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Pediatric colorectal surgery in low- and middle-income settings: Adaptation to the resources available
Published in Alejandra Vilanova-Sánchez, Marc A. Levitt, Pediatric Colorectal and Pelvic Reconstructive Surgery, 2020
Chris Westgarth-Taylor, Marion Arnold
Degenerative leiomyopathy is an acquired visceral myopathy of unknown etiology. It is predominantly identified in Southern and Southeastern Africa. It results in chronic intestinal pseudo-obstruction that is uniformly fatal. Patients usually present in the first or second decade of life and demise in the late second or early third decade. The presentation is usually colonic, but progresses to involve the entire gastrointestinal tract [5,6].
Functional Non-Malignant Large Bowel Obstruction
Published in Peter Sagar, Andrew G. Hill, Charles H. Knowles, Stefan Post, Willem A. Bemelman, Patricia L. Roberts, Susan Galandiuk, John R.T. Monson, Michael R.B. Keighley, Norman S. Williams, Keighley & Williams’ Surgery of the Anus, Rectum and Colon, 2019
Maysoon Gamaleldin, Luca Stocchi
In 1948, William Heneage Ogilvie published the first two cases of what subsequently became referred to as Ogilvie syndrome. In both cases, the presenting symptoms were strongly suggestive of a distal colonic obstruction, which prompted laparotomy, when he discovered unsuspected malignant infiltration into the crura of the diaphragm and the coeliac plexus without detecting any colonic masses. He hypothesised that colonic motility had been affected by ‘sympathetic deprivation’ due to malignant invasion by retroperitoneal tumors.1 In a subsequent series, Dudley described ‘intestinal pseudo-obstruction’ and cases of functional colonic obstruction in the absence of mechanical causes, which could be associated with known benign conditions but sometimes presented without any known associated co-morbidity.2 Amongst a number of definitions, such as acute colonic ileus, idiopathic large bowel obstruction, spastic ileus or ileus of the colon, the term acute colonic pseudo-obstruction (ACPO) has been reported at least since 19823 and has become increasingly accepted.
Megacystis microcolon intestinal hypoperistalsis syndrome
Published in Prem Puri, Newborn Surgery, 2017
Prem Puri, Jan-Hendrik Gosemann
The evaluation of the genetic background of MMIHS resulted in a number of recent publications that suggest the enteric smooth muscle actin gamma 2 (ACTG2) as the first gene to be clearly associated with MMIHS 15–17 and intestinal pseudo-obstruction. Some authors suggest to reorganize the clinical entities of MMIHS, prune belly syndrome, hollow visceral myopathy, and intestinal pseudo-obstruction into a spectrum of ACTG2-related disorders.15 The identification of a possible genetic background might have a relevant impact on prenatal counselling in the future.
The benefits and prospects of interleukin-6 inhibitor on systemic sclerosis
Published in Modern Rheumatology, 2019
Hardening and atrophy of the submucosal tissue and muscular layer of esophagus occur, which impair flexible movement of the esophagus [19]. In addition, the esophageal diameter is increased due to the decrease of contractile force associated with fibrosis of the muscular layer. In chest CT in such cases, we can observe expansion of the esophageal lumen on the left side of the trachea (Figure 2(B)). In addition, owing to expansion and atrophic change, the long-axis diameter of the esophagus is shortened, inevitably resulting in esophageal hiatal hernia [20]. Sclerosis of the lower esophageal sphincter makes it difficult to discharge undigested food into the stomach, and the digested food easily flows back to the esophageal side [21]. The esophageal mucosa is constantly exposed to strong acids due to the backflow of gastric juice, and structural reflux esophagitis occurs. The fibrotic change of the lower intestinal tract reduces the abilities to perform digestion and absorption. Overall, patients with SSc have problems with their nutritional status [22]. Owing to movement disturbances in the lower digestive tract, bowel movements tend to be stagnant. Some patients can develop pseudo-intestinal obstruction, called chronic intestinal pseudo-obstruction (CIPO), due to diminished peristalsis [23]. This diminished peristalsis decreases the amount of bacteria excreted with the stools, and the associated excess proliferation of bacteria causes the retention of gas in the intestinal tract. This phenomenon is called small intestinal bacterial overgrowth (SIBO) (Figure 3) [24].
Liposomal quercetin potentiates maxi-K channel openings in smooth muscles and restores its activity after oxidative stress
Published in Journal of Liposome Research, 2019
Mariia I. Melnyk, Dariia O. Dryn, Lina T. Al Kury, Alexander V. Zholos, Anatoly I. Soloviev
GI malfunction is known as a common disability which leads to uncomfortable life with a host of nonspecific symptoms that include abdominal pain, vomiting, nausea, constipation or diarrhea. Some illnesses, such as diabetes mellitus, can results in GI motility disorders (Camilleri et al.2011). Several rare diseases like an intestinal pseudo-obstruction cause rising of mortality chances (Beyder and Farrugia 2012). Maxi-K channelopathy is an important pathophysiological determinant or trigger of such unwanted complications. Up to date, there are only few K+ channel openers used in medicine. Therefore, the current challenge in pharmacology is to find safe and effective potassium channel openers, which would be able to treat cardiovascular complications in arterial hypertension, cardiac ischemia, diabetic vascular disease, overactive bladder, spastic colitis, etc.
What the internist should know about hereditary muscle channelopathies
Published in Acta Clinica Belgica, 2018
Véronique Bissay, Sophie C. H. Van Malderen
Digestive symptoms are the first signs in 28% of DM1 patients [26]. They are caused by motility dysfunction of the gastrointestinal tract and result in dysphagia, dyspeptic symptoms, delayed gastric emptying, abdominal pain, and an irritable bowel syndrome with diarrhea and constipation. Intestinal pseudo-obstruction can occur at any stage of the disease, sometimes many years before muscular symptoms appear. The mean features of DM1 are malabsorption, isolated elevated gamma-glutamyltransferase (GGT) levels, and symptomatic gall stones with a increased risk for acute cholecystitis. Whereas 25% of the DM1 patients consider gastrointestinal symptoms their most disabling complaints, a lot of patients with gastrointestal tract disturbances are not aware of it. This is probably due to the gradual impairment and their specific cognitive behavior, as mentioned before. There is less gastrointestinal involvement in DM2, which is commonly associated with dysphagia, constipation, and abdominal pain [27].