Insaf Mokhtar

Risk Factors for Erysipelas of the Leg in Tunisia: A Multicenter Case-Control Study

Background: Risk factors for erysipelas (cellulitis) were rarely evaluated in controlled studies. Regional variations of these risk factors have never be assessed. Objective: To assess risk factors for erysipelas of the leg in Tunisia. Subjects and Methods: Case-control study in seven hospital centers in Tunisia. Cases were 114 consecutive patients with erysipelas of the leg [sudden onset (<24 h) of a well-demarcated dermo-hypodermatitis with fever or chills]. Two controls were matched to each case for age, sex, and hospital (n = 208). Main outcome measures are local and general suspected risk factors for erysipelas of the leg. Results: In multivariate analysis, disruption of the cutaneous barrier (i.e. traumatic wound, toe-web intertrigo, excoriated leg dermatosis or plantar squamous lesions) and leg edema were independently associated with erysipelas of the leg, with respective odds ratios of 13.6 (95% confidence interval: 6.0–31) and 7.0 (1.3–38). No association was observed with diabetes, alcoholism, or smoking. Conclusions: We confirmed the major role of local risk factors and the minor role of general risk factors for erysipelas of the leg, in a setting different than the one previously studied. Detecting and treating toe-web intertrigo and traumatic wounds should be considered in the prevention of erysipelas of the leg.

Leishmaniose endonasale primitive à Leishmania infantum MON-80 en Tunisie

BACKGROUNDnMucocutaneous leishmaniasis is endemic in Central and South America. It causes massive mutilating and disfiguring lesions and can lead to destruction of facial structures. In Tunisia, leishmaniasis of the mucous membranes is rare, usually developing as a complication of cutaneous leishmaniasis via direct extension. We report the first case in Tunisia of isolated and primary nasal leishmaniasis.nnnCASE REPORTnA 70-year-old man with a history of nephrectomy for renal lithiasis was seen with a painless nodule that had been present for one month. The latter was erythematous, polypoid and firm, with a diameter of 2 cm, and was situated in the right endonasal mucosa. The diagnosis of leishmaniasis was confirmed by histological and direct examinations revealing high numbers of amastigotes of Leishmania. Culture of the offending organism in NNN medium and isoenzymatic characterization resulted in identification of MON-80 Leishmania infantum leishmaniasis. The outcome was good with treatment, and the nodule was deflated after six months.nnnDISCUSSIONnThere have been few reports of similar cases of primary and isolated mucosal leishmaniasis caused by Leishmania infantum. Our case is also unusual in that zymodeme MON-80 is only rarely a cause of Mediterranean leishmaniasis.

Bathing suit ichthyosis caused by a TGM1 mutation in a Tunisian child

Bathing suit ichthyosis (BSI) is an uncommon phenotype classified as a minor variant of autosomal recessive congenital ichthyosis (ARCI).

A case of linear atrophoderma of Moulin successfully treated with methotrexate

Linear atrophoderma of Moulin is an acquired rare and self‐limited skin condition. It is characterized by atrophic bandlike skin lesions that often show hyperpigmentation and always follow the lines of Blaschko. Usually it begins in childhood or adolescence and there is no evidence of any long term progression. We describe a case of a 21‐year‐old woman with clinical and histological features of linear atrophoderma of Moulin. The patient was successfully treated with methotrexate 20 mg/week during 6 months with an improvement of skin pigmentation and atrophy. Approximately, 30 cases of linear atrophoderma of Moulin were described in the literature. There is not a proven effective treatment of this dermatosis. High dose penicillin, topical corticosteroids, heparin, and oral potassium aminobenzoate have been used but found to be uneffective. To our knowledge, this is the first case of extensive linear atrophoderma of Moulin treated with methotrexate.

Erythroderma: A Clinical Study of 127 Cases and Review of the Literature

Background: Several publications reported different causes of erythroderma. Objective: The aim of this study was to determine the frequency of erythroderma and its aetiologies in Tunisian dermatology departments. Methods: This is a multicentric and retrospective study including all erythroderma patients in all Tunisian dermatology departments who consulted during a period of 5 years. Clinical and laboratory data were analysed. Results: Erythroderma was diagnosed in 127 patients; an incidence of 0.065% of patients is seen in dermatology consultations. In children (33 cases), the most frequent causes of erythroderma were ichthyosis (42.5%), seborrhoeic dermatitis (27.5%) and psoriasis (21%). In adults (94 cases), the main causes of erythroderma were psoriasis (41.5%), eczema (13%) and drug reactions (13%). Drug-related erythrodermas were specifically associated with fever and oedema (p = 0.0005) and eosinophilia (p = 0.01). Conclusion: No atopic erythroderma was observed, and eosinophilia was significantly associated with drug reactions.

Human herpesvirus-8 and hepatitis B and C virus infections in pemphigus.

we obtained clinical resolution. No recurrence was observed over the 11-month period. Pseudochromhidrosis is characterized by the secretion of colorless sweat, which becomes colored when it reaches the skin surface because of contact with dyes, exo-genous pigments, or products derived from chromogenic microorganisms (corynebacteria, Bacillus spp., Piedraia, Malassezia furfur). The differential diagnosis includes chromhidrosis, where it produces colored sweat from eccrine or apocrine sweat glands. The apocrine form is caused by the increased concentration or a change in the oxidation state of lipofuscin, the pigment normally present in the apocrine sweat. In the eccrine form, less commonly, sweat glands release sweat in the water-soluble pigments derived from the ingestion of drugs or dyes. Pseudochromhidrosis, eccrine chromhidrosis, and apocrine chromhidrosis differ not only in pathogenesis but also in terms of prognosis and treatment: in the first two forms, we can achieve complete healing by removing the cause of the pigmentation of the sweat; in the last one, we can act only with symptomatic drugs, such as pilocarpine, and reduce or inhibit sweating. Apocrine chromhidrosis is a chronic disease that occurs in puberty; when under hormonal stimulation the apocrine secretion activates and tends to resolve spontaneously in adulthood, when physiologically apocrine secretion is reduced. In our case, videodermoscopy was of great help, which allowed us to evaluate the distribution of pigment on the skin surface.

Bowen's disease of the digit successfully treated with immunocryosurgery.

rosus et atrophicus, vitiligo, rosacea, and rosacea-like eruptions). The precise mechanism by which tacrolimus improves CRP is unknown. A possible explanation is that tacrolimus modifies keratinocyte differentiation and induces normalization on epidermal proliferation, a fact that is reflected by a reduction in the expression of Ki-67, as occurs on psoriasis. In summary, CRP is a rare entity that involves several etiopathogenic factors. Topical tacrolimus is a new option for treating CRP. The effect is based on their ability to modify epidermal proliferation and keratinocyte differentiation. We need more studies that compare the efficacy of topical tacrolimus with other treatment options such as calcipotriol or topical retinoids.

Onychomadesis during bullous pemphigoid.

REFERENCES 1. Hillemanns P, Wang X, Staehle S, Michels W, Dannecker C. Evaluation of different treatment modalities for vulvar intraepithelial neoplasia (VIN): CO(2) laser vaporization, photodynamic therapy, excisionandvulvectomy. GynecolOncol 2006;100:271-5. 2. Andreasson B, Moth I, Jensen SB, Bock JE. Sexual function and somatopsychic reactions in vulvectomy-operated women and their partners. Acta Obstet Gynecol Scand 1986;65:7-10. 3. Kaufman RH. Intraepithelial neoplasia of the vulva. Gynecol Oncol 1995;56:8-21. 4. van Seters M, van Beurden M, de Craen AJ. Is the assumed natural history of vulvar intraepithelial neoplasia III based on enough evidence? A systematic review of 3322 published patients. Gynecol Oncol 2005;97:645-51. 5. Sheen MC, Sheu HM, Jang MY, Chai CY, Wang YW, Wu CF. Advanced penile verrucous carcinoma treated with intra-aortic infusion chemotherapy. J Urol 2010;183: 1830-5.

Subungueal haemorrhages following docetaxel (taxotere) treatment.

INTRODUCTIONnDocetaxel belongs to the taxane group of chemotherapeutic agents used in the management of various malignant diseases. Nail changes as a complication of such treatment are observed in about 44%. Subungual haemorrhages (SH), are very rare following docetaxel therapy and only a few cases have been previously reported.nnnOBSERVATIONnAn 80-year-old man suffering from prostate adenocarcinoma was treated with a 3-weekly cure of docetaxel started 3 months earlier. Nail changes occurred after the 5th cycle of docetaxel. Clinical examination revealed orange discoloration of the nail plates, subungueal haemorrhages (SH) and onycholysis involving nails of all the digits and toenails of both hands and feet. These features were highly suggestive of nail toxicity following docetaxel therapy.nnnDISCUSSIONnNail changes secondary to Taxane chemotherapy includes nail bed dyschromia, onycholysis, red or orange Beaus lines and subungueal hyperkeratosis. SH, as reported in this case, is related to the cumulative dose of docetaxel and should not be attributed to other systemic diseases. Clinicians should recognize this complication to avoid abusive treatment or investigations and inform the patients about the possibility of nail changes secondary to taxane drugs.

High B-cell-activating factor levels in endemic Tunisian pemphigus

References 1. Goodfield MJ, Jones SK, Veale DJ. Systemic sclerosis. In: Burns T, Breathnach S, Cox N, Griffiths C, editors. Rook’s Textbook of Dermatology. 8th ed. Oxford: Blackwell Scientific Publications; 2004. p. 91‐116. 2. Pasricha JS. Pulse therapy as a cure for autoimmune diseases. Indian J Dermatol Venereol Leprol 2003;69:323‐8. 3. Lopez‐Ovejero JA, Saal SD, D’Angelo WA, Cheigh JS, Stenzel KH, Laragh JH. Reversal of vascular and renal crises of scleroderma by oral angiotensin‐converting‐enzyme blockade. N Engl J Med 1979;300:1417‐9. 4. Cheung WY, Gibson IW, Rush D, Jeffery J, Karpinski M. Late recurrence of scleroderma renal crisis in a renal transplant recipient despite angiotensin II blockade. Am J Kidney Dis 2005;45:930‐4. 5. Pasricha JS, Ramam M. Variations of modifications of the standard regimen. In: Pasricha JS, editor. Pulse Therapy in Pemphigus and Other Diseases. 3rd ed. New Delhi: Mehta Publishers; 2006. p. 124‐7. 6. Pasricha JS, Ramam M. Variations of modifications of the standard regimen. In: Pasricha JS, editor. Pulse Therapy in Pemphigus and Other Diseases. 3rd ed. New Delhi: Mehta Publishers; 2006. p. 124‐7. 7. Das S, Giri PP, Roy AK. Dexamethasone‐ cyclophosphamide pulse in collagen vascular disease: An observation. Indian Dermatol Online J 2011;2:10‐2. 8. Viswanth V, Sonavane AD, Doshi AC, Parab MG. Dexamethasone – cyclophosphamide pulse therapy in progressive systemic sclerosis. Indian J Dermatol 2010;55:304‐5.