Because reoperative thyroid surgery can lead to potential complications, especially permanent RLN palsy or hypoparathyroidism, it should be reserved for patients who need it. The importance of respecting specific technical rules should be emphasized.

Background: Besides intestinal barrier function, the host tolerates gut commensals through both innate and adaptive immune mechanisms. It is now clear that gut commensals induce local immunoglobulin A (IgA) responses, but it remains unclear whether anti-microbiota responses remain confined to the gut. Objective: The aim of this study was to investigate systemic and intestinal responses against the whole microbiota under homeostatic conditions, and in the absence of IgA. Methods: We analyzed blood and feces from healthy donors, patients with selective IgA deficiency (SIgAd) and common variable immunodeficiency (CVID). Immunoglobulincoated bacterial repertoires were analyzed by combined bacterial fluorescence-activated cell sorting and 16S rRNA sequencing, and bacterial lysates were probed by western blot analysis with healthy donors serums. Results: Although absent from the healthy gut, serum anti-microbiota IgG are present in healthy individuals, and increased in SIgAd patients. IgG converge with non-overlapping secretory IgA repertoires to target the same bacteria. Each individual targets a diverse, microbiota repertoire whose proportion inversely correlates with systemic inflammation. Finally, Intravenous Immunoglobulin preparations (IVIG) target much less efficiently CVID gut microbiota than healthy microbiota. Conclusion: Secretory IgA is pivotal for induction of tolerance to gut microbiota. SIgAdassociated inflammation is inversely correlated with systemic anti-commensal IgG responses, which may thus serve as a second line of defense. We speculate that SIgAd patients could benefit from oral IgA supplementation. Our data also suggest that IVIG preparations might be supplemented with IgG from IgA deficient patients pools in order to offer a better protection against gut bacterial translocations in CVID. Key Messages:-Systemic IgG and secretory IgA bind a common spectrum of commensals.-Increased proportions of IgG+ microbiota and inflammatory markers in SIgAd.-IVIG poorly target CVID and SIgAd gut microbiota.

The revised Bethesda guidelines did not identify all HNPCC cases in our series. The molecular approach identified all HNPCC patients with MSI-positive tumors, increasing the workload for germline testing only slightly.

In humans, several grams of IgA are secreted every day in the intestinal lumen. While only one IgA isotype exists in mice, humans secrete IgA1 and IgA2, whose respective relations with the microbiota remain elusive. We compared the binding patterns of both polyclonal IgA subclasses to commensals and glycan arrays and determined the reactivity profile of native human monoclonal IgA antibodies. While most commensals are dually targeted by IgA1 and IgA2 in the small intestine, IgA1+IgA2+ and IgA1−IgA2+ bacteria coexist in the colon lumen, where Bacteroidetes is preferentially targeted by IgA2. We also observed that galactose-α terminated glycans are almost exclusively recognized by IgA2. Although bearing signs of affinity maturation, gut-derived IgA monoclonal antibodies are cross-reactive in the sense that they bind to multiple bacterial targets. Private anticarbohydrate-binding patterns, observed at clonal level as well, could explain these apparently opposing features of IgA, being at the same time cross-reactive and selective in its interactions with the microbiota.