The aim of this initial investigational study is to compare the effect of desloratadine on the inflammatory responses to heat stress in firefighters exercising in their personal protective equipment.
Significant heat strain where temperatures approach and exceed 39.0 degrees celsius is known to increase intestinal permeability and induce a graded systemic inflammatory response which includes increases in interleukin-6, tumor necrosis factor alpha, and c-reactive protein. Recent data examining firefighters found fire service instructors possessed greater resting levels of inflammatory markers and that 18-29% of the variation in these markers could be explained by frequency of heat strain. Firefighters themselves are susceptible to core temperatures ranging between 38.5 and 39.0C in as little as 2-3 work cycles. Considering resource limitation in the fire service, such workloads is a realistic possibility when at structural fires, particularly for first alarm apparatus. Though there is a well-defined role of the inflammatory response in adaptive changes, elevated resting levels begs the question of whether such frequency of exposure and acute inflammatory flux in fire service workers may contribute to chronic elevations of inflammatory markers and altered disease risk. Elevations in c-reactive protein are associated with cardiovascular risk with studies indicating a causative role of monomeric c-reactive protein in platelet activation and thrombus growth. Cooling methods save for cryotherapy have demonstrated limited to mild effectiveness for mitigating the inflammatory responses to heat strain resulting in no solution to attenuate acute inflammatory responses. The mast-cell stabilizing properties of desloratadine and its safety profile make it an interesting candidate for investigating its use in this context. This study seeks to determine whether 10mg desloratadine taken before and 24h after exertional heat strain to a core temperature to a core temperature of 39.5 degrees celsius reduces the associated inflammatory response measured over a 72-hour period.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
PREVENTION
Masking
DOUBLE
Enrollment
12
Oral ingestion 10mg pill 2 hours prior to heat strain trial. Second 10mg dose 24-hours later.
Oral ingestion 10mg inert pill 2 hours prior to heat strain trial. Second dose 24-hours later.
No pill ingestion during the trial - to discern the presence of a placebo effect from baseline inflammatory response
University of Victoria
Victoria, British Columbia, Canada
RECRUITINGChange in serum cortisol
Assessment of changes in serum cortisol within and between interventions measured via venipuncture and ELISA
Time frame: Before, immediately following, and 2-hours following exertional heat strain
Change in serum interleukin-6 and ELISA
Assessment of changes in serum interleukin-6 within and between interventions measured via venipuncture and ELISA
Time frame: Before, immediately following, and 2-hours following exertional heat strain
Change in serum c-reactive protein
Assessment of changes in serum c-reactive protein within and between interventions measured via venipuncture and ELISA
Time frame: Before, immediately following, and 24, 48, and 72-hours following exertional heat strain
Change in serum tumor necrosis factor alpha
Assessment of changes in serum tumor necrosis factor alpha within and between interventions measured via venipuncture and ELISA.
Time frame: Before, immediately following, and 2-hours following exertional heat strain
Change in body mass
Trial arm differences in fluid loss estimated via differences between before-after body mass.
Time frame: Before and immediately after exertional heat strain
Differences in core body heat storage
Trial arm differences in the change in core body temperature during heating.
Time frame: Before and immediately after exertional heat strain
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