Unexpected findings in dynamic vs baseline procalcitonin in obese patients

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Conference Proceeding

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PURPOSE: Obesity is an increasingly common comorbidity which can impact the host response to infection. Serum procalcitonin (PCT) can be an important heuristic when grounded in clinical context. Some comorbidities, such as advanced chronic kidney disease and certain malignancies, are known to alter PCT levels and are thereby accounted for when interpreting PCT levels; obesity is generally not among these variables and data are sparse whether it should be. In 2016, Boursier et al showed in 295 nonacutely-ill obese patients, the median baseline PCT level was above the 97.5th percentile previously documented in the general population and when comparing Grade I to Grade III obesity, Grade III had an odds ratio of 2.76 for being in the upper tercile. Less is known about the dynamic response of PCT levels in obese patients. Understanding is increasing about white adipose tissue as a robust endocrine organ, comprising 20% of body weight even in healthy-weight individuals, and notably capable of the production of TNF-alpha and IL-6, cytokines that stimulate PCT release. In the obese state, adipocytes hypertrophy leading to greater infiltration of adipose tissue macrophages (ATMs) yielding greater potential production of TNF-alpha and IL-6, while other macrophage functions, such as efferocytosis, may be increased as well. The differences in both the quality and quantity of adipose tissue in obese patients could account for the difference in baseline PCT levels shown by Boursier et al. It is unknown whether microbiologic stress on these relatively abundant ATMs would yield a higher or lower PCT response in obese patients. METHODS: Using retrospective chart review in a multi-campus, Midwestern hospital system from 2017 to 2019, a database of 281 patients was created; 165 non-obese and 116 obese using BMI above 30. The inclusion criteria included patients 18-89 who carried the diagnosis of “Sepsis” and had at least one measurement of PCT during that admission. RESULTS: The results of the investigation were unexpected. While not meeting the threshold for significance, the study showed a strong trend toward non-obese patients having higher PCT levels, despite prior studies showing the non-obese patients likely started from a lower baseline. The obese cohort had a mean PCT of 5.8 (3.3-8.6) while the non-obese 11.4 (6.2-16.6). Student’s ttest of the difference of cohort sample means of 5.6 showed a p-value of 0.0940 (CI -0.95 - 12.1); we are actively seeking to collect more data with the goal of meeting the threshold for statistical significance and accounting for potential confounders. CONCLUSIONS: In obese septic patients PCT levels were lower compared to non-obese septic patients despite possibly higher baseline values in obese non-septic patients. These findings are possibly due to the multifaceted role of ATMs at different stages of the inflammatory cascade. Obese patients are known to have more ATMs than non-obese patients, therefore in a bacterial septic milieu the ATM role of neutrophilic debris clean up may act to moderate PCT response, leading to lower PCT levels in obese septic patients. CLINICAL IMPLICATIONS: Better understanding of the host response to infection based on body habitus may improve treatments in the future for an increasingly obese population.




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CHEST Annual Meeting 2021 October 17-20, 2021. Abstract.

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