Clinics in gastroenterology最新文献

The muscle abnormality in diverticular disease is seen most often in surgically excised specimens in the sigmoid colon, though a pancolonic form of the disease without muscle thickening also exists in the elderly. In terms of physiopathology, the condition has a raised intraluminal pressure operating on the wall locally, this being most readily demonstrated in symptomatic patients. In Western societies the colon loses its tensile properties throughout life. The anatomical and functional evidence is that the colon is outstandingly strong in infancy in both Africans and Europeans, but later the mechanical properties of the African colon become superior and they remain so throughout ensuing decades. The diminished tensile strength and elasticity of the wall is no different in the diverticular and non-diverticular subjects and this suggests that an additional factor, such as pressure, may be necessary in Europeans to cause the mucosal extrusion which constitutes each diverticulum. Fiber fills the colon with bulkier, moister feces, which necessitates less work, especially as it operates for most of the time as a low-pressure system, only occasionally evacuating by mass peristalsis into the rectum. Cereal fiber binds salt and water and there is evidence that this is mostly a physicochemical process, dependent on particle size. Certain types of fibers undergo chemical degradation in the cecum and increase the bacterial population of the stool. Population studies show that diverticular disease subjects consume less fiber and in countries where the fiber intake is reduced, fecal output is lessened, transit is slower, and intraluminal pressure may be rising. As a result of the adoption of high-fiber diets and the use of bulking agents elective operations for diverticular disease are less commonly performed. The number of operations in most Western countries may be increasing because of increasing longevity. Complications often arise after a relatively short history; most are explicable on the basis of sudden pressure increments. The recent important finding in this disease is the change in colonic wall compliance, which probably occurs because of a collagen failure. Contraction of the taeniae may follow elastosis, which may relate to under-filling; this produces the contracted structure seen in the excised colonic specimen. The strength of the colonic wall diminishes throughout life, due to changes in its composition; some of these changes are hastened by self-imposed stresses, which currently seem to be mainly of dietary origin.

Rectal prolapse and solitary rectal ulcer syndrome are both benign conditions affecting the rectum, mainly in women; prolapse tends to occur late in life, while solitary rectal ulcer syndrome has a predilection for the younger adult. Complete rectal prolapse probably starts as a mid-rectal intussusception, although a combination of this theory and the 'sliding hernia' theory has been proposed by Altemeier et al (1971). The pelvic floor weakness associated with prolapse, which gives rise to incontinence, is most likely due to a traction injury to the pudendal nerve. Anorectal manometry will indicate those incontinent patients likely to benefit from rectopexy. Abnormal descent of the perineum may be found in rectal prolapse and solitary rectal ulcer syndrome as well as descending perineum syndrome per se. The clinical features of these three conditions can overlap. Solitary rectal ulcer syndrome is essentially due to prolapse and traumatization of the rectal mucosa. Inappropriate puborectalis contraction, abnormal perineal descent, and overt rectal prolapse have all been cited as possible mechanisms of development of the condition. Defecography is the radiologic investigation of choice. Electromyography, as in rectal prolapse, may show evidence of pudendal nerve damage although incontinence is rare.

The evidence shows that microbial fermentation of carbohydrates and endogenous substrates occurs in the large intestine of humans and that VFA represent a major endproduct. The large number of bacterial species, the complex nature of their interactions, and the endproducts of their fermentation processes are all likely to have significance in human health. Fermentation in the human intestine resembles rumen fermentation with respect to the metabolic pathways involved in anaerobic degradation of organic matter and in the concentrations of VFA endproducts. Thus, rumen bacteria are useful for understanding the dynamics and potential interactions of human intestinal bacteria. Current research is directed towards examining fermentation processes in animals, such as the pig and some species of monkey, since these animals most closely resemble the human. From such animal studies the metabolic activities of VFA and the processes by which they are produced and absorbed can be more clearly investigated and understood. The effects of diet on the microflora and on the metabolic pathways leading to the generation of VFA are under investigation. Modification of diet seems the most likely way of modifying the extent to which VFA are produced and absorbed by the human. As methodologies and protocols for evaluating human intestinal fermentation in vivo are revised and made more sensitive, the significance of fermentation will become more clearly understood. However, it appears that VFA make a physiologically significant contribution to the health of the colonic mucosa, and to the energy supply of the host. The magnitude of these effects is probably influenced by diet.

Colonic pseudoobstruction can occur as part of a generalized chronic intestinal pseudoobstruction syndrome or as an isolated entity. Isolated colonic pseudoobstruction can occur in two unrelated forms: the acute and chronic forms. Acute colonic pseudoobstruction is frequently a hospital-acquired disease that arises as a complication of other illnesses. The syndrome must be recognized and treated with early colonoscopic decompression to prevent cecal or colonic perforation. Chronic colonic pseudoobstruction is a syndrome of many causes. The prognosis of patients with chronic colonic pseudoobstruction is much better than that of generalized chronic intestinal pseudoobstruction, because the patients become asymptomatic with appropriate operations. The pathogenesis of acute colonic pseudoobstruction and several types of chronic colonic pseudoobstruction is not known. Further investigations should include bacteriologic study, histopathologic studies (examinations of smooth muscle and myenteric plexus), and examination of extrinsic nerves of the colon. With these approaches, a better understanding of the pathogenesis of these syndromes will be achieved.

There is growing evidence that colonic blood flow is controlled by both intrinsic and extrinsic factors. The existence of intrinsic vascular control mechanisms is evidenced by pressure-flow (and oxygen uptake) autoregulation, reactive hyperemia, vascular responses to acute venous hypertension, and a functional hyperemia. Although myogenic factors have long been considered to be solely responsible for the intrinsic ability of the colon to regulate its blood flow, recent developments indicate that metabolic mechanisms may be of equal importance in this regard. Both parasympathetic and sympathetic nerves play an important role in regulating colonic blood flow. The influence of circulating vasoactive agents and ischemia on colonic oxygenation are largely explained in terms of the relationship between oxygen uptake and blood flow. Colonic vascular dysfunction appears to be a major factor in the pathogenesis of inflammatory bowel diseases, chronic portal hypertension, and neonatal necrotizing enterocolitis. Future progress in this area will require the development of techniques for the measurement of colonic blood flow in man.