Prednisolone/salmeterol/fluticasone propionate
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Laryngeal leishmaniasis: case report A 71-year-old man developed laryngeal leishmaniasis following treatment with salmeterol/fluticasone propionate and prednisolone for chronic obstructive pulmonary disease (COPD) [dosages and durations of treatments to reactions onsets not stated]. The man was referred to the Ear, Nose and Throat (ENT) services due to progressive worsening of voice hoarseness for 4 years. He received comments from others for the severity of his dysphonia, and he also started having difficulty in swallowing. He denied weight loss or fever. He was first reviewed by the ENT team 5 years earlier and had undergone microlaryngoscopy and biopsy at that time, and again 3 years later due to persistent symptoms. On both occasions, investigations revealed evidence of oropharyngeal and laryngeal candidiasis with chronic inflammation and epithelial atypia of the right vocal fold but with no evidence of malignancy. He was treated for laryngopharyngeal reflux and had multiple courses of low-dose antifungal treatment [specific drug not stated]; however, his symptoms progressed. His past medical history included COPD, for which he had been receiving inhaled salmeterol/ fluticasone propionate and an average of 3–4 short courses per year of oral prednisolone for exacerbations of his COPD. He was an ex-smoker. He drank approximately 10 units of alcohol per week. On examination, flexible nasendoscopy revealed oedema and erythema of the post-cricoid area, diffuse erythema of both vocal cords, and swelling of the right vocal fold with normal mobility. There was also evidence of extensive oropharyngeal and laryngeal candidiasis. Blood tests were remarkable only for a mildly elevated CRP. An HIV antigen/antibody test was found to be negative negative. A differential diagnosis included recurrent or resistant laryngeal candidiasis, laryngeal neoplasia, laryngopharyngeal reflux or other causes of chronic laryngitis, including that related to environmental irritants. Due to the progressive symptoms, repeat direct microlaryngoscopy under general anaesthesia was performed which showed the similar findings to flexible nasendoscopy with polypoid oedema of the right true and false vocal fold. Biopsies were taken. Histopathological examination of the laryngeal biopsies showed hyperplastic and inflamed squamous epithelium with dense inflammation in the submucosa. The inflammation was predominantly chronic, comprising plasma cells, histiocytes and lymphocytes with illformed granulomatous reaction focally. Within macrophages and elsewhere, there were numerous tiny parasites seen. They had the morphology of leishmania amastigotes with basophilic nuclei and kinetoplasts. The organisms stained with Giemsa but not Grocott or DPAS stains confirming they were Leishman-Donovan bodies. There were also fungal pseudohyphae within the squamous epithelium, consistent with candidiasis. There was no evidence of epithelial dysplasia or malignancy. In view of these findings, the previous laryngeal biopsies were reviewed. Whilst both biopsies sho
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