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°£°æº¯ÁõÀÌ µ¿¹ÝµÈ Áö¼Ó¼º¿Ü·¡º¹¸·Åõ¼®(CAPD) ȯÀÚ¿¡¼­ÀÇ Ç÷û À¯»ê¿° ³óµµ Serum Lactate Levels in CAPD Patients with Liver Cirrhosis

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ÀÌÇö¼÷/Hyeon Suk Lee °­À翵/¾ç¿ø¼®/±è¼ø¹è/ÀÌ»ó±¸/¹ÚÁ¤½Ä/°­´öÈñ/À±°ßÀÏ/Jae Young Kang/Won Seok Yang/Soon Bae Kim/Sang Koo Lee/Jung Sik Park/Duk Hee Kang/Kyun Il Yoon

Abstract

¿ä¾à
º¹¸·Åõ¼®¿¡ ³Î¸® »ç¿ëµÇ°í ÀÖ´Â À¯»ê¿°Àº ´ëºÎºÐ °£¿¡¼­ ´ë»çµÈ ÈÄ ¿ÏÃæ ÀÛ¿ëÀ» ³ªÅ¸³»°Ô
µÇ¸ç, °£±â´É ÀÌ»óÀÌ ÀÖ´Â °æ¿ì Ç÷û À¯»ê¿° ³óµµ°¡ ¿À¸¦ °ÍÀ¸·Î ¿¹»óµÈ´Ù. ±×·¯³ª ÇöÀç±îÁö
´Â °£±â´É ÀÌ»óÀÌ µ¿¹ÝµÈ ÇÑ ¸íÀÇ ½ÅºÎÀü ȯÀÚ¿¡¼­ º¹¸·Åõ¼® ÈÄ Ç÷û À¯»ê¿°Ä¡°¡ ºñÁ¤»óÀû
À¸·Î Áõ°¡µÇ¾ú´Ù´Â º¸°í°¡ ÀÖÀ» »ÓÀÌ´Ù. ÀÌ¿¡ ÀúÀÚµéÀº °£°æº¯ÁõÀÌ µ¿¹ÝµÈ CAPD ȯÀÚ¿¡¼­
À¯»ê¿°ÀÌ Æ÷ÇÔµÈ Åõ¼®¾×ÀÌ Ç÷û À¯»ê¿° ³óµµ ¹× »ê¿°±â ´ë»ç¿¡ ¾î¶² ¿µÇâÀ» ¹ÌÄ¡´Â Áö¸¦ ¾Ë
¾Æº¸°íÀÚ ÇÏ¿´´Ù.
1996³â 5¿ùºÎÅÍ 1996³â 9¿ù±îÁö º¹¸·Åõ¼® ÁßÀÎ 42¿¹¿Í °£°æº¯Áõ 17¿¹¸¦ Æ÷ÇÔÇÑ ÃÑ 59¿¹¿¡
¼­ µ¿¸ÆÇ÷ À¯»ê¿°, pH, Áßź»ê¿° ¹× Á¤¸ÆÇ÷ ÃÑÀÌ»êȭź¼Ò ³óµµ¸¦ ÃøÁ¤ÇÏ¿© CAPD±º, °£°æº¯
ÁõÀÌ µ¿¹ÝµÈ CAPD±º ¹× °£°æº¯Áõ±ºÀ¸·Î ³ª´©¾î ºñ±³¡¤ºÐ¼®ÇÏ¿´´Ù. ¸ðµç ȯÀÚ´Â 40mmo1/L
ÀÇ À¯»ê¿°ÀÌ Æ÷ÇÔµÈ Åõ¼®¾×À» »ç¿ëÇÏ¿´´Ù.
µ¿¸ÆÇ÷ À¯»ê¿° ³óµµ´Â °£°æº¯ÁõÀÌ µ¿¹ÝµÈ CAPD±º¿¡¼­ Áß°£°ª(ÃÖÀú°ª-ÃÖ°í°ª)
4.19(2.39-5.2)mmol/L·Î CAPD±º 1.43(0.55-2.92)mmol/L, °£°æº¯Áõ±º 1.94(1.51-5.24)mmol/L
¿¡ ºñÇÏ¿© ³ôÀº °ªÀ» º¸¿´´Ù. µ¿¸ÆÇ÷ pH´Â ¼¼ ±º°£¿¡ Å« Â÷ÀÌ´Â ¾ø¾ú°í µ¿¸ÆÇ÷ Áßź»ê¿°
¹× Á¤¸ÆÇ÷ ÃÑÀÌ»êȭź¼Ò ³óµµ´Â °£°æº¯ÁõÀÌ µ¿¹ÝµÈ CAPD±º¿¡¼­ ´Ù¸¥ µÎ ±ºº¸´Ù ´Ù¼Ò ³·Àº
°á°ú¸¦ º¸¿´Áö¸¸ Åë°èÀû Â÷ÀÌ´Â ¾ø¾ú´Ù. À½ÀÌ¿Â °£°ÝÀº °£°æº¯ÁõÀÌ µ¿¹ÝµÈ CAPD±ºÀÌ ´Ù¸¥
µÎ ±º¿¡ ºñÇÏ¿© ³ô°Ô ³ªÅ¸³µÁö¸¸ Åë°èÀû Â÷ÀÌ´Â ¾ø¾ú´Ù.
ÀÌ»óÀÇ °á°ú¿Í »ó½ÂµÈ À¯»ê¿°ÀÌ ½É±Ù¼öÃà ÀúÇÏ, ÀúÇ÷¾Ð, ÁöÁú´ë»ç Àå¾Ö ¹× ³ú±â´É Àå¾Ö µî
À» ÀÏÀ¸Å³ ¼ö ÀÖÀ½À» °¨¾ÈÇÒ ¶§ °£°æº¯ÀÌ µ¿¹ÝµÈ ½ÅºÎÀü ȯÀÚ¿¡¼­ À¯»ê¿°ÀÌ Æ÷ÇÔµÈ Åõ¼®¾×
À» »ç¿ëÇÏ´Â µ¥´Â ÁÖÀÇ°¡ ÇÊ¿äÇÒ °ÍÀ¸·Î º¸ÀδÙ.

Lactate is the most commonly used buffer in CAPD. The buffering effect of lactate is
accomplished by its complete metabolism in liver and kidney. In patients with hepatic
disease the rate of metabolism may be lower with a consequent increase in plasma
lactate levels. Plasma lactate levels, however, have not been measured in CAPD patients.
This study was performed to evaluate the plasma lactate levels and acid-base status in
CAPD patients with liver cirrhosis.
The concentrations of arterial L-lactate, pH, bicarbonate and venous total
CO2 were measured in 6 CAPD patients with LC, 36 CAPD patients
without liver disease and 17 LC patients. All CAPD patients used commercially available
dialysate containing 40mmo1/L lactate(D,L-racemic solution).
Arterial lactate levels were 4.19mmol/L in CAPD patients with LC, 1.43mmol/L in
CAPD patients and 1.94mmo1/L in LC patients(p<0.05). Arterial pH were not different
among subgroups. Arterial bicarbonate concentrations were 20.5meq/L in CAPD patients
with LC, 24.2meq/L in CAPD patients and 24.4meq/L in LC patients. Venous total
CO2 levels were 21.4, 24.7 and 23.4meq/L, respectively. Anion gap were
13.1, 9.4 and 8.1, respectively.
From our results and possible toxicity of elevated lactate levels, lactate-containing PD
solutions should be used carefully to treat CAPD patients with LC.

Å°¿öµå

Lactate; CAPD; Liver Cirrhosis;

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