Desmoplastic cellular neurothekeoma: Clinicopathological analysis of twelve cases.

J Cutan Pathol. 2009 Mar 11; Zedek DC, White WL, McCalmont THBackground: Cellular neurothekeoma is a benign lesion most commonly found on the face and upper extremities in the first two decades of life. Methods: Retrospective clinicopathologic review of 12 examples of cellular neurothekeoma typified by prominent stromal sclerosis, a distinctive variant that we refer to as desmoplastic cellular neurothekeoma. Results: The mean age was 30 years (range, 3-55 years, 3 males, 9 females). The site was the head and neck in 3 cases, upper extremity in 4, lower extremity in 2, and trunk/abdomen in 3. All cases showed fascicles of slightly spindled and polygonal cells arrayed haphazardly in a prominent sclerotic background in the dermis and superficial subcutis. The cells displayed pale cytoplasm with indistinct membranes and vesicular nuclei with a single nucleolus. Lesional cells expressed NKI/C3, laminin, CD68, and CD10 and lacked expression of S-100 protein, EMA, and CD34. Clinical follow up was available on 10 cases with a mean duration of 24 months (range, 11-42 months) with no local recurrences or metastases. Conclusions: The immunohistochemical staining pattern, clinical findings, and benign nature are similar to "conventional" cellular neurothekeomas. The differential diagnosis includes desmoplastic melanocytic lesions, desmoplastic spindle cell carcinoma, dermatofibroma, "immature" scar, plexiform fibrohistiocytic tumor, perineurioma, and piloleiomyoma. Zedek DC, MD, White WL, MD, McCalmont TH, MD. Desmoplastic cellular neurothekeoma: Clinicopathological analysis of twelve cases.

[Cutaneous sarcoidosis through a hospital series of 28 cases]

Tunis Med. 2008 May; 86(5): 447-50Ben Jennet S, Benmously R, Chaâbane S, Fenniche S, Marrak H, Mohammed Z, Mokhtar IBACKGROUND: Sarcoidosis is a systemic disease, of unknown etiology, characterized by noncaseating epithelioid granulomas. It may affect many organs mainly lungs, lymph nodes and skin. AIM: The aim of our study is to evaluate retrospectively the epidemiological, clinical features and therapeutic particularities of cutaneous sarocidosis through a hospital series conducted in the dermatology department of Habib Thameur hospital. METHODS We have included 28 patients (23 females and 5 males) with a mean age of 45.5 years. RESULTS: The most frequent skin lesions were: papular sarcoidosis in 6 cases, nodular sarcoidosis in 8 cases and plaques in 6 cases. The other clinical types observed were: lupus pernio (2 cases), subcutaneous nodules (2 cases) and scar sarcoidosis (2 cases). Three patients presented erythema nodosum. Tuberculin skin test was negative in 77% of cases. Lymph nodes were palpable in 4 patients. Investigative exams revealed intrathoracic involvement in 8 cases and anterior uveitis sequels in 2 cases. Cutaneous manifestations were treated by chloroquin in 13 cases, allopurinol in 3 cases and intralesional betamethasone injections in 1 case. Five patients, with systemic involvement, underwent a therapy with oral corticosteroids. CONCLUSION: Sarcoidosis is a rare affection in Tunisia that affects mainly females. Cutaneous manifestations incite physicians to carry out complete investigations and to uphold a regular follow-up in order to detect systemic involvement.

Effects of antisense oligodeoxynucleotide to type I collagen gene on hypertrophic scars in the transplanted nude mouse model.

J Cutan Pathol. 2009 Mar 6; Xie J, Qi S, Yuan J, Xu Y, Li T, Li H, Liu X, Shu B, Liang HBackground: Antisense nucleic acids are effective in inhibiting harmful or uncontrolled gene expression. We had previously proved that the antisense DNA to type I collagen could effectively inhibit the synthesis of collagen type I in cultured hypertrophic scar fibroblasts, suggesting a potential role in anti-scarring, but there are no published reports of its effect on scar in the transplanted nude mouse model. Aims: To investigate the effects of antisense oligodeoxynucleotide (ASODN) to type I collagen gene on hypertrophic scars in the transplanted nude mouse model and clarify the potential of ASODN for the treatment of scars. Methods: The nude mouse model of hypertrophic scar was created and subjected to daily injections with ASODN and Lipofectamine for 2 ,4 or 6 weeks. We then examined the scars for changes in histopathological characteristics. The effects of ASODN on type I collagen gene expression were examined by reverse transcription-polymerase chain reaction and Western blots. Results: The ASODN could remarkably alleviate the scar in the nude mouse model and consistently inhibit type I collagen gene expression at both the mRNA and protein levels. Conclusion: ASODN was effective in downregulating type I collagen gene expression and could prove to be useful in the treatment of scars. Julin Xie, Shaohai Qi, Jishan Yuan, Yinbing Xu, Tianzeng Li, Houdong Li, Xusheng Liu, Bin Shu and Huizeng Liang.