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Background: Thyroid dysfunction is among the most common immune-related adverse events (irAEs) of immune checkpoint inhibitors (ICIs) therapy. Data regarding potential predictors of the development of thyroid irAEs are still limited and sometimes conflicting. Patients and methods: We assessed potential risk factors and clinical outcomes associated with the onset of thyroid irAEs in a cohort of patients with different types of cancer treated with ICIs at a single center. Clinical and biochemical data, including thyroid function tests and autoantibodies at baseline and during treatment, were collected, and the onset of thyroid irAEs was recorded. Patients with thyroid dysfunction and/or under levothyroxine therapy before starting ICI were excluded. Results: 110 patients (80 M, 30 F, aged 32–85 years; 56.4% non-small-cell lung cancer, 87% treated with anti-PD-1) with complete information were included in the study. Among them, 32 (29%) developed thyroid irAEs during ICIs therapy. Primary hypothyroidism was the most common irAEs, occurring in 31 patients (28.18% of the whole cohort), including 14 patients who experienced a transient thyrotoxicosis. About 60% of irAEs occurred within the first 8 weeks of therapy. At multivariate analysis, anti-thyroid autoantibodies positivity at baseline (OR 18.471, p= 0.022), a pre-existing (autoimmune and non-autoimmune) thyroid disorder (OR 16.307, p< 0.001), and a family history of thyroid diseases (OR = 9.287, p= 0.002) were independent predictors of the development of thyroid irAEs. Conclusion: Our data confirm the high frequency of thyroid dysfunctions (mostly hypothyroidism) during ICIs, and provide data on valuable predictors of thyroid toxicities that may help clinicians in identifying patients at risk for developing irAEs.

The cause of hyperintense magnetic resonance changes and reduced apparent diffusion coefficient (ADC) in specific brain regions of patients with Creutzfeldt-Jakob disease (CJD) is unknown. Our aim was to determine the neuropathologic correlates of antemortem water ADC and normalized T2-weighted changes in patients with CJD.

BACKGROUND & AIMS: Patients undergoing cardiac surgery frequently have pancreatic damage; several factors, including tissue hypoperfusion, have been implicated. The aim of this study is to better understand the effects of decreased blood supply on human pancreas. METHODS: Twenty- one consecutive patients undergoing surgery for thoracic or thoracoabdominal aortic aneurysm were studied. During surgery, the descending thoracic aorta was cross-clamped for a mean of 44 minutes (range, 15-85 minutes). Effects of the resultant pancreatic ischemia were assessed by examining the patients daily for evidence of acute pancreatitis for at least 20 days after surgery and by determining serum concentrations of amylase, pancreatic isoamylase, and lipase before clamping the aorta and at varying intervals after its release (1, 2, and 6 hours during the first day and once daily for the following 6 days). RESULTS: One patient died of acute necrotizing pancreatitis. None of the others had symptoms of pancreatitis postoperatively, but all showed a significant increase in serum pancreatic enzyme concentrations soon after declamping; this peaked about 24 hours later and persisted for all 7 days of the study. A significant relationship was found between the increase in pancreatic enzyme concentrations and the aortic clamping time. CONCLUSIONS: Acinar cell injury is a constant, rapidly appearing consequence of severe pancreatic ischemia, even that of brief duration; acinar cell injury is usually subclinical but may also present as severe acute pancreatitis. (Gastroenterology 1996 Oct;111(4):1033-8)