Secondary thyroidectomy is an operation generally considered to be associated with a significantly increased risk of damage to the recurrent laryngeal nerves and parathyroid glands. During a 20‐year period, to December, 1986, a total of 408 secondary thyroidectomies were performed. The majority (n=227) were for recurrent nodular goiter, followed by reoperations for thyroid cancer (n=151), and operations for secondary thyrotoxicosis (n=30). The incidence of operative recurrent laryngeal palsy was 1.5% over the 20‐year period, while the incidence of permanent hypoparathyroidism fell from 3.5% during the first 15 years to 1.6% over the last 5 years, with a similar fall in the incidence of transient hypocalcemia (8.4% down to 4.8%). The risk of complications can be minimized by careful attention to operative detail, employing the technique of capsular dissection with preservation of the vascular supply to the parathyroid glands while protecting the recurrent laryngeal nerve.

Vectors based on adeno-associated virus type 2 (AAV2) are powerful tools for gene transfer and genome editing applications. The level of interest in this system has recently surged in response to reports of therapeutic efficacy in human clinical trials, most notably for those in patients with hemophilia B (ref. 3). Understandably, a recent report drawing an association between AAV2 integration events and human hepatocellular carcinoma (HCC) has generated controversy about the causal or incidental nature of this association and the implications for AAV vector safety. Here we describe and functionally characterize a previously unknown liver-specific enhancer-promoter element in the wild-type AAV2 genome that is found between the stop codon of the cap gene, which encodes proteins that form the capsid, and the right-hand inverted terminal repeat. This 124-nt sequence is within the 163-nt common insertion region of the AAV genome, which has been implicated in the dysregulation of known HCC driver genes and thus offers added insight into the possible link between AAV integration events and the multifactorial pathogenesis of HCC.