Efficacy of curettage before excision in clearing surgical margins of nonmelanoma skin cancer.

OBJECTIVE: To determine whether curettage before excision of basal cell carcinoma (BCC) and squamous cell carcinoma (SCC) improves margin clearance rates. DESIGN: A retrospective, nonrandomized, case-control series of nonmelanoma skin cancers treated with preexcisional curettage followed by simple excision was identified using a computerized search of the database of a dermatopathology service. A validation cohort was established by manually identifying nonmelanoma skin cancers treated with wide excision on a given day. SETTING: All analyzed specimens were derived from the Dermatopathology Service at the University of California, San Francisco, a university-based laboratory that provides interpretation of skin biopsy specimens received directly from community (90%) and academic (10%) practices. PATIENTS: Our retrospective cohort consisted of all nonrecurrent nonmelanoma skin cancers diagnosed by biopsy and treated by simple excision between April 1, 1997, and April 30, 1999. There were 1983 BCCs and 849 SCCs included in our study. The validation cohort included skin cancers diagnosed by biopsy treated with simple excision on the 16th day of each month during the same period. INTERVENTION: Preexcisional curettage. MAIN OUTCOME MEASURE: We compared the frequency of tumor margin involvement of curetted vs noncuretted lesions. Margin involvement was considered surgical failure. RESULTS: Forty-two pecent of BCCs and 34% of SCCs were curetted before excision. In BCC, risks for surgical failure included head and neck lesions (P<.001), lesions treated by physicians performing fewer than 51 procedures (P<.001), and invasive subtypes (P<.01). Factors associated with surgical failure in SCC included in situ disease (P=.01) and an older (77 vs 74 years) patient population (P=.05). In univariate analysis, curettage before excision decreased the surgical failure rate for BCC by 24% (P=.03) but did not decrease the rate for SCC (P=.8). In multivariate analysis, curettage of BCC reduced surgical failure rates by 26% when the physician performed 50 skin cancer excisions or less during the study (odds ratio, 0.74; 95% confidence interval, 0.57-0.95;P=.02). CONCLUSION: Preoperative curettage decreases the frequency of positive margins in the management of BCC but not of SCC.

Photosensitivity in HIV-infected individuals.

OBJECTIVE: To characterize photosensitivity in HIV-infected individuals using minimal erythema dosage (MED) UVA (ultraviolet A light) and UVB (ultraviolet B light) photoprovocation light testing. DESIGN: Prospective, controlled analytical study. SETTING: University of California, San Francisco, between March 1995 and January 1997. PATIENTS: 13 HIV-seropositive patients with clinical and pathological features consistent with photodermatitis, 13 HIV-seropositive patients with biopsy-proven eosinophilic foliculitis (EF), and 10 HIV-seropositive patients with CD4 (T helper cell) count below 200 cells/uL and no history of photosensitivity or EF. INTERVENTION: Each patient underwent MED testing for UVB. All 13 patients with suspected photodermatitis underwent full photochallenge testing with UVA and UVB for up to 10 consecutive week days. RESULTS: Mean MED to UVB in patients with clinical photosensitivity and EF was lower (p = 0.004 and p = 0.022 respectively) than that of patients without a clinical history of photodermatitis. There were no significant differences in mean CD4 count or Fitzpatrick skin type. Positive photochallenge tests (papular changes at site of provocative light testing) to UVB (9 of 13 patients) were much more common than reactions to UVA (3 of 13 patients) in the photodermatitis group. All patients with clinically active photodermatitis developed papular changes at the site of UVB photochallenge testing, but only 1 of 5 patients with photodermatitis in remission developed papular changes with UVB photochallenge testing. Seven of the 13 patients with photodermatitis had Native American ancestry. Photosensitive patients were commonly taking trimethoprim-sulfamethoxazole (TMP-SMX), but no more commonly than EF or control patients. CONCLUSIONS: Photosensitivity in HIV-infected individuals appears to be a manifestation of advanced disease. Most patients are sensitive to UVB. The most severely affected individuals are both UVB and UVA sensitive, and may show reactions to visible light. A significant Native American ancestry may be a risk factor for development of photodermatitis in patients with advanced HIV disease. Finally, patients with eosinophilic folliculitis may be subclinically photosensitive.

Kaposiform hemangioendothelioma. An aggressive, locally invasive vascular tumor that can mimic hemangioma of infancy.

BACKGROUND: Kaposiform hemangioendothelioma is a rare, aggressive vascular proliferation in children that is clinically and histologically distinct from hemangioma of infancy. It often manifests later than infantile hemangioma, and complication by Kasabach-Merritt syndrome is common. OBSERVATIONS: We examined 3 children with kaposiform hemangioendothelioma, all of whom were initially misdiagnosed as having infantile hemangioma. All 3 children developed Kasabach-Merritt syndrome, in association with a rapidly growing cutaneous vascular mass. Treatment with systemic corticosteroids, interferon alfa, vincristine, and radiation therapy appeared to halt progression of the disease. None had evidence of human herpesvirus 8 infection. CONCLUSIONS: Cutaneous kaposiform hemangioendothelioma may appear in early infancy but often appears months to years later. It is frequently complicated by Kasabach-Merritt syndrome, has no known association with Kaposi sarcoma related to human immunodeficiency virus infection, and demonstrates aggressive local behavior with invasion but not distant metastasis. Awareness of this entity is important to prevent a mistaken diagnosis of common hemangioma of infancy.

Further evidence for the involvement of SmI cortical neurons in nociception: modifications of their responsiveness over the early stage of a carrageenin-induced inflammation in the rat.

In this electrophysiological study, changes in the responsiveness of neurons in the primary somatosensory (SmI) cortex in rats were analyzed during the development of carrageenin (CRG)-induced inflammation, an animal model of acute inflammatory hyperalgesia. SmI neurons were characterized as responding to non-noxious light touch, non-noxious articular movement, or noxious pinch. A total of 23 neurons so characterized in three groups were recorded for 60 min (17 of these neurons were recorded for up to 150 min) after an intraplantar injection of CRG. The possible modifications in their background and evoked activities were analyzed over this period of time. After CRG administration, cells responding to noxious pinch stimuli (n = 8) showed a nonsignificant increase in spontaneous activity, but a significant increase in their evoked response to pinch. These results were quite similar to past observations in the ventrobasal nucleus of the thalamus (VB). Cells responding to non-noxious articular stimulation (n = 6) showed variable modifications and no significant increase in the mean evoked response for up to 60 min. These results for articular cells were also quite comparable to results seen for VB responses for similar cells. However, mean spontaneous activity, which showed a highly variable increase, was significantly increased after 60 min. The depressive effect of a local anesthetic, Xylocaine, was tested on the activities of four cells (one pinch, three light touch units) 60 min after CRG administration over a 20-min interval. Xylocaine was found to depress both spontaneous activity and responses to the effective somatic stimulus, thereby implying that the observed central modifications in neuronal discharge are linked to the peripheral inflammation. Modifications observed for each group of cells are compared with past observations in peripheral fibers, in spinal dorsal horn neurons, and especially in the VB under similar inflammatory conditions. These data confirm that the SmI cortex is involved in the nociceptive process. Furthermore, the contrast between some modifications observed at this level and past observations under similar inflammatory conditions suggests a unique role of some cortical neurons, which might partially account for mechanical allodynia.