Ibuprofen Prevents Altitude Illness: A Randomized Controlled Trial for Prevention of Altitude Illness With Nonsteroidal Anti-inflammatories

Lipman, Grant S.; Kanaan, Nicholas C.; Holck, Peter; Constance, Benjamin B.; Gertsch, Jeffrey H.

doi:10.1016/j.annemergmed.2012.01.019

Cited by 76 publications

(72 citation statements)

References 50 publications

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“…Reported rates of AMS range from 25%-70% in tourists, trekkers, and climbers (Honigman et al, 1993;Wagner et al, 2008;Jackson et al, 2010;Lipman et al, 2012;McDevitt et al, 2014). While the best prevention of AMS is a gradual ascent, rapid ascent may provoke AMS despite the use of acetazolamide ( Jackson et al, 2010).…”

Section: Introductionmentioning

confidence: 94%

Study Looking at End Expiratory Pressure for Altitude Illness Decrease (SLEEP-AID)

Lipman

Kanaan

Phillips

et al. 2015

High Altitude Medicine & Biology

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Lipman, Grant S., Nicholas C. Kanaan, Caleb Phillips, Dave Pomeranz, Patrick Cain, Kristin Fontes, Becky Higbee, Carolyn Meyer, Michael Shaheen, Sean Wentworth, and Diane Walsh. Study Looking at End Expiratory Pressure for Altitude Illness Decrease (SLEEP-AID). High Alt Med Biol 16:154-161, 2015.--Acute mountain sickness (AMS) affects 25%-70% of the tens of millions of high altitude travelers annually, with hypoxia and nocturnal desaturations as major contributing factors. This is the first double blind randomized placebo controlled trial to assess expiratory positive airway pressure (EPAP) for AMS prevention and nocturnal hypoxic events. Healthy adult participants trekking in the Khumbu region of the Himalayas were randomized to a single-use EPAP nasal strip, or a visually identical sham device (placebo) prior to first night sleeping between 4371-4530 m (14,340-14,800 ft). The primary outcome was AMS incidence, measured by Lake Louise Questionnaire (LLQ), with secondary outcomes of AMS severity (by LLQ) and physiologic sleep indices measured by continuous sleep monitor. Intent-to-treat analysis included 219 participants with comparable demographic characteristics, of which 115 received EPAP and 104 placebo. There was no decrease in AMS with EPAP intervention (14% EPAP vs. 17% placebo; p=0.65; risk difference (-)3.15%, 95% CI (-)12.85%-6.56%). While overall AMS severity was not different between groups, EPAP reported decreased incidence of headache (64% vs. 76%; p<0.05, OR 0.51, 95% CI 0.27-0.95) and dizziness (81% vs. 98%; p<0.03, OR 0.29, 95% CI 0.09-0.78). During sleep, EPAP resulted in significant improvements in average peripheral oxygenation (Spo(2)) (80% versus 78%; p<0.01, mean difference=2, 95% CI 0.58-3.63) and a reduced percentage of time below 80% Spo(2) (31% vs. 46%; p<0.03, median difference=16, 95% CI 2.22-28.18). This lightweight and inexpensive EPAP device did not prevent acute mountain sickness, but did reduce the subgroup incidence of headache and dizziness while improving average nighttime peripheral oxygenation.

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Section: Introductionmentioning

confidence: 94%

Study Looking at End Expiratory Pressure for Altitude Illness Decrease (SLEEP-AID)

Lipman

Kanaan

Phillips

et al. 2015

High Altitude Medicine & Biology

Self Cite

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“…Recent studies have suggested that ibuprofen at a dose of 1800 mg·day −1 may be effective at preventing AMS [122], but studies have yet to establish superiority over acetazolamide or dexamethasone. In addition, safety with prolonged use at high altitude and, in particular the risk of gastrointestinal bleeding, remain unclear.…”

Section: Pharmacological Measuresmentioning

confidence: 99%

Acute high-altitude sickness

2017

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At any point 1-5 days following ascent to altitudes ⩾2500 m, individuals are at risk of developing one of three forms of acute altitude illness: acute mountain sickness, a syndrome of nonspecific symptoms including headache, lassitude, dizziness and nausea; high-altitude cerebral oedema, a potentially fatal illness characterised by ataxia, decreased consciousness and characteristic changes on magnetic resonance imaging; and high-altitude pulmonary oedema, a noncardiogenic form of pulmonary oedema resulting from excessive hypoxic pulmonary vasoconstriction which can be fatal if not recognised and treated promptly. This review provides detailed information about each of these important clinical entities. After reviewing the clinical features, epidemiology and current understanding of the pathophysiology of each disorder, we describe the current pharmacological and nonpharmacological approaches to the prevention and treatment of these diseases.

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“…NF-κB is a critical transcriptional activator of HIF-1α and basal NF-κB activity is required for HIF-1α protein accumulation during hypoxia in the brain of hypoxic animals (Rius et al, 2008). Conversely, HIF-1α promotes the inflammatory response within a hypoxic environment, at least in peripheral immune cells (Cramer et al, 2003; Lipman et al, 2012; Peyssonnaux et al, 2005; Walmsley et al, 2005; Zinkernagel et al, 2007). …”

Section: Models Of Inflammationmentioning

confidence: 99%

The impact of inflammation on respiratory plasticity

Hocker

Stokes

Powell

et al. 2017

Experimental Neurology

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Breathing is a vital homeostatic behavior and must be precisely regulated throughout life. Clinical conditions commonly associated with inflammation, undermine respiratory function may involve plasticity in respiratory control circuits to compensate and maintain adequate ventilation. Alternatively, other clinical conditions may evoke maladaptive plasticity. Yet, we have only recently begun to understand the effects of inflammation on respiratory plasticity. Here we review some of common models used to investigate the effects of inflammation and discuss the impact of inflammation on nociception, chemosensory plasticity, medullary respiratory centers, motor plasticity in motor neurons and respiratory frequency, and adaptation to high altitude. We provide new data suggesting glial cells contribute to CNS inflammatory gene expression after 24 hours of sustained hypoxia and inflammation induced by 8 hours of intermittent hypoxia inhibits long-term facilitation of respiratory frequency. We also discuss how inflammation can have opposite effects on the capacity for plasticity, whereby it is necessary for increases in the hypoxic ventilatory response with sustained hypoxia but inhibits phrenic long term facilitation after intermittent hypoxia. This review highlights gaps in our knowledge about the effects of inflammation on respiratory control (development, age, and sex differences). In summary, data to date suggest plasticity can be either adaptive or maladaptive and understanding how inflammation alters the respiratory system is crucial for development of better therapeutic interventions to promote breathing and for utilization of plasticity as a clinical treatment.

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Ibuprofen Prevents Altitude Illness: A Randomized Controlled Trial for Prevention of Altitude Illness With Nonsteroidal Anti-inflammatories

Cited by 76 publications

References 50 publications

Study Looking at End Expiratory Pressure for Altitude Illness Decrease (SLEEP-AID)

Study Looking at End Expiratory Pressure for Altitude Illness Decrease (SLEEP-AID)

Acute high-altitude sickness

The impact of inflammation on respiratory plasticity

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