Pravastatin-induced lichenoid drug eruption

SUMMARY A 64-year-old woman presented with diffuse and numerous pigmented macules on her face and upper back. Histopathological examination of a skin punch biopsy of the rash showed a lichenoid dermatitis. The most likely offending drug was pravastatin. Cessation of pravastatin resulted in gradual fading of the pigmentation. 3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors have previously been reported to cause lichenoid drug eruptions.     

Simvastatin-induced lichenoid drug eruption

Cutaneous drug eruptions have a variety of clinical features. Lichenoid drug eruptions are rare and may be difficult to diagnose. A case of a simvastatin-induced lichenoid eruption with skin and mucosal involvement is reported.     

Diffuse inflammatory lesions in patients treated with interferon alfa and ribavirin for hepatitis C: a series of 20 patients

BACKGROUND: Cutaneous side-effects of treatment with interferon alfa or interferon alfa plus ribavirin in patients with hepatitis C have already been reported but they are mostly local with inflammation and, much less frequently, necrosis at the injection points. By contrast, very few data are available with regard to distant skin reactions, particularly inflammatory lesions on other parts of the body. OBJECTIVES: To assess the clinical and histological pattern of inflammatory skin lesions outside the injection points in patients treated with interferon alfa and ribavirin for chronic hepatitis C. METHODS: Twenty patients attending a University Hospital in Southern France (secondary referral centre) were evaluated regard to clinical history, type and localization of lesions, progression and histology. Skin testing was performed in some patients and the relevance of the results was evaluated. RESULTS: Eczema-like skin lesions were mainly distributed on the extremities, sometimes associated with photosensitivity. They usually occurred between 2 and 4 months of treatment. Histology was nonspecific, with a dermal, mainly perivascular, mononuclear infiltrate. Skin testing was poorly informative and was not predictive of relapse. Treatment had to be interrupted in half the patients, of whom two of three relapsed on resuming therapy. CONCLUSIONS: The incidence of inflammatory skin lesions at a distance from injection sites in patients treated with interferon alfa and ribavirin for chronic hepatitis C is currently unknown, but this adverse event must be taken into consideration as it may lead to the transient or definitive interruption of treatment.     

Generalized lichenoid drug eruption following Blaschko lines

A 16‐year‐old girl was referred for evaluation of a widespread rash of 1 month duration. Its onset was on the trunk, but it rapidly generalized to cover virtually the entire body. It was intensely pruritic. The girl had a history of recurrent frontal headaches and had been taking ibuprofen 1 month prior to and during the onset of the rash. She was in otherwise good health. She apeared to be a healthy adolescent with flat topped violaceous papules scattered on her entire body following an arch line unilateral pattern on the right cheek, band‐shaped on the neck and ‘‘S’' shaped lines on the frontal chest and abdomen ( Fig. 1 ). They were ‘‘V’' shaped on the back, and had a linear pattern on all limbs. The nails, scalp, oral and genital mucosa were clear.

Figure 1 Open in figure viewer PowerPoint Band‐shaped violaceous papules on the neck and arms     

Mixed lichenoid and psoriasiform drug eruption induced by rifampicin

Rifampicin is an essential first line anti-tuberculosis drug. However, several cases of adverse reactions associated with this drug have been reported, the most common of which are cutaneous drug reactions. We report a case of mixed lichenoid and psoriasiform drug eruption induced by rifampicin.     

A case of lichenoid drug eruption associated with sildenafil citratus

A 53-year-old man developed lichenoid lesions on the upper chest, posterior surfaces of the trunk, and abdominal region about three months before his first visit. Physical examination and laboratory findings were normal; histopathology showed vacuolar degeneration of basal keratinocytes in association with a dense lympho-histioid infiltrate arranged in a lichenoid pattern with a few melanophages and eosinophils. The fact that our patient had been irregularly taking sildenafil citratus (Viagra) led to the hypothesis of a lichenoid drug-induced eruption. Our hypothesis was confirmed by clinical resolution three weeks after discontinuation of sildenafil citratus; moreover, the patient avoided the drug for about four months, and the eruption didn't reappear. Subsequently, we performed a challenge test with the drug, and the patient developed similar lichenoid lesions. Lichenoid eruptions are rather common dermatoses that can be induced by a great number of environmental agents and are clinically but not pathogenetically well defined. We report the present case because, despite the great number of drugs that can be implicated in the development of lichenoid eruptions, the association of such dermatoses and sildenafil citratus had been described only once previously in the literature until now. Furthermore, we wish to remark on the significance of a detailed anamnestic history to make the correct differential diagnosis between lichenoid drug-induced eruptions and lichen planus. This has a great clinical importance because simple discontinuation or substitution of the drug causes lichenoid drug-induced eruption resolution.     

8例苔藓样药疹的临床病理分析

详细分析了８例苔藓样药疹的临床与病理，并与１２例特发性扁平苔藓做了比较，发现在临床表现，组织病理，治疗及预后等方面两者存在的一定的差异，在组织病理中如发现嗜酸粒细胞，表皮破裂，角质层和颗粒层出现胶样小体常提示ＬＤＥ的诊断，而ＩＬＰ无１例出现上述病理特点。     

Granulocyte colony-stimulating factor-producing cutaneous angiosarcoma with leukaemoid reaction arising on a burn scar

We report a 46-year-old man with a giant tumour in a burn scar on his buttock. Pathological examination revealed that the dermis was filled with anastomosing vascular channels and round- or spindle-type atypical cells, which were compatible with the diagnosis of cutaneous angiosarcoma. Based on prominent leucocytosis (up to 113 000 microL-1), we measured serum granulocyte colony-stimulating factor (G-CSF). The highly elevated serum G-CSF of 303 ng L-1 (normal, 6.1-21.5 ng L-1) and positive immunohistochemical staining of the tumour tissue for G-CSF indicated that G-CSF was produced by the cutaneous angiosarcoma. To our knowledge, this is the first reported case of G-CSF-producing cutaneous angiosarcoma.     

人类疱疹病毒-2对HaCaT细胞表达GCSF和GMCSF的影响

目的探讨HaCaT细胞在人类疱疹病毒-2(HSV-2)刺激前后粒细胞集落刺激因子(GCSF)和粒/巨噬细胞集落刺激因子(GMCSF)的表达变化及意义。方法以VERO细胞进行HSV-2扩增,采用RT-PCR和荧光实时定量PCR检测HSV-2感染HaCaT细胞前及感染后24h、48h、72h时GCSF和GMCSF的表达量。结果HaCaT细胞可自分泌GCSF和GMCSF;HSV-2感染后24h,HaCaT细胞表达GCSF及GMCSF的水平增高,72h时又明显上升,且实验组与对照组相比两种细胞因子的表达有显著性差异。结论HaCaT细胞可以自发表达GCSF和GMCSF;HSV-2刺激对HaCaT细胞表达GCSF和GMCSF有促进作用。     

Cutaneous sarcoidosis during interferon alfa and ribavirin treatment of hepatitis C virus infection: two cases

Interferon-induced sarcoidosis is well documented. We report two new cases of sarcoidosis in two patients with hepatitis C virus infection treated with interferon alfa and ribavirin. These patients developed cutaneous sarcoidosis about 3 months after the beginning of the combination therapy. Spontaneous regression of the lesions was noted after discontinuation of the treatment. There have been more than 20 observations of the appearance or aggravation of this granulomatosis with interferon alfa and more recently with the combination of interferon alfa plus ribavirin. Dermatological signs are found in 50% of cases, and are often diagnostic. Other clinical symptoms of sarcoidosis resemble side-effects of interferon. The evolution is fairly stereotypical and is marked by a regression of the lesions following a dose reduction or curtailment of interferon. Interferon alfa acts by stimulating the T-helper (Th) 1 immune response. In addition to its antiviral action, ribavirin also enhances the Th1 response. Indeed, the superiority of the combination of interferon alfa and ribavirin in terms of antiviral action is corroborated by the enhancement of a Th1-type immune reaction by this combination. At the same time, this immune cell reaction triggers a greater granulomatous reaction.     

A drug eruption due to acebutolol with combined lichenoid and lupus erythematosus features

Many drugs have been implicated in the genesis of eruptions resembling lichen planus (Gange & Wilson Jones, 1978; Almeyda & Baker, 1970) and lupus erythemarosus (Raferty & Denman, 1973; Tuffanelli, 1972).
We report the development of both the above in the same patient during treatment with a beta blocking agent. On withdrawal of the drug the lesions resolved.     

Impaired cutaneous wound healing in granulocyte/macrophage colony-stimulating factor knockout mice

BACKGROUND: Wound healing involves various cells and cytokines, resulting in the regular progression of remodelling events. Granulocyte/macrophage colony-stimulating factor (GM-CSF) is a multifunctional pleiotropic cytokine and is known to facilitate wound healing, although the precise molecular and cellular mechanisms remain to be explored. OBJECTIVES: To use GM-CSF gene knockout (GM-CSF KO) mice to investigate the role of GM-CSF in cutaneous wound healing following full-thickness skin injury. METHODS: Full-thickness skin wounds were made in GM-CSF KO and wild-type mice. The wound closure, leucocyte infiltration, vascularization and extent of cytokine production were determined. RESULTS: Wound healing was significantly delayed in GM-CSF KO mice, accompanied by reduced cytokine production (interleukin-6, monocyte chemoattractant protein-1 and macrophage inflammatory protein-2), and platelet-endothelial cell adhesion molecule-1 expression. Consequently there was reduced recruitment of neutrophils and macrophages and reduced vascularization in the wounds of GM-CSF KO mice. Although collagen deposition was delayed, it was significantly increased in the wounds of the GM-CSF KO mice in the later stages of wound healing. CONCLUSIONS: We conclude that GM-CSF plays an important role in the complex network of effector molecules that regulate keratinocyte proliferation and the inflammatory response. These data have important implications for further development of the therapeutic manipulation of wound healing using GM-CSF.