These findings, combined with a lack of significant correlation between leptin and appetite, suggest that leptin reductions in TB are a reflection of wasting seen in TB disease, rather than a driving force behind appetite and nutritional dysregulation. We found that ghrelin in TB patients is elevated compared to controls, falls with treatment, and correlates negatively with BMI and BF. Our findings conflict with the one prior study we found on ghrelin levels in TB, which reported no differences in baseline or post-treatment ghrelin concentrations in TB patients and reported lower ghrelin levels in malnourished cases compared to wellnourished cases. Our results do agree with studies examining ghrelin in other pulmonary disorders, which found elevated ghrelin in malnourished patients with COPD and lung cancer. While no other published studies have examined resistin in infections, our finding of elevated resistin in the disease state agreed with prior studies showing elevations in gastrointestinal cancers, direct correlations between resistin and cancer stage and resistin and BMI loss. In summary, our data show that patients with pulmonary TB display clear AbMole alpha-Cyperone alterations in energy regulatory hormones in comparison to healthy controls, and these alterations coincide with changes in appetite and nutritional status. As altered hormone levels normalized during treatment, appetite and nutritional status also improved. PYY was the strongest predictor of appetite in these patients and high PYY was an indicator of poor prognosis, with high levels predicting reduced gains in appetite and body fat during treatment. While previous studies have examined various combinations of energy-regulatory hormones in patients with TB, we are unaware of any studies which have evaluated PYY, leptin, ghrelin, and resistin in the same population, or any that have three longitudinal data points during treatment. This broad view provides valuable insight into the patterns of disrupted energy regulation and inflammation in TB. In addition, this was the first published study to examine PYY in TB and our results suggest this hormone is a key player in appetite and energy dysregulation in TB. The relatively short follow-up time of this study limited our ability to measure long-term correlations between hormones, appetite, and nutritional status during treatment. While we found strong correlation trends between PYY and appetite as well as BF, we did not detect a correlation between PYY and BMI gain, nor could we detect correlations between appetite and BMI/BF gain during treatment. BMI and BF likely lag behind appetite, with appetite improving first during treatment and weight gain happening as a result. Thus, a longer follow-up time may have demonstrated stronger correlations between initial PYY and appetite and weight changes during or following treatment. To rule out the possibility that changes in hormones reflect differences in body composition rather than the disease state itself, it would have been ideal to match cases and controls by BMI and BF. However, as TB generally causes cachexia, healthy subjects by nature do not have equivalent body composition to TB patients and thus BMI was not a feasible option to use as matching criteria. A future study comparing TB patients with those with other cachexia-inducing disease states could further explore the hormonal abnormalities specific to TB.