Basal Cell Carcinoma. Analysis of 395 cases localized in the neck, ear and nose region.

BACKGROUND AND OBJECTIVES: To test if there are different outcomes in basal cell carcinoma for lesion size, histopathology, localization, and recurrence rates. MATERIALS AND METHODS: A total of 395 patients with BCC localized in the neck, nose and ear regions who were surgically treated in Latvian Oncology Centre between 2006-2011 were analyzed retrospectively. The data were analyzed using modified classification based on Clarks et al. (2014) and McKenzie et al. (2016). RESULTS: Three hundred and ninety-five cases of BCC that were surgically treated in head and neck region were reviewed. Results were tabulated in four categories: anatomical region, histopathology, lesion size, and recurrence rates. Classification by anatomical region: 228 cases in the nose region, 82 cases in the neck region, 82 cases in the ear region. Classification by histopathology: 259 cases presented as low risk BCC [nodular, pigmented, adenoid, keratotic and cystic], 21 cases presented as superficial, 94 cases presented as mixed, and 21 cases presented as high-risk BCC (metatypical, morphea form). Mann-Whitney U test was used to compare recurrent BCC cases to non-recurrent cases. Significantly higher recurrence rates were observed if BCC at the time of the excision was ≥10 mm (p<0.001). Significance was also noted in cases where histopathology was mixed BCC and in cases where mixed BCC was localized to the nose region (p<0.001). CONCLUSION: More attention should be brought to assessing classification and clinical treatment synergy. Higher recurrence rates are observed when lesions occur in high risk anatomical region (H zone), when lesion size reaches or exceeds 20 mm in diameter, and when lesion is subtyped as mixed BCC. It is crucial to evaluate risk factors such as BCC subtype and localization, as these are associated with a higher rate of recurrence when present in a single lesion. These risk factors, together with pre-treatment lesion evaluation will enable formulation of better treatment plan and prognostic aspects in each case.

Effect of acute systemic hypoxia on human cutaneous microcirculation and endothelial, sympathetic and myogenic activity.

The regulation of cutaneous vascular tone impacts vascular vasomotion and blood volume distribution as a challenge to hypoxia, but the regulatory mechanisms yet remain poorly understood. A skin has a very compliant circulation, an increase in skin blood flow results in large peripheral displacement of blood volume, which could be controlled by local and systemic regulatory factors. The aim of this study was to determine the acute systemic hypoxia influence on blood flow in skin, local regulatory mechanism fluctuations and changes of systemic hemodynamic parameters. Healthy subjects (n=11; 24.9±3.7years old) participated in this study and procedures were performed in siting position. After 20min of acclimatization 15min of basal resting period in normoxia (pO2=21%) was recorded, followed by 20min in acute systemic hypoxia (pO2=12%), and after 15min of recovery period in normoxia (pO2=21%). HRV was used to evaluate autonomic nervous system activity to heart from systemic hemodynamic parameters which continuously evaluated cardiac output, total peripheral resistance and mean arterial blood pressure. Regional blood flow was evaluated by venous occlusion plethysmography and skin blood flow by laser-Doppler flowmetry. To evaluate local factor influences to cutaneous circulation wavelet analysis was used; fluctuations in the frequency intervals of 0.0095-0.021, 0.021-0.052, and 0.052-0.145Hz correspondingly represent endothelial, sympathetic, and myogenic activities. Our results from HRV data suggest that acute systemic hypoxia causes statistically significant increase of sympathetic (LF/HF; N1=0.46±0.25 vs. H=0.67±0.36; P=0.027) and decrease of parasympathetic (RMSSD; 80.0±43.1 vs. H=69.9±40.4, ms; P=0.009) outflow to heart. Acute hypoxia causes statistically significant increase of heart rate (RR interval; N1=960.3±174.5 vs. H=864.7±134.6, ms; P=0.001) and cardiac output (CO; N1=5.4 (5.2; 7.9) vs. H=6.7±1.4, l/min; P=0.020). Regional blood flow and vascular conductance were not changed during acute systemic hypoxia, but forearm skin blood flow (skin blood flow; N1=39.7 (34.0; 53.2) vs. H=51.6±13.9, PU; P=0.002) increases however local regulatory factor activity was not changed by acute systemic hypoxia. Acute systemic hypoxia causes sympathetic stimulation to heart which results in increased heart rate and larger cardiac output which could be the reason of forearm skin blood flow increase in acute systemic hypoxia without impact of local regulatory factors.

Nail fold capillary diameter changes in acute systemic hypoxia.

The present study was undertaken to determine the effect of arterial blood hypoxemia induced by acute systemic hypoxia (pO2=12%) on capillary recruitment and diameter, and red blood cell (RBC) velocity in human nail fold capillaries during rest, arterial post-occlusive reactive hyperemia (PRH), and venous occlusion (VO) using intravital video-capillaroscopy. Capillary recruitment was unchanged in acute systemic hypoxia (H) versus normoxia (N). There was no difference in RBC velocity measurements between normoxia and hypoxia (P<0.63). However, a statistically significant increase in nail fold capillary total width (N, 39.9±9.1 vs. H, 42.7±10.3 µm; P<0.05), apical diameter (N, 15.5±4.3 vs. H, 16.8±4.3 µm; P<0.05), arterial diameter (N, 11.9±3.5 vs. H, 13.9±4.1 µm; P<0.05), and venous diameter (N, 15.5±4.3 vs. H, 17.2±4.8 µm; P<0.05) was observed and continued to be significant most often during post-occlusive reactive hyperemia (PRH) and venous congestion (VO). These data suggest that acute systemic hypoxia does not increase capillary recruitment, but instead increases capillary diameter, resulting in increased capillary blood flow.