Machet Mc

Fasciite à éosinophiles survenue secondairement à une infection par Borrelia burgdorferi

Resume Introduction La fasciite a eosinophiles associe un aspect sclerodermiforme de la peau, une hypereosinophilie et une atteinte des fascias constatee a l’imagerie par resonance magnetique (IRM) et par l’examen histologique. L’etiologie est inconnue mais quelques observations ont suggere une origine infectieuse. Nous rapportons l’association d’une fasciite a eosinophile a une infection a Borrelia burgdorferi . Observation Un homme de 54 ans consultait pour un œdeme indure et un enraidissement des mollets associes a un œdeme de la main gauche et de la face dorsale des doigts evoluant depuis 4 mois et apparus apres une morsure de tique sur le dos du pied gauche. Il y avait une hypereosinophilie a 1 010/mm 3 et un syndrome inflammatoire modere. La serologie de la maladie de Lyme etait positive par les methodes ELISA et Western Blot. Le diagnostic de fasciite a eosinophiles etait conforte par l’aspect en IRM et affirme par l’examen histologique d’une biopsie cutaneo-musculaire du mollet. La presence de B. burgdorferi n’a pas ete recherchee dans le tissu atteint. Discussion Il s’agit d’une fasciite a eosinophiles associee a une infection par B. burgdorferi sensu lato. Il peut s’agir d’une association fortuite mais la piqure de tique ayant precede le debut des signes de fasciite, il peut y avoir un lien de causalite. Des cas similaires ont ete decrits dans la litterature avec notamment mise en evidence du spirochete au sein du tissu atteint. La frequence de la fasciite a eosinophiles reste rare en regard de la prevalence de l’infection en zone d’endemie. On peut cependant supposer que chez certains malades, peut-etre genetiquement predisposes, l’infection par B. burgdorferi puisse etre a l’origine de fasciites.

Florid marginal zone differentiation in follicular lymphoma mimicking marginal zone lymphoma of MALT type in the lung

Up to 20% of laparoscopic procedures for tubal ectopic pregnancy are associated with persistent trophoblastic tissue. This is usually tubal in origin but cases of implantation of trophoblastic tissue in other intraabdominal sites have been described—usually on pelvic peritoneum. The secondary implantation of trophoblast tissue in omentum is very rare, with only two histologically described cases reported to date. We wish to report the first case of implantation of fetal parts in omentum following laparoscopic salpingectomy for a ruptured ectopic pregnancy. A 36-year-old woman presented with lower abdominal pain at 7 (+ 4) weeks’ gestation. A left ectopic pregnancy and an intrauterine pregnancy were detected on ultrasound scan. On laparoscopy a left ruptured ectopic pregnancy with fetal parts was seen. The left fallopian tube was removed piecemeal. A tubal ectopic pregnancy was confirmed histologically. Ten days later she presented with signs of peritonitis. On laparotomy a congested appendix and an omental mass, initially thought to be a left adnexal abscess, were seen. Both were removed and sent for histological examination. Macroscopically, the appendix showed a congested surface with pus-like organized material seen over the serosal fat. The omentum measured 170 · 60 · 20 mm and showed small areas of organized exudates and lobulated fat. Histologically, the appendix had acute inflammation with fibrinous exudates and fat necrosis on the serosal surface. The omentum showed an infiltrate of acute inflammatory cells and fat necrosis. Two deposits of mature cartilage were seen within the omentum. These were surrounded by immature mesenchymal cells. This was thought to represent a deposit of fetal parts from the previous ruptured ectopic pregnancy (Figure 1). Our case is unique in that fetal parts as opposed to trophoblastic tissue were found in omentum and this probably represents the implantation of fetal parts seen at the time of laparoscopy. Persisting trophoblastic tissue following laparoscopic procedures for tubal ectopic pregnancy can present as haemoperitoneum or peritonitis. This case report illustrates the point that the diagnosis must be suspected in any patient presenting with peritonism following treatment for ectopic pregnancy and a search for persistent tissue must be made.

Périartérite noueuse cutanée associée à une infection par le virus de l'hépatite C, régressive après une bithérapie antivirale

Resume Introduction Le virus de l’hepatite C (VHC) est souvent responsible de vasculites leucocytoclasiques par le biais d’une cryoglobulinemie de type II ou III. Les vasculites liees au VHC sans cryoglobulinemies sont plus rares. Observation Une femme âgee de 33 ans consultait pour un purpura infiltre necrotique des membres inferieurs, responsable d’ulcerations infracentimetriques des membres inferieurs. L’examen anatomopathologique montrait une vasculite touchant les arterioles hypodermiques, correspondant a une periarterite noueuse. Il n’y avait pas d’atteinte extracutanee. La malade avait une infection par le VHC (genotype 3) asymptomatique et non traitee depuis deux ans. Le traitement antiviral permettait la negativation de la viremie et la guerison des lesions cutanees avec un recul de deux ans par rapport a la fin du traitement. Commentaires Il s’agissait d’une vasculite repondant aux criteres de la periarterite noueuse cutanee, liee au VHC sans cryoglobulinemie. L’atteinte hepatique etait peu severe et ne necessitait pas un traitement antiviral. L’atteinte cutanee n’ayant pas regresse avec la colchicines et le genotype viral etant favorable, nous avons decide d’instituer un traitement antiviral. Cette option therapeutique doit etre connue des dermatologues, en pesant toutefois le risque potentiel d’aggravation de la vasculite par l’interferon.

Périartérite noueuse cutanée et maladie de Crohn : une association à ne pas méconnaître

INTRODUCTION Cutaneous polyarteritis nodosa (CPAN) is an entity which needs to be acknowledged, since it can have a spontaneously adverse outcome. We report two cases of CPAN associated with Crohns disease. CASE REPORTS The first patient was suffering from Crohns disease for 9 years when she was referred for a necrotic toe. A diagnosis of necrotizing angeitis was confirmed by histological examination of a skin biopsy. Despite systemic corticosteroids, the lesions became more severe, requiring immunosuppressive treatment. The second patient was a female patient referred with forefoot ischemia. Cutaneous histology confirmed the diagnosis of necrotizing angeitis that responded favourably to corticosteroid treatment. The patient had been diagnosed with Crohns disease 2 months previously. CONCLUSION CPAN differed from systemic PAN by the absence of visceral involvement. Its association with Crohns disease, although uncommon, must be recognized as it affects treatment and monitoring.

Extensive, erosive congenital self‐healing cell histiocytosis

Case 1 A newborn full-term male, with no family history of skin disease, presented multiple erosive lesions on 40% of the cutaneous surface, predominantly on the face and scalp. He showed discrete erosions in the oral and nasal mucosal membranes. The suspected diagnoses were congenital bullous epidermolysis, diffuse impetigo, staphylococcal scaled-skin syndrome or neonatal pemphigus. Histopathology examination revealed, underlying a slightly acanthosic epidermis, a massive infiltration of Langerhans histiocytosis cells (large cells with kidney-shaped nuclei) intermixed with infiltrates of eosinophils. Sporadic ulceration was observed, with a disruption of the basal membrane. Immunohistochemical staining of cells revealed positivity for S-100 and CD1a protein. Electron microscopy examination of a skin sample showed lobulated nuclei inside the histiocytes, with Birbeck granules. The skin erosions resolved spontaneously (Fig. 1). After 3 months, the crusted lesions had completely disappeared, leaving non-inflammatory scars with numerous small epidermal cysts (Fig. 2).