Abstract
The role of malnutrition in IPF remains uncertain and should be considered a consequence of the disease and not a comorbid condition. However, given the high prevalence of malnutrition in IPF its impact on mortality should be further evaluated. http://ow.ly/5CKe30okjma
From the authors:
We appreciate the thoughtful comments of S. Jouneau and co-workers in their correspondence addressing the importance of nutritional status in idiopathic pulmonary fibrosis (IPF). We agree with the authors that nutritional status is of great interest in chronic diseases such as IPF [1].
The two most accepted methods to assess nutritional status are body mass index (BMI) and fat-free mass (FFM) [2–5]. Although BMI is the most widely used and simplest method, several factors such as ethnicity, gender and social status may influence it [6]. Moreover, it remains unestablished what cut-off value is the most appropriate to identify malnutrition [7]. Fat-free mass, a more sophisticated assessment technique using bioelectrical impedance, is not routinely performed in IPF patients. Thus, evidence for FFM is very limited in patients with IPF [8].
We agree that the central question of “what are the best indicators to assess malnutrition in IPF?” has to be addressed [1]. It was not possible to assess most indicators of malnutrition in the TORVAN study (e.g. FFM, weight loss, low energy intake, mid-arm circumference, triceps skinfold, etc.) as they were not routinely collected in the cohort [9]. In addition, only variables previously proven to be associated with survival were considered for our analytical model. While nutritional status is known to influence prognosis in some pulmonary diseases, such as chronic obstructive pulmonary disease and tuberculosis [3, 10], its impact on IPF remains uncertain. Furthermore, it should be considered that malnutrition in IPF is rather a consequence of the disease and not a comorbid condition per se. However, given the high prevalence of malnutrition in IPF patients, this “forgotten factor” is of great interest and we agree that its impact on mortality should be further evaluated.
Footnotes
Conflict of interest: S.E. Torrisi has nothing to disclose.
Conflict of interest: B. Ley has nothing to disclose.
Conflict of interest: M. Kreuter reports grants from Galapagos, grants and personal fees from Boehringer Ingelheim and from Hoffman la Roche, outside the submitted work.
Conflict of interest: M. Wijsenbeek reports grants and other from Hoffman la Roche, grants and other from Boehringer Ingelheim, other from Galapagos, outside the submitted work; all grants and fees were paid to her institution.
Conflict of interest: E. Vittinghoff has nothing to disclose.
Conflict of interest: H.R. Collard reports personal fees from Bayer, Boehringer Ingelheim, Bristol-Myers Squibb, Global Blood Therapeutics, Genoa, ImmuneWorks, Navitor, Parexel, PharmAkea, Prometic, Toray, Unity, Patara, Veracyte, Roche/Genentech, aTyr, Advance Medical, Aeolus and MedImmune, grants from the Pulmonary Fibrosis Foundation, and grants and personal fees from Three Lakes Partners, all outside the submitted work.
Conflict of interest: C. Vancheri has nothing to disclose.
- Received March 27, 2019.
- Accepted March 27, 2019.
- Copyright ©ERS 2019
