We have read with great interest the article by Kim et al. 1 on the relationship between changes in parameters reflecting nutritional deficit, such as hypocholesterolaemia and prognosis in miliary tuberculosis. We wonder if the value of hypocholesterolaemia in predicting progression to respiratory failure and poor outcome in their patients was not exclusively related to malnutrition (intended as nutritional deficit), but was also related to more severe underlying infection. Indeed, in recent years conventional markers of malnutrition, such as hypocholesterolaemia, have also become recognised as markers of inflammation and severity of illness, for instance in severe infection 2–4. Curiously, a historical reference for this more recent concept is a 1911 article on febrile tuberculosis 5.
We are involved in using hypocholesterolaemia as a marker of sepsis and severity of illness in critically ill postoperative patients. We often find that sepsis is associated with cholesterol levels even below 1.0 mmol·L−1, independently of the underlying nutritional state, and find that persistently severe hypocholesterolaemia is associated with poor outcome 3, 4.
Perhaps a more severe underlying infection might help to explain, at least in part, the poor prognostic implications of hypocholesterolaemia in tuberculosis 1. It would be interesting to observe the correlation with the level of C-reactive protein.
In sepsis, an unresolved issue is whether acute hypocholesterolaemia merely reflects severity of disease, or it actively contributes to poor outcome. The differences between tubercular infection and surgical sepsis do not allow generalisations, however the article by Kim et al. 1 also offers an interesting insight into this problem. Several hypotheses support the view that the low availability of cholesterol in sepsis may impair adequate synthesis of stress hormones, and the adequate synthesis and function of cells taking part in host defence 4. The latter also seems to be the case with tubercular infection 6, 7 and, interestingly, oral or parenteral cholesterol supplementation has been used or proposed in both conditions 6, 8.
This aspect still deserves satisfactory assessment although, despite the apparent modernity of the issue, a 1920 article on pneumonia patients 9 was already observing that hypocholesterolaemia is a marker of the activity of infection and is associated with prognosis, white blood cells and pus have a high content of cholesterol and that cholesterol might be associated with anti-toxic properties.
Of course, the importance of an adequate nutritional state in tubercular infection 1 remains fundamental, independently of the interpretation of the components of hypocholesterolaemia, and we congratulate again the authors of the Kim et al. 1 study for their interesting work.
Statement of interest
None declared.
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