Post-colonoscopy diverticulitis: A systematic review

BACKGROUNDPost-colonoscopy diverticulitis is increasingly recognized as a potential complication. However, the evidence is sparse in the literature.AIMTo systematically review all available evidence to describe the incidence, clinical course with management and propose a definition.METHODSThe databases PubMed, EMBASE and Cochrane databases were searched using with the keywords up to June 2020. Additional manual search was performed and cross-checked for additional references. Data collected included demographics, reason for colonoscopy, time to diagnosis, method of diagnosis (clinical vs imaging) and management outcomes.RESULTSA total of nine studies were included in the final systematic review with a total of 339 cases. The time to diagnosis post-colonoscopy ranged from 2 h to 30 d. Clinical presentation for these patients were non-specific including abdominal pain, nausea/vomiting, per rectal bleeding and chills/fever. Majority of the cases were diagnosed based on computed tomography scan. The management for these patients were similar to the usual patients presenting with diverticulitis where most resolve with non-operative intervention (i.e., antibiotics and bowel rest).CONCLUSIONThe entity of post-colonoscopy diverticulitis remains contentious where there is a wide duration post-procedure included. Regardless of whether this is a true complication post-colonoscopy or a de novo event, early diagnosis is vital to guide appropriate treatment. Further prospective studies especially registries should include this as a complication to try to capture the true incidence.     

Comparative 13-week cigarette smoke inhalation study in Sprague-Dawley rats: evaluation of cigarettes with two banded cigarette paper technologies.

This study compared the toxicological responses of Sprague-Dawley rats exposed nose-only to mainstream smoke (MS) from Test cigarettes (1, 2, and 3) to those of Control cigarettes without banded cigarette paper technologies (BCPT). Test cigarettes 1 and 2 had bands based on one technology (different band weight application) while Test cigarette 3 had bands based on another technology. The banded papers are representative of current marketed technologies. Rats were exposed to humidified HEPA filtered air (Sham) or to MS at concentrations of 0.06, 0.20, or 0.80 mg wet total particulate matter per liter air. Each exposure group contained 30 animals/sex (sentinel had 20 animals/sex). The study had two phases (13 weeks each): MS exposure (1 h/day, 5 days/week) and recovery without smoke exposure. Endpoints included clinical observations, respiratory physiology, hematology, serum chemistry, blood carboxyhemoglobin (COHb), serum nicotine, body/organ weights, gross pathology, and histopathology. Comparisons conducted were: Sham exposed vs. all cigarettes, Control cigarette vs. all Test cigarettes, and Test 1 vs. Test 2. Control and Test MS had comparable effects on respiratory physiology, COHb, serum nicotine, serum chemistry, and hematology. While some minor differences were observed, Control and Test MS had comparable effects on clinical signs, body/organ weights, and gross pathology/histopathology. Consequently, exposure of rats to equivalent MS concentrations from the four cigarettes induced similar toxicological responses in this study.     

Novel characterization of a breakpoint in F8: an individualized approach to gene analysis when PCR and MLPA results contradict

Haemophilia A is an X‐linked bleeding disorder caused by heterogeneous mutations in the F8 gene. Two inversion hotspots in intron 22 and intron 1, as well as point mutations, small insertions and deletions in the F8 gene account for causal mutations leading to severe haemophilia A. Rarely, novel molecular mechanisms lead to a haemophilia A phenotype which cannot be completely characterized by routine molecular diagnostic methods. Here, we characterized the molecular abnormality in a boy with a severe haemophilia A phenotype. On investigation by PCR and DNA sequencing, exon 18 of F8 repeatedly failed to amplify. However, analysis by multiplex ligation‐dependent probe amplification demonstrated the presence of exon 18 sequence, suggesting a more complex rearrangement than a single exon deletion. The analysis of exon 18 and its flanking regions by inverse PCR revealed a complex mutation comprising insertions of extragenic sequences from Xq28 along with a partial duplication of exon 18. Based on the successful analysis and characterization of the familial breakpoint, we developed a PCR‐based diagnostic approach to detect this defect in family members in whom no diagnostic test could be offered until this time.