INTRODUCTION

Cyclosporine became a reference treatment for transplant patients from the beginning of the 1980s. In the blood, cyclosporine is 90% bound with proteins and is found in plasma in a proportion of 33-47%. Its main side effects are kidney failure and high blood pressure. Many skin complications have also been described. Some, such as the occurrence of carcinomas, are a non-specific consequence of immunosuppression. They are observed with other immunosuppressive drugs such as azathioprine [1]. Other complications, such as damage to the pilosebaceous follicle, seem on the contrary to be specific to ciclosporin. The most frequently reported damage to the pilosebaceous follicle are hypertrichosis, keratosis pilaris, acne and folliculitis [2]. Cyclosporine can more rarely cause profuse sebaceous hyperplasia.

CASE REPORT

A 33-year-old man, with a personal or family history of skin, monitored for a rheumatological problem, was put on ciclosporin. Consulted for a non-pruritic papular eruption that had been developing for 6 weeks.

Dermatological examination found yellow or flesh-colored papules, two to five millimeters in diameter, umbilical, sometimes centered by a comedo (Fig. 1a). There were no inflammatory lesions, in particular no pustules. The papules converged on almost the entire surface of the cheeks, forehead, e. Three diagnostic hypotheses were suggested: molluscum contagiosum, multiple adnexal tumors of the face and profuse sebaceous hyperplasia.

Figure 1: (a) Clinical image of Papular eruption of the face occurring during treatment with ciclosporin. (b) Dermoscopic image: Central yellowish aspect and vascularization in crown.

Dermoscopic examination showed an aggregation of yellowish-white clumps with linear vessels in a crown (Fig. 1b). Dermoscopic examination confirmed the diagnosis of sebaceous hyperplasia.

The patient was treated with isotretinoin at a dose of 20 mg per day. This dose was then reduced to 10 mg per day due to an increase in cholesterolaemia to 2.6 g/l. but the patient was lost sight of.

DISCUSSION

Sebaceous hyperplasia (SH) is a benign proliferation of the sebaceous glands, which in most cases is idiopathic and affects middle-aged men. SH results from intrinsic aging and extrinsic aging. In addition, this condition can occur in the context of genetic diseases such as Muir-Torre syndrome or familial HS. Some data reported in the literature suggest that ciclosporin could also be a causal factor. The mechanism of action of ciclosporin linked to the accumulation of the highly lipophilic molecule in the sebaceous gland [1]. Ciclosporin is a 5-alpha reductase inducer. It stimulates sebaceous secretion, which probably contributes to damage to the pilosebaceous follicle [2].

The classic manifestations of GHS are flesh-colored or whitish-yellow papules, normally umbilical, ranging in size from 2 to 9 mm [3]. Diagnosis is usually based on clinical features. Dermoscopy is a non-invasive diagnostic tool that allows the visualization of many yellowish-white lobulated structures on a pale yellow or yellowish-red background, corresponding to the sebaceous lobules and the umbilication at the center of the lesion, corresponds to a dilated follicular infundibulum, and the crown or the linear-irregular vessels, correspond to the dilated vessels [3].

Treatment modalities include photodynamic therapy with aminolevulinate methyl, topical dichloroacetic acid, cryotherapy, electrodesiccation, Pulsed dye laser or carbon dioxide laser and also Isotretinoin by inhibition of sebaceous secretion [4].

CONCLUSION

HS is a skin lesion that should be added to the possible rare but specific pilosebaceous changes occurring during cyclosporin treatment. Our case is exceptional because of the extension and rapid development of the lesions. Moreover, these lesions are essentially described in renal transplant recipients. To our knowledge, this is only the first case of disseminated HS observed after treatment for a rheumatological problem and not after bone marrow transplantation.

REFERENCES