Geriatric Nutritional Risk Index is a predictor of tolerability of antifibrotic therapy and mortality risk in patients with idiopathic pulmonary fibrosis.

BACKGROUND AND OBJECTIVE: Idiopathic pulmonary fibrosis (IPF) is characterized by progressive lung fibrosis of unknown aetiology. Epidemiological studies have suggested that IPF progression may negatively affect nutritional status. Weight loss during antifibrotic therapy is also frequently encountered. The association of nutritional status and outcome has not been fully evaluated in IPF patients. METHODS: This retrospective multicohort study assessed nutritional status of 301 IPF patients receiving antifibrotic therapy (Hamamatsu cohort, n = 151; Seirei cohort, n = 150). Nutritional status was evaluated using the Geriatric Nutritional Risk Index (GNRI). The GNRI was calculated based on body mass index and serum albumin. The relationship between nutritional status and tolerability of antifibrotic therapy as well as mortality was explored. RESULTS: Of 301 patients, 113 (37.5%) had malnutrition-related risk (GNRI < 98). Patients with malnutrition-related risk were older, had increased exacerbations and worse pulmonary function than those without a GNRI status <98. Malnutrition-related risk was associated with a higher incidence of discontinuation of antifibrotic therapy, particulary due to gastrointestinal disturbances. IPF patients with malnutrition-related risk (GNRI < 98) had shorter survival than those without such risk (median survival: 25.9 vs. 41.1 months, p < 0.001). In multivariate analysis, malnutrition-related risk was a prognostic indicator of antifibrotic therapy discontinuation and mortality, independent of age, sex, forced vital capacity, or gender-age-physiology index. CONCLUSION: Nutritional status has significant effects on the treatment and outcome in patients with IPF. Assessment of nutritional status may provide important information for managing patients with IPF.

[A case of primary pulmonary nocardiosis with multiple pulmonary nodules successfully treated with moxifloxacin].

A 18-year-old man was admitted with fever. His chest radiograph and CT scan showed consolidation shadow in the right middle lobe and multiple nodules in both lungs. He was treated with meropenem and minocycline. After this antibiotic therapy, the consolidation shadow disappeared and the multiple nodules were slightly reduced in their size. Since filamentous bacteria suspicious of Nocardia grew transiently in the initial sputum culture, we started to treat him with oral sulfametoxazole-trimethoprim. However, because agranulocytosis was caused by sulfametoxazole-trimethoprim therapy, we had to change the anti-bacterial therapy to minocycline. Minocycline was not effective, and the nodules enlarged. For accurate diagnosis, we employed video-assisted thoracic surgery (VATS) to investigate the histological and bacterial analyses of the pulmonary nodules. Histological findings of the pulmonary nodule obtained by VATS revealed granuloma with central necrosis associated with neutrophilic micro-abscess. Filamentous gram-positive bacteria in pulmonary nodule tissue was stained positively with both Grocott and Ziehl-Neelsen staining. Taking these findings together, we diagnosed primary pulmonary nocardiosis. Three months after initiating moxifloxacin, the size of the multiple pulmonary nodules was markedly reduced. Our experience with this case suggests that moxifloxacin can be recommended for the treatment of pulmonary nocardiosis.