Low fasting serum triglyceride and high free fatty acid levels in pulmonary fibrosis: a previously unreported finding.

OBJECTIVE

The authors describe here the occurrence of low fasting serum triglyceride (TG) and high free fatty acid (FFA) levels in pulmonary fibrosis, a finding that has never been reported before.

PATIENTS AND METHODS

TGs were measured in: (a) 44 patients (3 male and 41 female; mean age SEM: 63.06 +/- 4.04 years) who have been hospitalized in the authors' department in the past 2 years for chronic interstitial or fibrosing pulmonary disease (FP); (b) 20 patients (4 male and 16 female; mean age: 69.80 +/- 2.96 years) affected by various nonfibrosing pneumopathies or bronchopathies (NFP); (c) 110 control subjects (CS), composed of 15 male and 95 female consecutive patients (mean age: 67.52 +/- 1.52 years) hospitalized in 1999 for minor nonlung-related illnesses. In 24 FP and 36 CS patients, FFA have also been measured. All subjects investigated had no clinical or laboratory evidences of liver, kidney, or thyroid diseases, nor a history of hormonal treatment, alcohol consumption, smoking, or dietary disorders. None of the subjects investigated was under treatment with lipid lowering agents or with other drugs that could affect the levels of TG or FFA or their measurement (including ascorbic acid).

RESULTS

Compared with CS, the FP group showed a 61% reduction of TG (0.64 +/- 0.03 vs 1.63 +/- 0.08 mmol/L; P <.001), whereas no significant difference was observed between NFP and CS groups. Serum FFA in FP showed a 63% increase compared with CS (P <.01). In the FP group, TGs were also low in 5 patients with type 2 diabetes (0.76 +/- 0.11 mmol/L, -53%, P <.001) and in 6 obese (body mass index [BMI] > 29 kg/m2) subjects (0.51 +/- 0.03, -69%, P <.01), although it is known that TGs are often elevated in diabetes and obesity.

CONCLUSIONS

Chronic interstitial or pulmonary fibrosis is associated with low TG and high FFA levels. Although it is known that the lung contains lipoprotein lipase and is a significant source of plasma postheparin lipase activity, the mechanisms of this change remain to be clarified. Since insulin-like growth factor-I (IGF-I) is known to lower TG and increase FFA, a role could be played by the enhanced production of IGF-I that has been reported to occur in pulmonary fibrosis.