ABSTRACT
We report a very rare fatal case of reactive AA amyloidosis following pulmonary non-tuberculous mycobacteriosis (PNTM). A 61-year-old woman with a history of PNTM since 1992, whose treatment was difficult because of liver dysfunction and drug eruption caused by antibiotics, had been hospitalized due to recurrent pulmonary bacterial infection. She complained of leg edema in January, 2000, and nephrotic syndrome was diagnosed in February. After diarrhea and abdominal pain appeared in March, she was admitted to our hospital with worsening edema, and dizziness on April 28. Despite treatment, she died on May 5, 2000. Autopsy revealed PNTM and diffuse systemic depositions of amyloid A protein in heart, kidney and gastrointestinal tract. PNTM, often resistance to antibacterial agents, is increasing recently. This case suggests that it is necessary to take care of amyloidosis when various systemic symptoms are observed in chronic inflammatory disease.
Subject(s)
Amyloidosis/etiology , Lung Diseases/complications , Mycobacterium avium-intracellulare Infection/complications , Serum Amyloid A Protein/metabolism , Amyloidosis/blood , Arthritis, Rheumatoid/complications , Fatal Outcome , Female , Humans , Middle Aged , Nephrotic Syndrome/complicationsABSTRACT
Although many investigators reported the diagnostic and therapeutic value of bronchoscopy in the early stage of inhalation injury, few findings in the late stage of inhalation injury have been reported. We investigated histopathological changes of in trachea and bronchi after inhalation injury. Five survivors with inhalation injury underwent bronchoscopic examinations combined with biopsies from the early stage to the late stage. Although the bronchotracheal membranes improved to near normal under the bronchoscopic findings in the late or recovery stage, invasion of inflammatory cells and the capillary dilatation in the subepithelial region were still remarkable histologically. Goblet cells also increased on the surface of mucous membranes. In cases of the inhalation injury with severe burn, pulmonary edema, bronchial edema and secretions tended to be prolonged. Results suggested that continuous secretions in the respiratory tracts sometimes cause airway obstruction. Bronchoscopic and histologic findings in the healing process of inhalation injury predict long-term pulmonary functional outcome. Moreover, the aggressive pulmonary toilet seemed to be effective in removing foreign particles and accumulated secretions which also cause the inflammatory response and the obstruction in inhalation injury.
Subject(s)
Bronchi/pathology , Burns, Inhalation/pathology , Wound Healing/physiology , Adult , Aged , Aged, 80 and over , Bronchoscopy/methods , Burns, Inhalation/physiopathology , Female , Fiber Optic Technology , Humans , Male , Middle AgedSubject(s)
Anti-Inflammatory Agents/therapeutic use , Drugs, Chinese Herbal/therapeutic use , Phytotherapy , Pulmonary Disease, Chronic Obstructive/drug therapy , Administration, Oral , Aged , Biomarkers/blood , C-Reactive Protein/analysis , Humans , Pulmonary Disease, Chronic Obstructive/blood , Tumor Necrosis Factor-alpha/bloodABSTRACT
Left vocal cord palsy is a rare complication of pulmonary hypertension (also known as Ortner syndrome). Here we report a case of a patient with Ortner syndrome caused by primary pulmonary hypertension (PPH). The patient was a 28-year-old woman, who complained of persistent hoarseness and dyspnea on effort. A left vocal cord palsy, as well as PPH, was diagnosed, suggesting that pulmonary artery dilatation associated with PPH led to left recurrent laryngeal nerve palsy. This case suggests that PPH should be suspected in any case with unexplained left vocal cord palsy.
