pulmicort and Hyperplasia

Mucous membrane plasmacytosis (MMP) is rare condition characterized by diffuse plasma cell infiltration of upper aero-digestive tract mucosa. It results in epithelial hyperplasia that has a classic papillary appearance. We describe a case of MMP primarily affect laryngeal and oropharyngeal mucosa resulting in progressive airway obstruction. We highlight airway management and histopathology. The patient had near complete clinical response with inhaled budesonide, which has not yet been described as a treatment option in the literature. Laryngoscope, 133:70-72, 2023.

Topics: Budesonide; Humans; Hyperplasia; Larynx; Mucous Membrane

Tracheal stenosis following injury cannot be effectively treated. The current study compared the protective effects of different anti‑inflammatory drugs on tracheal stenosis and investigated their possible mechanisms. Rabbit tracheal stenosis models following injury were constructed and confirmed using hematoxylin and eosin (H&E) staining. A total of 30 rabbits were divided into the control (CON), penicillin (PEN), erythromycin (ERY), budesonide (BUD) and PEN + ERY + BUD groups (n=6). Stenotic tracheal tissue, serum and bronchoalveolar lavage fluid (BALF) were collected 10 days after continuous treatment. Pathological changes in the tracheas were observed by H&E staining. Histone deacetylase 2 (HDAC2) expression in tracheal tissues was detected by immunofluorescence. Immunohistochemistry was performed to detect collagen I (Col‑I) and collagen III (Col‑III) levels in tracheal tissues. Transforming growth factor β1 (TGF‑β1), vascular endothelial growth factor (VEGF) and interleukin 8 (IL‑8) levels in serum and BALF samples were determined using ELISA kits. Western blotting detected HDAC2, IL‑8, TGF‑β1 and VEGF levels in tracheal tissues. H&E staining demonstrated that tracheal epithelial hyperplasia and fibroblast proliferation in the ERY and PEN + ERY + BUD groups markedly improved compared with the CON group. Furthermore, in tracheal tissues, HDAC2 expression was significantly increased and IL‑8, TGF‑β1, VEGF, Col‑I and Col‑III levels were significantly decreased in the ERY and PEN + ERY + BUD groups compared with the CON group. Additionally, the results for the PEN + ERY + BUD were more significant compared with the ERY group. In serum and BALF samples, IL‑8, TGF‑β1 and VEGF levels in the ERY and PEN + ERY + BUD groups were significantly lower compared with the CON group, with the results of the PEN + ERY + BUD group being more significant compared with the ERY group. There were no significant differences between the PEN, BUD and CON groups. ERY inhibited tracheal granulation tissue proliferation and improved tracheal stenosis following injury and synergistic effects with PEN and BUD further enhanced these protective effects. The mechanism may involve HDAC2 upregulation and inhibition of local airway and systemic inflammatory responses.

Topics: Animals; Anti-Inflammatory Agents; Bronchoalveolar Lavage Fluid; Budesonide; Collagen; Disease Models, Animal; Erythromycin; Granulation Tissue; Histone Deacetylase 2; Hyperplasia; Interleukin-8; Penicillins; Protective Agents; Rabbits; Trachea; Tracheal Stenosis; Transforming Growth Factor beta1; Up-Regulation; Vascular Endothelial Growth Factor A

Micronodular lesions are common findings in lung imaging. As an important differential diagnosis, we describe a case of diffuse idiopathic pulmonary neuroendocrine cell hyperplasia; it is notable that the diagnosis of diffuse idiopathic pulmonary neuroendocrine cell hyperplasia is often delayed. This case provides supporting evidence to establish lung biopsy by cryotechnique as the option of first choice when considering a diagnostic strategy for micronodular lung lesions.. We report a case of a 65-year-old white woman who presented with obstructive symptoms of chronic coughing and dyspnea confirmed by conventional lung function tests. A computed tomography scan presented disseminated micronodules in all the lobes of her lungs. With the help of bronchoscopic cryobiopsy it was possible to obtain a high yield sample of lung parenchyma. On histologic examination, the micronodules correlated with a diffuse neuroendocrine cell hyperplasia. In the context of clinical symptoms, radiological aspects, and histomorphological aspects we made the diagnosis of a diffuse idiopathic pulmonary neuroendocrine cell hyperplasia. Obstructive symptoms were treated with inhaled steroids and beta-2-mimetics continuously. A comparison between current computed tomography scans of our patient and scans of 2014 revealed no significant changes. Last ambulatory checks occurred in January and May of 2016. The course of disease and the extent of limitation of lung function have remained stable.. The diagnosis of diffuse idiopathic pulmonary neuroendocrine cell hyperplasia is best made in a multidisciplinary review including clinical presentation, lung imaging, and histomorphological aspects. This report and current literature indicate that transbronchial lung cryobiopsy can be used as a safe and practicable tool to obtain high quality biopsies of lung parenchyma in order to diagnose micronodular lesions of the lung.

Topics: Aged; Albuterol; Anti-Inflammatory Agents; Biopsy; Bronchodilator Agents; Budesonide; Cough; Cryosurgery; Dyspnea; Female; Formoterol Fumarate; Humans; Hyperplasia; Lung; Lung Diseases, Interstitial; Neuroendocrine Cells; Prognosis; Respiratory Function Tests; Thoracic Surgery, Video-Assisted; Tiotropium Bromide; Tomography, X-Ray Computed; Treatment Outcome

Lymphocytic colitis is a chronic inflammatory disease affecting the bowel. The clinical course of lymphocytic colitis is believed to be benign with watery diarrhoea. We report herein what is, to the best of our knowledge, the first case of lymphocytic colitis complicated by a terminal ileal mass. A 23-year-old man presented with diarrhoea. Blind biopsies of samples taken from the terminal ileum, caecum and ascending colon showed features of lymphocytic colitis. He declined treatment with budesonide or 5-aminosalicylates. He presented 14 months later with pain over the right lumbar region and nausea. Computed tomographic enteroclysis showed a focal soft tissue enhancing mass at the terminal ileum. Excision of the soft tissue mass revealed that it was reactive nodular lymphoid hyperplasia with fibrous granulation tissue. In conclusion, an untreated lymphocytic colitis may result in the formation of an inflammatory mass lesion.

Topics: Biopsy; Budesonide; Cecum; Colitis, Lymphocytic; Colonoscopy; Diarrhea; Fibrosis; Granulation Tissue; Humans; Hyperplasia; Ileum; Inflammation; Intestinal Mucosa; Male; Nausea; Tomography; Treatment Outcome; Young Adult

The cause-and-effect relationship between airway smooth muscle (ASM) remodeling and airway hyperresponsiveness (AHR) following allergen challenge is not well established. Using a rat model of allergen-induced ASM remodeling we explored the relationship between the site of ASM remodeling and AHR. Brown Norway rats, sensitized and challenged (3 times at 5-day intervals) with ovalbumin, were intranasally administered 0.1 mg/kg budesonide 24 and 1 h before challenge. Airway responses to aerosolized methacholine were assessed 48 h or 1 wk after three challenges. Airways were stained and analyzed for total airway wall area, area of smooth muscle-specific α-actin, and goblet cell hyperplasia, and the constant-phase model was used to resolve the changes in respiratory system mechanics into large airway and peripheral lung responses. After three ovalbumin challenges, there was a significant increase in ASM area and in the total wall area in all sized airways as well as an increase in goblet cells in the central airways. Budesonide inhibited ASM growth and central airway goblet cell hyperplasia following ovalbumin challenges. Budesonide also inhibited small but not large airway total wall area. AHR was attributable to excessive responses of the small airways, whereas responsiveness of the large airways was unchanged. Budesonide did not inhibit AHR after repeated challenge. We conclude that ASM remodeling induced by repeated allergen challenges involves the entire bronchial tree, whereas AHR reflects alterations in the lung periphery. Prevention of ASM remodeling by corticosteroid does not abrogate AHR.

Topics: Airway Remodeling; Animals; Asthma; Bronchial Hyperreactivity; Bronchial Provocation Tests; Bronchoalveolar Lavage Fluid; Bronchodilator Agents; Budesonide; Cell Proliferation; Chemokines; Cytokines; Disease Models, Animal; Goblet Cells; Hyperplasia; Inflammation Mediators; Lung; Male; Muscle, Smooth; Ovalbumin; Rats; Rats, Inbred BN; Time Factors

The effects of aerosol budesonide and dietary myo-inositol on progression of benzo[alpha]pyrene (B[alpha]P) induced carcinogenesis were studied in A/J mouse lung. First, we determined when to intervene in the carcinogenesis process by exposing several animals to B[alpha]P at 100 and 150 mg/kg of body wt. Groups of these animals were necropsied from 1 to 36 weeks post-carcinogen. The presence of different categories of lung tumors was noted over the 36 week time period. Hyperplasia first appeared approximately 6 weeks post-carcinogen followed by adenoma at 9 weeks, then by carcinoma at 26 weeks. From this temporal sequence we determined we could test for effects of preventive agents on progression to hyperplasia by intervening at 3 weeks, for effects on progression to adenoma by intervening at 6 weeks and for effects on progression to carcinoma by intervention at 12 weeks. Intervention at 3 weeks post-carcinogen with aerosolized budesonide delayed both hyperplasia and adenoma formation. Once hyperplasia appeared in budesonide treated animals, however, it increased at the same rate as in control animals, indicating a delay in progression. Progression from adenoma to carcinoma was reduced when budesonide was given 12 weeks post-carcinogen. Dietary myo-inositol failed to suppress progression from adenoma to carcinoma when started 12 weeks post-carcinogen. In summary, budesonide is a chemopreventive agent that has inhibitory effects on B[alpha]P induced carcinogenesis of the lung in A/J mice at all stages of progression from hyperplasia formation to cancer.

Topics: Adenoma; Aerosols; Animals; Anti-Inflammatory Agents; Benzo(a)pyrene; Budesonide; Carcinogens; Disease Progression; Female; Hyperplasia; Inositol; Lung; Lung Neoplasms; Mice; Mice, Inbred A; Neoplasm Staging

To study the expression of transforming growth factor alpha, beta 1 in hyperplastic tissue after endoscopic polypectomy and the effect of corticosteroid.. Forty patients with nasal polyps were divided into two groups randomly: corticosteroid group (n = 20) with topical application of Budesonide (BUD, 400 micrograms/d) after endoscopic polypectomy and control group (n = 20) without corticosteroid after surgery. The hyperplastic tissues in operative cavity obtained in the 1st and 8th weeks after operation were studied with HE staining and immunohistochemistry technique respectively.. Morphological changes of hyperplastic tissue after endoscopic polypectomy included pseudostratified epithelium, highly edematous lamina proper and inflammatory cells infiltration, in which the main infiltrative cells were eosinophils (67.5%). Transforming growth factor alpha(TGF alpha) protein was highly expressed in epithelial cells, grand cells and inflammatory cells in the hyperplastic tissue. Transforming growth factor beta 1 (TGF beta 1) protein was highly expressed in inflammatory cells in the hyperplastic tissue. The expression of TGF alpha and beta 1 was significantly decreased after topical BUD spray (P < 0.01, 0.05).. Transforming growth factor alpha and beta 1 may play an important role in the formation and recurrence of nasal polyps.

Topics: Adult; Anti-Inflammatory Agents; Budesonide; Female; Humans; Hyperplasia; Male; Nasal Mucosa; Nasal Polyps; Transforming Growth Factor alpha; Transforming Growth Factor beta

We studied the antiinflammatory effect of a Russian-made glucocorticoid budesonide administered by inhalation and intraperitoneal injection to rats with experimental noninfectious pulmonary granulomatosis. The antiinflammatory effects of budesonide at both administration routes were similar. Intraperitoneal injection, in contrast to inhalation, produced a systemic effect manifested in suppression of hyperplasia of non-encapsulated lymphoid formations in the mucosa.

Topics: Administration, Inhalation; Animals; Anti-Inflammatory Agents; Bronchoalveolar Lavage Fluid; Budesonide; Hyperplasia; Infusions, Parenteral; Lung; Lymphomatoid Granulomatosis; Male; Rats; Rats, Wistar; Time Factors