High-Risk Cutaneous Squamous Cell Carcinoma without Palpable Lymphadenopathy: Is There a Therapeutic Role for Elective Neck Dissection?

PURPOSE: The beneficial role of elective neck dissection (END) in the management of high-risk cutaneous squamous cell carcinoma (CSCC) of the head and neck remains unproven. Some surgical specialists suggest that END may be beneficial for patients with clinically node-negative (N0) high-risk CSCC, but there are few data to support this claim. We reviewed the available literature regarding the use of END in the management of both CSCC and head and neck SCC (HNSCC). METHODOLOGY: The available medical literature pertaining to END in both CSCC and HNSCC was reviewed using PubMed and Ovid Medline searches. RESULTS: Many surgical specialists recommend that END be routinely performed in patients with N0 HNSCC when the risk of occult metastases is estimated to exceed 20%; however, patients who undergo END have no proven survival benefit over those who are initially staged as N0 and undergo therapeutic neck dissection (TND) after the development of apparent regional disease. There is a lack of data regarding the proper management of regional nodal basins in patients with N0 CSCC. In the absence of evidence-based data, the cutaneous surgeon must rely on clinical judgment to guide the management of patients with N0 high-risk CSCC of the head and neck. CONCLUSIONS: Appropriate work-up for occult nodal disease may occasionally be warranted in patients with high-risk CSCC. END may play a role in only a very limited number of patients with high-risk CSCC.     

Goldenhar’s Syndrome associated with congenital cyanotic heart disease

A case of Goldenhar’s Syndrome in a 10 year old girl is reported. The unusual features are the absence of epibulbar dermoid which is one of the major hallmarks of the Syndrome and the presence of an associated Cyanotic Heart disease.     

Immunohistological identification of cell subsets in human gingival after local treatment for gingivitis or periodontitis

The cellular infiltrate present in human diseased gingiva was analyzed in biopsies from 12 patients with gingivitis or periodontitis. The samples studied had been obtained in the course of surgery at inflammatory sites remaining after institution of periodontal treatment. Histological and immunological techniques were used to identify macrophages, B-cells, plasma-cells, T-cells and T cell subsets, as well as cells expressing class II HLA membrane antigens. T-cells appeared as the predominant population, but plasma-cells were also visualized in nearly all samples. Both OKT4+ and OKT8+ cells were seen in all cases, the latter being more numerous in periodontitis patients. Interdigitating-like cells were observed, positively labelled for class II antigens, as well as macrophages which were more numerous in periodontitis patients. These results suggest the participation of all components of the immune response in gingival disease, in a way resembling chronic recurrent inflammatory diseases.     

Role of pylorus in mediating cholecystokinin-stimulated satiety in the Zucker rat

Obese Zucker rats are less responsive than their lean littermates to the effects of cholecystokinin-octapeptide on satiety and pancreatic growth and exocrine function. We hypothesized that the hyperphagia observed in obese Zucker rats may be caused by a decreased pyloric contractile response to cholecystokinin, resulting in an increased rate of gastric emptying, decreased postprandial gastric distention, and thus decreased satiety. Pyloric muscle strips from six obese Zucker rats and six lean littermates were mounted in separate tissue baths and isometric contraction was measured in response to acetylcholine and cholecystokinin-octapeptide. The dose-response curves for acetylcholine-and cholecystokinin-octapeptide-stimulated pyloric muscle contraction were similar for both the obese and the lean rats. (For cholecystokinin, D₅₀ obese=4.0±0.6 nM, D₅₀ lean=3.4±0.2 nM;P=0.16). We conclude that the decreased satiety response to cholecystokinin-octapeptide observed in obese Zucker rats is not secondary to a decreased pyloric responsiveness to cholecystokinin.This work was supported by NIH grant AM28303-03.