pulmicort and Atrophy

The purpose of this expert review is to summarize the diagnosis and management of refractory celiac disease. It will review evaluation of patients with celiac disease who have persistent or recurrent symptoms, differential diagnosis, nutritional support, potential therapeutic options, and surveillance for complications of this condition.. This expert review was commissioned and approved by the American Gastroenterological Association (AGA) Institute Clinical Practice Updates Committee (CPUC) and the AGA Governing Board to provide timely guidance on a topic of high clinical importance to the AGA membership and underwent internal peer review by the CPUC and external peer review through standard procedures of Gastroenterology. These Best Practice Advice (BPA) statements were drawn from a review of the published literature and from expert opinion. Since systematic reviews were not performed, these BPA statements do not carry formal ratings of the quality of evidence or strength of the presented considerations. Best Practice Advice Statements BEST PRACTICE ADVICE 1: In patients believed to have celiac disease who have persistent or recurrent symptoms or signs, the initial diagnosis of celiac disease should be confirmed by review of prior diagnostic testing, including serologies, endoscopies, and histologic findings. BEST PRACTICE ADVICE 2: In patients with confirmed celiac disease with persistent or recurrent symptoms or signs (nonresponsive celiac disease), ongoing gluten ingestion should be excluded as a cause of these symptoms with serologic testing, dietitian review, and detection of immunogenic peptides in stool or urine. Esophagogastroduodenoscopy with small bowel biopsies should be performed to look for villous atrophy. If villous atrophy persists or the initial diagnosis of celiac disease was not confirmed, consider other causes of villous atrophy, including common variable immunodeficiency, autoimmune enteropathy, tropical sprue, and medication-induced enteropathy. BEST PRACTICE ADVICE 3: For patients with nonresponsive celiac disease, after exclusion of gluten ingestion, perform a systematic evaluation for other potential causes of symptoms, including functional bowel disorders, microscopic colitis, pancreatic insufficiency, inflammatory bowel disease, lactose or fructose intolerance, and small intestinal bacterial overgrowth. BEST PRACTICE ADVICE 4: Use flow cytometry, immunohistochemistry, and T-cell receptor rearrangement studies to distinguish between subtypes of refractory celiac disease and to exclude enteropathy-associated T-cell lymphoma. Type 1 refractory celiac disease is characterized by a normal intraepithelial lymphocyte population and type 2 is defined by the presence of an aberrant, clonal intraepithelial lymphocyte population. Consultation with an expert hematopatholog

Topics: Albumins; Atrophy; Budesonide; Celiac Disease; Enteropathy-Associated T-Cell Lymphoma; Glutens; Humans; Inflammatory Bowel Diseases; Lactose; Micronutrients; Prednisone; Receptors, Antigen, T-Cell; United States

In adults, asthma treatment with high doses of inhaled corticosteroids has resulted in dermal thinning. The aim of this study was to investigate the skin thickness in children with asthma during budesonide treatment. In a double-blind study, 113 children, 5-10 y old, with persistent asthma received budesonide 400 microg twice daily for 1 mo and thereafter 200 microg twice daily for 5 mo. Thereafter, 56 children received 100 microg twice daily for 1 y, whereas 57 other children used budesonide periodically for exacerbations. An additional 54 children were treated with disodium cromoglycate (DSCG) for 18 mo. Skin thickness was measured on each forearm before and after treatment for 6, 12, and 18 mo using a 20-MHz high-resolution ultrasonic device. The initial 6-mo budesonide treatment resulted in a greater reduction in mean skin thickness in the forearms compared with DSCG (right: -35.9 versus -5.9 microm; p = 0.004; left: -30.6 versus -7.3 microm; p = 0.03). At month 18, the inter-group differences were no longer significant. Budesonide inhalations in daily doses of 400-800 microg in prepubertal children with newly detected asthma may cause minor dermal thinning. The changes were reversible during low dose or periodic treatment with budesonide.

Topics: Administration, Inhalation; Anti-Asthmatic Agents; Asthma; Atrophy; Bronchodilator Agents; Budesonide; Child; Child, Preschool; Cromolyn Sodium; Double-Blind Method; Drug Administration Schedule; Drug Therapy, Combination; Female; Finland; Forearm; Humans; Male; Severity of Illness Index; Skin; Skinfold Thickness; Time Factors; Treatment Outcome; Ultrasonography

This study aims to assess voice changes and laryngeal abnormalities in asthmatic patients using inhaled corticosteroids (ICSs).. This study included 30 patients (15 females; mean age 21.3±2.6 years; range, 17 to 26 years and 15 males; mean age 20.7±2.3 years; range, 16 to 27 years) with bronchial asthma treated with ICSs between May 2013 and December 2013. A speech sample from each patient was evaluated by two phoniatricians and the degrees of dysphonia were scored. Each patient's voice was acoustically analyzed using the multidimensional voice program software. Videolaryngoscopy was used to detect laryngeal abnormalities including the vocal folds.. A total of 53.3% of ICSs users had dysphonia; most of them had a mild degree dysphonia. Of patients, vocal folds erythema was present in 56.7%, interarytenoid thickening in 56.7%, vocal folds bowing in 5.3% and vocal fold atrophy in 5.5%. A total of 36.7% patients had manifestations of laryngopharyngeal reflux. The presence of vocal fold bowing and atrophy was significantly related to the duration of ICS use (p=0.048). Soft phonation index values were positively associated with the duration of the ICS use (p=0.013).. Inhaled corticosteroids have abnormally adverse effects both on the function and the structure of the vocal folds.

Topics: Administration, Inhalation; Adolescent; Adult; Anti-Asthmatic Agents; Asthma; Atrophy; Beclomethasone; Budesonide; Dysphonia; Erythema; Female; Glucocorticoids; Humans; Laryngeal Diseases; Laryngoscopy; Male; Nebulizers and Vaporizers; Phonation; Speech; Video Recording; Vocal Cords; Voice; Young Adult

Topics: Administration, Inhalation; Atrophy; Beclomethasone; Bronchodilator Agents; Budesonide; Female; Humans; Long-Term Care; Lung Diseases, Obstructive; Middle Aged; Skin

Skin atrophy has been observed after prolonged use of inhaled corticosteroids. We therefore studied the effect of inhaled budesonide and nedocromil in patients with asthma on concentrations of procollagen propeptides in suction blister fluid reflecting skin collagen synthesis in vivo. Both types I and III procollagen propeptide concentrations decreased significantly after 6 wk of either 1,600 micro g/day (n=10) or 400 micro g/day (n=9) of inhaled budesonide but not in control subjects using inhaled nedocromil 16 mg/day (n=9). The reduction in mean propeptide concentrations ranged from 39 to 63%; the effects of the two budesonide doses did not differ significantly. Thus, even a low dose of inhaled corticosteroid represses skin collagen synthesis within a relatively short period.

Topics: Administration, Inhalation; Administration, Topical; Adolescent; Adult; Anti-Asthmatic Agents; Anti-Inflammatory Agents; Asthma; Atrophy; Blister; Bronchodilator Agents; Budesonide; Collagen; Exudates and Transudates; Female; Glucocorticoids; Humans; Male; Nedocromil; Peptide Fragments; Pregnenediones; Procollagen; Skin

Current glucocorticoids are inactivated mainly in the liver. Results from studies of their catabolism; their concentration gradients in epidermis and upper and lower dermis after topical application to intact and injured skin; and the concentration needed to inhibit synthesis of human connective tissue by skin fibroblasts; suggest that their systemic and local adverse reactions would logically be reduced further by adding a rapid extrahepatic biotransformation. An ideal glucocorticoid should be locally inactivated during, or immediately after, absorption. The data available for three glucocorticoids with some extrahepatic metabolism suggest that such relatively labile steroids may have a more autoregulating absorption than that of the conventional, more stable, steroids. This means that in skin areas with a damaged stratum corneum, the balance between steroid influx and inactivation may favour anti-inflammatory activity, while that balance is insufficient in intact skin for a triggering of glucocorticosteroid activity. When the skin lesions heal, and the high influx rate tapers off, corticosteroid activity in the epidermis and dermis may be better cut off than with the conventional, metabolically stable, corticosteroids. The compounds subject to local metabolism available today appear to have only moderate topical corticosteroid activity. There are still no valid data to support a claim that their catabolic effects on the connective tissue of diseased skin are less than those of conventional topical steroids. However, novel glucocorticosteroids with a still better relation between high intrinsic glucocorticosteroid activity and rapid metabolic turnover in skin should be designed and tested.

Topics: Administration, Topical; Anti-Inflammatory Agents; Atrophy; Biotransformation; Budesonide; Carbonates; Carboxylic Acids; Connective Tissue; Fibroblasts; Forecasting; Glucocorticoids; Humans; Liver; Lung; Pregnenediones; Skin; Structure-Activity Relationship; Time Factors