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Biomedical subjects

W F Lever

Publications and source records attributed to W F Lever.

At least 19 recordsLinked to original sources

[Inflammatory skin diseases and hypereosinophilia].

Among the dermatoses associated with tissue eosinophilia are pemphigus vegetans, bullous pemphigoid, granuloma facial and Wells' syndrome. Eosinophilic spongiosis can occur in the early stage of pemphigus. Pemphigus herpetiformis, a recently introduced term, does not represent a well defined entity but develops into either pemphigus vulgaris or pemphigus foliaceus. Granuloma facial is basically vasculitis. Eosinophilic cellulitis or Wells' syndrome shows numerous eosinophils which degranulate and through confluence of their granules form the so-called flame figures.

Cellulitis

Cell surface carbohydrates in proliferative epidermal lesions. II. Masking of peanut agglutinin (PNA) binding sites in solar keratoses, Bowen's disease, and squamous cell carcinoma by neuraminic acid.

Seventy-six skin biopsies of proliferative lesions were studied by using 4 different lectins and an avidin-biotin-peroxidase complex. In solar keratosis, Bowen's disease and squamous cell carcinoma, malignant-appearing keratinocytes exhibited loss of membrane staining with Concanavalia ensiformis agglutinin (Con A), but revealed cytoplasmic staining. When incubated with peanut agglutinin (PNA), the malignant keratinocytes did not stain. However, the PNA binding sites were not absent, but masked by sialic acid. Following cleavage of the sialic acid with neuraminidase, free PNA binding sites could be demonstrated in the plasma membranes. In contrast, the keratinocytes in keratoacanthomas showed membrane staining with Con A and also contained free PNA binding sites. These histochemical findings confirm and extend our earlier observations regarding cell surface carbohydrates in premalignant and malignant epidermal lesions.

ABO Blood-Group System

Distribution of carbohydrate residues in normal skin.

Sections of biopsies of normal skin obtained from 11 individuals were incubated with 8 lectins using an avidin-biotin complex (ABC). All sections when incubated with the appropriate lectin showed the presence of the following carbohydrate residues: L-fucose, beta-(1-4)-D-GlcNAc)2 (N-acetylglucosamine), acetylneuraminic acid, Gal-beta-(1-3)-GalNAc (N-acetyl-galactosamine), beta-D-galactose, alpha-D-glucose, and alpha-D-mannose. In addition, sections of individuals with blood group A showed alpha-D-GalNAc and sections of individuals with blood group B showed alpha-D-galactose. In the stratum (str.) basale, carbohydrates were present in small quantities, but as the cells matured and moved upward, the incorporation of carbohydrates into the cell membranes increased considerably. In the str. granulosum, lectin reactivity was absent in many sections, probably due to masking by phospholipids. The dark cells in the eccrine glands showed reactivity with all lectins except in the one nonsecretor with blood group A1, whose dark cells showed no L-fucose and alpha-D-GalNAc. The endothelial cells of the blood vessels showed lectin reactivity except when incubated with concanavalin A. The sebaceous glands showed both cytoplasmic and membrane staining when incubated with various lectins.

Acetylgalactosamine

Cell surface carbohydrates in psoriasis. Defective cytoplasmic transport by glycoconjugates carrying fucose residues suggested by lectin staining.

Eleven biopsy specimens of normal skin and twenty-four biopsy specimens of psoriatic lesions were examined histochemically by using several lectins (Ulex europaeus, UEA-1; Dolichos biflorus, DBA; Bandeirea simplicifolia, BS-I; Concanvalia ensiformis, Con A; Triticum vulgaris, WGA; Ricinus communis, RCA; Arachis hypogoea, PNA) in order to evaluate the presence and distribution of various carbohydrates in normal and psoriatic keratinocytes. The findings revealed that keratinocytes from psoriatic lesions are distinguished by a different composition of carbohydrate residues incorporated in their plasma membranes. In particular, the intracellular transport of alpha-L-fucose, alpha-D-mannose, and alpha-D-glucose to the plasma cell membrane is impeded, whereas their synthesis in the cytoplasm of the psoriatic keratinocytes is largely unaltered. In addition, due to the lack of terminal alpha-L-fucose, the alpha-D-N-acetyl-galactosamine and alpha-D-galactose residues cannot be transferred to the plasma membranes and, therefore, the antigens for blood groups A and B remain incomplete in psoriatic epidermis. On the basis of these findings and in comparison with previous findings of our group on hyperproliferative, malignant keratinocytes, it is concluded that particularly the disordered cytoplasmic transport of alpha-L-fucose-carrying glycoconjugates may represent a specific defect in psoriasis, possibly linked with the pathogenesis of this disease.

Acetylgalactosamine

Cell-surface carbohydrates in proliferative epidermal lesions. Distribution of A, B, and H blood group antigens in benign and malignant lesions.

The distribution of A, B, and H blood group antigens was studied by means of peroxidase-antiperoxidase technique in normal skin and in lesions of carcinomas in situ (solar keratoses, Bowen's disease), squamous cell carcinoma, keratoacanthomas, and verrucae. In normal skin, the epidermis of persons of blood group O showed H antigens throughout the epidermis; of blood group A, H and A antigens; and of blood group B, H and B antigens. In lesions of solar keratoses, there were no antigens of blood groups in the irregular downward proliferations. In five of 11 cases of Bowen's disease, there were no antigens of blood groups in the epidermis. In eight out of 10 cases of squamous cell carcinoma, no antigens of blood groups were found in the islands of the neoplastic process, but in two cases they were present in a patchy distribution. In the benign lesions examined, the antigens of A, B, and H blood groups were always present, although in verrucae the staining was confined to the upper layers of the epidermis only.

ABO Blood-Group System

Correlation of antibodies in skin and serum with disease severity in pemphigus.

Direct and indirect immunofluorescence (IF) testing was performed on 63 patients with active or inactive pemphigus in order to determine the reliability of these tests for diagnosis and for monitoring disease severity. Direct IF was positive in 58 of 63 patients with pemphigus. The five patients with negative direct IF had been free of lesions for more than a year. Thus, the direct IF test is a reliable diagnostic procedure that shows positive findings early in the disease. Indirect IF is inferior to direct IF as a diagnostic test because it may be negative in early cases, as observed in four patients. Furthermore, indirect IF, contrary to claims, is not reliable for evaluating the status of the disease. Thus, in patients with lesions and receiving treatment, 41% of the determinations showed a negative titer; whereas in patients free of lesions, 45% of the determinations showed a positive titer. In particular, seven patients without lesions and without treatment for more than a year had a positive titer.

Antibodies

Immunosuppressants and prednisone in pemphigus vulgaris: therapeutic results obtained in 63 patients between 1961 and 1975.

Evaluation of the treatment in 63 patients with pemphigus vulgaris showed that six patients (9.5%) died of the consequences of high-dosage prednisone treatment, while 24 patients (38.1%) were free of lesions and not receiving treatment. Immunosuppressants (methotrexate, cyclophosphamide, and azathioprine) are of value in patients with severe pemphigus vulgaris since they often reduce the maintenance dose of prednisone required after high-dosage prednisone treatment. Immunosuppressants are of even greater value in patients in the early, stable stage of pemphigus vulgaris. Of 16 such patients initially treated with a combination of an immunosuppressant and maintenance doses of prednisone not exceeding 40 mg on alternate days, 13 at no time required treatment with higher doses of prednisone. The good results obtained with this method emphasize the importance of diagnosing and treating pemphigus vulgaris in its early stage.

Adult

Localized mycosis fungoides with prominent epidermotropism: Woringer-Kolopp disease.

A patient had a single, large, sharply demarcated lesion on one leg. Under the mistaken diagnosis of malignant melanoma in situ, the lesion was excised and the area grafted in 1956. There has been no recurrence in the past 20 years. Histologic reevaluation led to a diagnosis of mycosis fungoides with pronounced epidermotropism of the cellular infiltrate. This case has close clinical and histologic resemblance with three cases published in Europe and regarded as a special form of reticulosis as first described by Woringer and Kolopp. Mycosis fungoides with marked epidermotropism is not always a benign localized disease but may be widespread and lead to death.

Adult

Secretion from human apocrine glands: an electron microscopic study.

Electron microscopic examination of apocrine glands revealed three types of secretion: merocrine apocrine, and possible holocrine. In the merocrine type of secretion numerous vesicles originating in the Golgi area discharged their granular contents into the lumen of the gland. In the apocrine type of secretion three stages were observed: (1) formation of an apical cap; (2) formation of a dividing membrane at the base of the apical cap; and (3) formation of tubules avove the dividing membrand that extended parallel to the membrane and led to a separation of the apical cap from the underlying cell, In the holocrine type of secretion individual secretory cells or even strands of secretory cells were dischard into the lumen of the gland.

Adult

Ultrastructural localization of in vivo bound immunoglobulins in bullous pemphigoid--a preliminary report.

The ultrastructural location of in vivo bound immunoglobulins in a case of bullous pemphigoid was determined by coupling peroxidase to antihuman gamma globulin. Immunoglobulin deposits were found exclusively in the space between the basal cells and the basal lamina. The location of the immunoglobulin in bullous pemphigoid thus differs from that in lupus erythematosus where immunoglobulins are found mainly below the basal lamina.

Antibodies, Anti-Idiotypic