[A case of intubation granuloma treated with steroid inhalation].

A 36-year-old woman was given a diagnosis of hemophagocytic syndrome associated with systemic lupus erythematosus, and was treated with high-dose methylprednisolone and etoposide. She needed endotracheal intubation for mechanical ventilation because of respiratory failure. She developed hoarseness and stridor 69 days after extubation. A pedunculated mass under her glottis was observed by the laryngoscopy. Development of a laryngeal granuloma due to long-term contact with the endotracheal tube was considered, although she was continuously given oral prednisolone (22.5 mg/day) even after extubation. She was treated with inhalation of fluticasone propionate and her symptoms, e.g. hoarseness, decreased. Disappearance of the polypoid lesion was seen on day 26. A laryngeal granuloma due to intubation developed, even with the systemic administration of steroids; but it was successfully treated with steroid inhalation.

Activation of complement system in adult T-cell leukemia (ATL) occurs mainly through lectin pathway: a serum proteomic approach using mass spectrometry.

Adult T-cell leukemia (ATL) is a fatal malignancy caused by infection with human T lymphotropic virus type-1 (HTLV-1). To search for a new biomarker of ATL, we analyzed sera from ATL patients using ProteinChip arrays. The spectral comparison of ATL patients with HTLV-1 carriers and healthy volunteers showed that the intensities of five peaks (1779, 1866, 2022, 4467, and 8930 m/z) were significantly increased in ATL, while those of four peaks (4067, 4151, 8130, and 8597 m/z) were decreased. From these differentially expressed peaks, we chose peaks of 1779, 1866, and 2022 m/z as biomarker candidates of ATL. MS/MS ion search using tandem mass spectrometry and immunoprecipitation assay using anti-C3 antibody showed that factors derived from these candidate peaks were identified as C3f, which is a component of the complement system and a fragment of complement C3. These results indicate that the complement system was activated in ATL. Further analysis of markers specific to the activation pathways (classical, alternative, and lectin pathways) in the complement system showed that the serum concentration of the marker of the lectin pathway was significantly higher in ATL patients. These results suggest that activation of the complement system in ATL occurs mainly through the lectin pathway.