Morbidity of central neck dissection: primary surgery vs reoperation. Results of a case–control study

Purpose

Complication rate in reoperative central neck node surgery is one of the main arguments to favor prophylactic central neck dissection at first operation in patients with papillary thyroid carcinoma. We evaluated if reoperative central neck dissection implies an increased postoperative morbidity. Secondarily, we aimed also to verify the effectiveness of the surgical resection of reoperative central neck dissection.

Methods

Forty-one patients who underwent reoperative central neck dissection after initial thyroidectomy for papillary thyroid carcinoma between January 2008 and May 2012 were compared to 41 controls who underwent central neck dissection at initial operation.

Results

The two groups were well matched for age, sex, and pN stage (P?=?0.296, 0.199, and 1.000, respectively). Three patients had distant metastases at presentation. No significant difference was found concerning mean number of removed nodes (P?=?0.064). No significant difference was found between the reoperative and the control groups concerning transient hypocalcemia (17 vs 19, respectively) (P?=?0.901) and transient recurrent nerve palsy (2 vs 2) (P?=?0.608). Follow-up was completed in 69 out of all the included patients (85.2 %). At a mean follow-up of 33 months, two patients (2.9 %) experienced nodal recurrence.

Conclusions

Morbidity of central neck dissection is similar for primary surgery and reoperation. In high-volume centers, reoperative central neck dissection can be safely accomplished when needed, allowing to achieve locoregional control in most of patients.     

Insulin secretion and insulin sensitivity defects are a common feature of mild,clinically homogeneous,recently diagnosed type II (Non-insulin-dependent) diabetics

Summary Alteration in insulin secretion and reduced peripheral sensitivity to the hormone have been reported in type II diabetes. In this paper, a comparison is made of basal glucose production (³H-6 glucose), insulin secretion and insulin sensitivityin vivo (hyperglycemic clamp) andin vitro (binding to circulating monocytes) in 24 patients with recently diagnosed type II diabetes, matched for age and fasting glycemia and divided into non-obese (14 subjects) and moderately obese (10 subjects), and in 9 non-obese controls. The non-obese diabetics were slightly hyperinsulinemic during fasting (10.8±1.0vs 4.8±0.8 μU/ml in controls, p < 0.0005), with a significant reduction in early and late insulin secretion (14.0±1.5vs 20.8 ± 2.0 μU/ml, p<0.01 and 24.8±3.3vs 34.7±2.14 μU/ml, p<0.025). The insulin sensitivity index MCR/I was significantly reduced (2.30±0.32vs 4.14±0.40, p<0.005). Endogenous glucose production was significantly increased (107±10.2vs 84±3.7 mg/m² per min, p<0.025) and displayed a positive correlation with fasting glycemia (r=0.51, p<0.05). Insulin binding to monocytes was significantly lower than in controls (2.36±0.22%vs 4.06±0.32%, p<0.0005). Moderately obese diabetics also were significantly hyperinsulinemic in the fasting state (18.1±2.8 μU/ml, p<0.0005vs controls) but, typically, lacked the early secretory phase (20.6±3.6 μU/mlvs baseline, n.s.). A similar increase of hepatic glucose production (107±11.2 mg/m² per min, p<0.025vs controls, n.s.vs non-obese diabetics) and decrease of peripheral sensitivity to insulin (MCR/I=1.78±0.31, p<0.0005vs controls, n.s.vs non-obese diabetics) was found in moderately obsese diabetics, as well as a significant reduction of insulin binding to insolated monocytes (2.62±0.4% p<0.01vs controls, n.s.vs non-obese diabetics). These results confirm that common defects of both non-obese and moderately obese type II diabetics are: lack of early phase of glucose induced insulin secretion, increase in hepatic glucose production and decrease of peripheral insulin sensitivity together with reduction of insulin binding to circulating monocytes. The hypothesis of a unique defect as a cause of hyperglycemia in type II diabetes in early clinical phase is not borne out by the results of this study. Moderate obesity, even if able to reduce insulin sensitivity, seems to be less important in determining hyperglycemia. This study was supported by a grant fromConsiglio Nazionale delle Ricerche, P.F. Medicina Preventiva, SP4,Malattie Degenerative, N. 84.02449.56.     

High risk of early resistant relapse for leukaemic patients with presence of multidrug resistance associated P-glycoprotein positive cells in complete remission

The immunocytochemical detection of multidrug-resistance (MDR) associated P-glycoprotein (P-170) was longitudinally performed on bone marrow smears from 32 responsive patients with acute leukaemia in the different phases of the disease (at diagnosis, in complete remission, at relapse) by means of APAAP technique and monoclonal antibody C219. The whole group of eight patients with presence of P-170 positive cells while in complete remission rapidly relapsed with a high proportion of blasts showing MDR phenotype; they were resistant to further treatments. Twelve out of 24 subjects without cells with MDR phenotype in complete remission remained in this condition, six had a responsive relapse (without significant expression of P-170 in 5/6 patients) and six a resistant relapse. Four patients of this last group significantly expressed P-170. Our data indicate that the detection of scattered P-170 positive cells during complete remission might identify a subset of leukaemic patients with high risk of early and resistant relapse.