To the Editor:
We thank Drs. Sikri and Bhattachar for their response
1
to our recent study, “HMOX1 Promoter Microsatellite Polymorphism Is Not Associated with High Altitude Pulmonary Edema in Han Chinese,” published in Wilderness & Environmental Medicine.2
Our study has clarified the link between microsatellite polymorphism in the heme oxygenase-1 (HMOX1) gene promoter and high-altitude pulmonary edema (HAPE) in Han Chinese and may attempt to explore the pathogenesis of HAPE. The exact pathophysiologic mechanisms of HAPE are still unclear. Recently, increasing evidence has shown that HAPE is the result of a combination of genetic and environmental factors, but the role of genetics has not been clearly determined.3
, - Yu-jing S.
- Ming-wu F.
- Wen-quan N.
- Guang-ping L.
- Jing-liang L.
- Shou-quan D.
- et al.
Endothelial nitric oxide synthase gene polymorphisms associated with susceptibility to high altitude pulmonary edema in Chinese railway construction workers at Qinghai-Tibet over 4 500 meters above sea level.
Chin Med Sci J. 2010; 25: 215-221
4
We assumed that heme oxygenase-1 promoter region microsatellite polymorphism may be related to HAPE.The pathogenesis of HAPE is not only exaggerated hypoxic pulmonary hypertension, but may also involve the inflammatory response and the reduction of glucocorticoid release. We fully agree that the diagnosis and definition of HAPE require very strict criteria. In the present study, HAPE was diagnosed based on clinical symptoms and chest radiograph. All patients experienced illness within 3 to 5 days after arrival from low altitude to high altitude (3800 m). Blood samples were collected soon after patients were hospitalized. In the non-HAPE patients, measurements including hemoglobin, white blood cell count, oxygen saturation, and pulmonary artery pressure were collected at a hospital after they had been in Yushu for 5 to 7 days. Before travel to high altitude, all patients were healthy and had no clinical symptoms. According to our experience, the most satisfactory treatments of HAPE are field treatment using high-flow oxygen (8–12 L·min−1) or a hyperbaric chamber. At the same time, patients were given drug treatment including dexamethasom,
5
nifedipine/Regitin,6
and furosemide. Clinical observations of heart rate, blood pressure, respiratory rate, and body temperature were periodically recorded. After treatment using these methods, all patients improved significantly within 24 hours and continued treatment in the hospital using Tibetan herbs, such as Rhodiola rosea,7
ginkgo leaf tablets, and echinacoside8
until complete recovery.References
Sikri G, Bhattachar S. HMOX1 promoter microsatellite polymorphism and high altitude pulmonary edema in Han Chinese men. Wilderness Environ Med. In press
- HMOX1 promoter microsatellite polymorphism is not associated with high altitude pulmonary edema in Han Chinese.Wilderness Environ Med. 2017; 28: 17-22
- Endothelial nitric oxide synthase gene polymorphisms associated with susceptibility to high altitude pulmonary edema in Chinese railway construction workers at Qinghai-Tibet over 4 500 meters above sea level.Chin Med Sci J. 2010; 25: 215-221
- Rare mitochondrial DNA polymorphisms are associated with high altitude pulmonary edema (HAPE) susceptibility in Han Chinese.Wilderness Environ Med. 2012; 23: 128-132
- Sleep and breathing in high altitude pulmonary edema susceptible subjects at 4,559 meters.Sleep. 2012; 35: 1413-1421
- The effect of vasodilators on pulmonary hemodynamics in high altitude pulmonary edema: a comparison.Int J Sports Med. 1992; 13: S68-S71
- Salidroside attenuates chronic hypoxia-induced pulmonary hypertension via adenosine A2a receptor related mitochondria-dependent apoptosis pathway.J Mol Cell Cardiol. 2015; 82: 153-166
- Antiproliferative effect of echinacoside on rat pulmonary artery smooth muscle cells under hypoxia.J Pharmacol Sci. 2014; 126: 155-163
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Published online: April 10, 2018
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