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Background Fecal microbiota, live-jslm (RBL; REBYOTA™), the first microbiota-based live biotherapeutic approved by the US Food and Drug Administration to prevent recurrent Clostridioides difficile infection (rCDI) in adults, has been evaluated in 5 prospective clinical trials. A retrospective analysis considered the safety and efficacy of RBL administered under US Food and Drug Administration enforcement discretion to patients with rCDI and broad eligibility criteria mimicking real-world practice. Methods We retrospectively identified adults with rCDI treated with RBL under enforcement discretion between November 1, 2015, and September 30, 2019, across 5 study sites. CDI diagnosis was based on site-specific practice. The primary safety set (PSS) included all patients who were naïve to previous RBL treatment and had continuously comprehensive medical records for 6 months following treatment. Results The primary treatment cohort had 94 patients; the PSS included 64 patients with common comorbidities receiving diverse chronic therapeutics. Most treatment-emergent adverse events were mild to moderate in severity and comparable between comorbidity subgroups and the overall population. There were no serious adverse events related to RBL or the administration procedure. In the PSS, 82.8% of RBL-treated patients responded at 8 weeks, of whom 88.7% had sustained response through 6 months. The number of RBL doses administered had no marked effect on outcome. Conclusions Together with prospective clinical trial outcomes, these findings support the efficacy and safety of RBL to prevent rCDI, with diagnostics and comorbidities representative of real-world clinical practice.

Diverticular disease–associated segmental colitis is a unique variant of chronic colitis limited to segments of the left colon that harbor diverticula. Histologically, this disease mimics chronic idiopathic inflammatory bowel disease and can be indistinguishable from ulcerative colitis or Crohn's colitis on histologic grounds alone. Patients typically present with hematochezia and cramping abdominal pain, and colonoscopic evaluation reveals inflammatory changes limited to the segment of bowel containing the diverticula, with rectal sparing. Although this disease does not appear to be an unusual form of diverticulitis but possibly an immunologically mediated process, many patients respond to treatment directed toward diverticulitis. A subset of patients requires immunosuppressive therapy and/or surgery, and a small subset progresses to develop classic ulcerative colitis. Because of the histologic overlap with ulcerative colitis and occasionally Crohn's colitis, it is essential that endoscopists provide a full description of the macroscopic appearance of the inflammatory changes at endoscopy, such as limitation to a segment of diverticular disease, so that the pathologist can provide a more informative interpretation of the biopsy.

A new family with resistance to thyroid hormone (RTH) harboring a mutation in the thyroid hormone receptor (TR) beta gene (R320C) is reported. The phenotype of affected members is compared to that of affected members of an unrelated family with an identical mutation in the TR beta gene that occurred independently. In one of the two families higher concentrations of free T4 were required to maintain a normal TSH level in affected subjects and unaffected first degree relatives but not in relatives by marriage. While this finding suggests that genetic background modulated the relative insensitivity to thyroid hormone caused by the mutant TR beta, it is uncertain whether the higher thyroid hormone levels prevented the occurrence of hyperactivity and attention deficit.

The anticonvulsant effects of ketosis were first reported in 1921 by Geyelin and Wilder. The therapeutic ketogenic diet for epilepsy was achieved by significantly reducing caloric fractions supplied by carbohydrates while increasing those supplied by lipids, thus inducing free fatty acid mobilization and beta oxidation to ketone bodies. Although earlier dietary formulations with animal fats proved unacceptable to many patients, the introduction of medium-chain triglyceride or corn oil as the lipid source in the diet has made the diet more acceptable. Ketosis induced with the therapeutic diet produces metabolic effects similar to those described in ketotic diabetic patients. It follows that alterations of immune function seen in diabetes mellitus might also occur with other causes of ketosis. When severe, recurrent, Staphylococcus aureus skin infections developed in one of our patients treated with the ketogenic diet, we undertook an immunologic evaluation and found significant neutrophil dysfunction, which improved when the ketogenic diet was discontinued. Because of this observation, we examined neutrophil function in other patients receiving the ketogenic diet.