Travelers with cutaneous leishmaniasis cured without systemic therapy.

BACKGROUND: Cutaneous leishmaniasis (CL) is a disfiguring but not life-threatening disease. Because antileishmanial drugs are potentially toxic, the World Health Organization (WHO) recommends simple wound care or local therapy as first-line treatment, followed or replaced by systemic therapy if local therapy fails or cannot be performed. METHODS: To determine the feasibility and impact of the recommended approach, we analyzed the results of a centralized referral treatment program in 135 patients with parasitologically proven CL. RESULTS: Infections involved 10 Leishmania species and were contracted in 29 different countries. Eighty-four of 135 patients (62%) were initially treated without systemic therapy. Of 109 patients with evaluable charts, 23 of 25 (92%) treated with simple wound care and 37 of 47 (79%) treated with local antileishmanial therapy were cured by days 42-60. In 37 patients with large or complex lesions, or preexisting morbidities, or who had not been cured with local therapy, the cure rate with systemic antileishmanial agents was 60%. Systemic adverse events were observed in 15 patients, all receiving systemic therapy. CONCLUSIONS: In this population of CL patients displaying variable degrees of complexity and severity, almost two-thirds of patients could be initially managed without systemic therapy. Of these, 60 were cured before day 60. The WHO-recommended stepwise approach favoring initial local therapy therefore resulted in at least 44% of all patients being cured without exposure to the risk of systemic adverse events. Efforts are needed to further simplify local therapy of CL and to improve the management of patients with complex lesions and/or preexisting comorbidities.

[A case of neurological syphilis mimicking Horton's disease and polymyalgia rheumatica]. / Syphilis neurologique révélée par un tableau évocateur d'artérite temporale et de pseudopolyarthrite rhizomélique.

BACKGROUND: Syphilis has been making a comeback over the last 10 years. Neurosyphilis can occur at any stage of the infection but is difficult to diagnose because of the existence of misleading forms, of which we describe an example below. PATIENTS AND METHODS: A 56-year-old woman presented symptoms evoking polymyalgia rheumatica and giant-cell arteritis in a context of ibuprofen treatment for a few weeks. She also had myodesospsia, syphilids and syphilitic roseola, together with laboratory indicators of inflammation. A lumbar puncture revealed lymphocytic meningitis and a positive Treponema Pallidum Haemagglutination Assay (TPHA) for cerebrospinal fluid, thus confirming the diagnosis of neurosyphilis. Moreover, the ophthalmologic examination showed optic neuritis with papilla lesions of syphilitic origin. This was successfully treated with a 3-week course of penicillin G infusions. CONCLUSION: Symptoms evocative of Horton's disease and polymyalgia rheumatica can reveal syphilis, a disease dubbed "the great simulator" on account of the variety of clinical forms it can take.

[Non-cutaneous manifestations of secondary syphilis]. / Manifestations extra-cutanéomuqueuses de la syphilis secondaire.

BACKGROUND: The usual presentation of secondary syphilis is with cutaneous and mucosal symptoms. However, systematic symptoms can also occur. The purpose of this study was to describe non-mucocutaneous manifestations of secondary syphilis. PATIENTS AND METHODS: Patients from the Infectious Diseases Department of Tourcoing Hospital in whom secondary syphilis was diagnosed between January 2000 and December 2006 were enrolled in this study. Patients with secondary syphilis had the typical cutaneous and mucosal symptoms and a VDRLgreater than or equal to one quarter (or a fourfold increase in the VDRL if previously positive). RESULTS: Seventy-seven patients presenting a total of 80 cases of secondary syphilis were enrolled, 50 of whom were HIV-positive. Of these patients, 21 (26.3 p. 100) had neurological symptoms with three cases (3.8 p. 100) of uveitis, four (5 p. 100) of papillitis, two (2.5 p. 100) of retinitis and one (1.25 p. 100) of otosyphilis. In 14 of these 21 patients (67 p. 100), lumbar puncture was performed, confirming the diagnosis of neurosyphilis in six cases. Three patients (3.8 p. 100) had diarrhoea, four (5 p. 100) had abdominal pain and six (7.5 p. 100) had hepatomegaly. Seven (11.5 p. 100) patients had alanine aminotransferase levels above twice the normal upper limit and two above 10 times the normal upper limit. Three patients had bone pain and in one patient, osteitis was confirmed by technetium and gallium scintigraphy (osteolysis). CONCLUSION: In patients with secondary syphilis, clinicians should search for non-mucocutaneous symptoms. In the presence of these symptoms, appropriate syphilis treatment should be initiated.

[Toxic dermatitis caused by tramadol]. / Toxidermie au tramadol.

BACKGROUND: Tramadol chlorhydrate (Topalgic) is a powerful analgesic recently introduced in France where its use has spread rapidly. We report a case where this drug induced a maculopapulous toxic skin reaction with secondary erythrodermia. CASE REPORT: A 47-year-old man was treated for lower back pain with tramadol chlorhydrate (50 mg b.i.d.). Otherwise, he was in good general health and was taking no other medications. Shortly after beginning the treatment, he developed a highly pruriginous maculopapulous eruption involving the entire skin surface, hyperthermia and general degradation. There was no skin exfoliation, mucosal involvement nor nodal enlargement. Tramadol was withdrawn and the patient was given corticosteroid therapy. Secondary erythrodermia developed after termination of the corticosteroids. The lesions regressed after tramadol withdrawal. DISCUSSION: Tramadol-induced skin reactions are uncommon and usually benign. In our case, the delay from onset of tramadol and the development of the maculopapulous eruption was very short (four days). The patient was taking no other medication. We hypothesize that the patient had been sensitized by cross-reaction with another compound and recall the fundamental aspects of tramadol and opiate drugs.

[Symmetrical benign lipomatosis of the tongue and Launois-Bensaude lipomatosis]. / Lipomatose bénigne symétrique de la langue et lipomatose de Launois-Bensaude.

BACKGROUND: There are many causes of macroglossia, including fatty infiltration. Unlike unique or multiple lipomas of the tongue, non-encapsulated adipocyte masses develop in the tongue in symmetrical benign lipomatosis. Only six cases have been reported in the literature. CASE REPORT: A 69-year-old man with a history of chronic alcoholism developed a soft tumefied formation on the lateral margins of the tongue. A yellow-colored content was perceived through the thin mucosa. The formation was bilateral and had developed for more than 10 years. The patient also presented Launois-Bensaude lipomatosis localized on the neck, the nuchal region and the shoulders. DISCUSSION: This is, to our knowledge, the first reported case of symmetrical benign lipomatosis associated with Launois-Bensaude lipomatosis. An analogy between these two conditions has been suggested, but the six earlier cases of lipomatosis of the tongue reported in the literature developed in patients without cutaneous lipomatosis.

[Leg ulcers and antiphospholipid antibodies. Prospective study of 48 cases]. / Ulcères de jambes et anticorps anti-phospholipides. Etude prospective de 48 observations.

BACKGROUND: Leg ulcres can be seen as manifestations of antiphospholipid syndromes but their pathogenic relationship with vascular thrombotic events secondary to antiphospholipid antibodies remains to be defined with precision. A significant association between anticardiolipin antibodies and venous leg ulcers has been described. We conducted this study to determine whether such an association is found in venous ulcers and if it could also be present in cases involving the arterial and/or arteriolar circulation. PATIENTS AND METHODS: From December 1995 to March 1997, 48 patients with leg ulcers involving venous (27 cases), arteriovenous (9 cases) or arteriolar (12 cases) circulations were admitted. The etiologic diagnosis was based on clinical presentation and duplex Doppler findings examining the superficial and deep venous and arterial circuits. Antiphospholipid antibodies were searched for in all cases: VDRL, ELISA for IgG and IgM antiphospholipid antibodies, antiprothrombinase circulating anticoagulant. RESULTS: Circulating anticoagulants were found in 22 of the 48 patients (46%): 12/27 (44%) involved venous leg ulcers (anticardiolipin antibodies, 5 cases; circulating anticoagulants, 4 cases; both, 2 cases); 1/9 involved arteriovenous ulcers (anticardiolipin antibodies, 5 cases); 9/12 involved arteriolar ulcers (anticardiolipin antibodies, 3 cases; circulating anticoagulants, 6 cases; both, 3 cases). Seven of the 9 patients also had severe arteritis. A past history of venous thrombosis was found in 3 cases with venous ulcers and antiphospholipid antibodies. One patient among the 5 with arteriolar ulcers had a past history of arterial thrombosis. DISCUSSION: Our cohort is too small for a formal conclusion but underlines two points: 1. antiphospholipid antibodies can be associated with venous ulcers independently of thrombosis history. The hypothesis that leukocyte stasis and endothelial cell activation causes an immune reaction implicating antiphospholipid antibodies has been put forward. The usefulness of an antiaggregate treatment or an anticoagulant treatment should be discussed, 2. The possible association between arteriolar ulcers and antiphospholipid antibodies requires further large scale studies.