Small Intestinal Bacterial Overgrowth and Irritable Bowel Syndrome: A Bridge between Functional Organic Dichotomy.

The pathogenesis of irritable bowel syndrome (IBS), once thought to be largely psychogenic in origin, is now understood to be multifactorial. One of the reasons for this paradigm shift is the realization that gut dysbiosis, including small intestinal bacterial overgrowth (SIBO), causes IBS symptoms. Between 4% and 78% of patients with IBS and 1% and 40% of controls have SIBO; such wide variations in prevalence might result from population differences, IBS diagnostic criteria, and, most importantly, methods to diagnose SIBO. Although quantitative jejunal aspirate culture is considered the gold standard for the diagnosis of SIBO, noninvasive hydrogen breath tests have been popular. Although the glucose hydrogen breath test is highly specific, its sensitivity is low; in contrast, the early-peak criteria in the lactulose hydrogen breath test are highly nonspecific. Female gender, older age, diarrhea-predominant IBS, bloating and flatulence, proton pump inhibitor and narcotic intake, and low hemoglobin are associated with SIBO among IBS patients. Several therapeutic trials targeting gut microbes using antibiotics and probiotics have further demonstrated that not all symptoms in patients with IBS originate in the brain but rather in the gut, providing support for the micro-organic basis of IBS. A recent proof-of-concept study showing the high frequency of symptom improvement in patients with IBS with SIBO further supports this hypothesis.

Medical update and potential advances in the treatment of pediatric intestinal failure.

Short bowel syndrome (SBS) and intestinal failure are chronic malabsorption disorders with considerable nutritional and growth consequences in children. Intestinal failure occurs when the functional gastrointestinal mass is reduced even if there is normal anatomical gastrointestinal length. A number of management strategies are often utilized to achieve successful intestinal rehabilitation and maintain adequate nutrition to avoid intestinal transplant. These strategies include minimizing the effect of parenteral associated liver disease, limiting catheter complications, and treating bacterial overgrowth in the remaining small intestine. In addition, there continues to be significant research interest in enhancing intestinal adaptation with targeted therapies. The purpose of this review is to discuss current perspectives and to highlight recent medical advances in novel investigational therapies.

Rosacea treatments: What's new and what's on the horizon?

Rosacea is a common, chronic, cutaneous disorder presenting with recurrent episodes of facial flushing, erythema, papules, pustules and telangiectasias. It is a multifactorial disease and its various clinical presentations probably represent the consequence of combined different triggers upon a specific background. Its management is largely based on long-established treatments empirically tailored to the specific presenting symptoms and no real breakthrough has occurred to date. However, recent insights into the still rather obscure pathophysiology of rosacea seem to open the way for etiologically oriented treatments. These may include, on the one side, the more effective application of traditional drugs, such as tetracyclines and metronidazole, to specifically selected patients or, on the other side, new therapeutic options, such as vitamin D receptor antagonists. It is to be remarked that the quality of most studies evaluating rosacea treatment is rather poor, mainly due to a lack of proper standardization. For a major breakthrough to occur in the management of rosacea, we need both a better understanding of its pathogenesis and the adherence of future clinical trials to clearly defined grading and inclusion criteria, which are crucial for investigators to correctly compare and interpret the results of their work.

Small intestinal bacterial overgrowth syndrome.

Human intestinal microbiota create a complex polymicrobial ecology. This is characterised by its high population density, wide diversity and complexity of interaction. Any dysbalance of this complex intestinal microbiome, both qualitative and quantitative, might have serious health consequence for a macro-organism, including small intestinal bacterial overgrowth syndrome (SIBO). SIBO is defined as an increase in the number and/or alteration in the type of bacteria in the upper gastrointestinal tract. There are several endogenous defence mechanisms for preventing bacterial overgrowth: gastric acid secretion, intestinal motility, intact ileo-caecal valve, immunoglobulins within intestinal secretion and bacteriostatic properties of pancreatic and biliary secretion. Aetiology of SIBO is usually complex, associated with disorders of protective antibacterial mechanisms (e.g. achlorhydria, pancreatic exocrine insufficiency, immunodeficiency syndromes), anatomical abnormalities (e.g. small intestinal obstruction, diverticula, fistulae, surgical blind loop, previous ileo-caecal resections) and/or motility disorders (e.g. scleroderma, autonomic neuropathy in diabetes mellitus, post-radiation enteropathy, small intestinal pseudo-obstruction). In some patients more than one factor may be involved. Symptoms related to SIBO are bloating, diarrhoea, malabsorption, weight loss and malnutrition. The gold standard for diagnosing SIBO is still microbial investigation of jejunal aspirates. Non-invasive hydrogen and methane breath tests are most commonly used for the diagnosis of SIBO using glucose or lactulose. Therapy for SIBO must be complex, addressing all causes, symptoms and complications, and fully individualised. It should include treatment of the underlying disease, nutritional support and cyclical gastro-intestinal selective antibiotics. Prognosis is usually serious, determined mostly by the underlying disease that led to SIBO.

Nausea, bloating and abdominal pain in the Roux-en-Y gastric bypass patient: more questions than answers.

Bariatric surgery is the most effective treatment for severe obesity. After surgery, patients may complain of gastrointestinal symptoms but their altered anatomy can make investigations difficult to perform or interpret. In particular, the Roux-en-Y gastric bypass (RYGBP) creates an excluded segment that is not easily accessible. We present a case illustrating some of the difficulties encountered when investigating the RYGBP patient complaining of nonspecific GI symptoms. Options are discussed for examining the excluded segment, and the diagnosis and significance of small intestine bacterial overgrowth in the RYGBP patient is reviewed.

Síndrome da alça cega: superpopulaçäo de germes: observaçäo de quatro casos / Blind loop syndrome: germs superpopulation: four cases observation

O autor apresenta quatro casos comprovados de síndrome de alça cega (estagnante). Em três casos o tratamento foi clínico, com antibióticos, e o outro foi submetido a cirurgia corretiva. O acompanhamento foi longo (10 anos) e o resultado terapêutico ótimo

Malabsorption secondary to Meckel's diverticulum.

This case report of a patient with a large Meckel's diverticulum with associated stagnation and bacterial proliferation demonstrates the resultant metabolic and nutritional alterations that have classically been described with the blind loop syndrome. A lesion as large as the one presented herein has rarely been reported with iron, vitamin B12, and folic acid deficiency anemias secondary to the contaminated small bowel (ileum) syndrome. A discussion of the pathophysiology, diagnosis, and treatment of this disorder and the multiple disease entities incorporated in the contaminated small bowel syndrome are included.

Protein-losing enteropathy in the human and experimental rat blind-loop syndrome.

Protein-losing enteropathy in 2 human subjects with small intestine bacterial overgrowth is reported. Partial improvement in 1 and complete normalization in the 2nd, during long-term antibiotic therapy, demonstrate for the first time antibiotic reversibility of protein-losing enteropathy in the human blind-loop syndrome. Studies in rats with experimental jejunal blind loops revealed depressed serum protein levels and excessive fecal excretion of intravenously administered 51Cr as compared with nonoperated and surgical controls. Comparison of protein loss of rats with blind loops present for varying lengths of time and paired comparison of rats tested for protein loss at two different times revealed a relatively stable degree of protein loss once it was manifest. Reversal of protein loss with antibiotic therapy was accomplished in only a small percentage of rats, and in those only after prolonged therapy. Surgical extirpation of the blind loop from rats with protein-losing enteropathy consistently corrected the protein loss, although this correction was delayed up to 9 wk from the time of corrective surgery. These studies demonstrate (a) significant protein loss as one etiologic factor for protein metabolic disturbances in the human and experimental rat blind-loop syndrome, (b) the occurrence of intestinal protein loss as a manifestation of functionally significant mucosal injury in the contaminated nonstagnant small bowel as well as the stagnant part of the small intestine affected by bacterial overgrowth, and (c) the difficulty of reversing functionally significant mucosal injury in the blind-loop syndrome once it has been manifest.