배경/목적: 한국의 내시경적 역행성 담췌관 조영술(ERCP)의 질을 평가한 전국적인 실태 조사 결과를 표준 질지표와 비교하여 기술하고자 한다. 방법: 건강보험심사평가원의 자료를 분석하였고, 이후에 무기명으로 전국적인 설문 조사를 시행하였다. 결과: ERCP 의사 157명 중에서 129명이 설문에 응답하여 82.2%의 회수율을 보였다. 한국에서 ERCP 시행률은 지속적으로 증가하였다. 약 반수의 의사는 1인당 ERCP 양이 연간 200예 이상으로 시술량이 많은 ERCP 의사에 속하였다. 대부분의 ERCP 의사들은 1단계의 ERCP 시술을 시행하였으나 담췌관 내압 측정, 담관-췌관경 및 췌장 시술은 많은 양의 시술을 하는 병원에서만 시행하였다. 대부분의 ERCP 의사들은 90% 이상의 성공률을 보였으나, 예비 괄약근 절개율이 약 25%로 표준 질지표보다 높았다. 12명의 ERCP 의사들이 최근 1년간 ERCP 후 환자가 사망하는 합병증을 경험하였다. 또한 ERCP 수련과 시술량이 낮거나 중등도인 병원의 방사선 차폐는 표준 질지표에 도달하지 못하였다. 결론: 한국의 ERCP 술기는 표준적인 질지표를 충족하였으나, ERCP 수련과 방사선 차폐 문제는 향후 개선이 필요하다.

내시경역행담췌관조영술과 관련된 심폐 합병증은 드물지만 심각한 장애나 심지어 사망까지 발생할 수 있다. ERCP 연 관 심폐합병증으로는 부정맥, 저혈압, 심근 경색, 호흡부전, 저산소증, 흡인 등이 있으며 이런 합병증들은 주로 진정 또는 마취와 관련하여 발생한다. 시술 관련 심폐합병증을 예방 하기 위해서 사용 약물 및 투여 용량에 신중을 기해야 하며, 시술 전 위험인자에 대한 평가는 물론 시술 중, 시술 후 철저한 심폐 활력징후에 대한 모니터링이 필요하다.

Calcium concentration in the bone resorption lacunae is high and is in the mM concentration range. Both osteoblast and osteoclast have calcium sensing receptor in the cell surface, suggesting the regulatory role of high extracellular calcium in bone metabolism. In vitro, high extracellular calcium stimulated osteoclastogenesis in coculture of mouse osteoblasts and bone marrow cells. Therefore we examined the genes that were commonly regulated by both high extracellular calcium and 1.25(OH)₂vitaminD₃(VD3) by using mouse oligo 11 K gene chip. In the presence of 10 mM [Ca²+]e or 10 nM VD3, mouse calvarial osteoblasts and bone marrow cells were co-cultured for 4 days when tartrate resistant acid phosphatase-positive multinucleated cells start to appear. Of 11,000 genes examined, the genes commonly regulated both by high extracellular calcium and by VD3 were as follows; 1) the expression of genes which were osteoclast differentiation markers or were associated with osteoclastogenesis were up-regulated both by high extracellular calcium and by VD3; trap, mmp9, car2, ctsk, ckb, atp6b2, tm7sf4, rab7, 2) several chemokine and chemokine receptor genes such as sdf1, scya2, scyb5, scya6, scya8, scya9, and ccr1 were up-regulated both by high extracellular calcium and by VD3, 3) the genes such as mmp1b, mmp3 and c3 which possibly stimulate bone resorption by osteoclast, were commonly up-regulated, 4) the gene such as c1q and msr2 which were related with macrophage function, were commonly down-regulated, 5) the genes which possibly stimulate osteoblast differentiation and/or mineralization of extracellular matrix, were commonly down-regulated; slc8a1, admr, plod2, lox, fosb, 6) the genes which possibly suppress osteoblast differentiation and/or mineralization of extracellular matrix, were commonly up-regulated; s100a4, npr3, mme, 7) the genes such as calponin 1 and tgfbi which possibly suppress osteoblast differentiation and/or mineralization of extracellular matrix, were up-regulated by high extracellular calcium but were down-regulated by VD3. These results suggest that in coculture condition, both high extracellular calcium and VD3 commonly induce osteoclastogenesis but suppress osteoblast differentiation/mineralization by regulating the expression of related genes.

Recently, we reported that high extracellular calcium increased receptor activator of nuclear factor- xB ligand (RANKL) expression via p44/42 mitogen-activated protein kinase (p44/42 MAPK) activation in mouse osteoblasts. However, the mechanism for p44/42 MAPK activation by high extracellular calcium is unclear. In this study, we examined the role of intracellular calcium increase in high extracellular calcium-induced RANKL induction and p44/42 MAPK activation. Primary cultured mouse calvarial osteoblasts were used. RANKL expression was highly induced by 10 mM calcium treatment. Ionomycin, a calcium ionophore, also increased RANKL expression and activated p44/42 MAPK. U0126, an inhibitor of MEK1/2, an upstream activator of p44/42 MAPK, blocked the RANKL induction by both high extracellular calcium and ionomycin. High extracellular calcium increased the phosphorylation of proline-rich tyrosine kinase 2 (Pyk2), one of the known upstream regulators of p44/42 MAPK activation. Bisindolylmaleimide, an inhibitor of protein kinase C, did not block RANKL induction and p44/42 MAPK activation induced by high extracellular calcium. 2-Aminoethoxydiphenyl borate, an inhibitor of inositol 1,4,5-trisphosphate (IP3) receptor, blocked the RANKL induction by high extracellular calcium. It also partially suppressed the activation of Pyk2 and p44/42 MAPK. Cyclosporin A, an inhibitor of calcineurin, also inhibited high calcium-induced RANKL expression in dose dependent manner. However, cyclosporin A did not affect the activation of Pyk2 and p44/42 MAPK by high extracellular calcium treatment. These results suggest that 1) the increase in intracellular calcium via IP3-mediated calcium release is necessary for RANKL induction by high extracellular calcium treatment, 2) Pyk2 activation, but not protein kinase C, following the increase in intracellular calcium might be involved in p44/42 MAPK activation, and 3) calcineurin-NFAT activation by the increase in intracellular calcium is involved in RANKL induction by high extracellular calcium treatment.