Anal adenocarcinoma: case report, literature review and comparative survival analysis.

INTRODUCTION: Anal adenocarcinoma is a rare malignancy with a poor prognosis. METHODS: We present a case of rare anal adenocarcinoma in a patient with normal screening colonoscopy. Using the Surveillance, Epidemiology and End Result database between 2000 and 2016, we performed survival analysis among individuals>20 years old comparing anal and rectal cancers. RESULTS: Survival analysis showed that anal adenocarcinoma is associated with worse outcomes compared with rectal adenocarcinoma and anal squamous cell carcinoma. DISCUSSION: This case and survival data illustrate the importance of prompt investigation of symptoms irrespective of colorectal cancer screening status with careful attention to examination of the anal area.

Colonoscopy surveillance after polypectomy may be extended beyond five years.

OBJECTIVES: Colonoscopy surveillance interval data longer than 5 years are limited. We examined adenoma yield to identify factors that predict appropriate intervals for postpolypectomy surveillance greater than 5 years, including risk of advanced adenoma recurrence. METHODS: We identified patients with and without adenomas on an index colonoscopy who returned at 5 to 10 years for a follow-up colonoscopy. Multivariate logistic regression was used to identify variables that predict finding an adenoma on follow-up colonoscopy. RESULTS: Three hundred ninety-nine patients were identified with a follow-up colonoscopy at an interval of >5 years. Irrespective of surveillance interval, adenoma incidence occurred in 116 patients (29.1%) with 25 (6%) having advanced adenomas. Patients with nonadvanced adenomas on index colonoscopy had a similar risk of advanced adenoma on follow-up colonoscopy at 5 years versus 6 to 10 years, 5% versus 6.2% (P=0.39). The risk of advanced adenoma at 5 and 6 to 10 years in patients with a negative index colonoscopy was 7% versus 3.6% (P=0.15). Patients with an advanced adenoma at index colonoscopy had the highest rate of advanced adenoma detection at 5 years at 26%. Proximal polyp location (odds ratio 12.4, confidence interval 2.7-56.7) predicted advanced adenoma occurrence at 5 years. CONCLUSIONS: Postpolypectomy colonoscopy intervals can be extended beyond 5 years in patients with nonadvanced adenomas. Our findings also support a rescreening interval of 5 to 10 years in patients with a negative index colonoscopy. Patients with an index advanced adenoma are at highest risk for recurrent advanced adenoma and should have repeat colonoscopy before a 5 years interval.

Isolated colonic ulcers: diagnosis and management.

Isolated ulcers of the large intestine are not associated with an underlying colitis and may be an incidental finding on screening colonoscopy or present with abdominal pain, hematochezia, chronic gastrointestinal bleeding, and rarely, perforation. A common cause of isolated colonic ulcers is the use of nonsteroidal anti-inflammatory drugs (NSAIDs), with ulcers in the cecum and right colon. Isolated rectal ulcers are caused by ischemia, solitary rectal ulcer syndrome (SRUS), radiation, or fecal impaction. Stercoral ulceration and nonspecific ulcers of the colon are rare but can cause colonic perforation. Infectious causes include tuberculosis and amebiasis. Histology is important to rule out malignancy but is not helpful for diagnosis except in SRUS and certain infections. The approach to isolated colonic ulceration includes biopsy of the ulcer and surrounding tissue, cessation of any NSAIDs, management of constipation, and recognition of the patient with SRUS. Inflammatory bowel disease should be ruled out in appropriate patients.

Acute pancreatitis.

PURPOSE OF REVIEW: Acute pancreatitis is associated with a significant morbidity and a mortality as high as 10%. This review summarizes the most relevant articles in the past year that have contributed to understanding and management of this disease. RECENT FINDINGS: Pathologic activation of both digestive zymogens and the transcription factor nuclear factor kappaB are early events in acute pancreatitis; these pathologic processes are inhibited in experimental pancreatitis by curcumin and the pH modulator chloroquine. Primary sensory neurons may constitute a final common pathway for pancreatic inflammation. Experimental acute pancreatitis and associated lung injury are attenuated by inhibiting the prostanoid mediators cyclo-oxygenase-2 and 5-lipoxygenase and CC chemokine receptor antagonist Met-RANTES. Endoscopic retrograde cholangiopancreatography-induced acute pancreatitis can be reduced experimentally by intraductal neurokinin-1 receptor antagonist and clinically by use of diclofenac and pancreatic duct stenting. MRI in the setting of acute pancreatitis is a reliable method of staging disease severity. Distinct patterns of cytokine response are observed in acute pancreatitis. SUMMARY: Early events within the acinar cell and the regulation of inflammation by transcription factors continue to be elucidated. Although experimental acute pancreatitis can be successfully ameliorated by use of cytokine and inflammatory inhibitors, this has not been demonstrated in clinical disease. The finding of a compartmentalization of the inflammatory response in acute pancreatitis may be important for planning therapeutic interventions. Pancreatic duct stenting reduces the risk of developing postendoscopic retrograde cholangiopancreatography pancreatitis in high-risk people.

Acute pancreatitis.

Acute pancreatitis begins as acute pancreatic injury and may generate a systemic inflammatory response that evolves into multiorgan failure, leading to death. Multiple inciting factors such as toxins (alcohol), gallstones, or endoscopic retrograde cholangiopancreatography result in a cascade of events beginning with the intra-acinar activation of zymogens and the release of cytokines and other proinflammatory mediators. Their release is a major determinant of the systemic inflammatory response and distant organ failure. Attempts to attenuate the severity of acute pancreatitis by blocking specific inflammatory mediators have had limited success. This review is divided into experimental acute pancreatitis and clinical acute pancreatitis. The distinction is maintained because although animal models of disease have helped define the pathogenesis of acute pancreatitis, they do not completely reproduce the clinical syndrome of human acute pancreatitis or guarantee equal success of therapies in humans.