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C Marquart-Elbaz

Publications and source records attributed to C Marquart-Elbaz.

11 recordsLinked to original sources
PubMed2001

[Does subcutaneous cellular tissue exist?].

BACKGROUND: The definition of the "subcutaneous cellular tissue" is still debated. METHODS: In order to establish the localisation and composition of this tissue, or, merely its existence, we interviewed French dermatologists and conducted a bibliographic study on the historical definitions of the so-called "subcutaneous cellular tissue". A questionnaire was sent to French professors of dermatology to assess their definition of the "subcutaneous cellular tissue". They were also asked to make a simple cartoon showing the anatomy of the skin and "subcutaneous cellular tissue". RESULTS: We obtained 37 answers which could be classified in three main categories: 1) "subcutaneous cellular tissue" and hypodermis are synonymous, 2) "subcutaneous cellular tissue" is an autonomous tissue which separates the hypodermis from the tissues below and 3) "subcutaneous cellular tissue" designates all structures located below the hypodermis. In an historic perspective, the "cellular system" was a macroscopic concept described in the eighteenth century as whitish fibrils delimitating "cells". It was renamed loose connective tissue in the twentieth century and thus "cellular" became obsolete. The definition of skin, and of "subcutaneous cellular tissue" in particular, has greatly changed over time. In the eighteenth century, only epidermis and dermis were considered as belonging to the skin, although some included the tela subcutanea. In the twentieth century, the "subcutaneous cellular tissue" is considered either as a part of the hypodermis, or as the hypodermis itself or as a tissue located between the hypodermis and the fascia. DISCUSSION: The difficulty in defining "subcutaneous cellular tissue" is the result of a French semantic problem. The "cellular tissue" became loose connective tissue. For French dermatologists, the skin is composed of epidermis, dermis and hypodermis and the hypodermis can therefore not be subcutaneous. In order to check whether an autonomous tissue could be evidenced under the skin, we conducted an histologic study, which is presented in a second article.

Connective Tissue↗
PubMed2001

[Cellular subcutaneous tissue. Anatomic observations].

INTRODUCTION: We showed in a companion paper that the definition of the French "subcutaneous cellular tissue" considerably varied from the 18th to the end of the 20th centuries and has not yet reached a consensus. To address the anatomic reality of this "subcutaneous cellular tissue", we investigated the anatomic structures underlying the fat tissue in normal human skin. METHODS: Sixty specimens were excised from the surface to the deep structures (bone, muscle, cartilage) on different body sites of 3 cadavers from the Institut d'Anatomie Normale de Strasbourg. Samples were paraffin-embedded, stained and analysed with a binocular microscope taking x 1 photographs. Specimens were also excised and fixed after subcutaneous injection of Indian ink, after mechanic tissue splitting and after performing artificial skin folds. RESULTS: The aspects of the deep parts of the skin greatly varied according to their anatomic localisation. Below the adipose tissue, we often found a lamellar fibrous layer which extended from the interlobular septa and contained horizontally distributed fat cells. No specific tissue below the hypodermis was observed. Artificial skin folds concerned either exclusively the dermis, when they were superficial or included the hypodermis, but no specific structure was apparent in the center of the fold. India ink diffused to the adipose tissue, mainly along the septa, but did not localise in a specific subcutaneous compartment. DISCUSSION: This study shows that the histologic aspects of the deep part of the skin depend mainly on the anatomic localisation. Skin is composed of epidermis, dermis and hypodermis and thus the hypodermis can not be considered as being "subcutaneous". A difficult to individualise, fibrous lamellar structure in continuity with the interlobular septa is often found under the fat lobules. This structure is a cleavage line, as is always the case with loose connective tissues, but belongs to the hypodermis (i.e. fat tissue). No specific tissue nor any virtual space was observed below the skin. Thus, the commonly used term "subcutaneous cellular tissue" is inappropriate.

Adipose Tissue↗
PubMed1997

[Primary cutaneous monomelic B-cell lymphoma].

BACKGROUND: Cutaneous B cell lymphomas, especially when appearing as a monomelic papulonodular eruption, are rare. PATIENT: Ms H. 87-year-old, consulted for a papulonodular eruption of the left lower limb which developed during the past 5 months. This limb had been the site of a lymphedema since a traumatism 8 years ago. Histopathological analysis and immunostaining of a nodule showed that it was a large cell lymphoma of follicular stem cells. There was no extracutaneous involvement and the patient was successfully treated with radiotherapy. Two months after the completed radiotherapy a cutaneous relapse on the trunk and the upper limbs was treated with cyclophosphamide-vincristine-prednisone chemotherapy. DISCUSSION: Lymphedema probably played a role in the genesis of this lymphoma presumably by reducing the local immune response. It may have harmed endothelial cells and maintained an antigenic stimulation leading first to lymphocyte hyperplasia and eventually to a true lymphoma, in the same way this has been proved for some MALT lymphomas.

Aged↗
PubMed1997

[Macrophage activation syndrome disclosing leukemic transformation of mycosis fungoides].

BACKGROUND: Mycosis fungoides can mimic pigmented purpuric dermatitis. We report such a case which progressed to peripheral T-cell lymphoma; progression was revealed by reactive hemophagocytic syndrome (RHS). CASE REPORT: A 65-year old male patient was hospitalized for a pigmented and purpuric eruption. The skin lesions appeared 2 years earlier and at that time biopsy had shown pigmented and purpuric dermatitis. One month before hospitalization, general signs appeared. On admission, he had papular and purpuric rash, mainly on the trunk, hepatosplenomegaly, enlarged axillar and inguinal lymph nodes, and fever at 38.2 degrees. A skin biopsy showed histologic changes typical of mycosis fungoides. He also had bicytopenia, hepatitis, and increased triglyceride and ferritin levels suggesting RHS which was proved by means of bone marrow biopsy. These tests also evidenced peripheral T-cell lymphoma. The patient was treated with two courses of chemotherapy (CHOP) but the disease progressed and he deceased. DISCUSSION: Mycosis fungoides can occasionally begin with an eruption very closely resembling pigmented purpuric dermatitis. Therefore, repeated biopsies should be done in case of widespread permanent pigmented purpuric dermatitis of no apparent origin. RHS is a life-threatening disease. The diagnosis should be suspected in any cytopenic patient with fever, increased triglyceride levels and abnormal liver tests. A search for an etiology must then be undertaken a prompt treatment is needed.

Aged↗
PubMed1997

[Chloroquine-induced achromotrichia. An ultrastructural study].

BACKGROUND: Electron microscopy examination of scalp biopsies from a patient with chloroquine achromotrichia gave elements concerning the pathogenesis of chloroquine-induced achromotrichia. CASE REPORT: A 21-year old light brown-haired patient developed achromotrichia after four months of treatment with chloroquine for subacute lupus erythematosus. Hair bleaching completely regressed 5 months after discontinuing chloroquine despite replacement with hydroxychloroquine. During the achromatrichia phase, many ultrastructural anomalies were observed in the hair root melanocytes: the nuclei were small and densified, and there was an accumulation of immature melanosomes in the cytoplasm; these melanosomes, mainly in stage II, were rarely transferred to keratinocytes. After recovery from the achromotrichia, melanocytes displayed a normal aspect. DISCUSSION: Pathophysiological disturbances leading to chloroquine induced achromotrichia are still unclear. The ultrastructural study of hair follicles in our patient show that under chloroquine action melanocytes become unable to perform complete melanin synthesis and to produce normally melanized melanosomes which may be transferred to keratinocytes. Non-melanized or poorly melanized melanosomes accumulate in the melanocytes which finally become inactive cells. These findings suggest that achromotrichia is induced by a toxic effect of chloroquine on the melanocyte.

Adult↗
PubMedDate not supplied

[Oral ulcers induced by nicorandil: prevalence and clinicopathological aspects].

INTRODUCTION: The first observations of "giant buccal aphthosis" induced by nicorandil were published in 1996. Nicorandil is a potassium channel activator used in the treatment of angina pectoris, which seems to induce specific buccal ulcerations. The purpose of this study was to analyze the clinicopathologic data of patients with aphthosis induced by nicorandil and to study the prevalence of this side effect. PATIENTS AND METHODS: We have seen 3 patients who spontaneously consulted, and 5 patients who were addressed to us after a telephone survey. We have then examined 100 consecutive patients treated by nicorandil for at least 1 month, who were hospitalized in 3 departments of cardiology in Strasbourg, and 100 age- and sex-matched controls who were treated by other antianginal drugs. RESULTS: Our 8 patients suffered from large, chronic and painful ulcerations of a 4-week duration, located on the tongue, the gingiva and the cheeks despite various symptomatic treatments. In one case, histopathologic data were consistent with an eosinophilic ulcer. Prospective study: among 100 patients treated by nicorandil, 5 had unusual chronic buccal ulcerations, whereas none of the 100 controls had aphthosis (p = 0.03). The confidence interval (99 p. 100) of this side effect prevalence was therefore 1 p. 100 to 14 p. 100. DISCUSSION: Nicorandil can induce large and painful buccal ulcerations with severe dysphagia, weight loss, and depression. Dermatologists should be aware of this particular side-effect, since our study showed a high prevalence, and because lesions heal rapidly after withdrawal of nicorandil. Why nicorandil may be associated with mouth ulcers remains unanswered. A past history of aphthae could be a cofactor of this side-effect.

Aged↗
PubMedDate not supplied

[Painful edema of the feet revealing ankylosing spondylitis].

INTRODUCTION: Painful peripheral oligoarthritis can reveal ankylosing spondylitis. In some instances, an acral pitting edema can be the sign of this affection. CASE REPORT: A 39-year-old man, with no significant previous medical history, consulted in a dermatology department for acral pain and edema of both feet, which were exacerbated during the second part of the night. On examination, he had a pitting edema and a livedo of the distal part of the feet. Biological investigations revealed an inflammatory syndrome and the presence of the histocompatibility HLA-B27 antigen. Bone scintigraphy revealed distal hyperfixation on both feet. Diagnosis of ankylosing spondylitis was established. DISCUSSION: Late-onset ankylosing spondylitis, which appears in subjects older than 35 years, can manifest as peripheral arthritis with systemic signs, often in the absence of involvement of the axial skeleton. Peripheral pitting edema of lower limbs can be the presenting sign. Since cutaneous involvement can be the presenting sign, dermatologists should be aware of this entity.

Adult↗