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Concomitant thyroid pathology in patients with primary hyperparathyroidism is common. This study compares complications of patients who underwent parathyroidectomy to those who underwent parathyroidectomy with a concomitant thyroidectomy.A retrospective review of prospectively collected data on 709 patients who underwent parathyroidectomy was performed. Patients who had prior thyroid or parathyroid procedures were excluded. Chi-square, Fisher's exact, Student's t-test, and Wilcoxon rank-sum tests were used to compare cohorts.Of the 641 patients included, 90% underwent parathyroidectomy alone and 10% underwent parathyroidectomy with a concomitant thyroidectomy. Overall, 49% had preoperative thyroid disease and 22% of patients with thyroid disease had a thyroid procedure. When compared with parathyroidectomy alone, parathyroidectomy with a concomitant thyroidectomy was associated with longer operative times (91 min versus 57 min, P 0.001), increased rate of overnight stay (69% versus 17%, P 0.001), and increased rate of transient hypocalcemia (15% versus 3%, P 0.001).Parathyroidectomy with a concomitant thyroidectomy is associated with longer operative times, increased rate of overnight stay, and increased transient hypocalcemia.

HMGB1, a non-histone chromosomal protein, can bind to the receptor for advanced glycation end products (RAGE) and act as an inflammatory mediator. We examined the role of HMGB1 in incisional wound healing and its possible mechanism of action through receptor for advanced glycation end products (RAGE).Male Sprague-Dawley rats undergoing full-thickness incisional wounding with subcutaneous implantation of PVA sponges were given daily injections of ethyl pyruvate (EP) (40 mg/kg, i.p.), a potent inhibitor of HMGB1 release. At 7 d post-wounding, wound breaking strength, sponge collagen content, and wound fluid HMGB1 levels were assessed. In vitro rat dermal or wound-derived fibroblasts were cultured with recombinant HMGB1 or advanced glycation end product (AGE). Some cultures were co-treated with a RAGE-blocking antibody. Fibroblast proliferation and collagen synthesis were assayed.In vivo treatment with EP significantly decreased wound HMGB1 levels (P0.05), which was paralleled by increased wound breaking strength (P0.05) and wound collagen content (P0.05). In vitro treatment with HMGB1 (100 ng/mL) had no effect on fibroblast proliferation but significantly reduced collagen synthesis (P0.05). This effect was abrogated by co-treatment with anti-RAGE antibody. Fibroblasts treated with AGE had lower collagen synthesis (P0.01), which was restored by anti-RAGE antibody treatment.HMGB1 impairs fibroblast collagen synthesis. Reducing wound HMGB1 levels lead to increased tensile strength and collagen synthesis. The data suggest that HMGB1 affects collagen synthesis through activation of RAGE.