Intraoperative neuromonitoring does not reduce the incidence of recurrent laryngeal nerve palsy in thyroid reoperations: results of a retrospective comparative analysis.

PURPOSE: Recurrent laryngeal nerve (RLN) palsy is the major concern of reoperative thyroid surgery, and the introduction of neuromonitoring could reduce the rate of this complication. The present study is a retrospective analysis of the experience with completion thyroidectomy with and without neuromonitoring in a referral center. METHODS: Between October 1999 and April 2011, 246 patients [37 men, 209 women; mean age, 55 ± 12.5 (range, 25-80) years] underwent 250 reoperations for recurrent goiter (n = 203), hyperthyroidism (n = 26), or recurrent thyroid cancer (n = 17). The mean interval between the initial and the reoperative procedure was 17.5 years. According to the availability of the neuromonitoring system and to the surgeon preference, 91 operations were performed with neuromonitoring (NM-group), whereas 159 were performed with direct nerve visualization (NV-group) alone. Patients' characteristics, perioperative data, and postoperative complications were collected in a prospectively maintained database. RESULTS: In the NM-group, 51 unilateral and 40 bilateral resections were performed. The NV-group included 122 unilateral and 37 bilateral procedures. The number of nerves at risk after previous surgery was 128 (NM-group) and 161 (NV-group), respectively. We registered eight RLN palsy in the NM-group (6.2 %) and four in the NV-group (2.5 %; p = 0.1). CONCLUSIONS: The routine use of intraoperative neuromonitoring seems not to reduce the incidence of RLN during redo thyroid surgery, at least in the setting of a tertiary referral center.

Posterior retroperitoneoscopic adrenalectomy for clinical and subclinical Cushing's syndrome.

BACKGROUND: Because of co-morbidity, adrenalectomy for adrenal Cushing's syndrome may be associated with an increased complication rate and long operating times. In the present study we report our experience with the posterior retroperitoneoscopic adrenalectomy in a large group of patients with clinical or subclinical Cushing's syndrome. PATIENTS AND METHODS: Between July 1994 and June 2009, 170 patients (17 males, 153 females age 50 +/- 13 years; range: 12-78 years) affected by Cushing's syndrome underwent operation via posterior retroperitoneoscopic access. Patients were divided into two groups, those with manifest Cushing's syndrome (mCS) [99 patients: 6 male, 93 female; age 45 +/- 13 years] and those with subclinical Cushing's syndrome (sCS) [71 patients: 11 male, 60 female; age: 56 +/- 11 years]. The sCS classification was assumed in cases without typical clinical symptoms but with a pathological dexamethasone suppression test. Partial adrenalectomy was performed in 35 cases (24 in the mCS-group and 11 in the sCS-group). RESULTS: Mortality was zero; major complications did not occur. The incidence of postoperative minor complications was 5.3%. Mean operating time was 58 +/- 36 min (range: 20-230 min) and did not differ between mCS and sCS patients (58 versus 59 min; p = ns). Postoperative oral steroids supplementation (POSS) was administered in 136 patients (99 mCS, 37 sCS). If POSS was started, mean duration of therapy was 12.3 months (mCS) and 10.3 months (sCS) [p = 0.08], respectively. After a mean follow-up of 70.9 +/- 46.5 months the cure rate was 99.4%. CONCLUSIONS: The posterior retroperitoneoscopic approach is fast and safe even in patients with Cushing's syndrome. Partial adrenalectomy represents a new option in the treatment of cortisol-producing adenomas.

Activation of type I phosphatidylinositol 4-phosphate 5-kinase isoforms by the Rho GTPases, RhoA, Rac1, and Cdc42.

Type I phosphatidylinositol 4-phosphate 5-kinase (PIP5K) catalyzes the formation of the phospholipid, phosphatidylinositol 4,5-bisphosphate (PIP(2)), which is implicated in many cellular processes. The Rho GTPases, RhoA and Rac1, have been shown previously to activate PIP5K and to bind PIP5K. Three type I PIP5K isoforms (Ialpha,Ibeta, and Igamma) have been identified; however, it is unclear whether these isoforms are differentially or even sequentially regulated by Rho GTPases. Here we show that RhoA and Rac1, as well as Cdc42, but not the Ras-like GTPases, RalA and Rap1A, markedly stimulate PIP(2) synthesis by all three PIP5K isoforms expressed in human embryonic kidney 293 cells, both in vitro and in vivo. RhoA-stimulated PIP(2) synthesis by the PIP5K isoforms was mediated by the RhoA effector, Rho-kinase. Stimulation of PIP5K isoforms by Rac1 and Cdc42 was apparently independent of and additive with RhoA- and Rho-kinase, as shown by studies with C3 transferase and Rho-kinase mutants. RhoA, and to a lesser extent Rac1, but not Cdc42, interacted in a nucleotide-independent form with all three PIP5K isoforms. Binding of PIP5K isoforms to GTP-bound, but not GDP-bound, RhoA could be displaced by Rho-kinase, suggesting a direct and constitutive PIP5K-Rho GTPase binding, which, however, does not trigger PIP5K activation. In summary, our findings indicate that synthesis of PIP(2) by the three PIP5K isoforms is controlled by RhoA, acting via Rho-kinase, as well as Rac1 and Cdc42, implicating that regulation of PIP(2) synthesis has a central position in signaling by these three Rho GTPases.