPV)-induced hyperproliferative lesions and inflammatory skin conditions, HSP27 expression largely resembles the pattern observed in normal human skin. HSP27 is expressed in a differentiation-related pattern in normal human epidermis and hyperproliferative disorders of the epidermis. We conclude that HSP27 may be regarded as a marker of differentiation in epidermal keratinocytes. Absence of HSP27 in the upper epidermal layers may be a marker for epidermal malignancy.

Basal Cell Carcinoma↗
PubMed1995

Immunohistochemical detection of p53 in melanomas with rare p53 gene mutations is associated with mdm-2 overexpression.

Expression of mutant p53 detected by immunohistochemistry has been described in human malignant melanoma, but there are few reports of molecular analyses. To investigate the genetic basis for p53 expression in malignant melanoma, we examined 58 primary tumors and 5 cutaneous metastases. The entire coding sequence of the p53 gene was screened by single-strand conformation polymorphism analysis and direct genomic sequencing of polymerase chain reaction products. p53 and mdm-2 expression were studied by immunohistochemistry. Two p53 gene mutations could be found in 1/63 samples examined, both having occurred in the same specimen from a patient with a nodular melanoma. p53 and mdm-2 expression were found immunohistochemically to increase with tumor progression both in frequency and in the mean proportion of positive cells, with the same cases staining positively for both antibodies. Our results suggest that a) p53 gene mutations are a rare event in human melanoma; b) accumulation and thus immunohistochemically detectable expression of p53 may result from posttranslational mechanisms affecting the p53 gene product; and c) p53 and mdm-2 are more important in late events in melanoma carcinogenesis.

Base Sequence↗
PubMed1994

Hailey-Hailey disease. Eradication by dermabrasion.

BACKGROUND: Chronic benign familial pemphigus (Hailey-Hailey disease) is a rare dominant genodermatosis that bothers patients by chronic recalcitrant plaques occurring mainly in the intertriginous areas. We looked for a surgical treatment that is not impaired by the complications and disadvantages of radical excision and grafting of involved areas. In 10 patients with debilitating Hailey-Hailey disease (five men, five women; age, 36 to 57 years), nine different involved areas (neck, axilla, cubital area, inframammary area, periumbilical area, groin and adjacent inner thigh, scrotum, vulva, and the perineal/perianal area) were treated by dermabrasion for a total of 46 treated regions. The plane of abrasion was located in the upper to middle dermis as verified by random sampling before and after surgery, thus documenting removal of the entire epidermis. RESULTS: In most instances, reepithelialization was completed after 7 to 10 days followed by excellent functional and cosmetic long-term results. When examined 3 to 79 months (median, 42 months) later, all treated areas remained completely disease free since surgery, except for major recurrences in four sites and minor recurrences in another four sites. Four of these areas were dermabraded again without subsequent relapse. CONCLUSIONS: Our results show that dermabrasion may be considered an excellent treatment of Hailey-Hailey disease that is unresponsive to conservative therapy. As a probable explanation, the intrinsic defect of cell adhesion in Hailey-Hailey disease seems to be limited to epidermal keratinocytes but spares adnexal structures from which rapid reepithelialization occurs.

Adult↗
PubMed1993

Human keratinocytes in vivo and in vitro constitutively express the 72-kD heat shock protein.

Exposure of cells to elevated temperatures induces a physiologic response characterized by the synthesis of a specific set of proteins (heat shock or stress proteins, HSPs) mediating repair mechanisms and protection from cellular damage. In the present study upon immunohistochemistry using a specific monoclonal antibody, the constitutive and heat-induced expression of the 72-kD HSP (HSP72) in normal human skin and in human epidermal cell lines (KB, A431) was investigated. Normal (unstressed) epidermis and adnexal structures of normal human skin were found to constitutively express HSP72. In contrast, a substantial HSP72 expression could not be observed in the dermal cellular compartment. In vitro heat treatment of punch biopsies from normal skin (42 degrees C, 4 h) resulted in a further increase of epidermal HSP72 expression. In addition, dermal cells were found to be induced to express HSP72. To further evaluate the spontaneous HSP72 expression of epidermal cells two epidermoid carcinoma cell lines (A431, KB) were investigated. Upon immunohistochemistry and Western blot analysis a significant HSP72 expression could be detected in unstressed KB and A431 cells. In contrast, a human fibrosarcoma cell line (HT1080) was negative for HSP72 at 37 degrees C but upon heat treatment a strong induction was observed. Furthermore, Northern blot analysis using a cDNA probe specific for human HSP72 revealed a constitutive expression of HSP72 mRNA in both epidermal cell lines. These findings demonstrate a significant expression of the stress-inducible HSP72 in unstressed human skin as well as in epidermal cell lines, suggesting that HSP72 may inherently be involved in the protective function of normal human skin.

Blotting, Northern↗
PubMed1993

[Pemphigus herpetiformis].

Pemphigus herpetiformis is an unusual variant of pemphigus. Clinically it can resemble Duhring's disease, while histopathological examination and, in particular immunofluorescence yield findings diagnostic for pemphigus. As pemphigus herpetiformis responds quite well to sulfones, recognition of this rare disorder is of practical relevance. In the present report, a case of pemphigus herpetiformis with an unusually young age of onset is presented. In addition, clinical features, results of histopathological examination and immunofluorescence, differential diagnosis and treatment are discussed.

Adult↗
PubMed1991

Immunoglobulins coat microorganisms of skin surface: a comparative immunohistochemical and ultrastructural study of cutaneous and oral microbial symbionts.

Only recently have human sweat glands been demonstrated to secrete immunoglobulins (Ig), paralleling Ig secretion in mucosal epithelia. It is well established that Ig protect mucosal membranes against infections by binding to surface structures of microorganisms. In view of these findings immunohistochemical studies were performed to determine if microbes on the skin surface are coated by Ig as proposed for mucosal bacteria and fungi. Smear preparations from the skin and oral cavity rich in micro-organisms were subjected to immunoperoxidase staining using anti-secretory component (SC), -IgA, -IgM, -IgG antibodies. An immunogold labeling technique of microbial suspensions of sweat and saliva was adapted to correlate the results on an ultrastructural level. Negative controls included unsuccessful staining for IgA in preparations obtained from an IgA-deficient patient as well as nonreactivity of subcultured microorganisms for all Ig classes or SC. Smear preparations from both the oral cavity and skin surface exhibited labeling of bacterial or fungal elements with anti-IgA, -IgM, -IgG, and -SC antibodies. Skin bacteria revealed a lower number of reactive microbes as compared to saliva. Staining intensity for the different Ig classes exhibited intra- and interindividual variations. Immunoelectronmicroscopically, Ig and SC could be detected either directly along the cell wall of coccal, coryneform, and fungal elements or on floccular and fimbrial material adhering to the bacterial surface. It is concluded that secretory Ig of the skin cover surface structures of microorganisms and thus modify their adhesional and/or infectious properties, resembling humoral surface immunity on mucous membranes.

Adult↗
PubMed1991

[Angiolymphoid hyperplasia with eosinophilia. Histologic study and successful therapy with the argon laser].

We report a case of angiolymphoid hyperplasia with eosinophilia (AHE) with regional lymphadenopathy. The multiple papules were composed of both a lymphoid infiltrate of predominant T-cell type with eosinophils and anomalous vascular proliferation lined by "histiocytoid" endothelial cells, which were in close association with a ruined artery at the subcutaneous level in the largest nodule. Immunoelectron microscopy revealed factor-VIII-related antigen to be concentrated within the Weibel-Palade bodies of the endothelial cells. Their cytoplasmic filaments consisted of vimentin. In the pericytes large amounts of actin were demonstrable. Since AHE has a benign progressive course and only local recurrence is noted, the lesions were treated with argon laser. Subsequently, lymphadenopathy resolved spontaneously and the blood parameters normalized. There is no evidence of recurrence 1 year after treatment.

Angiolymphoid Hyperplasia with Eosinophilia↗
PubMed1990

Cutaneous aspergillosis.

We report a cutaneous infection by Aspergillus flavus in a tetraplegic but otherwise healthy young man. He presented with multiple erythematous to violaceous indurated papules and plaques which had progressed to central ulcers or black eschars. Lesional scrapings, biopsies and cultures demonstrated a fungus, Aspergillus flavus, as the aetiological agent. As the patient had to leave for his home country before diagnosis had been established, we cannot report on the results of therapy in this case.

Adult↗
PubMed1990

Disseminated syringomas of the upper extremities. Case history and immunohistochemical and ultrastructural study.

A case of disseminated syringomas with unusual distribution and high age of onset is reported. The 66-year-old male patient presented with multiple lesions confined to dorsum of both hands and flexor side of both forearms. Morphological and immunohistochemical studies using keratin, S-100, carcinoembryonic antigen, and epithelial membrane antigen antibodies were performed both at light microscopical and ultrastructural level. These investigations revealed the presence of keratin filament containing colloid bodies near syringomatous epithelia. Reactivity for carcinoembryonic antigen could be demonstrated on the membranes of intracytoplasmic vesicles as well as within luminal debris. Absence of S-100 and epithelial membrane antigen in the tumor and ultrastructural features indicate ductal origin of syringoma.

Adenoma, Sweat Gland↗
PubMed1989

Immunohistochemical demonstration of immunoglobulin A in human sebaceous and sweat glands.

Immunoglobulin A (IgA) mediated humoral defense mechanisms have been detected on all mucous membrane surfaces. There are only a few papers about the presence of IgA in human skin. In order to demonstrate the occurrence of IgA in sebaceous and sweat glands, biopsies of normal human skin were investigated and compared to intestinal mucosa. Two different commercially available anti-IgA antibodies were used. For light microscopy peroxidase-anti-peroxidase (PAP) or avidin-biotin complex (ABC) staining was used, and for electron microscopy protein-A-gold (PAG) labeling was performed on tissue sections. Specifically decorated IgA was found in sebaceous glands as well as in various portions of eccrine glands. In sebaceous glands, the maximum of IgA concentration was seen near the mouth of pilosebaceous ducts. Sweat ducts exhibited a continuous coat of IgA, whereas secretory portions contained only singular scattered IgA positive cells. Immunoelectron microscopy suggests endocytotic uptake and processing of IgA in the glandular cells. These results indicate strongly that IgA are secreted by normal human sebaceous and sweat glands. Because it is well known that IgA plays an important role in inactivation of invading viruses, bacteria, and other antigenic structures on mucous membranes, it appears that IgA in sebum and sweat fulfil a similar function on the outer body surface.

Adolescent↗
PubMed1989

Secretory immunoglobulin A in sweat gland tumors.

The presence of immunoglobulin A (IgA) and secretory component (SC) was investigated in normal human skin and in cutaneous neoplasms including a variety of sweat gland tumors. Immunohistochemistry in normal sweat glands revealed the occurrence of secretory IgA (sIgA) as indicated by reactivity for IgA and SC in serial sections. The majority of 28 cases of sweat gland tumors could be demonstrated to retain their ability to produce IgA and SC. In normal as well as in neoplastic sweat glands heaviest staining for sIgA could be found in the lumina and at the surface of lining epithelia. This is comparable with the presence of sIgA in breast or intestinal neoplasms. In contrast other epidermal cysts or solid tumors were not labelled. In view of recent immunohistochemical studies the demonstration of IgA and SC may be of differentiating value in cutaneous glandular neoplasms.

Breast Neoplasms↗