ABSTRACT
BACKGROUND AND AIM: A recent study using lactulose hydrogen-breath testing suggests that small intestine bacterial overgrowth (SIBO) is a common cause of nonresponsive celiac disease (CD). The prevalence of SIBO in CD diagnosed by quantitative culture of intestinal aspirate is unknown. The aim of this study is to evaluate the prevalence and significance of SIBO in CD based on the results of quantitative culture of intestinal aspirate. METHODS: We studied patients with CD in whom culture of intestinal aspirate was evaluated for the presence of anaerobes and aerobes. Bacterial overgrowth was diagnosed if culture demonstrated >10 colony forming units/mL. The causes of nonresponsive CD were investigated. RESULTS: We included 149 biopsy-confirmed CD patients. The intestinal aspirate was collected in 79 (53%) patients with nonresponsive CD, 47 (32%) as initial work-up for malabsorption, and in 23 (15%) asymptomatic treated CD. SIBO was diagnosed in 14 (9.3%). Nine (11%) with nonresponsive CD, 5 (11%) at initial work-up for malabsorption, and 0 in asymptomatic treated CD. Patients with a positive culture had evidence of worse malabsorption. A coexistent disorder was found in 67% of patients with both nonresponsive CD and bacterial overgrowth. CONCLUSIONS: The prevalence of SIBO diagnosed by quantitative culture of intestinal aspirate was 9.3% in patients with CD. Patients with symptomatic treated or untreated CD were affected. SIBO may coexist with other disorders associated with nonresponsive CD.
Subject(s)
Bacteria/growth & development , Bacterial Infections/diagnosis , Bacterial Infections/epidemiology , Celiac Disease/diagnosis , Celiac Disease/epidemiology , Intestine, Small/microbiology , Adult , Aged , Aged, 80 and over , Bacteria/isolation & purification , Bacterial Infections/microbiology , Bacterial Infections/physiopathology , Celiac Disease/microbiology , Celiac Disease/physiopathology , Colony Count, Microbial , Female , Humans , Intestine, Small/physiopathology , Male , Middle Aged , Respiratory Aspiration , Young AdultABSTRACT
This review focuses on the autoimmune connective tissue diseases, endocrine, and dermatologic conditions associated with celiac disease, as well as the related gut inflammatory disorders of refractory celiac disease, autoimmune enteropathy, collagenous enteritis, and collagenous colitis.
Subject(s)
Autoimmunity/immunology , Celiac Disease/diagnosis , Celiac Disease/epidemiology , Celiac Disease/immunology , Intestines/immunology , Autoimmune Diseases/complications , Autoimmune Diseases/immunology , Celiac Disease/complications , Humans , Prevalence , Risk FactorsABSTRACT
Celiac disease is characterized by small bowel enteropathy, precipitated in genetically susceptible individuals by the ingestion of "gluten," which is a term used to encompass the storage proteins of wheat, rye, and barley. Although the intestine heals with removal of gluten from the diet, the intolerance is permanent and the damage recurs if gluten is reintroduced. This damage causes a wide variety of consequence including maldigestion and malabsorption, resulting in the characteristic, although not universal, features of malnutrition. This article examines recent advances in the understanding of the spectrum of celiac disease, illustrates the impact of celiac disease on nutrition, and describes approaches to the management of the disease.
Subject(s)
Celiac Disease/complications , Malnutrition/etiology , Adult , Celiac Disease/diagnosis , Celiac Disease/diet therapy , Celiac Disease/epidemiology , Diet, Protein-Restricted , Female , Glutens/adverse effects , Humans , Malabsorption Syndromes/diagnosis , Malabsorption Syndromes/diet therapy , Malabsorption Syndromes/epidemiology , Malabsorption Syndromes/etiology , Male , Malnutrition/diagnosis , Malnutrition/diet therapy , Malnutrition/epidemiology , Middle AgedABSTRACT
To inhibit tumor-induced angiogenesis, the VEGF signaling pathway was targeted using AAV vectors encoding a VEGF decoy receptor, a truncated, soluble form of the murine VEGF receptor-2 (tsFlk-1). This approach initially had significant anti-neuroblastoma efficacy in murine xenograft models of local and metastatic disease, but when higher circulating levels of tsFlk-1 were established, tumor growth was more aggressive than even in control mice. Part of the mechanism for this apparent tumor resistance was increased human VEGF expression by the tumor cells. However, further investigation revealed that although a greater amount of VEGF could be bound by higher levels of tsFlk-1, more VEGF also existed in an unbound state and was, therefore, available to support angiogenesis. This novel, tumor-independent mechanism for resistance to antiangiogenic strategies suggests that careful titering of angiogenesis inhibitors may be required to achieve maximal antitumor efficacy and avoid therapy resistance mediated, in part, by ligand bioavailability. This has important implications for therapeutic strategies that use decoy receptors and other agents, such as antibodies, to bind angiogenic factors, in an attempt to inhibit tumor neovascularization.
