Gilbert De Dobbeleer

Value of Standard Laboratory Tests for the Early Recognition of Group A β-Hemolytic Streptococcal Necrotizing Fasciitis

The laboratory data for 17 patients with group A beta-hemolytic streptococcal necrotizing fasciitis (GAS NF) were compared with data for 145 patients hospitalized for cellulitis during the same period. Admission values of C-reactive protein and creatine kinase were higher for patients in the group with GAS NF than for patients in the group with cellulitis (P<.001), suggesting that standard laboratory tests may be useful for the early differential diagnosis of GAS NF and cellulitis.

Treatment of classical Kaposi's sarcoma with intralesional injections of cidofovir: Report of a case

The effect of intralesional injections of cidofovir, a nucleotide analog with potent in vitro activity against human herpesvirus 8 (HHV‐8), was studied in vivo in an HIV‐negative patient with classical Kaposis sarcoma (KS). After five weekly injections of the drug, no clinical, histological, immunohistological, or virological changes could be detected in comparison with saline‐injected lesions. These findings suggest that, once the KS tumor has developed, active viral replication is no longer involved in the pathogenesis of the disease. Alternative hypotheses are that HHV‐8 replication in blood‐borne cells may foster growth of spindle cells in the skin, or that blocking HHV‐8 may not affect existing lesions but may prevent new lesions from developing. J. Med. Virol. 55:215–218, 1998.

Disrupted Desmosomes in Induced Lesions of Familial Benign Chronic Pemphigus

An occlusive dressing was applied to the unaffected skin of the back of a patient with familial benign chronic pemphigus (FBCP). Small lesions of FBCP appeared after 48 h, and the ultrastructure of successive biopsies was studied. It was concluded that: (a) the initial phenomenon in FBCP is the result of an insufficiency of cellular adhesion. This confirms several previous reports. (b) desmosomes are separated in two halves, invaginated in vacuoles and later deeply included in the cell. The particular fate of these disrupted desmosomes has already been observed after the action of several enzymes on the epidermis and in Dariers disease.

Proliferating cell nuclear antigen distribution in verrucous carcinoma of the skin.

Verrucous carcinoma (VC) of the skin is a rare variety of well‐differentiated squamous cell carcinoma (SCC) characterized by aggressive local growth and a low metastatic potential. These tumours are known to have histological and virological features similar to classic warts or condylomata. The aim of the present study was to map the proliferative compartment in VC (n=7) in comparison with warts (n=10) and typical well‐differtntiated SCC (n=10). The proliferating cells were detected by immunostaining of proliferating cell nuclear antigen (PCNA) in formalin‐fixed, paraffin‐embedded tissue sections, using the commercially available anti‐PCNA monoclonal antibody PC10. Normal epidermis served as a positive control and reference. In VC and warts, the PCNA‐positive cells were principally located at the periphery of lesions, in the basal layer of the tumour islands. In some warts, however, stronger PCNA expressed was noted in the superficial layers, of the lesions corresponding to virus‐infected keratinocytes (koilocytotic cells). In contrast, in SCC, PCNA‐positive cells were randomly scattered throughout the tumours.

Fixed drug eruption: ultrastructural study of dyskeratotic cells

Electron microscopic studies have been carried out on three cases of fixed drug eruption, with particular regard to the dyskeratotic cells. The authors have tried to show the sequence of events leading from a normal basal keratinocyte to a dyskeratotic body. Ribosomes were first increased in number; then the the tonofbrillar system looked thicker, cytoplasmic organelles degenerated and numerous melanosomes appeared. Many dyskeratotic bodies were later found in epidermal macrophages and in the intercellular space. Several intra‐cytoplasmic desmosomes were found in the dyskeratotic cells and their evolution is discussed. The increased number of melanosomes seen in the dyskeratotic bodies could be due to injury to epidermal cell and thei evolution be due to injury to epidermal lysosomal catabolism or it could be due to an apparent increase in melanosome numbers, within cells whose volume has been reduced.

Juvenile elastoma (Weidman). An ultrastructural study.

Two cases of juvenile elastoma (nevus elasticus in disseminated tumors) were histologically and ultrastructurally investigated. The predominant components of this disseminated dysembryoplasia are abnormal elastic fibers. Both cases showed numerous large elastic fibers with an abundant background matrix. The elastic microfibrils were replaced by granular material. In one case, most of the abnormal elastic units remained isolated without forming elastic fibers.

Staphylococcal Scalded Skin Syndrome. An Ultrastructural Study

The authors investigated the ultrastructure of the epidermis of two children who suffered from the staphylococcal scalded skin syndrome (or the Ritters type of toxic epidermal necrolysis). This syndrome is attributed to the action of an exfoliative toxin produced by Staphylococcus aureus phage group II. A characteristic bullous cleavage was selectively observed at the level of the granular layer, without any damage in other epidermal layers. This cleavage was the result of disruption of desmosomes between granular cells in two halves, each half desmosome conserving the tonofilaments which were attached to its attachment plaque. No remarkable cytoplasmic alteration occurred in the granular layer, with the exception of the development of thickened tonofilaments among dilated endoplasmic reticulum. Odland bodies were particularly numerous in the areas of desmosomal disruption. This syndrome must be considered as an entity clinically, histologically and ultrastructurally separate from the drug form of toxic epidermal necrolysis.

In vitro acantholysis induced by D-penicillamine, captopril, and piroxicam on dead de-epidermized dermis

Drug‐induced pemphigus has been recognized for 20 years, hui the mechanisms leading to acantholysis are still unclear. It has recently been demonstrated that penicillamine, captopril, and thiopronin may produce acantholytic lesions, cither by direct toxic or biochemical died, in human skin explains. Our work confirms that penicillamine and captopril may induce acantholysis on the model of keralinocyte culture on dead, de‐epidermized dermis. Moreover, it demonstrates that piroxicam, a new non‐steroidal anti‐inflammatory drug, of which one side effect is a pemphigus vulgaris‐like eruption, is also able to produce in vitro acantholysis.

Classic Kaposi's sarcoma after multiple-partner heterosexual behavior in Central Africa

We present a case of a possible sexual transmission of classic Kaposis sarcoma. To our knowledge, this is the first report of such a case. We noted a long delay between the probable contaminant contact and onset of lesions, suggesting that human herpesvirus 8 has longer incubation periods in healthy individuals than in immunocompromised patients.

Long‐term prurigo in a returned expatriate with chronic strongyloidiasis

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