Manuel Almagro

Indinavir-induced retinoid-like effects: incidence, clinical features and management.

Since 1998, many cases of antiretroviral therapy-related paronychia of the toes or fingers and ingrown toenails have been reported. Most of them were related to indinavir. Other indinavir-induced mucocutaneous disorders resembling the adverse effects of systemic retinoid therapy have also been reported. Although there is some uncertainty in the literature regarding a cause-effect relationship, results of several epidemiological and in vitro studies, together with cumulated clinical experience leave no doubt that indinavir causes a retinoid-like effect and nail alterations. Indeed, indinavir is the only antiretroviral drug that produces these disorders, although ritonavir may enhance indinavir-induced retinoid-like effects through pharmacokinetic interactions leading to increased plasma indinavir concentrations.Approximately 30% of patients receiving indinavir show two or more retinoid-like manifestations and 4–9% develop paronychia. These adverse effects are not related to other epidemiological variables such as the patient’s sex, age or other risk factors or immune status. They seem to be exposure dependent and, therefore, largely dose-dependent.Chronic paronychia is considered generally to be caused by contact irritants and candidal infection. Nevertheless, indinavir is currently the most frequent cause of chronic or recurrent paronychia in HIV-infected patients. In addition, retinoid-like manifestations such as cutaneous xerosis and cheilitis are frequent mucocutaneous adverse effects related to indinavir.The exact mechanism of indinavir-induced retinoid-like effects is unclear. Hypotheses for pathogenesis include interference with retinoid metabolism by enhancing the retinoic acid signalling pathway, or by increasing retinoic acid synthesis, or by reducing cytochrome P450-mediated retinoic acid oxidative metabolism.Replacement of therapy by an antiretroviral regimen not containing indinavir, while retaining other protease inhibitors and lamivudine, resolves retinoid-like manifestations without recurrences.

Dermatomyositis and mucinosis

Abstract

Superficial white onychomycosis in a 3-year-old human immunodeficiency virus-infected child.

Superficial white onychomycosis is exceptional in children, although a few anecdotal cases have been reported in the literature. On the other hand, superficial white onychomycosis and proximal subungual onychomycosis, while unusual in the general population, often appear in adult human immunodeficiency virus (HIV)‐infected persons.

Systemic lupus erythematosus presenting with a reticular erythematous mucinosis-like condition.

We report the case of a woman with clinical and histopathological features of reticular erythematous mucinosis syndrome (REM) who six years later developed diagnostic criteria for systemic lupus erythematosus (SLE). Two biopsies performed at the same area initially showed mucin dermal deposits and further development of characteristic dermo-epidermal changes of lupus erythematosus. Our findings suggest that SLE may present with a REM-like condition.

Spontaneous healing of Kaposi's angiosarcoma of the penis

We report a case of Kaposis angiosarcoma of the penis. Few cases have been reported of the initial and exclusive involvement of Kaposis angiosarcoma of the glans penis and prepuce. Our case is unique because of the number of lesions and the spontaneous remission.

Linear Immunoglobulin a Bullous Dermatosis Induced by Gemcitabine

OBJECTIVE: To report a case of linear immunoglobulin (Ig) A bullous dermatosis (LABD) induced by gemcitabine. CASE SUMMARY: A 59-year-old man was diagnosed with squamous-cell carcinoma of the lung in T4N2M0 stage and treated with cisplatin, vinorelbine, and gemcitabine. Twenty-four hours after the administration of gemcitabine, a symmetric, bullous, herpetiform eruption appeared on his trunk and upper limbs. Histopathologic examination and direct immunofluorescence test were consistent with IgA bullous dermatosis. Cutaneous lesions resolved two weeks after the drug was withdrawn and topical steroid treatment was instituted. DISCUSSION: Drug-induced LABD is a variant of classic or idiopathic LABD. Vancomycin is the most frequently implicated drug, but other agents have been reported to cause LABD. According to the Naranjo probability scale, the relationship of gemcitabine treatment with cutaneous eruption in our patient is possible. CONCLUSIONS: We report the first case of gemcitabine-induced LABD. Clinicians should monitor patients receiving this drug for signs of LABD.

Neutrophilic pustulosis and ulcerative colitis

Neutrophilic pustulosis is currently considered as a part of the spectrum of Sweets syndrome, and has been associated with inflammatory bowel disease and several other diseases.

Metastatic tuberculous abscesses in an immunocompetent patient

The decreased incidence of infectious diseases in developed countries may make their diagnosis difficult. Cutaneous tuberculosis is an example of this fact. A 44‐year‐old man presented with two painful abscesses on his lower extremities, which developed into chronic ulcers. A cutaneous biopsy revealed necrotizing granulomas in the dermis. Ziehl–Neelsen and periodic acid–Schiff stain were negative. Mantoux test was positive. Tc‐99m scintigraphy showed increased uptake in the bone tissue of the left ankle and right tibiae, without direct relation to cutaneous lesions. Chest X‐ray showed micronodular, apical, bilateral infiltrates, reduced volume of the right lung, and cavitation of the right superior lobe. Mycobacterium tuberculosis was grown from sputum and skin biopsy samples. Isoniazid, rifampin and pyrazinamide treatment for 2 months, followed by isoniazid and rifampin for 12 months, resulted in complete resolution. The clinical features of cutaneous tuberculosis in our patient were characteristic of tuberculous abscesses. Some uncommon findings, such as the low number of lesions, negative acid‐fast resistant stains in cutaneous biopsy samples and his preserved general state of health, may be explained by a higher competence of the immune system than is usual in this clinical subset of disseminated tuberculosis. Cutaneous tuberculosis should be included in the differential diagnosis of cutaneous abscesses in immunocompetent patients.

Cutaneous T-cell lymphoma presenting as disseminated, pigmented, purpura-like eruption.

A 48‐year‐old man with a history of psoriasis, who had received no oral pharmacologic treatment, presented in March 2000 with a progressive, cutaneous, pruritic eruption that began on his arms and legs, and became generalized. Examination revealed discrete, purpuric elements disseminated over the entire cutaneous surface, and in some areas confluent, large, erythematous, purpuric patches ( Figs 1 and 2 ). The palmoplantar surfaces and mucous membranes were spared. No lesions suggesting parapsoriasis or the usual presentation of cutaneous T‐cell lymphoma (CTCL) were present.

Subcutaneous Sarcoidosis during Pegylated Interferon Alfa and Ribavirin Treatment for Chronic Hepatitis C

Interferon is used to treat hepatitis C virus infection and its cutaneous side effects are well known. Recently, interferon-induced sarcoidosis has been reported. We report a new case of sarcoidosis during pegylated interferon alfa and ribavirin treatment with an unusual presentation in a woman with previous episodes of erythema nodusum and nodular vasculitis related to HCV.