Incarceration of a rectal prolapse is an unusual entity that represents a surgical emergency. Even more rarely, it becomes strangulated, requiring emergency surgery. When surgery becomes inevitable, the choice of procedure varies. A 57-year-old man who presented with strangulated rectal prolapse is described. The patient underwent emergency perineal proctosigmoidectomy, the Altemeier operation, combined with diverting loop sigmoid colostomy. The postoperative course was uneventful. After a 6-month follow-up, there was no recurrence, but the patient continued with fecal incontinence. This case underlines the importance of the Altemeier procedure as treatment in the patient with a strangulated prolapsed rectal segment.

Oncogenes alters metabolic pathways while the resulted metabolites, in turn, modifies the expression and production of oncogenes or tumor suppressors. Metabolic reprogramming has been considered as a consequence of oncogenes’ activity more than a phenotypic change of cancer cells. Currently, three different metabolic alterations for cancer cells, i.e. an increased ability to acquire nutrients, preferred metabolic pathways or differentiation pathways, have been described. Melatonin is a molecule which has been extensively investigated since it was discovered more than 60 years ago. From the aggregation of melanophores to antioxidant chain reactions, melatonin has been proposed to be an important molecule affecting the physiology of mammals but also the biology of unicellular organisms. Thus, the decrease in melatonin synthesis in humans with age has been related to several diseases including neurodegeneration and cancer. For many years, it has been believed that melatonin crosses biological membranes easily to exert its functions. However, this notion has been challenged by recent discovery that majority of melatonin might cross biological membranes through glucose transporters. This initial observation has generated a new important idea about melatonin’s function, that is, the membrane transportation of melatonin and glucose by the same transporter in cancer cells would be a new promising mechanism of this indole by either reprogramming glucose metabolism, impeding nutrients uptake or assigning preferred metabolic pathways in cancer cells. In this review, we will focus the role of melatonin as an antiproliferative agent, and its connection with metabolic changes due to melatonin competition with glucose.

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