慢性高山病 chronic mountain sickness CMS
https://en.wikipedia.org/wiki/Chronic_mountain_sickness
高地民族有另一種慢性高山病，主要是紅血球增多引起，症狀有 頭痛、頭暈、耳鳴、呼吸困難、心悸、睡眠障礙、疲憊、食慾不振神智改變、發紺、靜脈擴張等等。通常發生在三千公尺以上海拔，居住數年之後 出現。
慢性高山病與基因有關，並非所有高地民族的盛行率都一樣，在安地斯山脈盛行率最高，西非伊索匹亞盛行率最低，西藏人 5.6％。
CMS特徵是紅血球增多以及低血氧，隨著海拔下降會改善，紅血球增多會造成血液黏滯度上升，肺部血管血流不均，VQ mismatch 是指，在某些氧氣不足的肺部有過多血液，這些多出的血液得不到氧氣交換，在某些氧氣過多的肺部血流不足，這些多出的氧氣沒有足夠的紅血球可以攜帶至全身
診斷
血色素>20 (正常男性通常 14 左右，女性通常 12 左右) 。動脈氧氣濃度低於 85％（正常人 95-100％）
治療
下降、放血、服用 CAI 碳酸酐酶抑制劑 Carbonic anhydrase inhibitors
Chronic mountain sickness (CMS) is a disease that can develop during extended time living at a high altitude. It is also known as "Monge's disease", after its first description in 1925 by Carlos Monge.[1] While acute mountain sickness is experienced shortly after ascent to high altitude, chronic mountain sickness may develop after many years of living at high altitude. In medicine, high altitude is defined as over 2500 metres (8200 ft), but most cases of CMS occur at over 3000 m (10000 ft). Recently it has been correlated with increased expression of the genes ANP32D and SENP1.[1]
Although CMS generally affects people native to altitudes higher than 3000 m, it does not affect populations around the world equally. A recent study by Sahota and Panwar (2013)[2] reviewed CMS prevalence rates around the world and found the highest rates were found in Andean countries of South America and the lowest rates in people native to the East African Mountains of Ethiopia. CMS prevalence rates from the study are summarized below:
Ethiopia [3600–4100 m]: 0%
Tibetan Plateau (Tibetans): 0.91–1.2%
Indian Himalayas [3000m-4200m]: 4–7%
Kyrgyzstan [3000–4200 m]: 4.6%
Tibetan Plateau (Han Chinese): 5.6%
La Paz, Bolivia [3600 m]: 6% to 8%
Bolivia: 8–10%
Cerro de Pasco, Peru [4300 m]: 14.8–18.2%
Tibetan Plateau (Tibetans): 0.91–1.2%
Indian Himalayas [3000m-4200m]: 4–7%
Kyrgyzstan [3000–4200 m]: 4.6%
Tibetan Plateau (Han Chinese): 5.6%
La Paz, Bolivia [3600 m]: 6% to 8%
Bolivia: 8–10%
Cerro de Pasco, Peru [4300 m]: 14.8–18.2%
CMS is characterised by polycythemia 紅血球增多症 (with subsequent increased hematocrit) and hypoxemia 低血氧, which both improve on descent from altitude. CMS is believed to arise because of an excessive production of red blood cells, which increases the oxygen carrying capacity of the blood[2] but may cause increased blood viscosity and uneven blood flow through the lungs (V/Q mismatch). However, CMS is also considered an adaptation of pulmonary and heart disease to life under chronic hypoxia at altitude.[3]
The most frequent symptoms and signs of CMS are headache, dizziness, tinnitus, breathlessness, palpitations, sleep disturbance, fatigue, anorexia, mental confusion, cyanosis, and dilation of veins.[4]
Clinical diagnosis by laboratory indicators have ranges of Hb > 200 g/L, Hct > 65%, and arterial oxygen saturation (SaO2) < 85% in both genders.[5]
Treatment[edit]
Treatment involves descent from altitude, where the symptoms will diminish and the hematocrit return to normal slowly. Acute treatment at altitude involves bleeding (phlebotomy), removal of circulating blood, to reduce the hematocrit; however this is not ideal for extended periods. Carbonic anhydrase inhibitors have been shown to improve chronic mountain sickness by reducing erythropoietin and the resulting polycytemia, which resulted in better arterial O2 and lower heart rate.[3]
Treatment involves descent from altitude, where the symptoms will diminish and the hematocrit return to normal slowly. Acute treatment at altitude involves bleeding (phlebotomy), removal of circulating blood, to reduce the hematocrit; however this is not ideal for extended periods. Carbonic anhydrase inhibitors have been shown to improve chronic mountain sickness by reducing erythropoietin and the resulting polycytemia, which resulted in better arterial O2 and lower heart rate.[3]
碳酸酐酶抑制劑 Carbonic anhydrase inhibitors
2010/11/25 15:56
碳酸酐酶抑制劑 Carbonic anhydrase inhibitors
碳酸酐酶(carbonic anhydrase)的作用主要是催化二氧化碳與水合成碳酸(同時也加速碳酸分解為二氧化碳與水)；碳酸在體內又可快速分解為氫離子與碳酸氫根離子。碳酸酐酶存在體內許多部位，與身體細胞水分的移動及酸鹼平衡有相當大的關聯。乙醯胺基硫唑嘧錠(acetazolamide)是最早被發現的碳酸酐酶抑制劑，其是因為在研究磺胺類藥物的副作用時意外被發現；抑制碳酸酐酶對身體的酸鹼平衡有明顯的影響，但同時也提供一定的臨床用途。
多噻磺胺(dorzolamide)及布林左胺(brinzolamide)亦屬於磺胺類藥物的碳酸酐酶抑制劑，由於具有較高的角膜穿透性，因而被研發作為局部眼用藥劑；抑制眼球內睫狀體的碳酸酐酶活性，可降低房水的產生，使得眼壓下降。
國內使用之口服碳酸酐酶抑制劑主要為乙醯胺基硫唑嘧錠，商品名包括Acetazolamide、Acetazolamox、Ailopan、Atenezol、Azol、Diamox、Diazamide等。國內目前之碳酸酐酶抑制劑眼藥水則包括愛舒壓點眼懸液劑(Azopt)及舒露瞳點眼液劑(Trusopt)等。
藥理機轉：
碳酸酐酶抑制劑可抑制碳酸酐酶的作用，進而影響氫離子及碳酸氫根離子的生成，最終影響其他離子與水分在細胞膜內外的移動；其作用在腎臟可降低水分的吸收而產生利尿，作用在眼睛睫狀體可抑制房水的分泌，進而降低眼壓。此外，由於碳酸酐酶抑制劑可使得身體血液產生代謝性偏酸的現象，因而可增加呼吸速率，預防高山症的發生。
碳酸酐酶抑制劑可抑制碳酸酐酶的作用，進而影響氫離子及碳酸氫根離子的生成，最終影響其他離子與水分在細胞膜內外的移動；其作用在腎臟可降低水分的吸收而產生利尿，作用在眼睛睫狀體可抑制房水的分泌，進而降低眼壓。此外，由於碳酸酐酶抑制劑可使得身體血液產生代謝性偏酸的現象，因而可增加呼吸速率，預防高山症的發生。
適應症：
眼用碳酸酐酶抑制劑主要用於治療高眼壓症及慢性隅角開放型青光眼。
口服碳酸酐酶抑制劑主要用於治療急性青光眼、高山症、高腦壓症、癲癇等；此外，亦有利尿之作用。
眼用碳酸酐酶抑制劑主要用於治療高眼壓症及慢性隅角開放型青光眼。
口服碳酸酐酶抑制劑主要用於治療急性青光眼、高山症、高腦壓症、癲癇等；此外，亦有利尿之作用。
副作用：
一、眼用碳酸酐酶抑制劑偶可見的副作用為眼睛刺痛感、灼熱感、癢、流淚、視力模糊、及角結膜炎等，極少會發生全身性副作用。
二、口服使用的副作用包括：頭痛、苦澀感、胃腸道不適、發熱、發疹、腎結石、骨髓抑制、血小板減少性紫斑、溶血性貧血、粒性白血球缺乏、全血球減少、及代謝性酸中毒等。
一、眼用碳酸酐酶抑制劑偶可見的副作用為眼睛刺痛感、灼熱感、癢、流淚、視力模糊、及角結膜炎等，極少會發生全身性副作用。
二、口服使用的副作用包括：頭痛、苦澀感、胃腸道不適、發熱、發疹、腎結石、骨髓抑制、血小板減少性紫斑、溶血性貧血、粒性白血球缺乏、全血球減少、及代謝性酸中毒等。
禁忌：
對磺胺藥曾有過敏病史、蠶豆症、孕婦、血鈉或血鉀過低、肝腎功能不良、腎上腺衰竭、以及血氯過高的患者，應避免使用。
對磺胺藥曾有過敏病史、蠶豆症、孕婦、血鈉或血鉀過低、肝腎功能不良、腎上腺衰竭、以及血氯過高的患者，應避免使用。
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