Hyperplastic Gastric Polyps

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ºŸâªÉ«¬À≠‘ß‰∑¬§ŸàÕ“¬ÿ 74 ªï Õ“™’æ‡°…μ√°√ ¿Ÿ¡‘≈”‡π“ Õ.æ∫æ√– ®.μ“° CC: ∂à“¬¥” 2 —ª¥“Àå PTA PI: 2 —ª¥“Àå PTA ¡’Õ“°“√∂à“¬Õÿ®®“√–‡ªìπ ’¥”«—π≈– 6-7 §√—Èß ª√‘¡“≥§√—Èß≈– §√÷Ëß∂÷ßÀπ÷Ëß°√–‚∂π ‰¡à¡’Õ“°“√Õ“‡®’¬π‡ªìπ‡≈◊Õ¥ ∂à“¬‡ªìπ‡≈◊Õ¥ ¥ ª«¥∑âÕß ‰¢â À√◊Õμ—«‡À≈◊Õßμ“‡À≈◊Õß ªí “«–‡ªìπª°μ‘¥’ ‰¥â‰ªμ√«®∑’Ë‚√ßæ¬“∫“≈™ÿ¡™πæ∫«à“´’¥ ¡“°®÷ß‰¥â√—∫‡≈◊Õ¥ ·μà¬—ß¡’Õ“°“√´’¥·≈–∂à“¬¥”Õ¬Ÿàμ≈Õ¥ ·æ∑¬å®÷ß àßμ—«¡“√—°…“μàÕ ·≈–μ√«®«‘π‘®©—¬‡æ‘Ë¡‡μ‘¡ PH: ‰¡à‡§¬¡’Õ“°“√∂à“¬¥”¡“°àÕπ ‰¡à‡§¬Õ“‡®’¬π‡ªìπ‡≈◊Õ¥ °àÕπ°“√‡®Á∫ªÉ«¬§√—Èßπ’È‰¡à‡§¬‰¥â√—∫‡≈◊Õ¥ ¡’‚√§ª√–®”μ—«§◊Õ§«“¡¥—π‚≈À‘μ Ÿß √—∫¬“∑’Ë‚√ßæ¬“∫“≈™ÿ¡™π Personal History: √—∫ª√–∑“π¬“·°âª«¥ diclofenac ‡π◊ËÕß®“°¡’Õ“°“√ª«¥‡¡◊ËÕ¬®“°°“√∑”ß“π ¡“π“π 5 «—π ™à«ß 2 —ª¥“Àå°àÕπ¡“‚√ßæ¬“∫“≈ ‰¡à¥◊Ë¡ ÿ√“·≈–‰¡à Ÿ∫∫ÿÀ√’Ë ‰¡à¡’ª√–«—μ‘ IVDU ‰¡à‡§¬ —°μ“¡μ—« FH: ªØ‘‡ ∏ª√–«—μ‘¡–‡√Áß„π§√Õ∫§√—«

PE: V/S: BT 37.3˚C, PR 80/min, RR 16/min, BP 120/70 mm Hg GA: good consciousness, markedly pale, no jaundice

8 ®ÿ≈ “√ ¡“§¡·æ∑¬å√–∫∫∑“ß‡¥‘πÕ“À“√·Ààßª√–‡∑»‰∑¬, æƒ…¿“§¡- ‘ßÀ“§¡ 2559 HEENT: markedly pale conjunctivae, no icteric sclerae, thyroid gland not enlarged, lymph node not palpable, no oral ulcer, no lip hyperpigmentation or telangiectasia Heart: regular rhythm, normal S1S2, no murmur Lungs: normal breath sound Abdomen: no abdominal distension, no spider nevi, no superfi- cial vein dilatation, active bowel sound, no shifting dullness, no tenderness, no mass, no hepaotosple- nomegaly Extremities:no pitting edema, no clubbing of fingers, no palmar erythema °“√μ√«®∑“ßÀâÕßªØ‘∫—μ‘°“√ CBC: Hb 6.0 g/dL, Hct 18.6%, MCV 84.3 fL, WBC 5,100/mm3 (Neutro- phil 56.8%, Lymphocyte 32.3%, Monocyte 9.4%, Eosinophil 1% Basophil 0.5%), platelets 191,000/mm3 BUN 11 mg/dL, Cr 0.6 mg/dL Na 140 mEq/L, K 3.3 mEq/L, Cl 114 mEq/L, CO2 25 mEq/L LFT: TB 0.52 mg/dL, DB 0.19 mg/dL, AST 31 U/L, ALT 16 U/L, AP 56 U/L, Alb 3.5 g/dL, globulin 3.0 g/dL PT 11.7 sec (9.4-13.2) INR 1.11, aPTT 31.5 sec (25.9-39.8) √ªªÿ≠À“í 1. ∂à“¬Õÿ®®“√–‡ªìπ melena ¡“ 2 —ª¥“Àå 2. Anemia 3. ª√–«—μ‘°“√„™â NSAIDs

A Woman with Melena for 2 Weeks 9 Õ¿‘ª√“¬ ºâªÉ«¬À≠‘ßÕ“¬Ÿ ÿ74 ªï¡“¥â«¬Õ“°“√∂à“¬¥”¡“ 2 —ª¥“Àå√à«¡°—∫¡’ª√–«—μ‘ √—∫ ª√–∑“π¬“ NSAIDs μ√«®√à“ß°“¬‰¡àæ∫ chronic liver stigmata æ¬“∏‘ ¿“æπà“ ®–Õ¬Ÿà∑’Ë upper GI tract ·≈–πà“®–‡ªìπ non variceal upper GI bleeding ‚¥¬ “‡Àμÿπà“®–‡ªìπ®“° peptic ulcer disease ¡“°∑’Ë ÿ¥®÷ß‰¥â∑”°“√μ√«® esophagogastroduodenoscopy (EGD) æ∫ duodenal diverticulum with healed ulcer (¿“æ∑’Ë 1) ´÷Ëß‰¡àπà“Õ∏‘∫“¬Õ“°“√¢ÕßºŸâªÉ«¬‰¥â Õ¬à“ß‰√°Áμ“¡Õ“°“√ ∂à“¬¥”Õ“®‡°‘¥‰¥â®“°æ¬“∏‘ ¿“æ à«π≈à“ß°«à“π—Èπ¡“®π∂÷ß≈”‰ â„À≠àΩíòß¢«“‰¥â ®÷ß‰¥â ∑”°“√μ√«® colonoscopy ‡æ‘Ë¡‡μ‘¡μàÕ æ∫«à“¡’ colonic diverticulosis μ—Èß·μà sig- moid colon ®π∂÷ß ascending colon ·≈–„π terminal ileum ¡’ blood stained Õ¬Ÿà (¿“æ∑’Ë 2) ´÷Ëß‡¡◊ËÕ∑”°“√≈â“ß·≈–¥Ÿ√Õ¬‚√§¿“¬„π colonic diverticulosis ·≈â« ‰¡àæ∫≈—°…≥–¢Õß active bleeding ™—¥‡®π · ¥ß«à“ GI bleeding „πºŸâªÉ«¬√“¬ π’Èπà“®–¡’ “‡Àμ¡“®“°√Õ¬‚√§¿“¬„π≈”‰ â‡≈Á°‡Õß‡¢â“‰¥â°—∫ÿ overt obscure GI bleeding (μ“√“ß∑’Ë 1) ´÷Ëß “‡Àμÿ∑’Ë‡ªìπ‰ª‰¥â„πºŸâªÉ«¬√“¬π’È ‰¥â·°à 1. Small bowel neoplasm ‡™àπ GIST, lymphoma, adenocarcinoma 2. NSIAD induced small bowel ulcer ‡π◊ËÕß®“°¡’ª√–«—μ‘√—∫ª√–∑“π ¬“ diclofenac

¿“æ∑’Ë 1 Duodenal bulb

10 ®ÿ≈ “√ ¡“§¡·æ∑¬å√–∫∫∑“ß‡¥‘πÕ“À“√·Ààßª√–‡∑»‰∑¬, æƒ…¿“§¡- ‘ßÀ“§¡ 2559 ¿“æ∑’Ë 2 Terminal ileum

μ“√“ß∑’Ë 1 Etiology of obscure GI bleeding Upper GI and lower Mid GI bleeding GI bleeding overlooked Upper GI lesions Younger than 40 years of age Cameronûs erosions Tumors Fundic varices Meckelûs diverticulum Peptic ulcer Dieulafoyûs lesion Angiectasia Crohnûs disease Dieulafoyûs lesion Celiac disease Gastric antral vascular ectasia Lower GI lesions Older than 40 years of age Angiectasia Angiectasia Neoplasms NSAID enteropathy Celiac disease Uncommon Hemobilia Hemosuccus pancreaticus Aortoenteric fistula

A Woman with Melena for 2 Weeks 11 3. Vascular lesion ‡™àπ angiodysplasia, Dieulafoy lesion ‡π◊ËÕß®“°æ∫ blood stained ∑’Ë terminal ileum ®÷ß‰¥â∑”°“√μ√«® retrograde enteroscopy ´÷Ëß “¡“√∂μ√«®‰ª‰¥â∂÷ßμ”·Àπàß 30 ´¡.‡Àπ◊ÕμàÕ IC valve ·≈–¬—ß‰¡àæ∫√Õ¬‚√§ ·μà‡æ√“–ºŸâªÉ«¬‡√‘Ë¡¡’Õ“°“√ª«¥·πàπ∑âÕß‰¡à “¡“√∂∑πμàÕ °“√ àÕß°≈âÕßμàÕ‰¥â ·≈–æ∫ green bile ‰¡à¡’ active bleeding ®÷ß‰¥âÀ¬ÿ¥°“√ àÕß°≈âÕß ·≈–‡≈◊Õ°∑”°“√μ√«® CT abdomen ‡æ‘Ë¡‡μ‘¡‡π◊ËÕß®“° ß —¬ small bowel tumor (¿“æ∑’Ë 3) ´÷Ëßæ∫«à“¡’ a large hypervascular mass „π small bowel loop (likely jejunum) ∫√‘‡«≥Ωíòß¢«“¢Õß™àÕß∑âÕß «—¥‰¥â¢π“¥ 4 × 2 ´¡.„π√–π“∫μ—¥ ¢«“ß ¡’ active contrast extravasation √Õ∫Ê °âÕπ ‡¢â“‰ª„π bowel lumen ‰¡àæ∫«à“¡’ abnormal dilatation ¢Õß proximal bowel loops ‰¡à¡’ ascites ‰¡à æ∫μàÕ¡πÈ”‡À≈◊Õß‚μº‘¥ª°μ‘ ‡π◊ÈÕμ—∫ª°μ‘ ®“°¿“æ CT «‘π‘®©—¬«à“‡ªìπ small bowel GIST ºâªÉ«¬‰¥â√—∫°“√√—°…“¥â«¬°“√ºà“μ—¥„π‡«≈“μàÕ¡“Ÿ º≈°“√ºà“μ—¥æ∫ submucosal mass ¢π“¥ 3 ´¡.¬◊ËπÕÕ°®“°ºπ—ß¢Õß≈”‰ â‡≈Á° à«π jejunum √à«¡°—∫¡’ end on artery (¿“æ∑’Ë 4) º≈°“√μ√«®∑“ßæ¬“∏‘«‘∑¬“«‘π‘®©—¬‡ªìπ GIST ‚¥¬æ∫μ—«‡π◊ÈÕ

¿“æ∑’Ë 3 CT scan of abdomen

12 ®ÿ≈ “√ ¡“§¡·æ∑¬å√–∫∫∑“ß‡¥‘πÕ“À“√·Ààßª√–‡∑»‰∑¬, æƒ…¿“§¡- ‘ßÀ“§¡ 2559 ¿“æ∑’Ë 4 Intraoperative finding

¿“æ∑’Ë 5 Follicular of spindle cell in muscularis mucosa, CD117 positive

ßÕ°¢π“¥ 4.7 × 3 × 2.7 ´¡. ‡®√‘≠¡“®“°™—Èπ muscularis propria ‡¢â“‰ª„π™—Èπ submucosa ·≈– serosa √à«¡°—∫¡’ mucosal ulceration ·μà‰¡à¡’ lymphovascular invasion ·≈–¡’ margin free ≈—°…≥–‡´≈≈å‡ªìπ spindle cell type ¬âÕ¡μ‘¥ CD117 (+) ¡’ mitotic count 3/50 HPF (¿“æ∑’Ë 5) Review Gastrointestinal stromal tumor (GIST) GIST ‡ªìπ mesenchymal tumor ∑’Ëæ∫‰¥â∫àÕ¬∑’Ë ¥„π√–∫∫∑“ß‡¥‘πÕ“À“√ÿ ‡°‘¥¡“®“° interstitial of Cajal ´÷ËßÕ¬Ÿà√Õ∫Ê myenteric plexus ·≈–„π muscularis propria μ≈Õ¥∑“ß‡¥‘πÕ“À“√·≈–¡’°“√· ¥ßÕÕ°¢Õß KIT protein1 ´÷Ëßæ∫ ‰¥â 95% ¡’Õ¬Ÿàª√–¡“≥ 5% ∑’Ë‰¡à¡’°“√· ¥ßÕÕ°¢Õß KIT protein ‡√’¬°«à“ KIT

A Woman with Melena for 2 Weeks 13 negative GIST ‡°‘¥®“°°“√°≈“¬æ—π∏ÿå¢Õß¬’π platelet derived growth factor receptor alpha (PDGFRA)2 à«π„À≠à‡°‘¥„π§πÕ“¬ÿ¡“°°«à“ 40 ªï ‚¥¬æ∫¡“° ∑’Ë ÿ¥∑’ËÕ“¬ÿª√–¡“≥ 60 ªï æ∫„πºŸâ™“¬¡“°°«à“ºŸâÀ≠‘ß3 GIST “¡“√∂æ∫‰¥â∑ÿ°∑’Ëμ≈Õ¥∑“ß‡¥‘πÕ“À“√‚¥¬æ∫¡“°∑’Ë ÿ¥∑’Ë°√–‡æ“– Õ“À“√ (60%) √Õß≈ß¡“§◊Õ∑’Ë≈”‰ â‡≈Á° (30%) æ∫¡“°∑’Ë∫√‘‡«≥ jejunum4 ‚¥¬ gastric GIST ®–¡’æ¬“°√≥å‚√§∑’Ë¥’°«à“ small bowel GIST Õ“°“√¢Õß‚√§¢÷ÈπÕ¬Ÿà°—∫μ”·Àπàß¢Õß°âÕπ ¢π“¥¢Õß°âÕπ ·≈–°“√°√–®“¬ μ—«¢Õß‚√§ Õ“°“√ à«π„À≠à∑’Ëæ∫¡—°¡“¥â«¬‡√◊ËÕß‡≈◊Õ¥ÕÕ°„π∑“ß‡¥‘πÕ“À“√ Õ“°“√Õ◊ËπÊ ∑’Ëæ∫‰¥â‡™àπ Õ◊¥·πàπ∑âÕß ‡≈◊Õ¥ÕÕ°¿“¬„π‡¬◊ËÕ∫ÿ™àÕß∑âÕß Õ“°“√ÕàÕπ‡æ≈’¬®“°¿“«– ´’¥ „π°√≥’∑’Ë¡’°“√·æ√à°√–®“¬¢Õß‚√§¡—°‰ª∑’Ëμ—∫À√◊Õ¿“¬„π™àÕß∑âÕß °“√·æ√à °√–®“¬‰ª∑’ËμàÕ¡πÈ”‡À≈◊Õßæ∫‰¥âπâÕ¬¡“° à«π°“√·æ√à°√–®“¬‰ª∑’ËªÕ¥·≈– Õ«—¬«–Õ◊ËππÕ°™àÕß∑âÕß¡—°æ∫„π°√≥’∑’Ë‡ªìπ advanced disease °“√μ√«®«‘π‘®©—¬‡æ‘Ë¡‡μ‘¡ 1. Radiologic imaging 1.1 Contrast enhanced CT abdomen ‡ªìπ imaging ∑’Ë¥’∑’Ë ÿ¥„π °“√«‘π‘®©—¬·≈–ª√–‡¡‘π√–¬–¢Õß‚√§ “¡“√∂∑’Ë®–∫Õ°≈—°…≥–·≈–¢Õ∫‡¢μ¢Õß°âÕπ μ≈Õ¥®π°“√·æ√à°√–®“¬¢Õß‚√§‰¥â ‚¥¬≈—°…≥–∑’Ë typical ®–‡ªìπ well-defined heterogeneous mass with peripheral enhancing border and central low attenuation 1.2 MRI æ∫«à“§≥¿“æ„π°“√μ√«®¥âÕ¬°«à“°“√μ√«®¥â«¬ÿ CT abdomen „π°“√«‘π‘®©—¬ gastric GIST Õ—π‡π◊ËÕß¡“®“° °“√‡§≈◊ËÕπ‰À«¢Õß gastric wall ·≈–‡π◊ÈÕ‡¬◊ËÕ∑’ËÕ¬Ÿà√Õ∫Ê ¢≥–μ√«® ·μàÕ“®®–¡’ª√–‚¬™πå„π°“√ª√–‡¡‘π°“√·æ√à °√–®“¬‰ª∑’Ëμ—∫‡π◊ËÕß®“°∫“ß§√—Èß√Õ¬‚√§Õ“®®–¡’≈—°…≥– isodensity „°≈â‡§’¬ß°—∫ ‡π◊ÈÕμ—∫ª°μ‘‰¥â∑”„Àâ‰¡à‡ÀÁπ√Õ¬‚√§®“°°“√μ√«®¥â«¬ CT abdomen 1.3 Positron emission tomography scan (PET scan) ™à«¬„π °“√·¬° active tumor ÕÕ°®“° necrotic À√◊Õ inactive scar tissue ·¬°√–À«à“ß

14 ®ÿ≈ “√ ¡“§¡·æ∑¬å√–∫∫∑“ß‡¥‘πÕ“À“√·Ààßª√–‡∑»‰∑¬, æƒ…¿“§¡- ‘ßÀ“§¡ 2559 malignant °—∫ benign ·≈– recurrent tumor ‰¥â °“√μ√«®¥â«¬ PET scan ¥’ °«à“ CT abdomen „π·ßà∑’Ë«à“ “¡“√∂æ∫°“√‡ª≈’Ë¬π·ª≈ß¢Õß metabolic activity ¿“¬„π°âÕπ‡π◊ÈÕßÕ°´÷Ëß¡—°®–æ∫°àÕπ anatomic change ®“° CT scan πÕ°®“°π’È PET scan ¬—ß™à«¬∫Õ°°“√·æ√à°√–®“¬¢Õß‚√§°àÕπ°“√ºà“μ—¥·≈–™à«¬·¬°√Õ¬ ‚√§∑’Ë‰¡à·πà„®®“°°“√μ√«®¥â«¬ CT scan À√◊Õ MRI ‰¥â √«¡∑—Èß¬—ß “¡“√∂„™â„π °“√μ√«®°√≥’∑’ËºŸâªÉ«¬·æâ “√∑÷∫√—ß ’‰¥â5 Õ¬à“ß‰√°Áμ“¡ PET scan ¬—ß‰¡à “¡“√∂ π”¡“„™â∑¥·∑π CT scan ‰¥â‡π◊ËÕß®“°‰¡à “¡“√∂μ√«®‰¥â„π∑ÿ° ∂“π∑’Ë 2. Esophagogastroduodenoscopy (EGD) ‡ªìπ°“√μ√«®√Õ¬‚√§„π °√–‡æ“–Õ“À“√À√◊Õ¥Ÿ‚Õ¥’π—¡ ≈—°…≥–¢Õß GIST ¡—°æ∫‡ªìπ submucosal mass °“√∑” biopsy Õ“®®–‡æ‘Ë¡§«“¡‡ ’Ë¬ßμàÕ tumor bleeding ‡π◊ËÕß®“°‡ªìπ hypervascularized tumor πÕ°®“°π’È°“√∑” FNA Õ“®®–‡æ‘Ë¡§«“¡‡ ’Ë¬ßμàÕ tumor rupture ·≈– tumor seeding μ“¡√Õ¬‡¢Á¡ ¥—ßπ—Èπ„π°√≥’∑’ËºŸâªÉ«¬®”‡ªìπ μâÕß‰ªºà“μ—¥Õ¬Ÿà·≈â«Õ“®®–‰¡à®”‡ªìπμâÕßμ—¥™‘Èπ‡π◊ÈÕ‰ªμ√«® ¬°‡«âπ„π°√≥’∑’Ë‡ªìπ unresectable tumor À√◊Õ ¡’°“√«“ß·ºπ®–„Àâ imatinib °àÕπºà“μ—¥ 3. Endoscopic ultrasound (EUS) °“√μ√«®¥â«¬ EUS ®–æ∫≈—°…≥– hypoechoic mass ∑’Ë‡™◊ËÕ¡μàÕ°—∫™—Èπ∑’Ë 2 (muscularis mucosae) À√◊Õ™—Èπ∑’Ë 4 (muscularis propria) ¢Õßºπ—ß∑“ß‡¥‘πÕ“À“√ πÕ°®“°π’È¬—ß™à«¬·¬°√–À«à“ß benign °—∫ malignant ‚¥¬„π benign ®–¡’≈—°…≥– regular margin homogeneous pattern ¢π“¥πâÕ¬°«à“ 3 ´¡. à«π malignant ®–¡’≈—°…≥– irregular margin ¢π“¥¡“°°«à“ 4 ´¡. æ∫ echogenic foci ·≈– cystic space Õ¬Ÿà¿“¬„π °“√æ¬“°√≥å‚√§ ªí®®—¬∑’Ë ”§—≠ ‰¥â·°à 1. μ”·Àπàß¢Õß‚√§ æ∫«à“ gastric GIST ¡’æ¬“°√≥å‚√§∑’Ë¥’°«à“ small bowel GIST 2. ¢π“¥¢Õß°âÕπ 3. Mitotic count per 50 high power field (HPF)

A Woman with Melena for 2 Weeks 15 μ“√“ß∑’Ë 2 NIH consensus classification of primary GIST by mitotic index and size6 Risk category Tumor size in greatest dimension Mitotic count (per 50 HPFs) Very low < 2 cm < 5 Low 2-5 cm < 5 Intermediate < 5 cm 6 - 10 5 -10 cm < 5 High > 5 cm > 5 > 10 cm Any mitotic Any size > 10

®“°ªí®®—¬¥—ß°≈à“« “¡“√∂·∫àßÕÕ°‡ªìπ§«“¡‡ ’Ë¬ß‰¥â¥—ßμ“√“ß∑’Ë 2 °“√√—°…“ 1. Surgical resection ‡ªìπ curative treatment §«√æ‘®“√≥“ºà“μ—¥°√≥’∑’ËºâªÉ«¬¡’Õ“°“√Ÿ ‡ªìπ gastric GIST ∑’Ë¡’¢π“¥¡“°°«à“ 2 ´¡. À√◊Õ small bowel GIST §«√„Àâ free margin Õ¬à“ßπâÕ¬ 2 ´¡. ‚¥¬∑’ËÕ“®®–‰¡à®”‡ªìπμâÕß∑” lymph node dissection ‡π◊ËÕß®“°‚Õ°“ „π°“√·æ√à°√–®“¬¡“∑’ËμàÕ¡πÈ”‡À≈◊Õßæ∫‰¥âπâÕ¬ À≈—ßºà“μ—¥∂â“‡ªìπ complete resection §«√æ‘®“√≥“ surveillance μàÕ¥â«¬ CT scan ∑ÿ° 6 ‡¥◊Õπ ‡ªìπ‡«≈“ 5 ªï „π°≈ÿà¡ low risk à«π„π°≈ÿà¡ moderate to high risk ®–μ‘¥μ“¡ ¥â«¬ CT scan ∑ÿ° 3 ‡¥◊Õπ‡ªìπ‡«≈“ 3 ªï ®“°π—Èπ∑ÿ° 6 ‡¥◊Õπ‡ªìπ‡«≈“ 5 ªï ·≈–ªï ≈–§√—Èß μ“¡≈”¥—∫7 2. Imatinib „™â√—°…“„π°≈ÿà¡ KIT positive GIST ∑’Ë‰¡à “¡“√∂ºà“μ—¥‰¥â ¡’°“√·æ√à °√–®“¬¢Õß‡π◊ÈÕßÕ°À√◊Õ„Àâ‡ªìπ adjuvant „π°√≥’∑’Ë°âÕπ‡π◊ÈÕßÕ°¡’≈—°…≥– high risk °àÕπºà“μ—¥8 ¢π“¥¢Õß¬“∑’Ë„™â§◊Õ 400 mg/d ®“°°“√»÷°…“«‘®—¬æ∫«à“°“√√—°…“¥â«¬ imatinib ¡’Õ—μ√“°“√μÕ∫ πÕßÕ¬à∑’Ëª√–¡“≥√âÕ¬≈–Ÿ 70-85 ·≈– median progres-

16 ®ÿ≈ “√ ¡“§¡·æ∑¬å√–∫∫∑“ß‡¥‘πÕ“À“√·Ààßª√–‡∑»‰∑¬, æƒ…¿“§¡- ‘ßÀ“§¡ 2559 sion free survival (PFS) ª√–¡“≥ 20-24 ‡¥◊Õπ6,9 πÕ°®“°π’È¬—ß¡’°“√»÷°…“„π √–¬–¬“«∑’Ë¡’°“√μ‘¥μ“¡ºŸâªÉ«¬∑’Ë‡ªìπ advanced GIST 147 √“¬‡ªìπ‡«≈“π“π 9 ªï æ∫«à“ ¡’ overall survival √âÕ¬≈– 35 ∑’Ë 9 ªï10 „π·ßà¢Õß adjuvant therapy À≈—ß ºà“μ—¥‰¥â¡’°“√»÷°…“‚¥¬„Àâ imatinib 400 mg/d ‡ªìπ√–¬–‡«≈“ 36 ‡¥◊Õπ‡∑’¬∫°—∫ 12 ‡¥◊Õπ„πºŸâªÉ«¬ high risk ‚¥¬ median follow up ∑’Ë 54 ‡¥◊Õπ æ∫«à“ „π°≈ÿà¡ ∑’Ë‰¥â¬“ 36 ‡¥◊Õπ¡’ recurrent free survival ·≈– overall survival ¥’°«à“°≈ÿà¡∑’Ë ‰¥â¬“ 12 ‡¥◊ÕπÕ¬à“ß¡’π—¬ ”§—≠∑“ß ∂‘μ‘11 ”À√—∫º≈¢â“ß‡§’¬ß∑’Ëæ∫∫àÕ¬‰¥â·°à diarrhea, fatigue, nausea, rash à«π „À≠àÕ“°“√¡—°®–¥’¢÷Èπ‡Õß‰¡à®”‡ªìπμâÕßÀ¬¥¬“ÿ à«πº≈¢â“ß‡§’¬ß∑’Ë√π·√ßÕ¬à“ß‡™àπÿ LFT abnormality, lung toxicity, cytopenia, GI bleeding ‡ªìπº≈¢â“ß‡§’¬ß∑’Ëæ∫‰¥â πâÕ¬¡“°·≈–Õ“°“√¡—°¥’¢÷ÈπÀ≈—ß®“°À¬ÿ¥¬“12

‡Õ° “√Õâ“ßÕ‘ß 1. Hirota S, Isozaki K, Moriyama Y, Hashimoto K, Nishida T, Ishiguro S, et al. Gain of function mutations of c-KIT in human gastrointestinal stromal tumors. Science. 1998;279:577-80. 2. Heinrich MC, Corless CL, Duensing A, McGreevey L, Chen CJ, Joseph N, et al. PDGFRA activating mutations in gastrointestinal stromal tumors. Science. 2003;299:708-10. 3. Lin S, Rocker DC. Obscure gastrointestinal bleeding. Gastroenterol Clin North Am. 2005;34:679-98. 4. Miettinen M, Lasota J. Gastrointestinal stromal tumors: review on morphology, molecular pathology, prognosis, and differential diagnosis. Arch Pathol Lab Med. 2006;130:1466-78. 5. Demetri GD, von Mehren M, Antonescu CR, DeMatteo RP, Ganjoo KN, Maki RG, et al. NCCN Task Force report: update on the management of patients with gastrointestinal stromal tumors. J Natl Compr Canc Netw 2010;8 Suppl 2:S1- 41:quiz S42-4.

A Woman with Melena for 2 Weeks 17 6. Fletcher C, Berman J, Corless C, Gorstein F, Lasota J, Longley BJ, et al. Diagno- sis of gastrointestinal stromal tumors: A consensus approach. Hum Pathol 2002;33:459-65. 7. Blay JY, Bonvalot, Casali H, Choi H, Debiec-Richter M, Dei Tos AP, et al. Con- sensus meeting for management of gastrointestinal stromal tumors. Report of the GIST Consensus Conference of 20-21 March 2004, under the auspices of ESMO. Ann Oncol 2005;16:566-78. 8. Eisenberg BL1, Harris J, Blanke CD, Demetri GD, Heinrich MC, Watson JC, et al. Phase II trial of neoadjuvant/adjuvant imatinib mesylate (IM) for advanced primary and metastatic/recurrent operable gastrointestinal stromal tumor (GIST): early results of RTOG 0132/ACRIN 6665. J Surg Oncol. 2009;99:42-7. 9. Croom KF, Perry CM. Imatinib mesylate: in the treatment of gastrointestinal stromal tumours. Drug. 2003;63:512-22. 10. von Mehren M, Heinrich MC, Joensuu H, Blanke CD, Wehrle E, Demetri GD. Follow-up results after 9 years (yrs) of the ongoing, phase II B2222 trial of imatinib mesylate (IM) in patients (pts) with metastatic or unresectable KIT+ gastrointestinal stromal tumors (GIST). J Clin Oncol 2011;29:15 suppl 10016. 11. Joensuu H, Eriksson M, Sundby HK, Hartmann JT, Pink D, Schütte J, et al. One vs three years of adjuvant imatinib for operable gastrointestinal stromal tumor: a randomized trial. JAMA. 2012;307:1265-72. 12. Guilhot F. Indications for imatinib mesylate therapy and clinical management. Oncologist. 2004;9:271-81.

18 ®ÿ≈ “√ ¡“§¡·æ∑¬å√–∫∫∑“ß‡¥‘πÕ“À“√·Ààßª√–‡∑»‰∑¬, æƒ…¿“§¡- ‘ßÀ“§¡ 2559 Review Article Buried Bumper Syndrome «√«√√≥ ∫ÿ≠√—°…“ ∏’√π—π∑å √√æ®‘μ

Àπà«¬‚√§∑“ß‡¥‘πÕ“À“√·≈–μ—∫ ‚√ßæ¬“∫“≈æ√–¡ß°ÿÆ‡°≈â“

○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○ ∫∑π” °“√„ à “¬„ÀâÕ“À“√∑“ßÀπâ“∑âÕß¥â«¬«‘∏’ àÕß°≈âÕß À√◊Õ percutaneous endoscopic gastrostomy (PEG) ‡ªìπ°“√„ÀâÕ“À“√∑“ßÀπâ“∑âÕß„π√–¬–¬“«·°àºŸâ∑’Ë ¡’ªí≠À“°“√‰¥â√—∫ “√Õ“À“√‰¡à‡æ’¬ßæÕ ∑—Èß®“°ªí≠À“°“√°≈◊πÀ√◊Õ°“√¡’¿“«–Õÿ¥ μ—π∫√‘‡«≥§Õ·≈–À≈Õ¥Õ“À“√®“° “‡Àμμà“ßÊÿ ‡™àπ ¡–‡√ÁßÀ≈—ß‚æ√ß®¡°Ÿ ¡–‡√Áß‚§π≈‘Èπ À√◊Õ ¡–‡√ÁßÀ≈Õ¥Õ“À“√ ‚¥¬«‘∏’π’È‰¥â‡√‘Ë¡¡’°“√π”¡“„™â‡¡◊ËÕªï §.».1980 ‚¥¬ Pongsky ·≈– Gauderer1 ´÷Ëß‡ªìπ«‘∏’∑’Ë¡’°“√π”¡“„™âÕ¬à“ß·æ√àÀ≈“¬„πªí®®ÿ∫—π ‡π◊ËÕß®“° “¡“√∂∑”‰¥âßà“¬ ª≈Õ¥¿—¬ „™â¬“√–ß—∫§«“¡√Ÿâ ÷°‡æ’¬ß‡≈Á°πâÕ¬ ·≈– “¡“√∂∑” ”‡√Á®¿“¬„π‡«≈“ 10-30 π“∑’2 Õ¬à“ß‰√°Áμ“¡ æ∫«à“¡’¿“«–·∑√°´âÕπ‡°‘¥¢÷Èπ‰¥â∑—Èß „π√–¬–©—∫æ≈—π (acute complication) ·≈–„π√–¬–À≈—ß (late complication) ´÷ËßÕ“®‡ªìπ ¿“«–·∑√°´âÕπ∑’Ë¡’§«“¡√ÿπ·√ß‡≈Á°πâÕ¬ ‡™àπ ¿“«–·º≈μ‘¥‡™◊ÈÕ (wound infection) ¿“«–·º≈√—Ë«´÷¡ (gastrostomy leakage) À√◊Õ‡ªìπ¿“«–·∑√°´âÕπ∑’Ë¡’ §«“¡√ÿπ·√ß¡“° ‡™àπ ¿“«–μ‘¥‡™◊ÈÕ¿“¬„π™àÕß∑âÕß (peritonitis) ¿“«– “¬„Àâ Õ“À“√‡≈◊ËÕπ Ÿà™—Èπ√–À«à“ßºπ—ß°√–‡æ“–Õ“À“√ ·≈–™—Èπ„μâº‘«Àπ—ß ∑”„Àâ‰¡à “¡“√∂„Àâ Õ“À“√‰¥â ·≈–‡°‘¥°“√μ‘¥‡™◊ÈÕμ“¡¡“ À√◊Õ∑’Ë‡√’¬°«à“ buried bumper syndrome ´÷Ëß∂◊Õ‡ªìπ¿“«–·∑√°´âÕπ∑’Ë‡°‘¥¿“¬À≈—ß °Áæ∫‰¥â‡™àπ°—π Buried bumper syndrome ·≈–Õÿ∫—μ‘°“√≥å ¿“«– buried bumper syndrome ∂°√“¬ß“πŸ §√—Èß·√°‡¡◊ËÕªï §.».19883,4

Buried Bumper Syndrome 19 ·≈–∂Ÿ°μ—Èß™◊ËÕ‚¥¬ Klein ·≈–§≥–2 ‡ªìπ¿“«–∑’Ëæ∫‰¥â‰¡à∫àÕ¬ ‚¥¬æ∫‡æ’¬ß√âÕ¬≈– 0.3-2.45 ®“°¿“«–·∑√°´âÕπ∑—ÈßÀ¡¥ ∑’Ëæ∫®“°°“√„ à “¬„ÀâÕ“À“√∑“ßÀπâ“∑âÕß (PEG) ‚¥¬æ∫°“√‡≈◊ËÕπμ”·Àπàß¢ÕßÕÿª°√≥å°—π°√–∑∫ (internal bumper) ®“° ¿“¬„π°√–‡æ“–Õ“À“√ ‡¢â“‰ª·∑√°À√◊ÕΩíß (bury) Õ¬Ÿà„π™—Èπ√–À«à“ßºπ—ß°√–‡æ“– Õ“À“√·≈–™—Èπ„μâº‘«Àπ—ß ∑”„Àâ‡°‘¥¿“«–·∑√°´âÕπμà“ßÊ μ“¡¡“ ‡™àπ Õ“°“√ª«¥∑âÕß Õ“À“√∑’Ë„Àâ∑“ß “¬¬“ß‰¡à “¡“√∂‡¢â“ Ÿà¿“¬„π°√–‡æ“–Õ“À“√ ·≈–‡¢â“‰ª¢—ßÕ¬Ÿà„π™—Èπ ¢Õßºπ—ß°√–‡æ“–Õ“À“√∑’Ë internal bumper ‰ªΩíßÕ¬Ÿà ‡°‘¥¿“«–√—Ë«´÷¡∑’Ëº‘«Àπ—ß ¿“«–μ‘¥‡™◊ÈÕÕ—°‡ ∫À√◊Õ‡ªìπÀπÕßμ“¡¡“ ´÷Ëß∂◊Õ‡ªìπ¿“«–·∑√°´âÕπ∑’Ë√ÿπ·√ß ¡—°æ∫ „π√“¬∑’Ë„™â “¬ PEG ¡“π“πμ—Èß·μà 3 —ª¥“Àå¢÷Èπ‰ª6 ·μà°Á¡’√“¬ß“π°“√‡°‘¥¿“«– buried bumper syndrome À≈—ß®“°∑” PEG ‰¥â‡æ’¬ß 6 «—π7 À“°‰¡à‰¥â√—∫°“√ ¥Ÿ·≈√—°…“∑’Ë∂Ÿ°μâÕßÕ“®‡°‘¥¿“«–·∑√°´âÕπ√ÿπ·√ß¥—ß∑’Ë‰¥â°≈à“« ·≈–∫“ß√“¬∂÷ß¢—Èπ ‡ ’¬™’«‘μ‰¥â8 “‡Àμÿ·≈–°≈‰≈°“√‡°‘¥¿“«– buried bumper syndrome °“√‡°‘¥¿“«– buried bumper syndrome ‡√‘Ë¡μâπ¡“®“°°“√¡’·√ßμ÷ß √–À«à“ß external ·≈– internal bumper ¡“°‡°‘π‰ª ∑”„Àâ‡°‘¥°“√¢“¥‡≈◊Õ¥ ¢Õß‡π◊ÈÕ‡¬◊ËÕ∫√‘‡«≥π—Èπ (pressure necrosis) ´÷Ëßπ—∫‡ªìπ “‡ÀμÿÀ≈—°9 πÕ°®“°π’Èæ∫ «à“°√¥„π°√–‡æ“–Õ“À“√¡’ à«π∑”„Àâ‡°‘¥°“√‡ª≈’Ë¬π·ª≈ß√ª√à“ß¢ÕßŸ internal bumper ®÷ß‡ √‘¡„Àâ°“√‡≈◊ËÕπμ”·Àπàß‡°‘¥ßà“¬¢÷Èπ10 ‡¡◊ËÕ¡’°“√‡≈◊ËÕπμ”·Àπàß‡°‘¥¢÷Èπ ®–∑”„Àâ ™àÕß ∑“ß∫√‘‡«≥„μâμàÕ internal bumper ´÷Ëß‡§¬‡ªìπ∑“ß‡™◊ËÕ¡ Ÿà¿“¬„π°√–‡æ“–Õ“À“√ (gastrostomy tract) Ÿ≠‡ ’¬‰ª ·≈–∫“ß√“¬æ∫«à“¡’°“√ √â“ß‡π◊ÈÕ‡¬◊ËÕ„À¡à (epithelization) ¢÷Èπ¡“ª°§≈ÿ¡∫√‘‡«≥π’È®π‰¡à‡À≈◊Õ∑“ßÕÕ° Ÿà°√–‡æ“–Õ“À“√Õ’°‡≈¬ ´÷Ëß æ∫„π√“¬∑’Ë°“√«‘π‘®©—¬≈à“™â“ ªí®®—¬ àß‡ √‘¡°“√‡°‘¥¿“«– buried bumper syndrome ®“°°√≥’μ—«Õ¬à“ß∑’Ëºà“π¡“ æ∫«à“¡’ªí®®—¬∫“ßÕ¬à“ß∑’Ëæ∫√à«¡°—∫¿“«– buried bumper syndrome Õ—π‰¥â·°à

20 ®ÿ≈ “√ ¡“§¡·æ∑¬å√–∫∫∑“ß‡¥‘πÕ“À“√·Ààßª√–‡∑»‰∑¬, æƒ…¿“§¡- ‘ßÀ“§¡ 2559 ªí®®—¬À≈—° ª√–°“√ ”§—≠§◊Õ°“√¥÷ß√—Èß “¬ PEG μ÷ß‡°‘π‰ª∑”„Àâ external ·≈– internal bumper ™‘¥°—π·πàπ ®π‡°‘¥ pressure necrosis πÕ°®“°π’È °“√¥·≈ “¬Ÿ PEG ∑’Ë‰¡à‡À¡“– ¡ ‡™àπ °“√«“ßºâ“°äÕ´∫√‘‡«≥„μâ external bumper Àπ“‡°‘π‰ª À√◊Õ °“√ª≈àÕ¬ “¬ PEG ‰«â‚¥¬‰¡à¡’ ‘Ëßª°§≈ÿ¡„πºŸâªÉ«¬∑’Ë‰¡à “¡“√∂¥Ÿ·≈À√◊Õ§«∫§ÿ¡ μπ‡Õß‰¥â ®÷ß‡°‘¥°“√¥÷ß “¬ PEG ‚¥¬μ—«ºŸâªÉ«¬‡Õß ªí®®—¬‡ √‘¡Õ◊ËπÊ °“√‡ª≈’Ë¬π√ª√à“ß¢ÕßŸ internal bumper ®“°°√¥„π°√–‡æ“–Õ“À“√ ≈—°…≥– ¢Õß “¬ PEG °Á¡’º≈ °≈à“«§◊Õ „π√“¬∑’Ëæ∫¿“«– buried bumper syndrome π—Èπ ‡¡◊ËÕæ‘®“√≥“∑’Ë√Ÿª√à“ß ·≈–≈—°…≥–¢Õß internal bumper ¡—°æ∫«à“√Ÿª√à“ß¢Õß internal bumper ‡ªìπ™π‘¥¡’¢π“¥‡≈Á° √ª√à“ß‡√’¬«Ÿ ¢Õ∫§¡ À√◊Õ„™âæ≈“ μ‘°∑’Ë¡’§«“¡·¢Áß ”À√—∫ internal bumper ™π‘¥∫Õ≈≈Ÿπ ‰¡àæ∫«à“‡ªìπªí®®—¬‡ ’Ë¬ß¢Õß¿“«– buried bumper syndrome7 πÕ°®“°π’È¬—ßæ∫«à“ ¿“«–‚√§Õâ«π·≈–‰Õ‡√◊ÈÕ√—ß °Á‡ªìπªí®®—¬ ‡ ’Ë¬ß¢Õß°“√‡°‘¥ buried bumper syndrome ¥â«¬6 (μ“√“ß∑’Ë 1)

μ“√“ß∑’Ë 1 ªí®®—¬∑’Ë‡°’Ë¬«¢âÕß°—∫°“√‡°‘¥¿“«– buried bumper syndrome ª®®í ¬¥— “π°“√¥â ·≈Ÿ °“√¥÷ß “¬ PEG μ÷ß‡°‘π‰ª∑”„Àâ external ·≈– internal bumper ™‘¥°—π·πàπ °“√¥Ÿ·≈ “¬ PEG ∑’Ë‰¡à‡À¡“– ¡ ªí®®—¬¥â“πÕÿª°√≥å Internal bumper ‡ ’¬√Ÿª∑√ß ®“°°√¥„π°√–‡æ“–Õ“À“√ ≈—°…≥–·≈–√Ÿª√à“ß¢Õß PEG tube - Internal bumper ¡’¢π“¥‡≈Á° - º≈‘μ®“°æ≈“ μ‘°™π‘¥·¢Áß - ¡’√Ÿª√à“ß‡√’¬« ¢Õ∫‡√’¬∫§¡ ªí®®—¬¥â“πºŸâªÉ«¬ Obesity Chronic cough

Buried Bumper Syndrome 21 Õ“°“√·≈–Õ“°“√· ¥ß¢Õß¿“«– buried bumper syndrome Õ“°“√¢ÕßºŸâªÉ«¬∑’Ë¡’¿“«– buried bumper syndrome ‡°‘¥®“°°“√∑’Ë “¬ PEG ‡°‘¥°“√Õÿ¥μ—π (clogging) „ÀâÕ“À“√·≈â«‰¡à≈ß (resistance) À√◊Õ°“√∑’Ë “¬ PEG ‰¡à “¡“√∂‡§≈◊ËÕπ∑’Ë¢÷Èπ≈ßμ“¡ª°μ‘‰¥â (immobilization) ‚¥¬Õ“°“√∑’Ë¡—°π”¡“§◊Õ ¡’°“√√—Ë«´÷¡ (leakage) ¢ÕßÕ“À“√∑’Ëº‘«Àπ—ß∫√‘‡«≥√Õ∫ PEG tube À√◊Õ ¡’≈—°…≥– ∑’Ë∫àß∂÷ß¿“«–μ‘¥‡™◊ÈÕ„π∫√‘‡«≥π—Èπ ‡™àπ ¡’°“√∫«¡À√◊Õº‘«Àπ—ß∫√‘‡«≥π—Èπ¡’ ’·¥ß ºŸâ ªÉ«¬Õ“®¡’Õ“°“√ª«¥∑âÕß ¡’¿“«–μ‘¥‡™◊ÈÕ„π™àÕß∑âÕß μ‘¥‡™◊ÈÕ„π°√–· ‚≈À‘μ7,11 ∫“ß √“¬¡’¿“«–‡≈◊Õ¥ÕÕ°„π°√–‡æ“–Õ“À“√ °“√‡°‘¥ÀπÕß∑’Ëº‘«Àπ—ß∫√‘‡«≥π—Èπ ·≈–‡§¬ ¡’√“¬ß“π°“√‡ ’¬™’«‘μ®“°¿“«–π’È12 ‚¥¬¿“«– buried bumper syndrome ¡—°‡°‘¥ ‡ªìπ late complication ¢Õß°“√„ à “¬ PEG μ—Èß·μàÀ≈—ß∑” 3 —ª¥“Àå¢÷Èπ‰ª ®π∂÷ß 50 ‡¥◊Õπ6,12 ·μà¡’∫“ß√“¬ß“π∑’Ëæ∫«à“‡°‘¥À≈—ß∑”‡æ’¬ß 6 «—π (acute buried bumper syndrome)7 °“√«‘π‘®©—¬¿“«– Buried bumper syndrome °“√«‘π‘®©—¬¿“«– Buried bumper syndrome ∑”‰¥â®“°Õ“°“√·≈–Õ“°“√ · ¥ß ¥—ß°≈à“«¡“ ·μà„π√“¬∑’Ë¡’ underlying disease ‡™àπ ‚√§∑“ß√–∫∫ª√– “∑ °“√ Ÿ≠‡ ’¬§«“¡√Ÿâ ÷°‡®Á∫ª«¥ Õ“®∑”„Àâ‰¡à¡’Õ“°“√ª«¥∑âÕß ·μàºŸâ¥Ÿ·≈¡—° —ß‡°μ ‡ÀÁπ®“°°“√¡’ ¿“«–√—Ë«´÷¡ ´÷Ëß‡ªìπÕ“°“√∑’Ëπ”¡“∫àÕ¬∑’Ë ÿ¥ °“√∑¥ Õ∫À√◊Õμ√«®¥â«¬ «‘∏’À¡ÿπ “¬„Àâ√Õ∫ ·≈–‡§≈◊ËÕπ “¬ PEG ¢÷Èπ≈ß (rotate and slide) ®–‰¡à “¡“√∂ ∑”‰¥â ‡π◊ËÕß®“° internal bumper ∂Ÿ°Ωíß·πàπ„π™—Èπ√–À«à“ß°√–‡æ“–Õ“À“√·≈–™—Èπ „μâº‘«Àπ—ßÀπâ“∑âÕß °“√„ àπÈ”≈ß‰ª„π “¬ PEG ®–∑”„ÀâºŸâªÉ«¬ª«¥∑âÕß¡“°¢÷Èπ ´÷Ëß ®–·μ°μà“ß®“°¿“«– localized wound infection À√◊Õ¿“«–√—Ë«´÷¡∑—Ë«Ê‰ª∑’Ë “¬ PEG ®–¬—ß “¡“√∂‡§≈◊ËÕπ¢÷Èπ≈ß‰¥âμ“¡ª°μ‘ ·≈– ‡¡◊ËÕ„ àπÈ”≈ß‰ª°Á‰¡à‡æ‘Ë¡§«“¡‡®Á∫ª«¥ „Àâ°—∫ºŸâªÉ«¬11 °“√ àÕß°≈âÕß (endoscopy) ™à«¬„Àâ°“√«‘π‘®©—¬·¡àπ¬”¬‘Ëß¢÷Èπ ‚¥¬®–æ∫«à“ internal bumper ∂Ÿ°ª°§≈ÿ¡¥â«¬ gastric mucosa ‡°◊Õ∫∑—ÈßÀ¡¥ À√◊Õ„π∫“ß

22 ®ÿ≈ “√ ¡“§¡·æ∑¬å√–∫∫∑“ß‡¥‘πÕ“À“√·Ààßª√–‡∑»‰∑¬, æƒ…¿“§¡- ‘ßÀ“§¡ 2559 √“¬¡Õß‰¡à‡ÀÁπ bumper ‡≈¬ ´÷ËßÕ“®æ∫‡æ’¬ß√Õ¬πŸπ„π∫√‘‡«≥π—Èπ‡π◊ËÕß®“°æ◊Èπº‘« ¡’≈—°…≥–‡À¡◊Õπ gastric mucosa ª°μ‘ ∑—Èßπ’È¢÷Èπ°—∫√–¬–‡«≈“∑’Ë¡“æ∫·æ∑¬å «‘∏’ °“√Õ◊ËπÊ∑’Ë™à«¬„π°“√«‘π‘®©—¬ ·μà‰¡à®”‡ªìπ„π∑ÿ°√“¬ ‡™àπ °“√∑”Õ—≈μ√â“´“«¥å °“√ ‡ÕÁ°´‡√¬å§Õ¡æ‘«‡μÕ√å ·≈–°“√∑”§≈◊Ëπ·¡à‡À≈Á°‰øøÑ“ ‡ªìπμâπ6,7,11

¿“æ∑’Ë 1 Internal bumper Ωíß„π™—Èπ„μâºπ—ß°√–‡æ“–Õ“À“√ ‡ÀÁπ‡ªìπ√Õ¬πŸπ ·≈–‡ªìπ·º≈ ‚¥¬‰¡à ‡ÀÁπ à«π¢Õßª≈“¬ “¬ PEG (¿“æ®“°Àπà«¬‚√§√–∫∫∑“ß‡¥‘πÕ“À“√ ‚√ßæ¬“∫“≈ æ√–¡ß°ÿÆ‡°≈â“. °ÿ¡¿“æ—π∏å 2557)

¿“æ∑’Ë 2 (´â“¬) ·≈– 3 (¢«“) ¿“æ‡Õ°´‡√¬å§Õ¡æ‘«‡μÕ√å· ¥ß„Àâ‡ÀÁπ internal bumper ΩíßÕ¬Ÿà„π™—Èπ „μºâ «Àπ‘ ß— ·≈–æ∫·ÕßÀπÕß„μà μâ Õà internal bumper (¿“æ®“°Àπ«¬‚√§√–∫∫∑“ß‡¥à πÕ“À“√‘ ‚√ßæ¬“∫“≈æ√–¡ß°ÿÆ‡°≈â“. °ÿ¡¿“æ—π∏å 2557)

Buried Bumper Syndrome 23 °“√√—°…“¿“«– buried bumper syndrome ªí®®ÿ∫—π¬—ß‰¡à¡’·π«∑“ß°“√√—°…“∑’Ë™—¥‡®π ”À√—∫¿“«– buried bumper syndrome ·μà°“√√—°…“∑’Ë‡ªìπ∑’Ë‡ÀÁπæâÕß°—π„π·μà≈–√“¬ß“π §◊Õ °“√‡Õ“ “¬ PEG ∑’ËΩíßÕ¬ŸàÕÕ°‰ª∑—ÈßÀ¡¥ ·¡â«à“ºŸâªÉ«¬®–‰¡à¡’Õ“°“√ª«¥∑âÕßÀ√◊Õμ‘¥‡™◊ÈÕ°Áμ“¡ ‚¥¬‡ªÑ“ À¡“¬∑’Ë ”§—≠ §◊Õ °“√«‘π‘®©—¬„Àâ‡√Á«æÕ∑’Ë®– “¡“√∂π”‡Õ“ “¬ PEG ÕÕ°¥â«¬«‘∏’∑’Ë ßà“¬·≈– àßº≈°√–∑∫μàÕ gastrostomy tract πâÕ¬∑’Ë ÿ¥ ‡æ◊ËÕ∑’Ë®–„ à “¬ PEG Õ—π „À¡à‡¢â“‰ª∑’Ë‡¥‘¡‰¥â ‚¥¬‡©æ“–„π°√≥’∑’Ë·º≈¬—ß‰¡àÕ—°‡ ∫‡ªìπÀπÕß ´÷Ëß®“°Õ¥’μ ®π∂÷ßªí®®ÿ∫—π¡’°“√√—°…“¿“«– buried bumper syndrome À≈“°À≈“¬«‘∏’μ“¡¬ÿ§ ¡—¬∑’Ë¡’°“√æ—≤π“¢ÕßÕÿª°√≥å¢÷Èπ¡“ „π∑’Ëπ’È®–°≈à“«·¬°‡ªìπ°≈ÿà¡Ê ¥—ßπ’È °“√√—°…“®”‡æ“– ‰¥â·°à °“√π” “¬ PEG ÕÕ°∑—π∑’∑’Ë«‘π‘®©—¬¿“«– buried bumper syndrome ´÷Ëß∑’Ëºà“π¡“¡’√“¬ß“π°“√√—°…“À≈“¬«‘∏’ æ∫«à“«‘∏’‡À≈à“π’È‰¡à‡°‘¥¿“«– ·∑√°´âÕπ·≈– “¡“√∂∑”‰¥â‰¡à¬“° ¥—ßπ’È 1. °“√¥÷ßÕÕ°®“°ºπ—ßÀπâ“∑âÕß‚¥¬μ√ß (Simple external traction) «‘∏’π’È‡≈◊Õ°∑”„π°√≥’∑’Ë internal bumper ‡ªìπ™π‘¥ÕàÕππÿà¡ (collapsible) À√◊Õ¡’√Ÿª√à“ß‡ªìπ dome-shape ´÷Ëß “¡“√∂¥÷ßÕÕ°ºà“π∑“ßÀπâ“∑âÕß‰¥âßà“¬‚¥¬°√’¥ ∑’Ëº‘«Àπ—ß√Õ∫ “¬ PEG ≈ß‰ª¬—ß internal bumper ‡æ’¬ß‡≈Á°πâÕ¬ √à«¡°—∫°“√ §≈âÕß “¬ guide wire À√◊Õ‰¡à°Á‰¥â ‚¥¬∂â“μâÕß°“√„ à “¬ PEG Õ—π„À¡à°Á “¡“√∂ „ àºà“π gastrostomy tract ‡¥‘¡ ¥â«¬°“√§≈âÕß “¬ guide wire ‰«â°àÕπ ·≈â« „ à “¬„À¡à‡¢â“‰ª∑’Ë‡¥‘¡∑“ßÀπâ“∑âÕß ∑—Èßπ’È§«√‡≈◊Õ° ‡©æ“–„π°√≥’∑’Ë·º≈‰¡àμ‘¥‡™◊ÈÕ À√◊Õ‡ªìπÀπÕß ·≈–¬—ßæÕ¡’∑“ßÕÕ° Ÿà°√–‡æ“–Õ“À“√‡À≈◊ÕÕ¬Ÿà∫â“ß3,12 2. °“√π” “¬ PEG ÕÕ°¥â«¬«‘∏’°“√ àÕß°≈âÕß (Endoscopic removal) ‡ªìπ«‘∏’∑’Ëæ—≤π“®“°«‘∏’¢â“ßμâπ ∑—Èßπ’È‡æ◊ËÕ„Àâ°√–∑∫°√–‡∑◊Õπ·º≈ PEG πâÕ¬ ∑’Ë ÿ¥ ·≈– “¡“√∂„ à “¬„À¡à„π‡«≈“‡¥’¬«°—π‰¥â ´÷Ëß¡’‡∑§π‘§μà“ßÊ ¥—ßπ’È

24 ®ÿ≈ “√ ¡“§¡·æ∑¬å√–∫∫∑“ß‡¥‘πÕ“À“√·Ààßª√–‡∑»‰∑¬, æƒ…¿“§¡- ‘ßÀ“§¡ 2559 2.1 Pushed technique ¡’√“¬ß“π°“√„™â«‘∏’π’È§√—Èß·√°‚¥¬ Klein ·≈–§≥–2 μ—Èß·μàªï §.».1988 ‚¥¬°“√ àÕß °≈âÕß‡¢â“‰ª æ∫«à“¬—ß¡’ à«πª≈“¬ ÿ¥¢Õß “¬ PEG ‚º≈à„Àâ‡ÀÁπÕ¬Ÿà ·μà à«π¢Õß internal bumper ∂Ÿ°Ωíß„π™—Èπ„μâºπ—ß°√–‡æ“–Õ“À“√ ®“°π—Èπ„ à guide wire ®“° ∑“ß¥â“πª≈“¬ PEG ∑’Ë∂Ÿ°μ—¥ ‡À≈◊Õª√–¡“≥ 3-5 ‡´πμ‘‡¡μ√ ‡Àπ◊Õº‘«Àπ—ß ·≈â« μ“¡¥â«¬°“√„ à Savary-Gilliard dilator (¿“æ∑’Ë 3) ‰ª∑’Ë “¬ PEG ·≈–¥—π≈ß Ÿà °√–‡æ“–Õ“À“√ ‚¥¬‡æ‘Ë¡¢π“¥¢Õß dilator ‡√◊ËÕ¬Ê®π∂÷ß 44 Fr ®–‡ÀÁπ internal bumper ∂Ÿ°¥—πÕÕ°®“° gastric wall (pushed) ®“°π—Èπ„™â snare §≈âÕß∑’Ë internal bumper ·≈â«‡Õ“ÕÕ°∑“ßª“° À≈—ß®“°π—Èπ®÷ß„ à PEG tube Õ—π„À¡à ºà“π guide wire ∑’Ë„ à‰«â∑“ßÀπâ“∑âÕß ‚¥¬®“°√“¬ß“ππ’È‰¡àæ∫¿“«–·∑√°´âÕπ ·≈– “¡“√∂°≈—∫ ¡“„™â PEG ‡æ◊ËÕ„ÀâÕ“À“√‰¥â„π 24 ™—Ë«‚¡ßÀ≈—ß°“√√—°…“¥â«¬«‘∏’π’È ‰¥â¡’°“√π”«‘∏’π’È¡“ª√–¬°μå‚¥¬‡ª≈’Ë¬π®“°ÿ Savary-Gilliard dilator ¡“‡ªìπ Probe ∑’Ë®–„™â‡ªìπμ—« push ·∑π (¿“æ∑’Ë 4-5) 2.2 Pulled technique «‘∏’π’È®–„™â«‘∏’¥÷ßÕÕ°®“°¿“¬„π°√–‡æ“– ¥â«¬°“√„™â balloon dilator13 (¿“æ∑’Ë 6) ‚¥¬‡√‘Ë¡®“°°“√μ—¥ª≈“¬ “¬ PEG ∑“ßÀπâ“∑âÕß„Àâ‡À≈◊Õª√–¡“≥ 3 ‡´πμ‘‡¡μ√®“°º‘«Àπ—ß ·≈â«„ à guide wire ºà“π‡¢â“¡“„π°√–‡æ“– ®“°π—Èπ„ à balloon dilator ∑“ß°≈âÕß ‡¢â“‰ª «¡ guide wire π—Èπ ·≈â«°“ß∫Õ≈≈Ÿπ®π‰¥â·√ß¥—π ∑’Ë Ÿß∑’Ë ÿ¥ —ß‡°μ«à“∫Õ≈≈Ÿπ ®–μ‘¥·πàπ°—∫ internal bumper ®÷ß∑”°“√¥÷ß bumper

¿“æ∑’Ë 3 Savary-Gilliard dilatators (¿“æ®“° Kabbaj N, et al. World J Gastrointest Pharmacol Ther. 2011;2:46-49)

Buried Bumper Syndrome 25 ¿“æ∑’Ë 4 The stainless steel probe ¢π“¥§«“¡¬“« 27 ´¡. ‡ âπºà“π»Ÿπ¬å°≈“ß 3 ¡¡. ∑’Ë¡’ª≈“¬ ‡≈Á°§«“¡¬“« 3 ´¡. ‡ âπºà“π»Ÿπ¬å°≈“ß 2 ¡¡. (¿“æ®“° Binnebösel M, et al. Endos- copy. 2010;42:E17-E18)

¿“æ∑’Ë 5 ¿“æ®“°°“√ àÕß°≈âÕß‡ÀÁπª≈“¬ probe ‚º≈àÕÕ°¡“∑’Ëª≈“¬ “¬ (¿“æ®“° Binnebösel M, et al. Endoscopy. 2010;42:E17-E18) ÕÕ°®“°ºπ—ß°√–‡æ“– ·≈–π”ÕÕ°∑“ßª“°¥â«¬°≈âÕß À≈—ß®“°π—Èπ®÷ß„ à “¬ PEG Õ—π„À¡àºà“π guide wire ∑“ßÀπâ“∑âÕß πÕ°®“°π’È¬—ß¡’«‘∏’°“√¥÷ß„Àâ internal bumper À≈ÿ¥ÕÕ°®“°°“√Ωíßμ—« ‚¥¬°“√„™â snare À√◊Õ forceps ´÷Ëß¡—°∑”√à«¡°—∫‡∑§π‘§Õ◊ËπÊ ¥—ß®–°≈à“«μàÕ‰ª

26 ®ÿ≈ “√ ¡“§¡·æ∑¬å√–∫∫∑“ß‡¥‘πÕ“À“√·Ààßª√–‡∑»‰∑¬, æƒ…¿“§¡- ‘ßÀ“§¡ 2559 ¿“æ∑’Ë 6 °“√¥÷ß bumper ¥â«¬∫Õ≈≈Ÿπ (¿“æ®“° Strock P, et al. Endoscopy. 2005;37:279.)

2.3 Push-pull T technique14 «‘∏’π’È‡ªìπ«‘∏’°“√¥÷ß “¬ PEG ÕÕ°¥â«¬°“√ª√– “π√–À«à“ß°“√¥—π “¬ PEG ≈ß Ÿà°√–‡æ“– ¥â«¬ Kelly clamp √à«¡°—∫°“√¥÷ß internal bumper „ÀâÀ≈ÿ¥ ‡¢â“¡“„π°√–‡æ“–¥â«¬ snare ‚¥¬‡√‘Ë¡®“°°“√μ—¥ª≈“¬ “¬ PEG „Àâ‡À≈◊Õ ª√–¡“≥ 3 ´¡. ®“°Àπâ“∑âÕß ·≈–μ—¥ “¬ PEG ∑’Ë®–∑‘Èß¡“ à«πÀπ÷Ëß „Àâ‡ªìπ™‘Èπ¢π“¥¬“« 2 ´¡. Àπ÷Ëß™‘Èπ ‡μ√’¬¡‰«â À≈—ß®“°π—Èπ àÕß°≈âÕß‡¢â“‰ª·≈â« „™â snare ≈Õ¥ºà“π∑“ß™àÕß∑’Ë ‡À≈◊ÕÕ¬Ÿà¢Õßª≈“¬ “¬ PEG ·≈–¥—πÕÕ°‰ª Ÿà∑“ßÀπâ“∑âÕß „Àâ snare ‰ª§≈âÕß°—∫ ™‘Èπ à«π¢Õß “¬ PEG ¢π“¥ 2 ´¡. π—Èπ‰«â ·≈–„™â Kelly clamp ®—∫„ÀâÕ¬Ÿà°÷Ëß°≈“ß ‡ªìπ√Ÿªμ—« T (¿“æ∑’Ë 7) ®“°π—Èπ ‡Õ“°≈âÕßÕÕ° ·≈–∑”°“√¥÷ß bumper ¥â«¬ snare „π¢≥–∑’Ë∑”°“√¥—π “¬ PEG ¥â«¬ clamp ∑“ßÀπâ“∑âÕß‰ªæ√âÕ¡°—π ®πª≈“¬ “¬ ∑“ßÀπâ“∑âÕß®¡À¡¥ ®÷ßª≈àÕ¬ clamp ·≈– àÕß°≈âÕß‡¢â“‰ª „™â snare §≈âÕß “¬ PEG ÕÕ°¡“∑“ßª“° ·≈– “¡“√∂„ à “¬„À¡à‰¥â∑“ß™àÕß‡¥‘¡ ®“°°“√√“¬ß“πºŸâªÉ«¬∑’Ë‰¥â √—∫°“√√—°…“¥â«¬«‘∏’π’È‰¡àæ∫«à“‡°‘¥¿“«–·∑√°´âÕπ ”À√—∫°√≥’∑’Ë¡’ complete epithelization ª°§≈ÿ¡ snare ®–‰¡à “¡“√∂ºà“π‰¥â Õ“®„™â «‘∏’Õ◊Ëπ‡ √‘¡ ¥—ß®–°≈à“«μàÕ‰ª

Buried Bumper Syndrome 27 ¿“æ∑’Ë 7 · ¥ß Push-pull T technique (¿“æ®“° Boyd JW, et al. Gastrointest Endosc 1995;41:508-11)

2.4 Pulled out and replace with pull-typed feeding tube ‡ªìπ°“√π” PEG ∑’ËΩíßμ—«ÕÕ°®“° gastric wall ‚¥¬°“√„™â “¬ PEG Õ—π„À¡à ¥—π¢Õß‡°à“ ÕÕ°∑“ßº‘«Àπ—ß ‚¥¬μ—¥ª≈“¬ “¬ PEG tube „Àâ‡À≈◊Õ 3 ‡´πμ‘‡¡μ√ ®“°º‘«Àπ—ß ·≈–°√’¥º‘«Àπ—ß ‡≈Á°πâÕ¬∑’Ë√Õ∫ “¬‡¥‘¡ ·≈â«„™â™ÿ¥‡¢Á¡§≈âÕß guide wire ¢Õß PEG kit ‡®“–‡¢â“∑“ß‡¥‘¡ ‚¥¬ «¡‡¢Á¡‡¢â“‰ª„π “¬‡°à“ Ÿà¿“¬„π °√–‡æ“–Õ“À“√ μ√«®¥Ÿμ”·Àπàß®“°°“√ àÕß°≈âÕß„Àâ‡¢Á¡ÕÕ°μ√ß°—∫ª≈“¬ “¬ „ à guide wire ºà“π∑“ß√Ÿ PEG Õ—π‡¥‘¡ ·≈–„™â«‘∏’ pull “¬ PEG Õ—π„À¡à‡¢â“¡“„π °√–‡æ“–Õ“À“√·≈â«¥÷ßÕÕ°∑“ßº‘«Àπ—ß ‚¥¬ª≈“¬ “¬ PEG Õ—π„À¡à®–‡¢â“‰ª§≈âÕß °—∫ª≈“¬ “¬ PEG Õ—π‡°à“ ·≈–®–∂Ÿ°¥—πÕÕ°‰ªæ√âÕ¡°—π16 (¿“æ∑’Ë 8) 2.5 Needle knife technique „π°√≥’∑’Ë àÕß°≈âÕß‡¢â“‰ªæ∫«à“ ‰¡à‡ÀÁπ à«π¢Õß internal bumper ‡À≈◊Õ Õ¬Ÿà‡≈¬ (complete buried) Õ“®æ∫‡æ’¬ß bulging ∑’Ë∫√‘‡«≥π—Èπ ‰¥â¡’√“¬ß“π°“√„™â Olympus pre-cut papillotomy needle knife ‡¢â“¡“™à«¬ ‚¥¬°“√∑” incision

28 ®ÿ≈ “√ ¡“§¡·æ∑¬å√–∫∫∑“ß‡¥‘πÕ“À“√·Ààßª√–‡∑»‰∑¬, æƒ…¿“§¡- ‘ßÀ“§¡ 2559 ‡ªìπ·©°Ê ®“°®ÿ¥°÷Ëß°≈“ß√Õ¬πŸπ ®π‡ÀÁπ à«π¢Õß internal bumper ·≈â«„™â alli- gator forceps À√◊Õ snare ¥÷ß PEG tube ∑’ËΩíßÕ¬Ÿà„ÀâÀ≈ÿ¥‡¢â“¡“„π°√–‡æ“–Õ“À“√ ·≈â«π”ÕÕ°∑“ßª“° (pulled by snare)6 (¿“æ∑’Ë 9) 3. °“√√—°…“¥â«¬«‘∏’ºà“μ—¥·≈–°“√ºà“μ—¥ºà“π°≈âÕß (surgical intervention and laparoscopic removal) „π°√≥’∑’Ë‰¡à “¡“√∂∑”°“√√—°…“¥â«¬«‘∏’ simple extraction À√◊Õ endoscopic technique μà“ßÊ ·≈â« À√◊Õ„π°√≥’∑’Ë‡°‘¥¿“«–·∑√°´âÕπ ‡™àπ °“√μ‘¥

¿“æ∑’Ë 8 The tapered tip of the PEG tube has engaged the bumper buried in the abdominal wall (¿“æ®“° Venu RP, et al. Gastrointest Endosc. 2002;56:582-4)

¿“æ∑’Ë 9 °“√„™â needle knife °√’¥ºπ—ß°√–‡æ“–Õ“À“√ „Àâ‡ªìπ·©°®“°®ÿ¥°÷Ëß°≈“ß¢Õß√Õ¬πŸπ (¿“æ ®“° Ma MM, et al. Gastrointest Endosc. 1995;41:505-8)

Buried Bumper Syndrome 29 ‡™◊ÈÕ¿“¬„π™àÕß∑âÕß (peritonitis) À√◊Õ‡°‘¥ÀπÕß °Á®–‡ªìπ∫∑∫“∑¢Õß∑“ß»—≈¬°√√¡ ‡™àπ °“√ºà“μ—¥ À√◊Õ°“√ºà“μ—¥ºà“π°≈âÕß (laparoscopic removal)17 ‚¥¬‰¡à¢Õ°≈à“« √“¬≈–‡Õ’¬¥„π∑’Ëπ’È °“√√—°…“‡ √‘¡ ‰¥â·°à °“√„Àâ “√πÈ” °“√„Àâ¬“ªØ‘™’«π–„π°√≥’∑’Ë¡’°“√μ‘¥‡™◊ÈÕ‚¥¬§√Õ∫§≈¡ÿ ‡™◊ÈÕ·∫§∑’‡√’¬™π‘¥·°√¡≈∫·≈–‡™◊ÈÕ·∫§∑’‡√’¬™π‘¥‰¡àæ÷ËßÕÕ°´‘‡®π ·≈–°“√„Àâ¬“≈¥ ª«¥ °“√„ à PEG tube „À¡à∑¥·∑π¢Õß‡¥‘¡ “¡“√∂∑”‰¥âæ√âÕ¡°—∫°“√π” PEG tube ‡°à“ÕÕ° ¥—ß‰¥â°≈à“«¡“¢â“ßμâπ ‚¥¬∑’Ë “¡“√∂„™â tract ‡¥‘¡‰¥â‡≈¬ ¬°‡«âπ°√≥’∑’Ë¡’°“√μ‘¥‡™◊ÈÕ„π™àÕß∑âÕßÀ√◊ÕΩï ÀπÕß∑’Ë™—Èπ„μâº‘«Àπ—ß ´÷ËßÀ≈—ß°“√π” “¬‡°à“ÕÕ°‚¥¬«‘∏’∑“ß»—≈¬°√√¡·≈â« §«√√Õ„Àâ ·º≈‡°à“À“¬‚¥¬°“√√—°…“¥â«¬¬“ªØ‘™’«π–‰ª°àÕπ ®÷ßæ‘®“√≥“∑” PEG ∑’Ëμ”·Àπàß Õ◊Ëπ·∑π¿“¬À≈—ß °“√ªÑÕß°—π°“√‡°‘¥¿“«– buried bumper syndrome 1. À≈—ß∑” PEG ®–¡’ tension √–À«à“ß external ·≈– internal bumper Õ¬à“ß¡“° „π«—π∂—¥¡“§«√§≈“¬ tension π’È ‡æ◊ËÕ„Àâ PEG tube ‡§≈◊ËÕπ¢÷Èπ≈ß‰¥â Õ¬à“ßÕ‘ √– ‚¥¬„Àâ external bumper ‡§≈◊ËÕπ Ÿß¢÷Èπ‰¥âÕ¬à“ßπâÕ¬ 1 ´¡. ‡Àπ◊Õ®“° º‘«Àπ—ßÀπâ“∑âÕß16 2. ‰¡à§«√«“ßºâ“°äÕ´„μâ external bumper Àπ“‡°‘π‰ª ‡π◊ËÕß®“°®–∑”„Àâ ·√ßμ÷ß√–À«à“ßºπ—ßÀπâ“∑âÕß°—∫ internal bumper ‡æ‘Ë¡¢÷Èπ16 3. °“√„Àâ§”·π–π”·°àºŸâ¥Ÿ·≈ºŸâªÉ«¬∑’Ë„™â PEG ‰¥â·°à °“√¥Ÿ·≈ “¬ PEG „π·μà≈–«—π §«√μ√«® Õ∫«à“ “¬ PEG “¡“√∂ ‡§≈◊ËÕπ¢÷Èπ≈ß‰¥â Ÿß®“°º‘«Àπ—ßÕ¬à“ßπâÕ¬ 1 ´¡. ·≈–À¡ÿπ‡ªìπ«ß√Õ∫‰¥â °“√‰¡à«“ß ºâ“°äÕ´„μâ external bumper ¥—ß∑’Ë‰¥â°≈à“«¡“ „π°√≥’∑’Ë¬—ß‰¡à„™â “¬ PEG §«√‰¥â

30 ®ÿ≈ “√ ¡“§¡·æ∑¬å√–∫∫∑“ß‡¥‘πÕ“À“√·Ààßª√–‡∑»‰∑¬, æƒ…¿“§¡- ‘ßÀ“§¡ 2559 √—∫°“√ªî¥À√◊Õª°§≈ÿ¡Õ¬à“ß¡‘¥™‘¥ ‡æ◊ËÕªÑÕß°—π‰¡à„ÀâºŸâªÉ«¬∑’Ë‰¡à “¡“√∂§«∫§ÿ¡ μπ‡Õß‰¥â¥÷ß “¬ PEG ÕÕ°‚¥¬‰¡à√Ÿâμ—« πÕ°®“°π’È À“°ºŸâ¥Ÿ·≈æ∫ªí≠À“°“√√—Ë«´÷¡ °“√‡§≈◊ËÕπ∑’Ë‰¡à‰¥â¢Õß PEG tube °“√„ÀâÕ“À“√‰¡à‡ªìπ‰ªμ“¡ª°μ‘ À√◊ÕÕ“À“√≈ß™â“ °“√¡’√Õ¬∫«¡·¥ß¢Õßº‘«Àπ—ß√Õ∫ “¬ À√◊ÕºâªÉ«¬¡’Õ“°“√ª«¥∑âÕßŸ §«√ª√÷°…“·æ∑¬å ∑—π∑’ ‡Õ° “√Õâ“ßÕ‘ß 1. Ponsky JL, Gauderer MW. Percutaneous endoscopic gastrostomy: a nonoperative technique for feeding gastrostomy. Gastrointest Endosc. 1981;27:9-11. 2. Klein S, Heare BR, Soloway RD. The ùûburied bumper syndromeé : a com- plica- tion of percutaneous endoscopic gastrostomy. Am J Gastroenterol. 1990;85:448- 51. 3. Gluck M, Levant J, Drennan F, et al. Retraction of Sacks-Vine gastrostomy tubes into the gastric wall: report of seven cases [abstract]. Gastrointest Endosc. 1988;34:215. 4. Shallman RW, NorFleet RG, Hardache JM. Percutaneous endoscopic gastrostomy feeding tubes migration and impaction in the abdominal wall. Gastrointest Endosc 1988;34:367-8. 5. Pop GH. çBuried bumper syndrome: can we prevent it?é Practical Gastroenterol- ogy 2010; 34:5:8-13. 6. Ma MM, Semlacher EA, Fedorak RN, et al. The buried gastrostomy bumper syndrome: prevention and endoscopic approaches to removal. Gastrointest Endosc. 1995;41:505-8. 7. Khalil Q, Kibria R, Akram S. Acute buried bumper syndrome. South Med J. 2010;13:1256-8. 8. Anagnostopoulous GK, Kostopoulos P, Arvanitidis DM. Buried bumper syndrome with a fatal outcome, presenting early as gastrointestinal bleeding after percutaneous endoscopic gastrostomy placement. J Postgrad Med. 2003;49:325-7. 9. Foutch PG, Woods CA, Talbert GA, et al. A critical analysis of the Sachs-Vine

Buried Bumper Syndrome 31 gastrostomy tube: a review of 120 consecutive procedures. Am J Gastroenterol. 1988;83:812-15. 10. Vargo JJ, Ponsky JL. Percutaneous endoscopic gastrostomy: clinical applica- tions. Medsc Gastroenterol. 2000;2:4. 11. Geer W, Jeanmanod R. Early presentation of buried bumper syndrome. West J Emerg Med. 2013;5:421-3. 12. Lee Tzong-His, Lin Jaw-Town. Clinical manifectations and management of buried bumpersyndrom in patients with percutaneous endoscopic gastrostomy. Gastrointest Endosc. 2008;68:580-4. 13. Strock P, Weber J. Buried bumper syndrome: endoscopic management using a balloon dilator. Endoscopy. 2005;37:279. 14. Boyd JW, DeLegge MH, Shamburek RD, et al. The buried bumper syndrome: a new technique for safe, endoscopic PEG removal. Gastrointest Endosc. 1995;41:508-11. 15. Binnebösel M, et al. Removal and replacement of a PEG tube after çburied bumper syndromeé. Endoscopy. 2010;42:E17-E18. 16. Venu RP, Brown RD, Pastika BJ, et al. The buried bumper syndrome: a simple management approach in two patients. Gastrointest Endosc. 2002;56:582-4. 17. Ehsan S, Dyall L, Ubhi S. A novel laparoscopic approach for the surgical management of buried bumper syndrome. Ann R Coll Surg Engl. 2012;94:61.

32 ®ÿ≈ “√ ¡“§¡·æ∑¬å√–∫∫∑“ß‡¥‘πÕ“À“√·Ààßª√–‡∑»‰∑¬, æƒ…¿“§¡- ‘ßÀ“§¡ 2559 Review Article Management of Gastric Polyps æ‘π‘® »√’æ∏Ÿ√“…Æ√å ‡æÁ™™√’ æ√¡≥’

Àπà«¬‚√§∑“ß‡¥‘πÕ“À“√ ‚√ßæ¬“∫“≈¿Ÿ¡‘æ≈Õ¥ÿ≈¬‡¥™

○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○

∫∑π” μ‘Ëß‡π◊ÈÕ°√–‡æ“–Õ“À“√ (gastric polyp) ‡ªìπ¿“«–°“√‡®√‘≠∑’Ëº‘¥ª°μ‘¢Õß ‡π◊ÈÕ‡¬◊ËÕ´÷Ëß¡’°“√¬◊Ëπ (projecting) ®“°º‘«‡¬◊ËÕ∫ÿ°√–‡æ“–Õ“À“√ (gastric mucosal membrane) ‡¡◊ËÕμ√«®æ∫μ‘Ëß‡π◊ÈÕ„π°√–‡æ“–Õ“À“√§«√μâÕßæ‘®“√≥“„π·ßà¢Õß ≈—°…≥–∑“ß‡π◊ÈÕ‡¬◊ËÕ«‘∑¬“ (histology) “‡Àμÿ ∏√√¡™“μ‘°“√°”‡π‘¥‚√§ √«¡∂÷ß æ‘®“√≥“«à“μ‘Ëß‡π◊ÈÕ¥—ß°≈à“«®”‡ªìπμâÕß‰¥â√—∫°“√√—°…“‡©æ“–‡®“–®ßÀ√◊Õ‰¡à „π∫∑§«“¡π’È®–°≈à“«∂÷ß fundic gland polyp, hyperplastic gastric polyp, gastric adenoma, gastrointestinal stromal tumor (GIST), inflammatory fibroid polyp ·≈– gastric neuroendocrine tumor (carcinoid) ‡ªìπ À≈—°1 Fundic Gland Polyps μ‘Ëß‡π◊ÈÕ™π‘¥π’È‡°‘¥®“°μàÕ¡∫√‘‡«≥°√–æÿâß°√–‡æ“–Õ“À“√ (fundic gland polyp) (¿“æ∑’Ë 1) ∂◊Õ‡ªìπμ‘Ëß‡π◊ÈÕ∑’Ëμ√«®æ∫¢≥–μ√«® àÕß°≈âÕß∑“ß‡¥‘πÕ“À“√ à«π ∫π‰¥â∫àÕ¬∑’Ë ÿ¥ „πª√–‡∑»·∂∫μ–«—πμ°¡’º≈°“√»÷°…“¢π“¥„À≠àæ∫«à“„π°≈ÿà¡ ºŸâªÉ«¬∑’Ë¡“√—∫°“√μ√«® àÕß°≈âÕß∑“ß‡¥‘πÕ“À“√ à«π∫πæ∫§«“¡™ÿ° (prevalence) ¢Õß°“√μ√«®æ∫μ‘Ëß‡π◊ÈÕ°√–‡æ“–Õ“À“√√âÕ¬≈– 6.35 ‚¥¬æ∫‡ªìπ fundic gland polyp √âÕ¬≈– 77 ‡ªìπ hyperplastic polyp/polypoid foveolar hyperplasia √âÕ¬≈– 17

Management of Gastric Polyps 33 ¿“æ∑’Ë 1 multiple fundic gland polyps ∑’Ëæ∫®“°°“√ àÕß°≈âÕß∫√‘‡«≥ gastric body

‡ªìπ adenoma √âÕ¬≈– 0.69 ·≈–‡ªìπ inflammatory fibroid polyp √âÕ¬≈– 0.12 fundic gland polyp ∑’Ëμ√«®æ∫®“°°“√ àÕß°≈âÕß¡—°æ∫®”π«πμ‘Ëß‡π◊ÈÕ§√—Èß≈–À≈“¬Ê μ‘Ëß ‚¥¬¡—°¡’¢π“¥‡≈Á° (<1 ´¡.) æ◊Èπº‘«¢Õßμ‘Ëß‡π◊ÈÕ®–¡’≈—°…≥–‡√’¬∫ (smooth) „ (glassy) ·≈–‰¡à¡’°â“π (sessile) À“°„™â°≈âÕß∑’Ë¡’√–∫∫ NBI (narrow band imaging) ®–‡ÀÁπ≈—°…≥–‡ªìπ√—ßº÷Èß (honeycomb appearance) ·≈–¡’À≈Õ¥‡≈◊Õ¥Õ¬Ÿà ·πàπÀπ“ (dense vasculature) ´÷Ëß‰¡à∂◊Õ«à“‡ªìπ≈—°…≥–®”‡æ“–‡π◊ËÕß®“° “¡“√∂ æ∫‰¥â„πμ‘Ëß‡π◊ÈÕ™π‘¥‰¡à‡ªìπ¡–‡√Áß (hyperplastic polyp) ‰¥â3 ·√°‡√‘Ë¡∑’Ë¡’°“√§âπæ∫ ¡’§«“¡‡™◊ËÕ«à“ fundic gland polyp ‡ªìπμ‘Ëß‡π◊ÈÕ™π‘¥Œ“¡“√å‚μ¡“ (hamartomatous polyp) Õ¬à“ß‰√°Áμ“¡®“°°“√»÷°…“μàÕ¡“æ∫«à“μ‘Ëß‡π◊ÈÕ™π‘¥π’È¡’§«“¡ —¡æ—π∏å°—∫ °“√„™â¬“≈¥°√¥™π‘¥ PPI (proton pump inhibitor) ´÷Ëß‰¥â¡’°“√‡ πÕ«à“°≈‰° ®“°°“√¬—∫¬—Èß°“√À≈—Ëß°√¥¥â«¬¬“™π‘¥¥—ß°≈à“«πà“®–‡°’Ë¬«¢âÕß°—∫æ¬“∏‘ ¿“æ∑’Ëμ√«® æ∫4 Fundic gland polyp ®–ª√–°Õ∫¥â«¬μàÕ¡ÕÁÕ°´‘πμ‘°∑’Ë¢¬“¬ (dilated oxyntic gland) ®”π«πÀπ÷ËßμàÕ¡À√◊ÕÀ≈“¬μàÕ¡ ‚¥¬‡√’¬ßμ—«¥â«¬‡´≈≈åæ“‰√∑Õ≈

34 ®ÿ≈ “√ ¡“§¡·æ∑¬å√–∫∫∑“ß‡¥‘πÕ“À“√·Ààßª√–‡∑»‰∑¬, æƒ…¿“§¡- ‘ßÀ“§¡ 2559 ¿“æ∑’Ë 2 ≈—°…≥– dilated oxyntic gland ∑’Ë‡√’¬ßμ—«¥â«¬ cuboidal parietal cells (a); ·≈– flattened mucous and parietal cells (b ·≈– c)

·≈–‡´≈≈å‡¬◊ËÕ‡¡◊Õ°∑’Ë·∫π√“∫ (flattened parietal and mucous cells) (¿“æ∑’Ë 2) °“√æ∫≈—°…≥–¥—ß°≈à“«®“°°“√¬âÕ¡ ‰≈¥å¥â«¬ hematoxylin ·≈– eosin (H&E) ∂◊Õ‡ªìπ«‘∏’°“√„™â®”·π°‰¥â ‘ËßÀπ÷Ëß∑’Ëæ÷ß√–«—ß§◊ÕÀ“°æ∫«à“æ◊Èπº‘«¢Õßμ‘Ëß‡π◊ÈÕ¡’ ≈—°…≥–∂Ÿ°°—¥‡´“– (eroded) ·≈–¡’≈—°…≥–¢Õß°“√ √â“ß‡π◊ÈÕ‡¬◊ËÕ„À¡à (regenera- tive appearance) Õ“®∑”„Àâ·ª≈º≈º‘¥§‘¥«à“‡ªìπ‡´≈≈åº‘¥ª°μ‘ (dysplasia) ‰¥â ´÷Ëß¿“«–‡´≈≈åº‘¥ª°μ‘∑’Ë·∑â®√‘ß‚¥¬‡©æ“–™π‘¥¢—Èπ Ÿß (high grade) ∂◊Õ«à“æ∫‰¥âπâÕ¬ ¡“°·≈–æ∫Õ¬à“ß®”°—¥‡©æ“–„π°≈ÿà¡ºŸâªÉ«¬∑’Ë‡ªìπ polyposis syndrome ·π«»÷°…“∑“ß§≈‘π‘° (Clinical approach) ‚¥¬∑—Ë«‰ª‡¡◊ËÕμ√«®æ∫μ‘Ëß‡π◊ÈÕ §«√ ÿà¡‡≈◊Õ°μ‘Ëß‡π◊ÈÕ·≈–∑”°“√μ—¥™‘Èπ‡π◊ÈÕ (biopsy) ‡æ◊ËÕπ”‰ªμ√«® Õ∫¬◊π¬—π°“√«‘π‘®©—¬ μ‘Ëß‡π◊ÈÕ∑’Ë¡’¢π“¥„À≠à (>1 ´¡.) §«√®–∑”°“√μ—¥ÕÕ°∑—ÈßÀ¡¥‡æ◊ËÕ¬◊π¬—π°“√«‘π‘®©—¬‡π◊ËÕß®“° fundic gland polyp

Management of Gastric Polyps 35 ®”π«ππâÕ¬¡“°∑’Ë®–¡’¢π“¥„À≠à‡°‘π 1 ´¡. °“√∑” biopsy „π°√≥’π’È®–‰¡à¡’§«“¡ ‡À¡“– ¡‡π◊ËÕß®“°À“°μ‘Ëß‡π◊ÈÕπ—Èπ‰¡à„™à fundic gland polyp °“√ ÿà¡ biopsy Õ“® ‰¡à§√Õ∫§≈¡æ◊Èπ∑’Ë∑’ËÕ“®®–¡’‚Õ°“ æ∫«à“‡ªìπÿ dysplasia À√◊Õ‡ªìπ‡π◊ÈÕßÕ° (neoplasia) §«√∑”°“√μ√«® Õ∫μ‘Ëß‡π◊ÈÕ∑’Ë‡À≈◊Õ«à“¡’μ‘Ëß‡π◊ÈÕÕ—π„¥∑’Ë¡’√Ÿª√à“ßÀπâ“μ“·μ°μà“ß®“°μ‘Ëß ‡π◊ÈÕ à«π„À≠àÕ¬à“ß™—¥‡®π·≈–§«√∑” biopsy ‡æ◊ËÕμ√«® Õ∫À√◊ÕÀ“°‡ªìπ‰ª‰¥â„Àâ °”®—¥μ‘Ëß‡π◊ÈÕ‡À≈à“π’ÈÕÕ° ‚¥¬‡©æ“–Õ¬à“ß¬‘Ëß„π°√≥’∑’Ëμ‘Ëß‡π◊ÈÕ¡’¢π“¥„À≠à°«à“ 1 ´¡. ¡’·º≈ ·≈–Õ¬à„πμ”·Àπàß∑’Ëæ∫‰¥â‰¡à∫àÕ¬Ÿ ‡™àπ antrum ‡ªìπμâπ ‡¡◊ËÕæ∫ fundic gland polyps „πºŸâªÉ«¬Õ“¬ÿπâÕ¬ ‚¥¬‡©æ“–Õ¬à“ß¬‘Ëß∂â“æ∫μ‘Ëß‡π◊ÈÕ¡’®”π«π¡“° (‡™àπ >20 μ‘Ëß) §«√§”π÷ß∂÷ß¿“«– polyposis syndrome ‰«â¥â«¬ ‚¥¬°≈ÿà¡ºŸâªÉ«¬∑’Ë‡ªìπ familial polyposis syndrome ¡—°®–¡’Õ“¬ÿπâÕ¬°«à“°≈ÿà¡ºŸâªÉ«¬∑’Ë¡’ fundic gland polyps (Õ“¬ÿ‡©≈’Ë¬ 40 ªï)5-6 ·≈–∫“ß§√—Èß®–æ∫μ‘Ëß‡π◊ÈÕ∫√‘‡«≥ antrum7 ‡¡◊ËÕ„¥°Áμ“¡ ∑’Ëæ∫«à“μ‘Ëß‡π◊ÈÕ°√–‡æ“–Õ“À“√¡’§«“¡‡°’Ë¬«‡π◊ËÕß°—∫‡π◊ÈÕßÕ°„π≈”‰ â‡≈Á° à«πμâπ (duodenal adenomas) §«√®–§‘¥∂÷ß¿“«– familial polyposis syndrome ‰«â‡ ¡Õ·≈– §«√∑”°“√ àÕß°≈àÕß≈”‰ â„À≠à√à«¡¥â«¬ Fundic gland polyps πâÕ¬§√—Èß¡“°∑’Ë®–æ∫„π°√–‡æ“–Õ“À“√‚¥¬‡ªìπº≈ ®“°°“√μ‘¥‡™◊ÈÕ Helicobacter pylori ¥â«¬ “‡Àμÿ¥—ß°≈à“«®÷ß∑”„ÀâÀ“°‡¡◊ËÕ„¥°Áμ“¡ ∑’Ë¬—ß‰¡àæ∫¿“«– familial polyposis syndrome °“√∑’Ë®–§‘¥∂÷ß¡–‡√Áß°√–‡æ“– Õ“À“√π—Èπ®÷ß¬—ßªìπ∑’Ë∂°‡∂’¬ß°—πÕ¬Ÿà8 Õ¬à“ß‰√°Áμ“¡°“√æ∫μ‘Ëß‡π◊ÈÕ®”π«π¡“°À√◊Õ¡’ ¢π“¥„À≠à (>1 ´¡.) ¡—°®–μâÕßÀ“ “‡Àμÿ∑’Ë‡°’Ë¬«¢âÕß¥â«¬‡ ¡Õ ·¡â®–¬—ß‰¡à¡’ ·π«∑“ßªØ‘∫—μ‘™—¥‡®π ¡’¢âÕ·π–π”«à“À“°‡¡◊ËÕ„¥∑’Ëæ∫μ‘Ëß‡π◊ÈÕ®”π«π¡“°°«à“ 20 μ‘Ëß ¢÷Èπ‰ªÀ√◊Õμ‘Ëß‡π◊ÈÕ¡’¢π“¥„À≠à°«à“ 1 ´¡. §«√∑”°“√≈¥¢π“¥À√◊ÕÀ¬ÿ¥¬“ PPI ‡æ◊ËÕ ª√–‡¡‘π«à“μ‘Ëß‡π◊ÈÕ®–¡’°“√≈¥¢π“¥À√◊Õ®”π«π≈ßÀ√◊Õ‰¡à À“°æ∫«à“¡’°“√≈¥≈ß¢Õß μ‘Ëß‡π◊ÈÕ°“√∑’Ë®–„Àâ¬“ PPI °≈—∫‡¢â“‰ª„À¡àπ—Èπ¬—ß‰¡à‡ªìπ∑’Ë∑√“∫·πà™—¥„π‡√◊ËÕß§«“¡ ‡À¡“– ¡ „π∑“ßªØ‘∫—μ‘À“°æ∫«à“°“√ºà“μ—¥‰¡à„™à∑“ß‡≈◊Õ° Õ“®≈Õßæ‘®“√≥“‡ª≈’Ë¬π ™π‘¥¢Õß¬“ PPI ·≈–≈¥¢π“¥¬“„Àâ‡À≈◊ÕπâÕ¬∑’Ë ÿ¥‡∑à“∑’Ë “¡“√∂∑”‰¥â §«√æ‘®“√≥“ μ√«®«—¥√–¥—∫ gastrin „π´’√—Ë¡√à«¡¥â«¬·¡â®–¬—ß‰¡àæ∫§«“¡ —¡æ—π∏å√–À«à“ß√–¥—∫ gastrin „π´’√—Ë¡·≈–°“√‡°‘¥ fundic gland polyps9 ‚¥¬√–¥—∫„π´’√—Ë¡∑’Ë Ÿß (>400

36 ®ÿ≈ “√ ¡“§¡·æ∑¬å√–∫∫∑“ß‡¥‘πÕ“À“√·Ààßª√–‡∑»‰∑¬, æƒ…¿“§¡- ‘ßÀ“§¡ 2559 æ‘‚§°√—¡/¡≈.) ®–∑”„Àâ§‘¥∂÷ß¿“«–∑’Ë‡°‘¥®“°°“√¬—∫¬—Èß°“√À≈—Ëß°√¥ À“°‰¡àæ∫«à“ºŸâ ªÉ«¬¡’¿“«–À≈—Ëß “√ gastrin ¡“°∑’Ë‡°‘¥®“°¿“¬„π√à“ß°“¬‡Õß (intrinsic hyper- secretor) ·≈–‰¡àæ∫«à“¡’‡π◊ÈÕßÕ°·°ä μ√‘‚π¡“ (gastrinoma) À√◊Õ°≈ÿà¡Õ“°“√‚´≈ ≈‘ß‡®Õ√å-‡Õ≈≈‘ —π (Zollinger-Ellison syndrome) °Á§«√∑’Ë®–À¬ÿ¥¬“ PPI ·≈–∂â“ À“°ºŸâªÉ«¬¡’Õ“°“√¢Õß‚√§°√¥‰À≈¬âÕπ (gastroesophageal reflux disease) °Á §«√®–„™â¬“°≈à¡¬—∫¬—Èßμ—«√—∫Œ‘ ∑“¡’π∑’Ëÿ 2 (H2-receptor antagonist) ·∑π ®“°°“√ ∑’Ë¡’√“¬ß“πæ∫§«“¡ —¡æ—π∏å√–À«à“ß‡π◊ÈÕßÕ°§“√å´‘πÕ¬¥å¢Õß°√–‡æ“–Õ“À“√ (gastric carcinoid) °—∫°“√¬—∫¬—Èß°“√À≈—Ëß°√¥®“°°“√„™â¬“ PPI10-11 ·≈–¡’°“√‡æ‘Ë¡§«“¡ μ√–Àπ—°‡°’Ë¬«°—∫º≈¢â“ß‡§’¬ß¢Õß¬“∑’ËÕ“®‡°‘¥¢÷Èπ∑”„Àâ¡’°“√ àß‡ √‘¡„Àâ≈¥°“√„™â¬“ „πºŸâªÉ«¬∑’Ë‰¡à¡’¢âÕ∫àß™’È™—¥‡®π·≈–À“°„™â¬“„Àâ„™â¢π“¥¬“„ÀâπâÕ¬∑’Ë ÿ¥‡∑à“∑’Ë “¡“√∂ ∑”‰¥â12-14 Hyperplastic Gastric Polyps μ‘Ëß‡π◊ÈÕ∑’Ë‰¡à°≈“¬‡ªìπ¡–‡√Áß (hyperplastic polyp) ‡°‘¥®“°°“√Õ—°‡ ∫∑’Ë¡’ °“√‡æ‘Ë¡®”π«π¢Õß‡´≈≈å‚ø«‘‚Õ≈“¢Õß°√–‡æ“–Õ“À“√ (gastric foveolar cell) ‚¥¬ ‡¡◊ËÕ¡’°“√Õ—°‡ ∫‡°‘¥¢÷ÈπÕ¬à“ß‡¥àπ™—¥Õ“®‡√’¬°μ‘Ëß‡π◊ÈÕ™π‘¥π’È«à“‡ªìπ inflammatory polyps ‡¡◊ËÕ„¥°Áμ“¡∑’Ë¡’¿“«–°“√‡æ‘Ë¡®”π«πÕ¬à“ß¡“° (hyperproliferation) ¢Õß foveolar cell Õ¬à“ß™—¥‡®π √àÕß¢ÕßμàÕ¡„π°√–‡æ“–Õ“À“√ (gastric pits) À√◊Õ ‡√’¬°«à“‚ø«‘‚Õ‡≈ (foveolae) ®–¡’≈—°…≥–¬◊¥¬“«ÕÕ° (elongation) §¥‡§’È¬« (tortuous) ·≈–¡’°“√¬°μ—«¢Õß™—Èπ‡¬◊ËÕ∫ÿº‘« (elevation of the mucosa) ´÷Ëß≈—°…≥– ∑—ÈßÀ¡¥π’ÈÕ“®√«¡‡√’¬°«à“ polypoid foveolar hyperplasia „πºŸâªÉ«¬∑’Ë‰¥â√—∫°“√ ºà“μ—¥°√–‡æ“–Õ“À“√¥â«¬«‘∏’ Billroth ™π‘¥∑’Ë 1 ·≈– 2 (Billroth I and II) ∫√‘‡«≥ à«πª≈“¬∑’Ë‡À≈◊Õ¢Õß°√–‡æ“–Õ“À“√ (gastric stumps) ‡¬◊ËÕ∫ÿ°√–‡æ“–Õ“À“√∑’ËÕ¬Ÿà „°≈â°—∫√Õ¬‡™◊ËÕ¡μàÕ (anastomosis) ®–¡’°“√ —¡º— °—∫πÈ”¥’ à«π∑’Ë‰À≈¬âÕπ°≈—∫ Ÿà °√–‡æ“–Õ“À“√ (bile reflux) Õ¬à“ßμàÕ‡π◊ËÕß·≈–‡ªìπ “‡Àμÿ∑”„Àâ‡°‘¥ foveolar hyperplasia Õ¬à“ß¡’π—¬ ”§—≠ „πºâªÉ«¬∫“ß√“¬Õ“®æ∫°“√¢¬“¬μ—«≈—°…≥–∂Ÿ ßπÈ”ÿ (cystic dilatation) ¢Õß foveolae ·≈–∑”„Àâ¡’≈—°…≥–§≈â“¬μ‘Ëß‡π◊ÈÕ (polypoid lesions)

Management of Gastric Polyps 37 ∑’Ëª√–°Õ∫¥â«¬∂ÿßπÈ” (cyst) √àÕß¢ÕßμàÕ¡∑’Ë§¥‡§’È¬« (tortuous pit) ·≈–¡—°¡’æ◊Èπ º‘«¢Õß‡¬◊ËÕ∫ÿº‘«∑’Ë¡’≈—°…≥–∂Ÿ°°—¥‡´“– (eroded surface epithelium) ´÷Ëß≈—°…≥– ¥—ß°≈à“«∫“ß§√—ÈßÕ“®‡√’¬°«à“ gastritis cystica polyposa ‡π◊ËÕß®“°¿“«–∑—ÈßÀ¡¥ ¥—ß°≈à“«¢â“ßμâπ‡°‘¥®“°√Õ¬‚√§∑’Ë¡’≈—°…≥–æ◊Èπ∞“π·∫∫‡¥’¬«°—π ‡æ◊ËÕªÑÕß°—π§«“¡ —∫ π∑’ËÕ“®‡°‘¥¢÷Èπ®÷ß‡√’¬°√«¡«à“ hyperplastic polyps §«“¡‡°’Ë¬«‡π◊ËÕß¥—Èß‡¥‘¡¢Õß hyperplastic polyps „π°√–‡æ“–Õ“À“√ ¡—°æ∫«à“¡’‡¬◊ËÕ∫ÿ∑’ËΩÉÕ‡À’Ë¬« (mucosal atrophy) ´÷ËßÕ“®¡’ “‡Àμÿ®“°°“√μ‘¥‡™◊ÈÕ Helicobacter pylori À√◊Õ°√–‡æ“–Õ“À“√Õ—°‡ ∫™π‘¥ÕÕ‚μÕ‘¡¡Ÿπ (autoimmune gastritis) °Á‰¥â15 Õ¬à“ß‰√°Áμ“¡‡√Á«Ê π’È‰¥â¡’°“√æ∫«à“°“√‡°‘¥μ‘Ëß‡π◊ÈÕ™π‘¥π’È„π ºâªÉ«¬∑’Ë¡’‡¬◊ËÕ∫Ÿ º‘«°√–‡æ“–Õ“À“√ª°μ‘À√◊Õ·∫∫μÕ∫ πÕßÿ (normal or reactive gastric mucosa) ∑’Ë‰¡àæ∫À≈—°∞“π°“√μ‘¥‡™◊ÈÕ Helicobacter pylori ¡’ —¥ à«π∑’Ë‡æ‘Ë¡ ¡“°¢÷Èπ „πª√–‡∑»·∂∫μ–«—πμ°æ∫«à“ hyperplastic polyps ∑’Ë∂◊Õ‡ªìπμ‘Ëß‡π◊ÈÕ °√–‡æ“–Õ“À“√™π‘¥∑’Ëæ∫∫àÕ¬∑’Ë ÿ¥¢≥–∑”°“√ àÕß°≈âÕß‰¥â‡ª≈’Ë¬π¡“æ∫πâÕ¬≈ß °«à“√âÕ¬≈– 202 hyperplastic polyps ¡—°æ∫∫àÕ¬∑—Èß„π‡æ»™“¬·≈–‡æ»À≠‘ß‰¥â„°≈â ‡§’¬ß°—π ‚¥¬æ∫¡“°™à«ßÕ“¬ÿ 60-70 ªï ‡¡◊ËÕ∑”°“√ àÕß°≈âÕß°√–‡æ“–Õ“À“√®–æ∫ μ‘Ëß‡π◊ÈÕ‰¥â∫àÕ¬∫√‘‡«≥ antrum ·≈–¡—°¡’®”π«πÀ≈“¬Ê μ‘Ëß ≈—°…≥–æ◊Èπº‘«®–‡√’¬∫ (smooth) ¡’≈—°…≥–§≈â“¬‚¥¡ (dome-shaped) ·≈–¡’¢π“¥√–À«à“ß 0.5-1.5 ´¡. (¿“æ∑’Ë 3) μ‘Ëß‡π◊ÈÕ∑’Ë¡’¢π“¥„À≠à¡—°¡’≈—°…≥–‡ªìπ≈ÕπÀ√◊Õ°≈’∫ (lobulated) ·≈–¡’ °â“π (pedunculated)16 ·≈–æ◊Èπº‘«‡¬◊ËÕ∫ÿ¡—°¡’√Õ¬°—¥‡´“– (eroded) ´÷Ëß‡ªìπ “‡Àμÿ ∑”„Àâ‡°‘¥°“√‡ ’¬‡≈◊Õ¥‡√◊ÈÕ√—ß (chronic blood loss) ·≈–¿“«–‚≈À‘μ®“ß®“°°“√ ¢“¥∏“μÿ‡À≈Á° (iron deficiency anemia) ‰¥â πâÕ¬§√—Èß∑’Ë®–æ∫ºŸâªÉ«¬∑’Ë¡’μ‘Ëß‡π◊ÈÕ ¢π“¥„À≠à∑’Ë¡“¥â«¬Õ“°“√°√–‡æ“–Õ“À“√ à«πª≈“¬Õ¥μ—πÿ (gastric outlet obstruction) ´÷Ëß‡°‘¥°“√∑’Ëμ‘Ëß‡π◊ÈÕÕ“®‰ªÕÿ¥°—ÈπÀ√◊Õ¬◊Ëπ¬âÕ¬ (prolapse) ‰ª¬—ß°√–‡æ“– Õ“À“√ à«π pylorus17 ¡’§«“¡‡™◊ËÕ«à“ hyperplastic polyp πà“®–‡°‘¥®“°°“√¡’ hyperproliferation ‡æ◊ËÕμÕ∫ πÕß°—∫°—∫°“√∑’Ë‡π◊ÈÕ‡¬◊ËÕ‰¥â√—∫∫“¥‡®Á∫®“°°“√∂Ÿ° °—¥‡´“–À√◊Õ‡ªìπ·º≈ (ulcer) ‚¥¬¡’°“√‡æ‘Ë¡°“√À≈¥≈Õ°¢Õß‡´≈≈åº‘«∑’Ëμ“¬(increasedÿ cellular exfoliation)18

38 ®ÿ≈ “√ ¡“§¡·æ∑¬å√–∫∫∑“ß‡¥‘πÕ“À“√·Ààßª√–‡∑»‰∑¬, æƒ…¿“§¡- ‘ßÀ“§¡ 2559 ¿“æ∑’Ë 3 ≈—°…≥–¢Õß hyperplastic polyp ∑’Ëμ√«®æ∫®“°°“√ àÕß°≈âÕß∫√‘‡«≥ gastric antrum

≈—°…≥–∑“ß®ÿ≈æ¬“∏‘«‘∑¬“·≈–‡°≥±å„π°“√«‘π‘®©—¬ ≈—°…≥–¢Õß hyperplastic polyp ¡—°¡’°“√¬◊¥¬“« (elongated) °“√º‘¥ √Ÿª (grossly distorted) °“√·μ°·¢πß (branching) ·≈–°“√¢¬“¬μ—«¢Õß hyperplastic foveolae ∑’Ë«“ßμ—«Õ¬Ÿà„π ‚μ√¡“∑’Ë¡’≈—°…≥–∫«¡ (edematous stroma) ´÷Ëßª√–°Õ∫¥â«¬∑àÕ®”π«π¡“° (rich in vasculature) ·≈–æ∫¡’°“√°√–®“¬μ—« ¢Õß°≈ÿà¡°≈â“¡‡π◊ÈÕ‡√’¬∫ (smooth muscle bundles) √à«¡°—∫¡’¿“«–°“√Õ—°‡ ∫ ¡’ √“¬ß“πæ∫«à“ª√–¡“≥√âÕ¬≈– 1-20 ¢Õß hyperplastic polyps ¡’≈—°…≥–∑’Ë‡ªìπ®ÿ¥ ·√°‡√‘Ë¡ (foci) ¢Õß dysplasia (¿“æ∑’Ë 4) ¥â«¬‡Àμÿπ’È®÷ßÕ“®‡ªìπ ‘Ëß –∑âÕπ„Àâ‡ÀÁπ ∂÷ß∑’Ë¡“¢Õß°“√„™â‡°≥±å°“√«‘π‘®©—¬∑’Ë¡’§«“¡·μ°μà“ß°—π‡æ◊ËÕ„™â„π°“√ª√–‡¡‘π¿“«– dysplasia ¡“°°«à“®–„™â§«“¡‡ª≈’Ë¬π·ª≈ß∑’Ë·∑â®√‘ß∑“ß¥â“π¿Ÿ¡‘»“ μ√åÀ√◊Õ™’«¿“æ (real geographic or biological variability) æ∫¡’°“√°≈“¬æ—π∏ÿå¢Õß¬’π å p53 (p53 gene) §«“¡º‘¥ª°μ‘¢Õß‚§√‚¡‚´¡ (chromosomal aberrations) ·≈–°“√

Management of Gastric Polyps 39 ¿“æ∑’Ë 4 ≈—°…≥–¢Õß hyperplastic polyp ∑’Ë‡®“–®ß„Àâ‡ÀÁπ∂÷ß≈—°…≥–¢Õß high grade dysplasia ‚¥¬‡ÀÁπ dysplastic epithelial cells

‡°‘¥ microsattelite instability ‰¥â„πμ‘Ëß‡π◊ÈÕ¥—ß°≈à“«¢â“ßμâπ19-20 ‚¥¬æ∫«à“¡’§«“¡ ™ÿ°∑—ÈßÀ¡¥ (overall prevalence) ¢Õß°“√‡°‘¥‡ªìπ¡–‡√Áß (carcinoma) ¢Õß hyperplastic polyps πâÕ¬°«à“√âÕ¬≈– 2 ·≈–¡—°®–æ∫‰¥â∫àÕ¬„πμ‘Ëß‡π◊ÈÕ∑’Ë¡’¢π“¥„À≠à‡°‘π 2 ´¡.21-22 ·π«»÷°…“∑“ß§≈‘π‘° Hyperplastic polyps ∑’Ë¡’¢π“¥„À≠à‡°‘π 1 ´¡. ¡’‚Õ°“ ‡ ’Ë¬ß„π°“√‡°‘¥ ‡ªìπ¡–‡√Áß §«√‰¥â√—∫°“√μ—¥∑‘Èß„ÀâÀ¡¥Õ¬à“ß ¡∫Ÿ√≥å (completely removed) ‚¥¬ À“°μ√«®æ∫«à“¡’ dysplasia À√◊Õ‡ªìπ¡–‡√Áß¿“¬„π‡¬◊ËÕ∫ ÿ(intramucosal carcinoma) ·μàμ√«®‰¡àæ∫„π°â“π (stalk) ¢Õßμ‘Ëß‡π◊ÈÕ „π°√≥’π’È®–∂◊Õ«à“¡’°“√μ—¥∑‘ÈßÕ¬à“ß ¡∫√≥å·≈â«À√◊Õ‡∑’¬∫‡§’¬ß°—∫§”«à“À“¬·≈â«π—Ëπ‡ÕßŸ 23 „π°“√μ—¥ (excision) √Õ¬‚√§ ∑’Ë¡’≈—°…≥–§≈â“¬μ‘Ëß‡π◊ÈÕ (polypoid lesion) §«√∑’Ë®– ÿà¡‡°Á∫ (sampling) ™‘Èπ

40 ®ÿ≈ “√ ¡“§¡·æ∑¬å√–∫∫∑“ß‡¥‘πÕ“À“√·Ààßª√–‡∑»‰∑¬, æƒ…¿“§¡- ‘ßÀ“§¡ 2559 ‡π◊ÈÕ‡¬◊ËÕ∑’Ë‰¡à¡’√Õ¬‚√§ (unaffected mucosa) √à«¡¥â«¬‡ ¡Õ‡æ◊ËÕ„Àâ‰¥â√“¬≈–‡Õ’¬¥ ¢Õß¢âÕ¡Ÿ≈∑’Ë‡™◊ËÕ∂◊Õ‰¥â‡°’Ë¬«°—∫¢âÕ¡Ÿ≈∑“ß°“¬¿“æ (topography) ·≈–§«“¡√ÿπ·√ß (severity) ¢Õß¿Ÿ¡‘À≈—ß (background) ¢Õß¿“«–°√–‡æ“–Õ“À“√Õ—°‡ ∫ (gastritis) ·≈–¿“«–ΩÉÕ‡À’Ë¬« (atrophy) ‡¡◊ËÕæ∫«à“ hyperplastic polyp ‡À≈à“π—Èπ‡°‘¥¢÷Èπ®“°¿Ÿ¡‘À≈—ß¢Õß°“√¡’ °√–‡æ“–Õ“À“√Õ—°‡ ∫·∫∫ΩÉÕ‡À’Ë¬«™π‘¥‡√◊ÈÕ√—ß (chronic atrophic gastritis) §«√ ª√–‡¡‘π§«“¡√ÿπ·√ß·≈–¢Õ∫‡¢μ°“√°√–®“¬ÕÕ° (extent) ¢Õß¿“«–°√–‡æ“– Õ“À“√Õ—°‡ ∫·∫∫ΩÉÕ‡À’Ë¬«¥â«¬ ´÷Ëß¡’ª√–‚¬™πå„π°“√®”·π°§«“¡‡ ’Ë¬ß (risk strati- fication) ¢Õß°“√‡°‘¥¡–‡√Áß°√–‡æ“–Õ“À“√ (gastric cancer) ‚¥¬ “¡“√∂ ª√–‡¡‘π‰¥â®“°∑“ß‡π◊ÈÕ‡¬◊ËÕ«‘∑¬“ (histology) „™â°“√ª√–‡¡‘π¢Õß Operative Link for Gastritis Assessment (OLGA) (μ“√“ß∑’Ë 1) À√◊Õ Operative Link on Gas- tritis/Intestinal Metaplasia Assessment staging systems24-25 ´÷Ëß·∫∫ª√–‡¡‘π ∑—Èß§ŸàμâÕßÕ“»—¬≈—°…≥–°“√·∫àß·¬° (grading) ∑“ß‡π◊ÈÕ‡¬◊ËÕ®“°™‘Èπ‡π◊ÈÕμ—«Õ¬à“ß∑’Ë

μ“√“ß∑’Ë 1 °“√ª√–‡¡‘π gastric staging ‚¥¬„™â OGLA system Corpus Atrophy score No Mild Moderate Severe atrophy atrophy atrophy atrophy (score 0) (score 1) (score 2) (score 3) No atrophy (score 0) Stage 0 Stage I Stage II Stage II (including incisura angularis) Mild atrophy (score 1) Stage I Stage I Stage II Stage III (including incisura angularis)

Antrum Moderate atrophy (score 2) Stage II Stage II Stage III Stage IV (including incisura angularis) Severe atrophy (score 3) Stage III Stage III Stage IV Stage IV (including incisura angularis)

Management of Gastric Polyps 41 ‡°Á∫®“°∫√‘‡«≥ antrum ·≈– corpus ¢Õß°√–‡æ“–Õ“À“√‚¥¬„™â«‘∏’ biopsy ™‘Èπ ‡π◊ÈÕμ“¡°“√·π–π”¢Õß Sydney system26 ≈—°…≥–∑“ß°“¬¿“æ∑’Ë·¬°°—π¢Õß™‘Èπ ‡π◊ÈÕμ—«Õ¬à“ß∑’Ë‰¥â®“°∫√‘‡«≥ antrum ·≈– corpus ∂◊Õ«à“‡ªìπ®ÿ¥ ”§—≠¬‘Ëß‡π◊ËÕß®“° ¿“«– pseudopyloric metaplasia ®–¡’≈—°…≥–∑’Ë‡≈’¬π·∫∫§≈â“¬ (mimics) °—∫‡π◊ÈÕ‡¬◊ËÕ∫√‘‡«≥ antrum ¡“° À“°æ∫«à“¡’°“√μ‘¥‡™◊ÈÕ Helicobacter pylori §«√„Àâ°“√√—°…“∑ÿ°√“¬·≈– μ‘¥μ“¡°“√√—°…“‡æ◊ËÕ¬◊π¬—π«à“ “¡“√∂°”®—¥‡™◊ÈÕ‰¥â ”‡√Á®‚¥¬∑”°“√ àÕß°≈âÕß‡æ◊ËÕ biopsy ´È”À√◊Õ„™â«‘∏’°“√‡ªÉ“≈¡À“¬„®·≈–«—¥√–¥—∫¬Ÿ‡√’¬ (urea breath test) ¡’ ºâªÉ«¬À≈“¬√“¬æ∫«à“Ÿ hyperplastic polyps À“¬‰ªÀ√◊Õ≈¥®”π«π≈ß‰¥â27-28 ºâªÉ«¬Ÿ ∑’Ë¡’ OLGA √–¥—∫ 3 ·≈– 4 (stage III and IV) §«√®–¡’°“√ àÕß°≈âÕß‡æ◊ËÕ‡ΩÑ“ √–«—ß‚√§„π√–¬–¬“« (long term endoscopic surveillance) ‚¥¬√–¬–‡«≈“ ‡À¡“– ¡∑’Ë ÿ¥∑’Ë®–„™â‡æ◊ËÕ surveillance π—Èπ¬—ß‰¡à‡ªìπ∑’Ë∑√“∫·πà™—¥·≈–¬—ß‰¡à¡’ ·π«∑“ßªØ‘∫—μ‘·∫∫À≈—°∞“π‡™‘ßª√–®—°…å (evidence-base guidelines) Gastric Adenomas (Raised Intraepithelial Neoplasia) μ‘Ëß‡π◊ÈÕ°√–‡æ“–Õ“À“√™π‘¥∑’Ë‡ªìπ‡π◊ÈÕßÕ° (gastric neoplastic polyp) ∑’Ë æ∫∫àÕ¬∑’Ë ¥§◊Õ‡¬◊ËÕ∫ÿ º‘«∑’Ë¡’°“√‡®√‘≠Õ¬à“ßº‘¥ª°μ‘ÿ (epithelial dysplastic growth) ´÷Ëß¡—°‡√’¬°μ‘Ëß‡π◊ÈÕ™π‘¥π’È«à“ adenoma ‚¥¬Õß§å°“√Õπ“¡—¬‚≈° (World Health Or- ganization) ‰¥â¡’°“√®—¥μ—Èß™◊ËÕ„À¡à‡æ◊ËÕ„™â‡√’¬° (new nomenclature) §◊Õ raised intraepithelial neoplasia29-30 „π°≈à¡ª√–‡∑»Ωíòßμ–«—πμ°æ∫ÿ gastric adenoma ™π‘¥∑’Ë‡°‘¥‡π◊ËÕß¡“®“°°“√μ‘¥‡™◊ÈÕ Helicobacter pylori πâÕ¬¡“° ‚¥¬æ∫πâÕ¬°«à“ √âÕ¬≈– 1 ¢Õßμ‘Ëß‡π◊ÈÕ°√–‡æ“–Õ“À“√∑’Ëμ√«®æ∫∑—ÈßÀ¡¥ ´÷Ëß·μ°μà“ß®“°°≈ÿà¡ ª√–‡∑»„π·∂∫‡Õ‡™’¬μ–«—πÕÕ°∑’Ë®–æ∫Õÿ∫—μ‘°“√≥å (incidence) ¢Õß°“√‡°‘¥ gastric cancer ß·≈–æ∫Ÿ gastric adenoma ‰¥âª√–¡“≥Àπ÷Ëß„π ’Ë¢Õßμ‘Ëß‡π◊ÈÕ°√–‡æ“– Õ“À“√31-32 gastric adenoma “¡“√∂æ∫∑—Èß„π‡æ»™“¬·≈–À≠‘ß‰¥â‡∑à“°—π·≈–¡—° æ∫∫àÕ¬„π™à«ßÕ“¬ ÿ60-70 ªï ®“°°“√ àÕß°≈âÕß®–æ∫≈—°…≥–‡ªìπ≈Õπ§≈â“¬°”¡–À¬’Ë (velvety lobulated appearance) ·≈–¡—°æ∫‡ªìπμ‘Ëß‡¥’Ë¬« (solitary) (¿“æ∑’Ë 5)

42 ®ÿ≈ “√ ¡“§¡·æ∑¬å√–∫∫∑“ß‡¥‘πÕ“À“√·Ààßª√–‡∑»‰∑¬, æƒ…¿“§¡- ‘ßÀ“§¡ 2559 ·¡â«à“®– “¡“√∂æ∫‰¥â∑ÿ°∫√‘‡«≥¢Õß°√–‡æ“–Õ“À“√·μà¡—°æ∫∫àÕ¬∫√‘‡«≥ antrum °“√®”·π°§ÿ≥≈—°…≥– (features) ¢Õß gastric adenoma ‚¥¬„™â°≈âÕß∑’Ë¡’√–∫∫ NBI π—Èπ¬—ß‰¡à¡’°“√°”Àπ¥‡ªìπ∑’Ë™—¥‡®π3 Gastric adenoma ®–ª√–°Õ∫¥â«¬‡´≈≈å‡¬◊ËÕ∫ÿ∑’Ëº‘¥ª°μ‘ (dysplastic epithelial cells) ´÷Ëß‡°‘¥®“°°“√¡’ atrophy ·≈– intestinal metaplasia ‚¥¬¡—° ®–¡’§«“¡ —¡æ—π∏å°—∫°“√μ‘¥‡™◊ÈÕ Helicobacter pylori ·≈– “¡“√∂‡ª≈’Ë¬π·ª≈ß®“° dysplasia ‡ªìπ carcinoma ‰¥â‡™àπ‡¥’¬«°—∫„π≈”‰ â„À≠à (colon) À“°μ‘Ëß‡π◊ÈÕ¬‘Ëß ¡’¢π“¥„À≠à‡∑à“‰√°Á®–¡’§«“¡‡ªìπ‰ª‰¥â∑’Ë®–æ∫ foci ¢Õß°“√‡°‘¥‡ªìπ¡–‡√Áß (adenocarcinoma) ¡“°¢÷Èπ‡∑à“π—Èπ ¡–‡√Áß∑’Ë‡°‘¥¢÷Èπ„π™à«ß‡«≈“‡¥’¬«°—π (synchronous adenocarcinoma) πÕ°‡Àπ◊Õ®“°∫√‘‡«≥∑’Ëæ∫„π°√–‡æ“–Õ“À“√¡’√“¬ß“π«à“æ∫ ‰¥â∂÷ß√âÕ¬≈– 30 ¢ÕßºâªÉ«¬∑’Ë¡’Ÿ adenoma ·≈–¡’ foci ¢Õß adenocarcinoma √à«¡¥â«¬ ·π«»÷°…“∑“ß§≈‘π‘° Gastric adenoma ¡—°æ∫«à“‡°‘¥„πºŸâªÉ«¬∑’Ë¡’¿Ÿ¡‘À≈—ß‡ªìπ chronic atrophic gastritis ‡π◊ËÕß®“°μ‘Ëß‡π◊ÈÕ™π‘¥π’È∂◊Õ‡ªìπ√Õ¬‚√§π” (precursor lesion) „π

¿“æ∑’Ë 5 A: ≈—°…≥–¢Õß flat gastric adenoma √à«¡°—∫¡’ velvety appearance ∑’Ë∫√‘‡«≥ distal body ¢Õß°√–‡æ“–Õ“À“√ B: ≈—°…≥–¢Õß gastric adenoma ∑’Ëª√–°Õ∫¥â«¬ dysplastic columnar epithelium ·≈–¡’≈—°…≥–∑’Ë∫àß∫Õ°«à“¡“®“°°√–‡æ“–Õ“À“√§◊Õ®–æ∫ à«π¢Õß gastric tissue remnant (≈Ÿ°»√)

Management of Gastric Polyps 43 °“√‡°‘¥ gastric adenocarcinoma ¥—ßπ—Èπ§«√ª√–‡¡‘π§«“¡√ÿπ·√ß·≈–¢Õ∫‡¢μ °“√°√–®“¬ÕÕ°¢Õß atrophic gastritis ¥â«¬∑ÿ°§√—ÈßπÕ°‡Àπ◊Õ‰ª®“°°“√μ—¥ adenoma Õ¬à“ß ¡∫Ÿ√≥å °“√ biopsy √«¡∂÷ß°“√„™â OLGA À√◊Õ Operative Link on Gastritis/Intestinal Metaplasia Assessment staging systems „π°“√ ª√–‡¡‘π°Á “¡“√∂„™âÀ≈—°°“√‡¥’¬«°—∫„π hyperplastic polyp24-25 ºŸâªÉ«¬∑ÿ°√“¬∑’Ë ‰¥â√—∫°“√«‘π‘®©—¬«à“¡’ gastric adenoma §«√‰¥â√—∫°“√μ‘¥μ“¡‡æ◊ËÕ‡ΩÑ“√–«—ß‚√§ √«¡∑—ÈßÀ“°æ∫«à“¡’°“√μ‘¥‡™◊ÈÕ Helicobacter pylori §«√„Àâ°“√√—°…“√à«¡¥â«¬‡ ¡Õ Gastrointestinal Stromal Tumors Gastrointestinal stromal tumors (GISTs) ‡ªìπ‡π◊ÈÕßÕ°∑’Ë¡’°“√‡®√‘≠·∫àß μ—«®“° interstitial cells of Cajal ´÷Ëß “¡“√∂æ∫‰¥âμ≈Õ¥™à«ß¢Õß∑“ß‡¥‘πÕ“À“√ (digestive tract) ·μàæ∫‰¥âπâÕ¬„π™àÕß∑âÕß (abdomen) ·≈–Õÿâß‡™‘ß°√“π (pelvic cavity)33 ‚¥¬æ∫„π°√–‡æ“–Õ“À“√√âÕ¬≈– 40-60 GISTs ¡—°æ∫∫àÕ¬„π‡æ»™“¬ ·≈– “¡“√∂æ∫‰¥â∑ÿ°∫√‘‡«≥„π°√–‡æ“–Õ“À“√·μà à«π„À≠à®–æ∫∫√‘‡«≥ fundus34 ¬—ß‰¡à∑√“∫ªí®®—¬‡ ’Ë¬ß (predisposing factors) ∑’Ë™—¥‡®π ‡¬◊ËÕ∫ÿº‘«°√–‡æ“–Õ“À“√ ¢Õß°âÕπ‡π◊ÈÕßÕ° (tumors) Õ“®¡’≈—°…≥–ª°μ‘À√◊Õ¡’≈—°…≥–¢Õß°√–‡æ“–Õ“À“√ Õ—°‡ ∫™π‘¥„¥°Á‰¥â ‡ªìπ∑’Ëπà“ π„®«à“¡’√“¬ß“π°“√æ∫ microscopic GISTs ‰¥â ∫àÕ¬„π°√–‡æ“–Õ“À“√ à«π∫π¢Õß§π≠’ËªÉπ∑’Ë‰¥â√—∫°“√ºà“μ—¥°√–‡æ“–Õ“À“√‡π◊ËÕß®“°ÿ gastric cancer ·≈–°“√»÷°…“π’È∑”„Àâ§‘¥«à“ ®√‘ßÊ ·≈â«¡’‚Õ°“ ‰¡à∫àÕ¬π—°∑’Ë®–æ∫ GIST ¢π“¥„À≠à·≈– “¡“√∂∑’Ë®–æ—≤π“»—°¬¿“æ°≈“¬‡ªìπ¡–‡√Áß (malignant potential) ‰¥â35 ®“°°“√ àÕß°≈âÕß®–æ∫ GISTs ¡’≈—°…≥–‡ªìπ°âÕπ„μâ‡¬◊ËÕ∫ÿº‘« (submucosal lesion) ¡’¢Õ∫‡√’¬∫™—¥‡®π (well-cicumscribed) æ◊Èπº‘«‡¬◊ËÕ∫ÿ°√–‡æ“– Õ“À“√∑’ËÕ¬Ÿà‡Àπ◊Õ√Õ¬‚√§¡—°¡’≈—°…≥–ª°μ‘ (normal overlying gastric mucosa) ·μà°ÁÕ“®æ∫√Õ¬°—¥‡´“– (eroded) À√◊Õ·º≈μ√ß°≈“ß√Õ¬‚√§ (ulcerated center) ‰¥â (¿“æ∑’Ë 6) °“√ biopsy °âÕπ‡π◊ÈÕßÕ°™π‘¥π’È¡—°∑”‰¥â¬“°‡π◊ËÕß®“°‡¬◊ËÕ∫º‘«∑’Ëª°§≈ÿ ¡ÿ Õ¬à¡—°®–≈◊Ëπ‰À≈Ÿ (slide over) ‡Àπ◊Õ°âÕπ‡π◊ÈÕßÕ° ·≈–ª“°§’∫∑’Ë„™âμ—¥™‘Èπ‡π◊ÈÕ (biopsy

44 ®ÿ≈ “√ ¡“§¡·æ∑¬å√–∫∫∑“ß‡¥‘πÕ“À“√·Ààßª√–‡∑»‰∑¬, æƒ…¿“§¡- ‘ßÀ“§¡ 2559 ¿“æ∑’Ë 6 ¿“æ®“°°“√ Õß°≈à Õß· ¥ß„Àâ ‡Àâ πÁ GIST ´ß¡Ë÷ ≈’ °…≥–‡ª— πì ulcerated submucosal mass ∫√‘‡«≥ gastric body forceps) ¡—°®–®—∫‰¡à§àÕ¬∂Ÿ°™‘Èπ à«π‡π◊ÈÕ‡¬◊ËÕ∑’Ë‡À¡“– ¡¢Õß GIST ´÷Ëß∑”„Àâæ¬“∏‘ ·æ∑¬å¡—°√“¬ß“πº≈™‘Èπ‡π◊ÈÕ∑’Ëμ√«®æ∫«à“ª°μ‘ ¥—ßπ—Èπ°“√∑’Ë®–„Àâ‰¥â¡“´÷Ëß™‘Èπ‡π◊ÈÕ∑’Ë ‡À¡“– ¡μàÕ°“√«‘π‘®©—¬§◊ÕμâÕß∑”°“√Õ—≈μ√“´“«πå√à«¡°—∫°“√„™â‡¢Á¡¢π“¥‡≈Á°‡®“– ¥Ÿ¥ºà“π∑“ß°“√ àÕß°≈âÕß (endosonographic fine-needle aspiration) À√◊Õ°“√ „™â‡¢Á¡™π‘¥¡’ª≈Õ°‡æ◊ËÕμ—¥™‘Èπ‡π◊ÈÕ (tru-cut needle biopsy) „π·ßà‡π◊ÈÕ‡¬◊ËÕ«‘∑¬“ GISTs ®–ª√–°Õ∫‰ª¥â«¬°≈à¡‡´≈≈å√ÿ ª°√– «¬Ÿ (spindle cells) ´÷Ëß®–Õ¬Ÿà‡°“–°≈ÿà¡°—πÕ¬à“ß·πàπÀπ“ (dense aggregate) ‚¥¬‡√’¬ßμ—«‡ªìπ° ≈ÿà¡ (arranged in bundles) „π∑‘»∑“ß∑’Ë·μ°μà“ß°—π (different direction) (¿“æ∑’Ë 7) “¡“√∂·∫àß GISTs ‰¥â‡ªìπ 2 ™π‘¥§◊Õ·∫∫°√– «¬ (spindled) ·≈–·∫∫Õ‘æ‘∏‘≈Õ¬¥å (epitheloid) ‚¥¬·μà≈–™π‘¥®–¡’§ÿ≥≈—°…≥–∑“ß‡π◊ÈÕ‡¬◊ËÕ (histologic characteris- tics) ∑’Ë„™â∑”π“¬æƒμ‘°√√¡ (behavior) ‰¥â34 ·π«°“√»÷°…“∑“ß§≈‘π‘° GISTs ∑’Ë¢π“¥‡≈Á°°«à“ 1 ´¡. à«π„À≠à‰¡à¡’Õ“°“√·≈–¡—°μ√«®æ∫‚¥¬

Management of Gastric Polyps 45 ¿“æ∑’Ë 7 ¿“ææ¬“∏‘«‘∑¬“· ¥ß≈—°…≥– stroma ∑’Ëª√–°Õ∫¥â«¬°≈ÿà¡¢Õß spindle cells ´÷Ëßæ∫‰¥â„π GIST

∫—ß‡Õ‘≠√–À«à“ß∑”°“√ àÕß°≈âÕß∑“ß‡¥‘πÕ“À“√¥â«¬¢âÕ∫àß™’ÈÕ◊Ëπ ‡¡◊ËÕ GISTs ‚μ¢÷Èπ®– ‡ªìπ “‡Àμÿ∑”„Àâ¡’√Õ¬°—¥‡´“– (erosion) À√◊Õ·º≈ (ulcerartion) ∑’Ë∫√‘‡«≥æ◊Èπº‘« ‡¬◊ËÕ∫ÿÀ√◊Õ°¥‡∫’¬¥Õ«—¬«–¢â“ß‡§’¬ß‰¥â ·≈–À≈“¬§√—Èß°Áæ∫«à“‡ªìπ “‡Àμÿ¢Õß¿“«– ‡≈◊Õ¥ÕÕ°À√◊Õ¡’Õ“°“√ª«¥‰¥â ∑°§√—Èß∑’Ëμ√«®æ∫ÿ GISTs §«√®–§”π÷ß∂÷ß°“√¡’»—°¬¿“æ°“√‡ªìπ¡–‡√Áß (malignant potential) √à«¡¥â«¬‡ ¡Õ ‚¥¬æ∫«à“¡“°°«à“√âÕ¬≈– 50 ¢ÕßºŸâªÉ«¬∑’Ë¡“ æ∫·æ∑¬å§√—Èß·√°·≈–¡’ GISTs ∑’Ë¡’¢π“¥„À≠à (> 2 ´¡.) ¡—°Õ¬à„π√–¬–·æ√à°√–®“¬Ÿ (metastasis) ‡√’¬∫√âÕ¬·≈â« ‚¥¬μ”·Àπàß∑’Ëæ∫«à“¡’°“√·æ√à°√–®“¬‰¥â∫àÕ¬§◊Õμ—∫ „π∑“ßªØ‘∫—μ‘æ∫«à“¡’¿“«–∑’Ë —¡æ—π∏å°—π¥’ (good correlation) √–À«à“ß¢π“¥ (size), §«“¡ “¡“√∂„π°“√·∫àßμ—« (mitotic activity) ·≈–æƒμ‘°√√¡∑“ß§‘≈π‘° (clinical behavior) ¢Õß GISTs ¡’¢âÕ·π–π”„Àâºà“μ—¥ ”À√—∫°âÕπ∑’Ë¡’¢π“¥„À≠à‡°‘π 2 ´¡. ‚¥¬¢π“¥∑’Ë‡≈Á°°«à“Õ“®„™â«‘∏’°“√‡Õ“°âÕπÕÕ°∑—Èß°âÕπºà“π∑“ß°“√ àÕß°≈âÕß (endoscopic enucleation) ·≈–μ“¡¥â«¬°“√μ‘¥μ“¡‡æ◊ËÕ‡ΩÑ“√–«—ß‚√§ (surveillance)

46 ®ÿ≈ “√ ¡“§¡·æ∑¬å√–∫∫∑“ß‡¥‘πÕ“À“√·Ààßª√–‡∑»‰∑¬, æƒ…¿“§¡- ‘ßÀ“§¡ 2559 ¡’°“√„™â¬“°≈ÿà¡∑’Ë¬—∫¬—Èß‰∑‚√´’π‰§‡π (tyrosine kinase inhibitors) ‡æ◊ËÕ‡ªìπ °“√√—°…“·∫∫‡®“–®ß‡ªÑ“À¡“¬ (targeted therapy) „π√“¬∑’ËºŸâªÉ«¬¡’¿“«–°“√·æ√à °√–®“¬¢Õß‚√§·≈â«À√◊Õ‰¡à “¡“√∂∑”°“√ºà“μ—¥ (unresectable) °âÕπ GIST ÕÕ° ‰¥â36 ¡’°“√„™â¬“ tyrosine kinase inhibitor ¿“¬À≈—ß°“√ºà“μ—¥μ—«°âÕπ„π√“¬∑’Ë ‡ªìπ GISTs ∑’Ë¡’§«“¡‡ ’Ë¬ß ßŸ (high-risk GISTs) ‡æ◊ËÕ∑’Ë®–¬—∫¬—Èß°“√°≈—∫‡ªìπ´È” (recurrence) ·μà√–¬–‡«≈“„π°“√„Àâ¬“∑’Ë‡À¡“– ¡¬—ß‰¡à‡ªìπ∑’Ë°”Àπ¥™—¥‡®π37 °“√¬âÕ¡™‘Èπ‡π◊ÈÕ¥â«¬«‘∏’°“√∑“ßÕ‘¡¡Ÿ‚πæ¬“∏‘«‘∑¬“ (immunohistochemical stains) ∂◊Õ‡ªìπÀ—«„® ”§—≠„π°“√„™â«‘π‘®©—¬ GISTs ‚¥¬∂◊Õ‡Õ“°“√°≈“¬æ—π∏ÿå ¢Õß c-kit proto-oncogene ‡ªìπ°ÿ≠·® ”§—≠„π√–¥—∫‚¡‡≈°ÿ≈∑’Ë “¡“√∂®–μ√«® æ∫‰¥â®“°°“√¬âÕ¡æ‘‡»…π’È ·Õπμ’È∫Õ¥’È (antibody) ∑’Ë„™â„π°“√¬âÕ¡§◊Õ CD117 ´÷Ëß ®–¬âÕ¡μ‘¥ GISTs ‰¥âª√–¡“≥√âÕ¬≈– 95 ‚¥¬∑’Ë‡À≈◊ÕÕ’°√âÕ¬≈– 5 (¡—°‡ªìπ™π‘¥ epitheloid) „™â antibody ∑’Ë¬âÕ¡μ‘¥ GIST protein À√◊Õ platelet-derived growth factor alpha34 ‚¥¬À“°‰¡àæ∫«à“¡’°“√¬âÕ¡μ‘¥¢Õßμ—« antibody ¥—ß°≈à“«¢â“ßμâπ §«√®– ß —¬«à“Õ“®‡ªìπ‡π◊ÈÕßÕ°¢Õß°≈â“¡‡π◊ÈÕ‡√’¬∫ (leiomyoma) À√◊Õ‡π◊ÈÕßÕ°¢Õß √–∫∫ª√– “∑ (neuroma, schwannoma) ´÷Ëß§«√ àß¬âÕ¡ actin ·≈– S-100 ‡æ‘Ë¡ ‡μ‘¡ §à“∑’Ë„™â∑”π“¬æƒμ‘°√√¡¢Õß GIST ∑’Ëæ¬“∏‘·æ∑¬å§«√π”¡“„™âª√–‡¡‘π ª√–°Õ∫¥â«¬ ¢π“¥¢Õß°âÕπ‡π◊ÈÕßÕ° (tumor size) ·≈–§à“π—∫°“√·∫àßμ—« (mitotic count) ‚¥¬∑—Ë«‰ª‡√“ “¡“√∂∑’Ë®–∫Õ°‰¥â«à“¬‘Ëß¢π“¥¢Õß‡π◊ÈÕßÕ°‚μ¡“°·π«‚πâ¡∑’Ë ®–¡’‚Õ°“ ‡°‘¥ metastasis °Á¡“°¢÷Èπμ“¡‰ª¥â«¬ ¡’¢âÕ¡Ÿ≈∫àß™’È«à“ GIST ∑’Ë¡’¢π“¥ ‡≈Á°°«à“ 2.5 ´¡.®–æ∫ metastasis √âÕ¬≈– 15 ·≈–‡æ‘Ë¡¢÷Èπ‡ªìπ√âÕ¬≈– 80 „π°≈ÿà¡ ∑’Ë¡’¢π“¥‡°‘π 6 ´¡.34 ¡’°“√»÷°…“æ∫«à“°“√¡’§à“ mitotic count ∑’Ë Ÿß®– —¡æ—π∏å °—∫°“√Õ¬Ÿà√Õ¥ (survival) ∑’Ë≈¥≈ß Õ¬à“ß‰√°Á¥’°“√√“¬ß“π§à“ mitotic count ·∫∫ ¥—Èß‡¥‘¡´÷Ëß®–√“¬ß“π‡ªìπ®”π«πμàÕÀπà«¬æ◊Èπ∑’Ë°”≈—ß¢¬“¬¢π“¥ ßŸ (per high-power field) π—Èπæ∫«à“¬—ß‰¡à¡’§«“¡∂Ÿ°μâÕß‡æ’¬ßæÕ·≈–¬—ß‰¡à‡ªìπ¡“μ√∞“π ¡’‡æ’¬ß§à“ mitotic count ∑’Ë Ÿß (‡™àπ >5 mitoses/50 high-power field) √à«¡°—∫¢âÕ¡Ÿ≈∑’Ë‰¥â ®“°μ”·Àπàß∑’Ë∂Ÿ°μâÕß (precise area) ®“° high-power field (´÷Ëß®–¡’§«“¡

Management of Gastric Polyps 47 º—π·ª√·μ°μà“ß°—π‰¥âª√–¡“≥ 3 ‡∑à“®“°Õÿª°√≥å°≈âÕß·μà≈–™π‘¥∑’Ë„™â) ∑’ËæÕ®– “¡“√∂π”¡“„™âª√–‡¡‘π‡°’Ë¬«°—∫°“√æ¬“°√≥å‚√§ (prognostic assessment) ‰¥â38 ¥—ßπ—Èπ‡¡◊ËÕ„¥∑’Ë·æ∑¬åºŸâ„Àâ°“√√—°…“‰¥â√—∫√“¬ß“πæ∫§à“ mitotic count ∑’Ë Ÿß„π√Õ¬ ‚√§ GIST ·æ∑¬å§«√∑”°“√·ª≈º≈¥â«¬§«“¡√–¡—¥√–«—ß·≈–§«√μ—Èß§”∂“¡„π„® ‡ ¡Õ«à“æ¬“∏‘·æ∑¬å‰¥â„™â«‘∏’°“√„¥„π°“√„Àâ‰¥â¡“´÷Ëß§”μÕ∫π—Èπ Inflammatory Fibroid Polyps Inflammatory fibroid polyps (À√◊Õ‡√’¬°Õ’°™◊ËÕ«à“ Vanek tumors) ∂◊Õ ‡ªìπμ‘Ëß‡π◊ÈÕ™π‘¥∑’Ë¡’‚Õ°“ æ∫‰¥âπâÕ¬¡“° ‚¥¬æ∫πâÕ¬°«à“√âÕ¬≈– 0.1 ®“°®”π«π μ‘Ëß‡π◊ÈÕ°√–‡æ“–Õ“À“√∑’Ëμ√«®æ∫∑—ÈßÀ¡¥39 ®“°°“√ àÕß°≈âÕß®–æ∫μ‘Ëß‡π◊ÈÕ¡’≈—°…≥– ·¢Áß (firm) ‡ªìπμ‘Ëß‡¥’Ë¬« (solitary) ¡’°â“πÀ√◊Õ‰¡à¡’°â“π°Á‰¥â (pedunculated or sessile) ·≈–¡—°®–æ∫·º≈ (ulcerated) ‰¥â∫àÕ¬ (¿“æ∑’Ë 8) §≥≈—°…≥–∑“ß‡π◊ÈÕ‡¬◊ËÕ«‘∑¬“¢Õßÿ μ‘Ëß‡π◊ÈÕ™π‘¥π’È®–¡’≈—°…≥–‡¥àπ§◊Õ ª√–°Õ∫¥â«¬°“√‡æ‘Ë¡®”π«πÕ¬à“ß√«¥‡√Á«¢Õß ‡´≈≈å√Ÿª°√– «¬ (spindle cells) À≈Õ¥‡≈◊Õ¥¢π“¥‡≈Á° (small vessels) ·≈–°“√ ·∑√°´÷¡¢Õß°“√Õ—°‡ ∫ (inflammatory infiltrate) ¥â«¬‡¡Á¥‡≈◊Õ¥¢“«™π‘¥Õ’‚Õ´‘‚πøî≈

¿“æ∑’Ë 8 A: ≈—°…≥–¢Õß inflammatory fibroid polyp ∑’Ëμ√«®æ∫®“°°“√ àÕß°≈âÕß∫√‘‡«≥ antrum ‚¥¬¡’≈—°…≥–‡ªìπ well-circumscribed submucosal lesion B: ≈—°…≥–∑“ß‡π◊ÈÕ‡¬◊ËÕ«‘∑¬“ ¡’≈—°…≥–·∫π√“∫ (flattend) √Õ¬°—¥‡´“– (eroded) ·≈– gastric epithelium ª√–°Õ∫ ¥â«¬ fibrous tissue Àπ“·πàπ√à«¡°—∫¡’ inflammatory cells C: À≈Õ¥‡≈◊Õ¥ (vessels) ∂Ÿ°≈âÕ¡√Õ∫¥â«¬ fibroblasts ·≈– stroma ∑’Ë®–æ∫√à«¡°—∫ eosinophils

48 ®ÿ≈ “√ ¡“§¡·æ∑¬å√–∫∫∑“ß‡¥‘πÕ“À“√·Ààßª√–‡∑»‰∑¬, æƒ…¿“§¡- ‘ßÀ“§¡ 2559 (eosinophils) Õ¬à“ß‡¥àπ™—¥„μâ‡¬◊ËÕ∫ÿº‘« ¥â«¬‡Àμÿ¥—ß°≈à“«μ‘Ëß‡π◊ÈÕ‡À≈à“π’È∫“ß§√—Èß®– ∂Ÿ°‡√’¬°Õ’°™◊ËÕÀπ÷Ëß«à“ eosinophilic granuloma æ¬“∏‘°”‡π‘¥ (pathogenesis) π—Èπ¬—ß‰¡à∑√“∫‡ªìπ∑’Ë·πà™—¥ À“°¬âÕ¡¥â«¬«‘∏’°“√∑“ßÕ‘¡¡Ÿ‚πæ¬“∏‘«‘∑¬“®–æ∫«à“ μ‘Ëß‡π◊ÈÕ‡À≈à“¡’‡´≈≈å‡¥Áπ‰¥√μ‘° (dendriticcell) ‡ªìπ·À≈àß°”‡π‘¥40 ¡’√“¬ß“πæ∫«à“ √âÕ¬≈– 70 ¢Õß inflammatory fibroid polyps ∑’Ëμ√«®æ∫®–¡’ gain-of-function mutation „π∫√‘‡«≥¢Õß platelet-derived growth factor receptor alpha polypeptide gene ´÷Ëß¡’§«“¡§≈â“¬§≈÷ß°—∫ GIST ™π‘¥∑’Ëμ√«®‰¡àæ∫ CD117 (CD117 negative) ®÷ß‡ªìπ à«π∑’Ë∑”„Àâ§‘¥«à“πà“®–¡’§«“¡‡ªìπ‰ª‰¥â∑’Ë®–∑”„Àâ‡°‘¥°√–∫«π °“√°“√°≈“¬‡ªìπ‡π◊ÈÕßÕ° (neoplastic process) ‰¥â41 ·π«»÷°…“∑“ß§≈‘π‘° Inflammatory fibroid polyps à«π„À≠à¡—°‰¡à¡’Õ“°“√ (asymptomatic) ·μà¢π“¥∑’Ë„À≠à “¡“√∂∑”„Àâ‡°‘¥Õ“°“√ª«¥∑âÕß (abdominal pain) Õ“°“√Õ‘Ë¡‡√Á« (early satiety) ‚≈À‘μ®“ß (anemia) ·≈–°√–‡æ“–Õ“À“√ à«πª≈“¬Õÿ¥μ—π (gastric outlet obstruction) ‰¥â42 ≈—°…≥–∑’Ëμ√«®æ∫®“°°“√μ√«®Õ—≈μ√“´“«¥åºà“π∑“ß°“√ àÕß°≈âÕß®–æ∫≈—°…≥–¢Õ∫‡¢μ∑’Ë‰¡à™—¥ (indistinct margin) √Õ¬‚√§¥Ÿ‡ªìπ‡π◊ÈÕ ‡¥’¬«°—π·≈–„Àâ ’¥” (hypoechoic homogeneous lesion) ·≈–®–Õ¬Ÿà„π™—Èπ∑’Ë Õß À√◊Õ “¡ (second or third layer) ‚¥¬∑’Ë™—Èπ∑’Ë ’Ë®–æ∫«à“Õ¬Ÿà„π ¿“æ∑’Ë ¡∫Ÿ√≥å¥’ (in- tact fourth layer) ´÷Ëß®–¡’ª√–‚¬™πå„π°“√π”¡“„™â™à«¬«‘π‘®©—¬43-44 Gastric Neuroendocrine Tumors (Carcinoids) Carcinoids ‡ªìπ‡π◊ÈÕßÕ°μàÕ¡‰√â∑àÕ (neuroendocrine tumors) ∑’Ë¡“®“° ‡´≈≈å enterochromaffin-like (ECL cell)45 °“√®—¥·∫àß™π‘¥¢ÕßÕß§å°“√Õπ“¡—¬ ‚≈°§√—Èß≈à“ ÿ¥ (æ.». 2553) ‰¥â¡’°“√¬°‡≈‘°„™â§”«à“ carcinoid ‡π◊ËÕß®“°§”«à“ neuroendocrine tumor ¥¡’§«“¡‡À¡“– ¡¡“°°«à“Ÿ 46 ¡’°“√»÷°…“æ∫«à“ neuroendocrine tumors ¢Õß°√–‡æ“–Õ“À“√æ∫‰¥âπâÕ¬°«à“√âÕ¬≈– 2 ®“°®”π«π√Õ¬‚√§∑’Ë¡’ ≈—°…≥–§≈â“¬μ‘Ëß‡π◊ÈÕ (polypoid lesions) ∑’Ëμ√«®æ∫∑—ÈßÀ¡¥

Management of Gastric Polyps 49 Gastric neuroendocrine tumors ·∫àßÀ≈—°Ê ÕÕ°‡ªìπ 3 ™π‘¥ ‰¥â·°à 1. ™π‘¥∑’Ë 1 (type I) æ∫‰¥â√âÕ¬≈– 70-80 ®“°®”π«π¢Õß¡–‡√ÁßμàÕ¡‰√â ∑àÕ¢Õß°√–‡æ“–Õ“À“√∑’Ëμ√«®æ∫‰¥â ¡—°¡’§«“¡ —¡æ—π∏å°—∫°“√¡’·°ä μ√‘π„π‡≈◊Õ¥∑’Ë ßŸ (hypergastrinemia) ´÷Ëß‡ªìπº≈¡“®“° autoimmune atrophic gastritis ·≈– æ∫∫àÕ¬„π§π ŸßÕ“¬ÿ ·≈–¡—° —¡æ—π∏å°—∫¿“«–‚≈À‘μ®“ß‡æÕ√åπ‘‡™’¬ (pernicious anemia)47-48 ‡π◊ÈÕßÕ° (¿“æ∑’Ë 9) ‡À≈à“π’È®–¡’¢π“¥‡≈Á° (< 1 ´¡.) Õ¬à®”°—¥„π∫√‘‡«≥Ÿ ¢Õß‡¬◊ËÕ∫ÿÕÁÕ°´‘πμ‘° (oxyntic mucosa) ·≈–¡’·π«‚πâ¡æ∫®”π«π¡“°°«à“Àπ÷Ëß (multiple) ·≈–¡—°æ∫√à«¡°—∫ multifocal ECL cell hyperplasia à«π„À≠à‡π◊ÈÕ ßÕ°π’È¡—°æ∫‚¥¬∫—ß‡Õ‘≠·≈–∫àÕ¬§√—Èßæ∫‰¥â®“°°“√ àÕß°≈âÕß∑“ß‡¥‘πÕ“À“√ à«π∫π ‡æ◊ËÕÀ“ “‡Àμÿ¢Õß‚≈À‘μ®“ß „π∑“ß‡π◊ÈÕ‡¬◊ËÕ«‘∑¬“®–ª√–°Õ∫¥â«¬°≈ÿà¡¢Õß‡´≈≈åμàÕ¡ ‰√â∑àÕ (nest of endocrine cells) ·≈–¡’¥—™π’°“√·∫àßμ—«∑’ËμË”¡“° (very low prolif-

¿“æ∑’Ë 9 A: ≈°…≥–¢Õß— gastric carcinoid ∑¡Ë’ ’ surface ulceration ∫√‡«≥‘ distal body ¢Õß°√–‡æ“– Õ“À“√ B: · ¥ß°“√√«¡‡¢â“¥â«¬°—π¢Õß ECL cells ´÷Ëß®–Õ¬Ÿà‡√’¬ßμ—«„π™—Èπ∑’Ë≈÷°¢Õß carcinoid tumor C: ≈—°…≥–¢Õß‡´≈≈å neuroendocrine ´÷Ëß¬âÕ¡μ‘¥ ’‰´·πæ‚μ‰ø´‘π (synaptophysin)

50 ®ÿ≈ “√ ¡“§¡·æ∑¬å√–∫∫∑“ß‡¥‘πÕ“À“√·Ààßª√–‡∑»‰∑¬, æƒ…¿“§¡- ‘ßÀ“§¡ 2559 eration index) 2. ™π‘¥∑’Ë 2 (type II) æ∫«à“¡’§«“¡ —¡æ—π∏å°—∫¿“«– hypergastrinemia ´÷Ëß‡°‘¥®“° gastrin ∑’ËÀ≈—Ëß¡“®“°‡π◊ÈÕßÕ° à«π„À≠à¡—°μ√«®æ∫„πºŸâªÉ«¬∑’Ë‰¥â√—∫ °“√ ß —¬·≈–μâÕß°“√ ◊∫§âπ«à“¡’°≈ÿà¡Õ“°“√ MEN-1 (MEN-1 syndrome) À√◊Õ °≈à¡Õ“°“√‚´≈≈‘ß‡®Õ√å-‡Õ≈≈‘ —πÿ (Zollinger-Ellison syndrome) À√◊Õ‰¡à49 ´÷Ëß°≈à¡ÿ Õ“°“√¥—ß°≈à“«¡—°¡’°âÕπ‡π◊ÈÕßÕ°∑’Ë¡’¢π“¥‡≈Á° (<1 ´¡.) ·≈–‰¡àæ∫≈—°…≥–¢Õß°“√ ·∑√°´÷¡ (infiltrating) À√◊Õ pleomorphic features „πºâªÉ«¬∑’Ë¡’°≈Ÿ à¡Õ“°“√ÿ MEN- 1 ®–æ∫‡¬◊ËÕ∫ÿ°√–‡æ“–Õ“À“√¡’≈—°…≥–ª°μ‘À√◊Õ°“√Õ—°‡ ∫‰¥â‡≈Á°πâÕ¬ ·μà®–‰¡àæ∫ °“√ΩÉÕ‡À’Ë¬«¢Õß‡¬◊ËÕ∫ÿ∫√‘‡«≥°√–æÿâß¢Õß°√–‡æ“–Õ“À“√ (fundic mucosa) „π ºâªÉ«¬∑’Ë¡’°≈Ÿ à¡Õ“°“√‚´≈≈‘ß‡®Õ√å-‡Õ≈≈‘ —π¡—°®–æ∫«à“¡’°“√¢¬“¬¢π“¥¢Õß‡´≈≈åÿ (hy- pertrophy) √à«¡°—∫¡’°“√‡°“–°≈ÿà¡°—πÕ¬à“ß·πàπÀπ“¢ÕßμàÕ¡ÕÁÕ°´‘πμ‘° (oxyntic gland) ·≈–‰¡àæ∫°“√Õ—°‡ ∫∑’Ë™—¥‡®π ‡π◊ÈÕßÕ°™π‘¥π’È∂◊Õ«à“‡ªìπ™π‘¥∑’Ëæ∫‰¥âπâÕ¬∑’Ë ¥ÿ ‚¥¬æ∫‡æ’¬ß√âÕ¬≈– 5-8 ¢Õß‡π◊ÈÕßÕ°μàÕ¡‰√â∑àÕ¢Õß°√–‡æ“–Õ“À“√50 3. ™π‘¥∑’Ë 3 (type III) ‰¡àæ∫«à“¡’§«“¡ —¡æ—π∏å°—∫ hypergastrinemia ·≈–¡—°æ∫‡ªìπ°âÕπ‡¥’Ë¬« ‚¥¬ “¡“√∂æ∫‰¥â„π∫√‘‡«≥‡¬◊ËÕ∫ÿ°√–‡æ“–Õ“À“√¢Õß§π ª°μ‘·≈–‰¡àæ∫ ECL cell hyperplasia ®–æ∫‡π◊ÈÕßÕ°™π‘¥π’Èª√–¡“≥√âÕ¬≈– 20 ¢Õß‡π◊ÈÕßÕ°μàÕ¡‰√â∑àÕ¢Õß°√–‡æ“–Õ“À“√ à«π„À≠à®–μ√«®æ∫‡¡◊ËÕºâªÉ«¬¡’Õ“°“√·≈â«Ÿ ‚¥¬‡°‘¥®“°°“√∑’Ë¡’°“√°—¥‡´“–¢Õß‡¬◊ËÕ∫ ÿ(mucosal erosion) ·≈–°“√‡ ’¬‡≈◊Õ¥ (blood loss) À√◊Õ°“√·æ√à°√–®“¬ (metastasis) ´÷Ëß¡—°®–æ∫Õ“°“√¥—ß°≈à“«‡¡◊ËÕ°âÕπ‡π◊ÈÕ ßÕ°¡’¢π“¥„À≠à‡°‘π 1.5 ´¡. ·≈–¡’√ª·∫∫°“√‡®√‘≠·∑√°´÷¡Ÿ (infiltrating growth pattern) √à«¡°—∫æ∫æ◊Èπ∑’Ë¢Õß‡π◊ÈÕμ“¬ (area of necrosis) ·≈–¡’√–¥—∫¢Õß pleo- morphism ∑’ËÀ≈“°À≈“¬ ¥—™π’°“√·∫àßμ—«®– Ÿß¡“° (high proliferation index) æ∫«à“‡π◊ÈÕßÕ°™π‘¥π’È¡’°“√æ¬“°√≥å‚√§‰¡à¥’ (poor prognosis) ‚¥¬¡’°“√Õ¬à√Õ¥‡©≈’Ë¬Ÿ (mean survival) ∑’Ë 28 ‡¥◊Õπ51 ·π«»÷°…“∑“ß§≈‘π‘° ‡π◊ÈÕßÕ°™π‘¥∑’Ë 1 ·≈– 2 ¡—°®– “¡“√∂μ—¥∑‘Èßºà“π∑“ß°“√ àÕß°≈âÕß‰¥â „π

Management of Gastric Polyps 51 ºŸâªÉ«¬∫“ß√“¬∑’Ëæ∫¡’‡π◊ÈÕßÕ°®”π«π¡“°·≈–¡’°“√°≈—∫‡ªìπ´È”¢Õß‡π◊ÈÕßÕ°™π‘¥∑’Ë 1 °“√∑”°“√ºà“μ—¥°√–‡æ“–Õ“À“√ à«π antrum (antral resection) ®—¥‡ªìπ∑“ß‡≈◊Õ° ∑’Ë‡À¡“– ¡ °“√∑” antrectomy ®–∑”„Àâ®”π«π°âÕπ‡π◊ÈÕ∑’Ëº≈‘μ·°ä μ√‘π (gastrin- producing mass) ≈¥≈ß ®÷ß‡ªìπ°“√°”®—¥ ‘Ëß°√–μâπÿ (stimulus) ∑’Ë®–∑”„Àâ‡°‘¥ECL cell proliferation52 ·π«∑“ß°“√√—°…“„À¡àÊ Õ“∑‘ °“√„™â¬“μâ“πμ—«√—∫·°ä μ√‘π (gastrin receptor antagonist: netazepide) °”≈—ßÕ¬Ÿà„π™à«ß°“√§âπ§«â“«‘®—¬·≈–Õ“® ∂◊Õ‡ªìπ·π«∑“ß°“√√—°…“„À¡à„πºâªÉ«¬∑’Ë¡’‡π◊ÈÕßÕ°μàÕ¡‰√â∑àÕ¢Õß°√–‡æ“–Õ“À“√™π‘¥∑’ËŸ 1 (type 1 gastric carcinoids) ‰¥â53 ºŸâªÉ«¬∑’Ë‡ªìπ‡π◊ÈÕßÕ°™π‘¥∑’Ë 3 (type III) Õ“® ¡’Õ“°“√¢Õß‚≈À‘μ®“ß ª«¥∫√‘‡«≥≈‘Èπªïò À√◊Õ¡’Õ“°“√·≈–Õ“°“√· ¥ß¢Õß°“√·æ√à °√–®“¬¢Õß‡π◊ÈÕßÕ° (metastasis) ´÷Ëß‡ªìπÕ“°“√∑’Ëæ∫‰¥âπâÕ¬¡“° ‚¥¬®–¡’≈—°…≥– Õ“°“√∑’Ëμ√«®æ∫‰¥â§◊Õ º‘«Àπ—ß·¥ß (cutaneous flushing) ∑âÕß‡ ’¬ ¿“«– À≈Õ¥≈¡‡°√Áßμ—« (bronchospasm) ·≈–√Õ¬‚√§∑’Ë≈‘ÈπÀ—«„® (cardiac valvular lesions) ∑“ß‡≈◊Õ°„π°“√√—°…“§◊Õ°“√ºà“μ—¥·≈â«μ“¡¥â«¬°“√„Àâ‡§¡’∫”∫—¥ «‘∏’∑’Ë¥’∑’Ë ÿ¥∑’Ë„™â„π°“√«‘π‘®©—¬ neuroendocrine tumor §◊Õ°“√¬âÕ¡ ’ ∑“ßÕ‘¡¡Ÿ‚πæ¬“∏‘«‘∑¬“ ´÷Ëß®–¬âÕ¡μ‘¥ ’¢Õß‰´·πæ‚μ‰ø´‘π (synaptophysin) ‚§√‚¡·°√π‘π‡Õ (chromogranin A) À√◊Õ´’¥’ 56 (CD56) ‚¥¬°“√¬âÕ¡μ‘¥ ’¥—ß°≈à“« ¢â“ßμâπ®–‡ªìπμ—«∫àß™’È≈—°…≥–¢Õß neuroendocrine (neuroendocrine marker) ‰¥â ·π«°“√«‡§√“–À‘ μå ß‡πË‘ Õ°√–‡æ“–Õ“À“√∑È◊ æ∫®“°°“√ Ë’ Õß°≈à Õßâ (Approach to Gastric Polyps Found at Endoscopy) ‡π◊ËÕß®“°μ‘Ëß‡π◊ÈÕ à«π„À≠à¡—°®–∂°μ√«®æ∫‚¥¬∫—ß‡Õ‘≠¢≥–∑”°“√ àÕß°≈âÕßŸ ∑“ß‡¥‘πÕ“À“√ à«π∫π ®÷ß‡ªìπ ‘Ëß®”‡ªìπ∑’Ë·æ∑¬åºŸâ∑”°“√ àÕß°≈âÕß (endoscopist) §«√®–»÷°…“·≈–‡°Á∫¢âÕ¡Ÿ≈√“¬≈–‡Õ’¬¥„Àâ‰¥â¡“°∑’Ë ÿ¥¢≥–∑”°“√ àÕß°≈âÕß‡æ◊ËÕ∑’Ë®– ‰¥âπ”¢âÕ¡Ÿ≈¡“™à«¬‡ªìπ·π«∑“ß„π°“√∫√‘À“√®—¥°“√°—∫μ‘Ëß‡π◊ÈÕ„πÕπ“§μ‰¥â À“°≈—°…≥–¢Õßμ‘Ëß‡π◊ÈÕ∑”„Àâ§‘¥∂÷ß fundic gland polyps °Á§«√∑” biopsy ∑’Ëμ‘Ëß‡π◊ÈÕπ—ÈπÊ À√◊Õμ‘Ëß‡π◊ÈÕ∫√‘‡«≥Õ◊ËπÊ √à«¡¥â«¬ ‚¥¬¢π“¥∑’Ë„À≠à‡°‘π 1 ´¡.§«√®–∑”°“√μ—¥∑‘Èß„Àâ ¡∫Ÿ√≥å ‚¥¬§«√„Àâ§«“¡ π„®°—∫ fundic gland polyp

52 ®ÿ≈ “√ ¡“§¡·æ∑¬å√–∫∫∑“ß‡¥‘πÕ“À“√·Ààßª√–‡∑»‰∑¬, æƒ…¿“§¡- ‘ßÀ“§¡ 2559 ∑’Ë¡’≈—°…≥–√Õ¬‚√§º‘¥·º°®“°ª°μ‘ (atypical-looking lesions) À“°μ√«®æ∫°Á §«√®–∑”°“√ biopsy ‡æ◊ËÕμ√«® Õ∫‡æ‘Ë¡‡μ‘¡‡ ¡Õ À“°≈—°…≥–∑’Ëæ∫‰¡à‡¢â“°—∫ fundic gland polyps ·æ∑¬åºâ àÕß°≈âÕß§«√æ‘®“√≥“∑”°“√μ—¥μ‘Ëß‡π◊ÈÕ∑’Ë¡’¢π“¥„À≠àŸ >1 ´¡.ÕÕ°∑—ÈßÀ¡¥ À“°‰¡à “¡“√∂∑”‰¥âÕ¬à“ßπâÕ¬°Á§«√∑”°“√μ—¥‡°Á∫™‘Èπ‡π◊ÈÕμ—«Õ¬à“ß àßμ√«®‡ ¡Õ„π°√≥’¢Õßμ‘Ëß‡π◊ÈÕ¢π“¥„À≠àÀ≈—ß®“°∑’Ë∑√“∫º≈°“√«‘π‘®©—¬∑“ßæ¬“∏‘ ‡π◊ÈÕ‡¬◊ËÕ (histopathlogic diagnosis) ·≈â« §«√æ‘®“√≥“μàÕ„π‡√◊ËÕß°“√√—°…“«à“ ®”‡ªìπ∑’Ë®–μâÕßμ—¥μ‘Ëß‡π◊ÈÕÕÕ° (polypectomy) À√◊Õ‰¡à ·≈–À“°μâÕß∑”§«√∑”„π √Ÿª·∫∫„¥√–À«à“ß∑”¥â«¬«‘∏’°“√ àÕß°≈âÕßÀ√◊Õ„™â«‘∏’ºà“μ—¥ ‚¥¬¡’ªí®®—¬∑’Ë “¡“√∂π” ¡“„™â™à«¬„π°“√μ—¥ ‘π„®§◊Õ (1) §«“¡‡ ’Ë¬ß„π‡√◊ËÕß‚Õ°“ ∑’Ë®–‡°‘¥§«“¡º‘¥æ≈“¥ ¥â“πæ¬“∏‘«‘∑¬“„π°√≥’μ‘Ëß‡π◊ÈÕ¢π“¥„À≠à55 (2) μ‘Ëß‡π◊ÈÕ∑”„Àâ‡°‘¥Õ“°“√À√◊Õ‰¡à (3) ¿“«–¢ÕßºŸâªÉ«¬·≈– ÿ¢¿“æ‚¥¬√«¡ ·≈– (4) §«“¡™”π“≠¢Õß·æ∑¬å À“° ·æ∑¬åºŸâ àÕß°≈âÕß à«π„À≠à¬—ß‰¡à¡’ª√– ∫°“√≥å‡æ’¬ßæÕ„π°“√μ—¥μ‘Ëß‡π◊ÈÕ∑’Ë¡’¢π“¥ „À≠à¡“° √«¡∑—Èß¡’§«“¡°—ß«≈μàÕ¿“«–·∑√°´âÕπ∑’ËÕ“®‡°‘¥¢÷Èπ‡π◊ËÕß®“°√Õ¬‚√§∑’Ë¡’ ¢π“¥„À≠à∑—ÈßÀ≈“¬ à«π„À≠à¡’À≈Õ¥‡≈◊Õ¥¡“‡≈’È¬ß¡“°·≈–¡’·π«‚πâ¡‡°‘¥‡≈◊Õ¥ÕÕ° Ÿß‚¥¬‡©æ“–°≈ÿà¡ inflammatory fibroid polyps, carcinoids ·≈– GISTs ∫“ß §√—Èß°≈ÿà¡∑’Ë‡ªìπ°âÕπ„μâ‡¬◊ËÕ∫ÿ°Á¡’‚Õ°“ ‡ ’Ë¬ßμàÕ°“√·μ°∑–≈ÿ (perforation) ‰¥â °“√ ∑”°“√μ—¥™‘Èπ‡π◊ÈÕ°àÕπ°Á∂◊Õ‡ªìπ ‘Ëß∑’Ë‡À¡“– ¡‡π◊ËÕß®“° “¡“√∂∑’Ë®–∑”„Àâ·æ∑¬å¡’ ‡«≈“«“ß·ºπ°“√√—°…“∑’Ë‡À¡“– ¡À≈—ß∑√“∫º≈°“√«‘π‘®©—¬∑“ßæ¬“∏‘√«¡∑—Èß‰¥âæŸ¥ §ÿ¬·≈–„Àâ§”ª√÷°…“„π‡√◊ËÕß√Õ¬‚√§∑’Ëæ∫°—∫ºŸâªÉ«¬·≈â« °“√μ‘¥μ“¡Õ“°“√ (Follow-Up Evaluation) ªí®®∫—π¬—ß‰¡à¡’·π«∑“ßªØ‘∫—μ‘∑’Ë‡ªìπ‡™‘ßÀ≈—°∞“πª√–®—°…åÿ (evidence-based guideline) Õ¬à“ß‰√°Á¥’°“√ àÕß°≈âÕß‡æ◊ËÕ‡ΩÑ“√–«—ß‚√§ (surveillance) „πμ‘Ëß‡π◊ÈÕ∑’Ë‰¡à„™à fundic gland polyps ¿“¬„π√–¬–‡«≈“ 1 ªï∂◊Õ«à“πà“®–‡ªìπ·π«ªØ‘∫—μ‘∑’Ëπà“®– „™â‰¥â‡æ◊ËÕ∑’Ë®–ª√–‡¡‘π«à“¡’°“√‡°‘¥¢÷Èπ´È” (recurrence) ¢Õß√Õ¬‚√§À√◊Õ¡’μ‘Ëß‡π◊ÈÕ „À¡à‡°‘¥¢÷ÈπÀ√◊Õ‰¡à °“√μ‘¥μ“¡Õ“°“√À≈—ß∑”°“√μ—¥μ‘Ëß‡π◊ÈÕ‰ª·≈â«‚¥¬‡©æ“–°≈à¡∑’Ë‡ªìπÿ high-grade dysplasia À√◊Õ¡–‡√Áß√–¬–·√° (early cancer) §«√æ‘®“√≥“

Management of Gastric Polyps 53 ·π«∑“ß‡ªìπ√“¬Ê‰ª ‚¥¬Õ¬à“ßπâÕ¬§«√¡’°“√μ‘¥μ“¡„π™à«ß 2-3 ªï·√°·≈–„™â™à«ß √–¬–‡«≈“∑’Ë —Èπ (short duration) ‡™àπ 6 ‡¥◊Õπ ‡ªìπμâπ °≈ÿà¡ gastric carcinoids §«√¡’°“√ àÕß°≈âÕß‡æ◊ËÕμ‘¥μ“¡Õ“°“√∑ÿ° 1-2 ªï

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Management of Gastric Polyps 59 Review Article Recurrent Pyogenic Cholangitis °π°æ®πå ®âπ∑√å¿‘«—≤πå ‡©≈‘¡√—∞ ∫—≠™√‡∑«°ÿ≈

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∫∑π” Recurrent Pyogenic Cholangitis (RPC) ‡ªìπ‚√§∑’Ë¡’≈—°…≥– ”§—≠ §◊Õ‡°‘¥π‘Ë«„π∑àÕπÈ”¥’¿“¬„πμ—∫ ∑”„Àâ‡°‘¥°“√Õ—°‡ ∫‡√◊ÈÕ√—ß®π‡°‘¥°“√μ’∫μ—π¢Õß √–∫∫∑àÕ∑“ß‡¥‘ππÈ”¥’ √à«¡°—∫Õ“®¡’°“√Õ—°‡ ∫¢Õß∑àÕπÈ”¥’®“°‡™◊ÈÕ·∫§∑’‡√’¬‡ªìπÊÀ“¬Ê ´÷Ëß‡ªìπ “‡Àμÿ¢Õß‚√§μ—∫‡√◊ÈÕ√—ß·≈–‚√§¡–‡√Áß¢Õß∑àÕπÈ”¥’ ‚√§π’È¡’°“√√“¬ß“π§√—Èß ·√°„πªï §.».1930 ‚¥¬ Digby1 „π§π‡™◊ÈÕ “¬®’π μàÕ¡“ Cook2 ·≈–§≥–‡√‘Ë¡ ‡√’¬°‚√§π’È«à“ RPC „πªï §.».1950 ‚¥¬μàÕ¡“‰¥â¡’°“√‡√’¬°™◊ËÕ‚√§π’ÈÕ¬à“ßÀ≈“°À≈“¬ ‡™àπ oriental cholangiohepatitis, oriental cholangiopathy, Hong Kong disease, biliary obstruction syndrome of the Chinese, hepatolithiasis ·≈– oriental infestational cholangitis ‡ªìπμâπ √–∫“¥«‘∑¬“ Recurrent pyogenic cholangitis ‡ªìπ‚√§∑’Ëæ∫‰¡à∫àÕ¬ ‚¥¬¡—°‡°‘¥„π ª√–™“°√„πª√–‡∑»·∂∫¿¡‘¿“§‡Õ‡™’¬μ–«—πÕÕ°Ÿ ‚¥¬‡©æ“–‡™◊ÈÕ “¬®’π3-8 ·μà„π¬§ÿ ªí®®ÿ∫—π‡π◊ËÕß®“°¡’°“√Õæ¬æ¬â“¬∂‘Ëπ∑’ËÕ¬ŸàÕ“»—¬¢Õßª√–™“°√„π¿Ÿ¡‘¿“§‡Õ‡™’¬·≈– ‡Õ‡™’¬μ–«—π«—πÕÕ°‡©’¬ß„μâ‰ª Ÿà°≈ÿà¡ª√–‡∑»„π´’°‚≈°μ–«—πμ°¡“°¢÷Èπ ®÷ß∑”„Àâ¡’ ‚Õ°“ æ∫‚√§ RPC ‡æ‘Ë¡ Ÿß¢÷Èπ„πª√–‡∑»´’°‚≈°μ–«—πμ°μ“¡‰ª¥â«¬ Õ¬à“ß‰√°Áμ“¡ ¬—ß‰¡à¡’°“√√“¬ß“πÕÿ∫—μ‘°“√≥å¢Õß‚√§π’È‡ªìπ∑’Ë·πà™—¥ „π¢≥–∑’ËÕÿ∫—μ‘°“√≥å„π°≈ÿà¡

60 ®ÿ≈ “√ ¡“§¡·æ∑¬å√–∫∫∑“ß‡¥‘πÕ“À“√·Ààßª√–‡∑»‰∑¬, æƒ…¿“§¡- ‘ßÀ“§¡ 2559 ª√–‡∑»‡Õ‡™’¬μ–«—πÕÕ°(‰μâÀ«—π ·≈–≠’ËªÿÉπ) ¡’·π«‚πâ¡≈¥≈ß ´÷Ëß‡™◊ËÕ«à“‡°‘¥®“°°“√ ª√—∫‡ª≈’Ë¬πæƒμ‘°√√¡°“√∫√‘‚¿§Õ“À“√·∫∫μ–«—πμ° ·≈–¡’ ÿ¢Õπ“¡—¬∑’Ë¥’¢÷Èπ°«à“„π Õ¥’μ8,20 ‚¥¬ RPC ¡’‚Õ°“ ‡°‘¥„π‡æ»¢“¬·≈–‡æ»À≠‘ß„°≈â‡§’¬ß°—π (1:1.2)26-28 ·≈– æ∫‰¥â∫àÕ¬∑’Ë ¥„π™à«ßÕ“¬ÿ ÿ30-40 ªï ·μà¬—ß “¡“√∂æ∫‰¥â„πºâªÉ«¬∑’Ë¡’Õ“¬Ÿ ¡“°°«à“ÿ 60 ªï¥â«¬9-12 ‚√§ RPC æ∫‰¥â∫àÕ¬„π‡¢μæ◊Èπ∑’Ë™π∫∑ ™“¬·¥π ·≈–„π°≈ÿà¡ª√–™“°√∑’Ë ¿“«–∑ÿæ‚¿™π“°“√À√◊Õ‡»√…∞“π–‰¡à¥’13-15 æ¬“∏‘°”‡π‘¥ Recurrent pyogenic cholangitis ‡°‘¥®“°¿“«–πÈ”¥’§—Ëß ·≈–¡’°“√°àÕ μ—«¢Õßπ‘Ë«„πμ”·Àπàß à«πμâπμàÕ°“√μ’∫μ—π ‚¥¬æ¬“∏‘°”‡π‘¥¢Õßæ¬“∏‘ ¿“æ¥—ß °≈à“«π—Èπ¬—ß‰¡à∑√“∫∑’Ë¡“Õ¬à“ß·πà™—¥ “¡“√∂·∫àß≈—°…≥–¢Õßπ‘Ë«„π∑àÕπÈ”¥’„πμ—∫‰¥â ‡ªìπ™π‘¥ª∞¡¿Ÿ¡‘´÷Ëß‡™◊ËÕ«à“π‘Ë«‡°‘¥¢÷Èπ‡Õß¿“¬„π∑àÕπÈ”¥’„πμ—∫ æ∫¡“°„π°≈ÿà¡ª√–‡∑» ‡Õ‡™’¬μ–«—πÕÕ° ·≈–™π‘¥∑ÿμ‘¬¿Ÿ¡‘´÷Ëßπ‘Ë«‡°‘¥¢÷Èπ®“°°“√¬âÕπ°≈—∫¢Õßπ‘Ë«®“°∑àÕ∑“ß ‡¥‘ππÈ”¥’πÕ°μ—∫·≈–∂ÿßπÈ”¥’ √à«¡°—∫°“√‡°‘¥π‘Ë«„π∑àÕπÈ”¥’„πμ—∫´÷Ëß‡°‘¥μ“¡À≈—ß æ∫ ∫àÕ¬„π°≈ÿà¡ª√–‡∑»´’°‚≈°μ–«—πμ°5,16-17 °“√‡°‘¥π‘Ë«™π‘¥ª∞¡¿Ÿ¡‘ ·≈–°“√μ’∫μ—π¢Õß∑àÕπÈ”¥’ “¡“√∂π”‰ª Ÿà°“√μ‘¥ ‡™◊ÈÕ·∫§∑’‡√’¬¢Õß∑àÕπÈ”¥’ °“√μ‘¥‡™◊ÈÕ„π°√–· ‡≈◊Õ¥ ·≈–‡°‘¥π‘Ë«™π‘¥∑μ‘¬¿ÿ ¡‘μ“¡¡“‰¥âŸ ‡™◊ÈÕ·∫§∑’‡√’¬∑’Ëæ∫‰¥â∫àÕ¬ ®“°°“√‡æ“–‡™◊ÈÕ‰¥â®“°πÈ”¥’ ‰¥â·°à Escherichia coli (>95%), Klebsiella spp., Pseudomonas spp. ·≈– Proteus spp. à«π·∫§∑’‡√’¬ ™π‘¥‰¡àæ÷Ëßæ“ÕÕ°´‘‡®π ·≈–°“√μ‘¥‡™◊ÈÕ·∫§∑’‡√’¬À≈“¬™π‘¥√à«¡°—ππ—Èπæ∫‰¥â≈¥≈ßμ“¡ ≈”¥—∫9,18-19 ≈—°…≥–∑“ßæ¬“∏‘«‘∑¬“ ®–æ∫§«“¡º‘¥ª°μ‘¢Õß∑àÕπÈ”¥’∑—Èß¿“¬„πμ—∫ (intrahepatic) ·≈–¿“¬πÕ°μ—∫ (extrahepatic) ¡’®ÿ¥μ’∫μ—π ·≈–¡’°“√¢¬“¬μ—« ¢Õß∑àÕπÈ”¥’¿“¬„πμ—∫ à«πºπ—ß¢Õß∑àÕ∑“ß‡¥‘ππÈ”¥’®–¡’°“√Õ—°‡ ∫‡√◊ÈÕ√—ß ¡’æ—ßº◊¥ – ¡·≈–Àπ“μ—«¢÷Èπ ≈—°…≥–¢ÕßπÈ”¥’®–¢âπ¡“°¢÷Èπ æ∫·∫§∑’‡√’¬ ‡»…´“°¢Õß ‡´≈≈å™—Èπ‡¬◊ËÕ∫ÿº‘« ·≈–μ–°Õπ¢ÕßπÈ”¥’ ∫“ß§√—ÈßÕ“®æ∫πÈ”¥’‡ªìπÀπÕß ∑—Èßπ’È∑àÕπÈ”¥’ ¥â“π´â“¬„πμ—∫‚¥¬‡©æ“–„πμ”·Àπàß°≈’∫μ—∫´â“¬¥â“π¢â“ß¡—°æ∫„π‚√§√–¬–‡√‘Ë¡·√°

Recurrent Pyogenic Cholangitis 61 ·≈–¡’æ¬“∏‘ ¿“æ‡¥àπ™—¥¡“°°«à“μ”·ÀπàßÕ◊ËπÊ ¢Õß∑àÕ∑“ß‡¥‘ππÈ”¥’„πμ—∫·≈–πÕ° μ—∫21 ‚¥¬‰¡à∑√“∫‡Àμº≈∑’Ë™—¥‡®πÿ ·μà§”Õ∏‘∫“¬∑’Ëπà“®–‡ªìπ‰ª‰¥â¡“°∑’Ë ¥πà“®–‡°‘¥ÿ ®“°∑àÕπÈ”¥’¢Õßμ—∫¥â“π´â“¬∑”¡ÿ¡™—π°«à“¥â“π¢«“®÷ß‡°‘¥°“√§—Ëß·≈–μ’∫μ—π¢Õß∑àÕ∑“ß ‡¥‘ππÈ”¥’‰¥âßà“¬7,22 πÕ°®“°π’ÈÕ“®æ∫°“√¢¬“¬¢π“¥¢Õß·Õ¡æ≈“Ÿ (ampulla hyper- trophy) ‡π◊ËÕß®“°¡’°“√À≈ÿ¥¢Õßπ‘Ë«´È”Ê ∑”„Àâ‡°‘¥°“√Õ—°‡ ∫∫àÕ¬·≈–¡’æ—ßº◊¥À√◊Õ ·º≈‡ªìπ∑’Ë∫√‘‡«≥π’È °“√√«∫√«¡¢âÕ¡Ÿ≈®“°‡Õ‡™’¬μ–«—πÕÕ° æ∫«à“ √âÕ¬≈– 69 ¡’π‘Ë« ∑—Èß∑àÕπÈ”¥’∑—Èß¿“¬„π·≈–¿“¬πÕ°μ—∫√à«¡°—π √âÕ¬≈– 78 ¡’π‘Ë«∑’Ë∫√‘‡«≥μ—∫°≈’∫´â“¬‡¥àπ √âÕ¬≈– 45 ¡’π‘Ë«∑’Ëμ—∫°≈’∫„¥°≈’∫Àπ÷Ëß √âÕ¬≈– 48 ¡’π‘Ë«„πμ—∫√à«¡°—∫π‘Ë«„π∂ÿßπÈ”¥’ ·≈–√âÕ¬≈– 76 ¡’°“√μ’∫μ—π¢Õß∑àÕπÈ”¥’¿“¬„πμ—∫√à«¡¥â«¬86 ≈—°…≥–¢Õß°âÕππ‘Ë«„π∑àÕπÈ”¥’ “¡“√∂æ∫‰¥â®”π«π¡“°·≈–¡’À≈“° À≈“¬¢π“¥ ‚¥¬°âÕππ‘Ë« à«π¡“°¡’Õß§åª√–°Õ∫‡ªìπ·§≈‡´’¬¡∫‘≈‘√Ÿ∫‘‡πμ (°âÕππ‘Ë« ’ πÈ”μ“≈ π‘Ë¡ ·≈–·μ°ßà“¬) ´÷Ëß·μ°μà“ß®“°°âÕππ‘Ë«™π‘¥‚§≈‡≈ ‡μÕ√Õ≈∑’Ë¡—°æ∫„π ºŸâªÉ«¬‚√§π‘Ë«„π∂ÿßπÈ”¥’23-24 “‡Àμ¢Õß‚√§ÿ “‡Àμÿ¢Õß‚√§ RPC ¬—ß‰¡à∑√“∫·πà™—¥ ·μà°Á¡’À≈“¬ ¡¡ÿμ‘∞“π´÷Ëß‡™◊ËÕ«à“πà“ ®–‡ªìπ “‡Àμÿ¢Õß‚√§‰¥â ‚¥¬‡©æ“–ªí®®—¬¥â“π ¿“«–·«¥≈âÕ¡∑’Ëπà“®–¡’§«“¡ ”§—≠ ·≈– —¡æ—π∏åμàÕ°“√‡°‘¥‚√§ Õ—π‰¥â·°à ¿Ÿ¡‘¿“§‡Õ‡™’¬μ–«—πÕÕ°‡©’¬ß„μâ æ◊Èπ∑’Ë™π∫∑ ·≈–‡»√…∞“π–‰¡à¥’ ·≈–æ∫«à“ “‡Àμÿ¥—ßμàÕ‰ªπ’Èπà“®–‡ªìπ “‡Àμÿ¢Õß RPC 1. °“√μ‘¥‡™◊ÈÕª√ ‘μ ≈—°…≥–∑“ß¿Ÿ¡‘»“ μ√å¢Õß°≈ÿà¡ºŸâªÉ«¬‚√§∑àÕπÈ”¥’Õ—°‡ ∫™π‘¥°≈—∫‡ªìπ´È”¡’ §«“¡ —¡æ—π∏å°—∫æ◊Èπ∑’Ë´÷Ëß¡’°“√μ‘¥‡™◊ÈÕª√ ‘μ„π∑àÕπÈ”¥’‡ªìπ‚√§‡©æ“–∂‘Ëπ ‚¥¬‡©æ“– °“√μ‘¥‡™◊ÈÕæ¬“∏‘„∫‰¡â„πμ—∫‰¥â·°à Clonochis sinensis, Opisthorchis spp., ·≈– Fascioliasis ´÷Ëß∑”„Àâ‡°‘¥°“√Õ—°‡ ∫μàÕ‡¬◊ËÕ∫ÿº‘«¢Õß∑àÕπÈ”¥’ √â“ß‡¡◊Õ°„π∑àÕπÈ”¥’ ‡æ‘Ë¡¢÷Èπ π”‰ª à°“√‡°‘¥∑àÕπÈ”¥’Õ—°‡ ∫‡√◊ÈÕ√—ßŸ ‡°‘¥π‘Ë«‰¥âßà“¬¢÷Èπ ·≈–‡°‘¥°“√Õ¥μ—πμ“¡¡“ÿ ‰¥â19,25

62 ®ÿ≈ “√ ¡“§¡·æ∑¬å√–∫∫∑“ß‡¥‘πÕ“À“√·Ààßª√–‡∑»‰∑¬, æƒ…¿“§¡- ‘ßÀ“§¡ 2559 C. sinensis æ∫¡“°„π¿¡‘¿“§‡Õ‡™’¬μ–«—πÕÕ°Ÿ ‚¥¬‡©æ“–„πª√–‡∑»®’π ≠’ËªÉπÿ ‰μâÀ«—π ‡«’¬¥π“¡ ·≈–‡°“À≈’ §π®–‰¥â√—∫‡™◊ÈÕæ¬“∏‘®“°°“√√—∫ª√–∑“πÕ“À“√¥‘∫ À√◊Õ ÿ°Ê ¥‘∫Ê ´÷Ëß¡’´’ μå¢Õßæ¬“∏‘°àÕπ∑’Ë®–‡®√‘≠‡μ‘∫‚μ„π≈”‰ â‡≈Á° à«π¥Ÿ‚Õ¥’π—¡ Opisthorchis spp. æ∫ 2 “¬æ—π∏ÿå´÷Ëß¡—°∑”„Àâ‡°‘¥‚√§„π§π‰¥â·°à O. felineus ·≈– O. viverrini æ∫¡“°„π¿Ÿ¡‘¿“§‡Õ‡™’¬μ–«—πÕÕ°‡©’¬ß„μâ ¬ÿ‚√ª°≈“ß ·≈–¬ÿ‚√ªμ–«—πÕÕ° ‚¥¬‡©æ“–„π‰´∫’‡√’¬ ·≈–∫“ß à«π¢Õß°≈ÿà¡ª√–‡∑»´÷Ëß‡§¬Õ¬Ÿà “∏“√≥√—∞‚´‡«’¬μ¡“°àÕπ O. viverrini ‡ªìπæ¬“∏‘´÷Ëßæ∫‰¥â„πª√–‡∑»‰∑¬ ‚¥¬‡©æ“– „π¿“§μ–«—πÕÕ°‡©’¬ß‡Àπ◊Õ §πμ‘¥‡™◊ÈÕ®“°°“√√—∫ª√–∑“π‡π◊ÈÕª≈“¥‘∫ À√◊Õ °Êÿ ¥‘∫Ê ∑’Ë¡’μ—«ÕàÕπ¢Õßæ¬“∏‘ Fascioliasis ‡ªìπ°“√μ‘¥‡™◊ÈÕ∑’Ë‡°‘¥®“°æ¬“∏‘„∫‰¡â„πμ—∫ Fasciola hepatica À√◊Õ F. gigantica ‚¥¬ F. hepatica æ∫‰¥â∫àÕ¬°«à“·≈–¡’°“√°√–®“¬μ—«Õ¬Ÿà∑—Ë« ‚≈° √«¡∑—Èßª√–‡∑»‰∑¬‚¥¬‡©æ“–„π¿“§μ–«—πÕÕ°‡©’¬ß‡Àπ◊Õ §πμ‘¥‡™◊ÈÕ®“°°“√ √—∫ª√–∑“πæ◊™πÈ”∑’Ë¡’μ—«ÕàÕπ¢Õßæ¬“∏‘‡°“–Õ¬Ÿà Ascaris lumbricoides ‡ªìπæ¬“∏‘μ—«°≈¡„π≈”‰ â ·≈–‡ªìπæ¬“∏‘∑’Ë°àÕ‚√§ „π¡πÿ…¬å∑—Ë«‚≈°‰¥â∫àÕ¬‡ªìπÕ—π¥—∫μâπÊ ‚¥¬§π®–μ‘¥‡™◊ÈÕ®“°°“√√—∫ª√–∑“π‰¢à¢Õß æ¬“∏‘´÷Ëß¡—°ªπ‡ªóôÕπ¡“°—∫¥‘π A. lumbricoides “¡“√∂∑”„Àâ‡°‘¥∑àÕπÈ”¥’Õ—°‡ ∫‰¥â ‚¥¬°“√‰™®“°≈”‰ â‡¢â“ Ÿà∑àÕπÈ”¥’ºà“π∑“ß ampulla of vater ∑”„Àâ‡°‘¥°“√μ‘¥‡™◊ÈÕ ·∫§∑’‡√’¬μ“¡¡“ ·≈–Õ“®‡°’Ë¬«¢âÕß°—∫¿“«– RPC ‰¥â ∂÷ß·¡â«à“¢âÕ¡Ÿ≈∑“ß√–∫“¥«‘∑¬“®–¡’§«“¡ —¡æ—π∏å·≈–¡’À≈—°∞“π«à“°“√μ‘¥ ‡™◊ÈÕª√ ‘μ‡À≈à“π’È‡ªìπæ¬“∏‘°”‡π‘¥¢Õß RPC ·μà°Á¬—ß‰¡à “¡“√∂∑’Ë®– √ÿª‰¥â™—¥‡®π ‡π◊ËÕß®“°æ∫°“√μ‘¥‡™◊ÈÕª√ ‘μ‡æ’¬ß√âÕ¬≈– 20-45 ‡∑à“π—Èπ„πºŸâªÉ«¬ RPC ¡’ªí®®—¬ ∫“ßª√–°“√´÷Ëß‡™◊ËÕ«à“πà“®–‡ªìπ§”Õ∏‘∫“¬„π‡√◊ËÕß¢Õß§«“¡·μ°μà“ß„π°“√μ√«®æ∫ °“√μ‘¥‡™◊ÈÕª√ ‘μ„πºŸâªÉ«¬‚√§μ‘¥‡™◊ÈÕ∑àÕπÈ”¥’™π‘¥°≈—∫‡ªìπ´È” §◊Õ §«“¡™ÿ°„π°“√ μ√«®π—Èπ¢÷ÈπÕ¬Ÿà°—∫§«“¡‰«¢Õß™ÿ¥°“√μ√«®´÷ËßÕ“®®–¡’§«“¡·μ°μà“ß°—π„π·μà≈– √“¬ß“π ·≈–°“√μ‘¥‡™◊ÈÕª√ ‘μ„πºŸâªÉ«¬ RPC Õ“®®–‰¡àæ∫√àÕß√Õ¬À√◊Õμ—«æ¬“∏‘„π °âÕππ‘Ë« (∫“ß√“¬ß“π “¡“√∂· ¥ß„Àâ‡ÀÁπ«à“ “¡“√∂æ∫‰¢à À√◊Õμ—«æ¬“∏‘„π·°π °≈“ß¢Õßπ‘Ë«‰¥â)10-11, 19

Recurrent Pyogenic Cholangitis 63 2. °“√μ‘¥‡™◊ÈÕ·∫§∑’‡√’¬ π‘Ë«™π‘¥¡’ ’ (pigment stone) æ∫„πºŸâªÉ«¬ RPC ‡π◊ËÕß®“°°“√μ‘¥‡™◊ÈÕ ·∫§∑’‡√’¬‚¥¬‡©æ“–Õ¬à“ß¬‘Ëß Escherichia coli æ∫«à“πÈ”¥’¢ÕßºâªÉ«¬¡’√–¥—∫‡Õπ‰´¡åŸ β-glucorodinase Ÿß¢÷Èπ ∑”„Àâ‡°‘¥ unconjugated bilirubin Ÿß¢÷Èπ„π√–∫∫∑àÕ πÈ”¥’·≈–√«¡μ—«°—∫·§≈‡´’¬¡‡ªìπ°âÕππ‘Ë« πÕ°®“°π’È‡¡◊ËÕ¡’π‘Ë«‡°‘¥¢÷Èπ¬—ß àßº≈„Àâ‡°‘¥ ¿“«–Õÿ¥°—Èπ¢Õß°“√‰À≈¢ÕßπÈ”¥’ àßº≈„Àâ¡’°“√‡°‘¥π‘Ë«‰¥âßà“¬¢÷Èπ ·≈–¡’°“√μ‘¥‡™◊ÈÕ ™π‘¥°≈—∫‡ªìπ´È”‰¥â35-36 à«ππ‘Ë«„π∑àÕπÈ”¥’„πμ—∫™π‘¥ª∞¡¿Ÿ¡‘·∫∫‚§‡≈ ‡μÕ√Õ≈π—Èπ¬—ß‰¡à∑√“∫ æ¬“∏‘°”‡π‘¥∑’Ë™—¥‡®π ‡™◊ËÕ«à“‡°‘¥§«“¡º‘¥ª°μ‘·≈–§«“¡‰¡à —¡æ—π∏å°—π¢Õß°“√ —ß‡§√“–Àå‚§‡≈ ‡μÕ√Õ≈·≈–°“√ —ß‡§√“–Àå‡°≈◊ÕπÈ”¥’„πμ—∫ (up-regulation of cho- lesterol synthesis ·≈– down-regulation of bile-acid synthesis) ‚¥¬Õ“® ‡°’Ë¬«¢âÕß°—∫§«“¡∫°æ√àÕß„π°“√À≈—ËßøÕ ‚ø≈‘ªî¥ºà“π canalicular transporter ·≈–‚ª√μ’π MDR3 (multidrug resistance protein)37 “‡Àμÿ·≈–∑’Ë¡“¢Õß°“√μ‘¥‡™◊ÈÕ·∫§∑’‡√’¬¬—ß‰¡à™—¥‡®π ∫“ß°“√»÷°…“æ∫«à“ ‡™◊ÈÕ·∫§∑’‡√’¬·∑√°´÷¡ºà“π√–∫∫æÕ√å∑—≈®“°≈”‰ â À√◊Õ‡™◊ËÕ«à“Õ“®®–μ‘¥‡™◊ÈÕ ·∫§∑’‡√’¬„π∑àÕπÈ”¥’´÷Ëß‡ªìπº≈®“°¡’°“√μ‘¥‡™◊ÈÕª√ ‘μπ”¡“°àÕπ25, 31-34 ·¡â®–¬—ß‰¡à∑√“∫·πà™—¥«à“°“√μ‘¥‡™◊ÈÕ·∫§∑’‡√’¬π—Èπ‡ªìπ “‡ÀμÿÀ√◊Õ‡ªìπº≈ ®“°°“√‡°‘¥π‘Ë«°Áμ“¡ ·μà¡’°“√»÷°…“Àπ÷Ëßæ∫«à“°“√μ‘¥‡™◊ÈÕ„π∑àÕπÈ”¥’‡°‘¥¢÷Èπ¿“¬À≈—ß ¡’°“√‡°‘¥π‘Ë«38 πÕ°®“°π’È¬—ß¡’°“√μ√«®æ∫«à“ºâªÉ«¬‚√§Ÿ RPC ¢“¥°“√¬—∫¬—Èß¢Õß√–¥—∫ ‡Õπ‰´¡å β-glucorodinase ´÷Ëßæ∫„ππÈ”¥’ª°μ‘ ∑”„Àâ¡’‚Õ°“ ‡°‘¥π‘Ë« ß¢÷Èπ¥—ß∑’Ë‰¥â°≈à“«Ÿ ¢â“ßμâπ11-13, 39-43 3. °“√§—Ëß¢ÕßπÈ”¥’ °“√§—Ëß °“√μ’∫μ—π À√◊Õ°“√Õÿ¥°—Èπ¢ÕßπÈ”¥’‡ªìπ à«π ”§—≠∑’Ë‡™◊ËÕ«à“∑”„Àâ‡°‘¥ RPC11,44-46 ‚¥¬‡™◊ËÕ«à“°“√μ’∫μ—ππ—Èπ¡—°¡’ “‡ÀμÕ◊Ëππ”¡“°àÕπÕ—π‰¥â·°àÿ ¡’°“√Õ—°‡ ∫ ‡ªìπÊ À“¬Ê ¡“°àÕπÀ≈“¬§√—Èß ·≈–∑”„Àâ‡°‘¥π‘Ë« √à«¡°—∫¡’°“√μ‘¥‡™◊ÈÕ´È”Ê ¢÷Èπ‰¥â „π ¢≥–∑’Ë¡’°“√»÷°…“„π —μ«å∑¥≈Õß´÷Ëß∑”„Àâ¡’°“√μ’∫μ—π¢Õß∑àÕπÈ”¥’√à«¡ à«πª≈“¬®π

64 ®ÿ≈ “√ ¡“§¡·æ∑¬å√–∫∫∑“ß‡¥‘πÕ“À“√·Ààßª√–‡∑»‰∑¬, æƒ…¿“§¡- ‘ßÀ“§¡ 2559 ‡°‘¥π‘Ë«„π∂ßπÈ”¥’·≈–∑àÕ∑“ß‡¥‘ππÈ”¥’„πμ—∫ÿ ·μà°≈—∫‰¡àæ∫À≈—°∞“π¢Õß°“√μ‘¥‡™◊ÈÕ¢Õß πÈ”¥’47-48 Õ“°“√·≈–Õ“°“√· ¥ß ºŸâªÉ«¬‚√§ RPC ¡—°®–¡’Õ“°“√¢Õß∑àÕπÈ”¥’Õ—°‡ ∫‡©’¬∫æ≈—π‡π◊ËÕß®“°¡’ °“√Õÿ¥μ—π·≈–¡’°“√μ‘¥‡™◊ÈÕ·∫§∑’‡√’¬„π∑àÕπÈ”¥’‡°‘¥¢÷Èπ ´÷ËßÕ“°“√·≈–Õ“°“√· ¥ß ‰¥â·°à ‰¢â ŸßÀπ“« —Ëπ ª«¥∑âÕß„μâ≈‘ÈπªïòÀ√◊Õ™“¬‚§√ß¢«“ ·≈–¥’´à“π (´÷Ëß‡√’¬°Õ“°“√/ Õ“°“√· ¥ß “¡Õ¬à“ßπ’È √à«¡°—π«à“ Charcotûs triad) À“°¡’ Charcotûs triad √à«¡ °—∫§«“¡¥—π‚≈À‘μμË”·≈–√–¥—∫°“√√—∫√Ÿâ≈¥≈ß‡√’¬°«à“ Reynoldûs pentad ´÷Ëßæ∫‰¥â „π¿“«–∑’Ë¡’°“√Õ—°‡ ∫√ÿπ·√ß„π∑àÕπÈ”¥’ ‡√‘Ë¡¡’¿“«– sepsis ·≈â« (toxic cholangitis) ‚¥¬Õ“°“√·≈–Õ“°“√· ¥ß∑’Ëæ∫∫àÕ¬ ‰¥â·°à °“√μ‘¥‡™◊ÈÕ∑àÕπÈ”¥’ (√âÕ¬≈– 44) ª«¥∑âÕß·μà‰¡àæ∫∑àÕπÈ”¥’Õ—°‡ ∫ (√âÕ¬≈– 32) ·≈–μ—∫ÕàÕπÕ—°‡ ∫ (√âÕ¬≈– 17)49 ‡π◊ËÕß®“°ºŸâªÉ«¬ à«π„À≠à¡—°¡’Õ“°“√‡√‘Ë¡μâπ∑’Ë‰¡à√ÿπ·√ßÀ√◊Õ‰¡à™—¥‡®π ®÷ß ∑”„ÀâºŸâªÉ«¬Õ“®‰¡à‰¥â√—∫°“√«‘π‘®©—¬·≈–√—°…“Õ¬à“ß∂Ÿ°μâÕß„π§√—Èß·√° ®÷ß∑”„Àâ ºŸâªÉ«¬ à«π¡“°‰¥â√—∫°“√«‘π‘®©—¬‡¡◊ËÕ‚√§‡ªìπ¡“°·≈â« ‚¥¬æ∫«à“‡æ’¬ß√âÕ¬≈– 15-30 ¢ÕßºŸâªÉ«¬ RPC ‡∑à“π—Èπ∑’Ë‰¥â√—∫°“√«‘π‘®©—¬„π√–¬–‡√‘Ë¡μâπ¢Õß‚√§ ºŸâªÉ«¬∫“ß√“¬ Õ“®¡“¥â«¬¿“«–·∑√°´âÕπ¢Õß RPC ‰¥â·°à ΩïÀπÕß∑’Ëμ—∫ μ—∫ÕàÕπÕ—°‡ ∫ μ—∫·¢Áß ¡–‡√Áß„π∑àÕ∑“ß‡¥‘ππÈ”¥’ ‡ªìπμâπ ¿“«–·∑√°´âÕπ¢Õß RPC ∑’Ëæ∫∫àÕ¬ ‰¥â·°à ΩïÀπÕß∑’Ëμ—∫ (liver abscesses) ¡’°“√·μ°¢ÕßÀπÕß„π∑àÕπÈ”¥’∑’ËÕÿ¥μ—π‡¢â“ Ÿà™àÕß∑âÕßÀ√◊Õ¡’∑“ß‡™◊ËÕ¡μàÕ√–À«à“ß∑àÕ πÈ”¥’°—∫Õ«—¬«–¢Õß√–∫∫∑“ß‡¥‘πÕ“À“√„π™àÕß∑âÕß (choledocho-enteric fistula) À√◊Õºπ—ßÀπâ“∑âÕß (choledocho-cutaneous fistula)9,12,49 ‡ªìπμâπ πÕ°®“°π’È°Á¡’ √“¬ß“π°“√‡°‘¥°“√Õÿ¥μ—π¢ÕßÀ≈Õ¥‡≈◊Õ¥¥”æÕ√å∑—≈ ·≈–¡’‡≈◊Õ¥ÕÕ°„π∑àÕπÈ”¥’ (hemobilia)12-18 °“√μ√«®√à“ß°“¬ “¡“√∂æ∫ ‰¢â μ—«‡À≈◊Õßμ“‡À≈◊Õß °¥‡®Á∫∫√‘‡«≥„μâ™“¬ ‚§√ß¢«“À√◊Õ∫√‘‡«≥≈‘Èπªïò ·≈–μ—∫‚μ πÕ°®“°π—Èπ„π°√≥’∑’Ëæ∫«à“¡’¿“«–·∑√°´âÕπ¢Õß RPC √à«¡¥â«¬·≈â« Õ“®®–μ√«®æ∫¢“∫«¡ πÈ”„π™àÕß∑âÕß À√◊Õ≈—°…≥–¢Õß‡¬◊ËÕ∫ÿ

Recurrent Pyogenic Cholangitis 65 ™àÕß∑âÕßÕ—°‡ ∫ (peritonitis) ‡ªìπμâπ ‚¥¬¢÷ÈπÕ¬Ÿà°—∫¿“«–·∑√°´âÕπ·μà≈–™π‘¥ °≈à¡ºÿâ«‘®—¬‡°’Ë¬«°—∫π‘Ë«„πμ—∫®“°ª√–‡∑»≠’ËªŸ Éπÿ (Hepatolithiasis Research Group) ‰¥â‡ πÕ°“√·∫àß‚√§ RPC μ“¡§«“¡√ÿπ·√ß‡ªìπ 4 √–¥—∫ (μ“√“ß∑’Ë 1)50 ‚¥¬ æ∫ºŸâªÉ«¬®“°°“√»÷°…“Õ¬Ÿà„π√–¥—∫ 1 √âÕ¬≈– 20 √–¥—∫ 2 √âÕ¬≈– 25 ·≈–Õ¬Ÿà„π √–¥—∫ 3 ·≈– 4 √âÕ¬≈– 55 °“√«‘π‘®©—¬ °“√«‘π‘®©—¬‚√§ RPC Õ“»—¬Õ“°“√·≈–Õ“°“√· ¥ß º≈°“√μ√«®‡≈◊Õ¥ μ√«®Õÿ®®“√– ·≈–°“√μ√«®∑“ß√—ß ’«‘∑¬“ °“√μ√«®Õ—≈μ√“´“«¥å‡ªìπ°“√μ√«®‡∫◊ÈÕß μâπ∑’Ë∑”‰¥âßà“¬·≈–¡’ª√–‚¬™πå ‚¥¬ “¡“√∂æ∫∑àÕπÈ”¥’¡’¢π“¥„À≠à¢÷Èπ (bile duct dilatation) ·≈–μ√«®æ∫π‘Ë«‰¥â√âÕ¬≈– 85-9011,51 (¿“æ∑’Ë 1) πÕ°®“°π’È¬—ß “¡“√∂ μ√«®æ∫ΩïÀπÕß∑’Ëμ—∫‰¥â¥â«¬ °“√μ√«®«‘π‘®©—¬¥â«¬‡ÕÁ°´‡√¬å§Õ¡æ‘«‡μÕ√å (computer tomography) ‡¡◊ËÕ‡ª√’¬∫‡∑’¬∫°—∫°“√©’¥ ’∑àÕπÈ”¥’æ∫«à“°“√μ√«®‡ÕÁ°´‡√¬å§Õ¡æ‘«‡μÕ√å “¡“√∂ ∫Õ°∂÷ß≈—°…≥–¢Õß∑àÕπÈ”¥’∑’Ë¡’°“√¢¬“¬¢π“¥ ¡’°“√μ’∫·§∫¢Õß∑àÕπÈ”¥’∫√‘‡«≥√Õ∫ πÕ° °“√Àπ“μ—«¢Õßºπ—ß∑àÕπÈ”¥’ ΩïÀπÕß∑’Ëμ—∫ °âÕπ´÷Ëß‡°‘¥®“°πÈ”¥’§—Ëß °âÕππ‘Ë« ≈—°…≥–¢Õß‡π◊ÈÕμ—∫ ·≈–μ”·Àπàß∑’Ë¡’§«“¡º‘¥ª°μ‘„πμ—∫ ‰¥â¥’°«à“°“√©’¥ ’∑àÕ∑“ß‡¥‘π πÈ”¥’9,12,52 ´÷Ëß‡ªìπ¢âÕ¡Ÿ≈∑’Ë ”§—≠μàÕ°“√«“ß·ºπ°“√√—°…“ (¿“æ∑’Ë 2) °“√μ√«®‡æ◊ËÕ¥Ÿ≈—°…≥–¢Õß∑àÕ∑“ß‡¥‘ππÈ”¥’¥â«¬°“√©’¥ ’ (¿“æ∑’Ë 3-4) Õ—π ‰¥â·°à endoscopic retrograde cholangiopancreatography (ERCP), percutaneous transhepatic cholangiography (PTC), ·≈– magnetic resonance

μ“√“ß∑’Ë 1 °“√·∫àß§«“¡√ÿπ·√ß¢Õß‚√§ recurrent pyogenic cholangitis √–¥—∫ 1 ‰¡à¡’Õ“°“√ √–¥—∫ 2 ¡Õ“°“√ª«¥∑’ Õßâ √–¥—∫ 3 ¡’Õ“°“√‡À≈◊Õß™—Ë«¢≥– (transient jaundice) À√◊Õ∑àÕπÈ”¥’Õ—°‡ ∫ (cholangitis) √–¥—∫ 4 ¡’Õ“°“√‡À≈◊Õß ¡’°“√μ‘¥‡™◊ÈÕ√ÿπ·√ß À√◊Õ¡–‡√Áß∑àÕ∑“ß‡¥‘ππÈ”¥’

66 ®ÿ≈ “√ ¡“§¡·æ∑¬å√–∫∫∑“ß‡¥‘πÕ“À“√·Ààßª√–‡∑»‰∑¬, æƒ…¿“§¡- ‘ßÀ“§¡ 2559 ¿“æ∑’Ë 1 π‘Ë«„π∑àÕπÈ”¥’„πμ—∫ √à«¡°—∫¡’°“√¢¬“¬„À≠à¢Õß∑àÕπÈ”¥86’

¿“æ∑’Ë 2 ¿“æ‡Õ°´‡√¬å§Õ¡æ‘«‡μÕ√å· ¥ß„Àâ‡ÀÁπ∑àÕπÈ”¥’„πμ—∫¢â“ß´â“¬¢¬“¬„À≠à¢÷Èπ ·≈–æ∫π‘Ë«Õ¬Ÿà ¿“¬„π (≈Ÿ°»√ ’·¥ß)

Recurrent Pyogenic Cholangitis 67 ¿“æ∑’Ë 3 ERCP æ∫°“√¢¬“¬„À≠à¢Õß∑àÕπÈ”¥’„πμ—∫¢â“ß´â“¬ ·≈–æ∫π‘Ë«À≈“¬°âÕπ„π∑àÕπÈ”¥’

¿“æ∑’Ë 4 MRCP · ¥ß„Àâ‡ÀÁπ°“√¢¬“¬ „À≠à¢Õß∑àÕπÈ”¥’ ·≈–æ∫π‘Ë«„π ∑àÕπÈ”¥’„πμ—∫87

68 ®ÿ≈ “√ ¡“§¡·æ∑¬å√–∫∫∑“ß‡¥‘πÕ“À“√·Ààßª√–‡∑»‰∑¬, æƒ…¿“§¡- ‘ßÀ“§¡ 2559 cholangiopancreatography (MRCP) π—Èπ æ∫«à“ MRCP ‡ªìπ°“√μ√«®∑’Ë‰¡à in- vasive ·≈– “¡“√∂∫Õ°√“¬≈–‡Õ’¬¥¢Õß∑àÕπÈ”¥’‰¥â¥’°«à“ ERCP ·≈– PTC ‚¥¬ ‡©æ“–°√≥’∑’Ë‰¡à “¡“√∂©’¥ ’‡¢â“‰ª„π∑àÕπÈ”¥’∑’Ë¡’°“√μ’∫μ—π¬“«À√◊Õμ’∫μ—π·∫∫ ¡∫Ÿ√≥å πÕ°®“°π’È „π°√≥’∑’Ë©’¥ ’‡¢â“‰ª„π∑àÕπÈ”¥’∑’Ëμ’∫μ—π·≈â« ’‰¡à “¡“√∂‰À≈ °≈—∫¡“À¡¥ Õ“®∑”„Àâ‡°‘¥°“√μ‘¥‡™◊ÈÕ¢Õß∑àÕπÈ”¥’‰¥â ¥—ßπ—Èπ°“√μ√«® ERCP À√◊Õ PTC ®÷ß§«√‰¥â√—∫¬“ªØ‘™’«π–°àÕπ∑”°“√μ√«®‡æ◊ËÕ≈¥‚Õ°“ °“√μ‘¥‡™◊ÈÕ¥—ß∑’Ë‰¥â°≈à“«¡“53- 54 °“√»÷°…“„πºŸâªÉ«¬ primary slerosing cholangitis æ∫«à“ °“√∑” ERCP ¡’ ‚Õ°“ ‡°‘¥¿“«–·∑√°´âÕπ (cholangitis ·≈– pancreatitis) ‰¥â∂÷ß√âÕ¬≈– 10 ¢Õß ºŸâªÉ«¬55 ”À√—∫¢âÕ¥âÕ¬¢Õß MRCP §◊Õ‰¡à “¡“√∂∑’Ë®–„Àâ°“√√—°…“æ√âÕ¡°—∫°“√ «‘π‘®©—¬‰¥â ≈—°…≥–∑’Ëæ∫‰¥â®“°°“√©’¥ ’∑àÕ∑“ß‡¥‘ππÈ”¥’ ‡™àπ ∑àÕπÈ”¥’¿“¬„π ·≈–/ À√◊Õ¿“¬πÕ°μ—∫¢¬“¬„À≠à¢÷Èπ ‚¥¬Õ“®æ∫≈—°…≥–∑àÕπÈ”¥’„πμ—∫¥¬◊¥¢÷ÈπŸ ·≈–·μ°°‘Ëß °â“π‡ªìπ¡ÿ¡·À≈¡πâÕ¬≈ß (straightened intrahepatic duct with less acute or right-angled branching pattern) ´÷Ëß‡ªìπº≈®“°º—ßæ◊¥√Õ∫∑àÕπÈ”¥’ (periductal fibrosis) ·≈–∑àÕπÈ”¥’„πμ—∫ à«π√Õ∫πÕ°¡’¢π“¥‡≈Á°≈ß·≈–·μ°°‘Ëß°â“ππâÕ¬ (de- creased arborization and acute tapering of peripheral ducts)53,55 ®–‡ÀÁπ ≈—°…≥–∑’Ë‡√’¬°«à“ çarrowheadé à«π„π°√≥’∑’Ë¡’°“√μ’∫μ—π¢Õß∑àÕπÈ”¥’Õ¬à“ß ¡∫Ÿ√≥å®–æ∫≈—°…≥–∑’Ë‡√’¬°«à“ çmissing ducté °“√»÷°…“·∫∫¬âÕπÀ≈—ß‚¥¬ Sugiyama ·≈–§≥–56 æ∫«à“°“√μ√«® MRCP ‡æ◊ËÕ«‘π‘®©—¬π‘Ë« ·≈–μ”·Àπàß¢Õßπ‘Ë«„π∑àÕπÈ”¥’„πμ—∫ ¡’§«“¡‰«√âÕ¬≈– 97 §«“¡®”‡æ“–√âÕ¬≈– 99 ·≈–§«“¡·¡àπ¬”√âÕ¬≈– 98 ·≈–°“√μ√«® MRCP ‡æ◊ËÕ «‘π‘®©—¬°“√μ’∫·§∫ ·≈–μ”·Àπàß¢Õß°“√μ’∫·§∫¢Õß∑àÕπÈ”¥’„πμ—∫ ¡’§«“¡‰«√âÕ¬≈– 93 §«“¡®”‡æ“–√âÕ¬≈– 97 ·≈–§«“¡·¡àπ¬”√âÕ¬≈– 97 ¡’°“√®”·π°π‘Ë«„π∑àÕπÈ”¥’„πμ—∫ ‡æ◊ËÕ™à«¬ª√–‡¡‘π·≈–μ‘¥μ“¡º≈°“√√—°…“ (¿“æ∑’Ë 5)57 ·μà°Á¬—ß‰¡à¡’°“√®”·π°¢Õßπ‘Ë«„π∑àÕπÈ”¥’„πμ—∫Õ¬à“ß‡ªìπ√–∫∫∑’Ë‡ªìπ ¡“μ√∞“π·≈–™—¥‡®π ´÷Ëß∂â“∑√“∫μ”·Àπàß ¢π“¥ ·≈–®”π«π¢Õßπ‘Ë«„π∑àÕπÈ”¥’Õ¬à“ß ≈–‡Õ’¬¥ ¡’ª√–‚¬™πåÕ¬à“ß¡“°„π∑“ß§≈‘π‘°·≈–¡’ª√–‚¬™πåÕ¬à“ß¬‘Ëß„π°“√√—°…“‚¥¬

Recurrent Pyogenic Cholangitis 69 ¿“æ∑’Ë 5 ª√–‡¿∑¢Õßπ‘Ë«„π∑àÕπÈ”¥’„πμ—∫ ·∫àßμ“¡°“√°√–®“¬μ—«¢Õßπ‘Ë«57 A: π‘Ë«„π∑àÕπÈ”¥’°âÕπ‡¥’¬«À√◊ÕÀ≈“¬°âÕπ √à«¡°—∫¡’∑àÕ∑“ß‡¥‘ππÈ”¥’„πμ—∫¢¬“¬¢π“¥À√◊Õ μ’∫μ—π ‚¥¬Õ¬Ÿà„π°≈’∫μ—∫‡¥’¬«°—π√à«¡¥â«¬À√◊Õ‰¡à°Á‰¥â B: π‘Ë«À≈“¬°âÕπ¿“¬„π∑àÕπÈ”¥’„πμ—∫∑—Èß Õß¢â“ß √à«¡°—∫¡’°“√μ’∫μ—π¢Õß∑àÕπÈ”¥’„πμ—∫ ¢â“ßÀπ÷Ëß¢â“ß„¥ C: π«À≈“¬°Ë‘ Õπ¿“¬„π∑â Õπà ”¥È „πμ’ ∫∑— ß Õß¢È— “ßâ √«¡°à ∫°“√μ— ∫μ’ π¢Õß∑— Õπà ”¥È ∑’ ß Õß¢È— “ßâ

‡©æ“–„π°“√ºà“μ—¥ ·π«∑“ß°“√√—°…“ °“√√—°…“‚√§ RPC §«√¡’°“√¥Ÿ·≈·∫∫Õß§å√«¡ ·≈–¡’ À “¢“«‘™“™’æ ‡™àπ Õ“¬ÿ√·æ∑¬å∑“ß‡¥‘πÕ“À“√·≈–μ—∫ »—≈¬·æ∑¬å ·≈–√—ß ’·æ∑¬å ¡“√à«¡„π°“√¥Ÿ·≈ºŸâ ªÉ«¬ ‚¥¬¡’‡ªÑ“À¡“¬‡æ◊ËÕ√—°…“‚√§∑àÕπÈ”¥’Õ—°‡ ∫„π√–¬–·√°Ê §«∫§ÿ¡¿“«– ·∑√°´âÕπ™π‘¥‡©’¬∫æ≈—π ªÑÕß°—π°“√°≈—∫‡ªìπ´È” ·≈–ªÑÕß°—π¿“«–·∑√°´âÕπ„π √–¬–¬“«

70 ®ÿ≈ “√ ¡“§¡·æ∑¬å√–∫∫∑“ß‡¥‘πÕ“À“√·Ààßª√–‡∑»‰∑¬, æƒ…¿“§¡- ‘ßÀ“§¡ 2559 1. °“√√—°…“¿“«–·∑√°´âÕπ‡©’¬∫æ≈—π ºâªÉ«¬ à«π„À≠à¡—°¡’Õ“°“√·≈–Õ“°“√· ¥ß¢Õß∑àÕπÈ”¥’Õ—°‡ ∫™π‘¥‡©’¬∫æ≈—πŸ ®÷ß§«√„Àâ°“√√—°…“¥â«¬°“√„Àâ “√πÈ” °“√„Àâ¬“ªØ‘™’«π– ·≈–°“√√–∫“¬∑àÕ∑“ß‡¥‘π πÈ”¥’‡¡◊ËÕ¡’¢âÕ∫àß™’È ®“°π—Èπ®÷ß‡μ√’¬¡ºŸâªÉ«¬·≈–ª√–‡¡‘π‡æ◊ËÕ„Àâ°“√√—°…“ªÑÕß°—π„π √–¬–¬“«μàÕ‰ª °“√„Àâ¬“ªØ‘™’«π–§«√‡≈◊Õ°„Àâ¬“ªØ‘™’«π–·∫∫§√Õ∫§≈ÿ¡ ‚¥¬¡’ªí®®—¬„π ‡√◊ËÕß¢Õß§«“¡√ÿπ·√ß¢Õß‚√§ ·≈–√Ÿª·∫∫°“√μ‘¥‡™◊ÈÕ‡ªìπ à«π™à«¬„π°“√‡≈◊Õ°„™â¬“ ·μà‡π◊ËÕß®“° RPC π—Èπ‰¡à‰¥â¡’·π«∑“ß°“√„Àâ¬“ªØ‘™’«π–∑’Ë‡ªìπ¡“μ√∞“π ®÷ß·π–π” °“√‡≈◊Õ°¬“ªØ‘™’«π–μ“¡°“√√—°…“°“√μ‘¥‡™◊ÈÕ∑“ß‡¥‘ππÈ”¥’ ‚¥¬§«√„Àâ§√Õ∫§≈ÿ¡ ‡™◊ÈÕ°≈ÿà¡¥◊ÈÕ¬“ ·≈– Enterococci spp. ‡ªìπæ‘‡»… (μ“√“ß∑’Ë 2)93-94

μ“√“ß∑’Ë 2 °“√‡≈◊Õ°„™â¬“ªØ‘™’«π– Severity Host Organism Mild Moderate and Severe First-line drugs Second-line drugs Hospital-acquired multiple and/or penicillin/β-lactamase third- and fourth- fluoroquinolones resistant inhibitor combination generation and carbapenems (Pseudomonas spp., (i.e.piperacillin/ cephalosporins methicillin-resistant tazobactam or or penicillin/ Staphylococcus ampicillin/sulbactam) β-lactamase aureus, and inhibitors vancomycin-resistant enterococci) Community- single species of penicillin/β-lactamase third- and fourth- fluoroquinolones acquired intestinal organisms inhibitor combination generation and carbapenems (E. coli, Klebsiella (i.e.piperacillin/ cephalosporins and Enterococcus tazobactam or or penicillin/ spp.) ampicillin/sulbactam) β-lactamase inhibitors

Recurrent Pyogenic Cholangitis 71 ”À√—∫°“√√–∫“¬∑àÕ∑“ß‡¥‘ππÈ”¥’„πºŸâªÉ«¬ RPC ‡¡◊ËÕ¡’¢âÕ∫àß™’Èπ—Èπ æ∫«à“¡’ §«“¡¬ÿàß¬“°æÕ ¡§«√·≈–¡’‚Õ°“ ≈â¡‡À≈«§àÕπ¢â“ß Ÿß„π°“√√–∫“¬¥â«¬«‘∏’°“√ àÕß°≈âÕß∑àÕ∑“ß‡¥‘ππÈ”¥’ (ERCP) ‡π◊ËÕß®“°°“√μ’∫·§∫¢Õß∑àÕπÈ”¥’´÷ËßÕ“®Õ¬Ÿà≈÷°„π μ—∫¡’§«“¡¬“«À√◊Õ¡’À≈“¬®ÿ¥ °âÕππ‘Ë«Õ“®¡’®”π«π¡“° ¢π“¥„À≠à ·¢Áß ·≈–√«¡ °—π·πàπ„π∑àÕπÈ”¥’¿“¬„πμ—∫58-60 ‡ªìπμâπ ¥—ßπ—Èπ„π°√≥’∑’Ë°“√√–∫“¬πÈ”¥’ºà“π∑àÕπÈ”¥’ ÕÕ°∑“ß≈”‰ â‰¥â‰¡à‡æ’¬ßæÕ ·π–π”„Àâ√—°…“¥â«¬«‘∏’°“√Õ◊Ëπ ‡™àπ °“√‡®“–ºà“πº‘«Àπ—ß (percutaneous transbiliary drainage) À√◊Õ°“√ºà“μ—¥ 2. °“√ªÑÕß°—π¿“«–·∑√°´âÕπ„π√–¬–¬“« °“√ªÑÕß°—π¿“«–·∑√°´âÕπ„π√–¬–¬“«¢Õß RPC ‚¥¬°”®—¥π‘Ë« ªÑÕß°—π °“√‡°‘¥π‘Ë«´È” ≈¥‚Õ°“ „π°“√μ‘¥‡™◊ÈÕ´È”Ê ´÷Ëß¡’À≈“¬·π«∑“ß ‡™àπ °“√√—°…“¥â«¬«‘∏’ °“√ àÕß°≈âÕßºà“π∑àÕ∑“ß‡¥‘ππÈ”¥’ °“√ºà“μ—¥ °“√„™â§≈◊Ëπ‡ ’¬ß À√◊Õ„™â√à«¡°—πÀ≈“¬ «‘∏’ ‡ªìπμâπ 2.1 °“√°”®—¥π‘Ë« °“√°”®—¥π‘Ë«¥â«¬°≈âÕß ”À√—∫∑àÕπÈ”¥’ (choledochoscope) ‚¥¬ “¡“√∂ ∑”‰¥âÀ≈“¬«‘∏’ ‰¥â·°à ºà“π∑“ß∑àÕ√–∫“¬™π‘¥μ—«∑’ (T-tube)61-63 ºà“π∑“ß hepaticocutaneous jejunostomy site64 (¿“æ∑’Ë 6) À√◊Õºà“π∑“ß transpapillary √–À«à“ß°“√∑” ERCP65 ‚¥¬Õ“®®–μâÕß∑”À≈“¬§√—Èß‡æ◊ËÕ°”®—¥π‘Ë«®πÀ¡¥ ·≈– πÕ°®“°π’È«‘∏’π’È¬—ß “¡“√∂∑”°“√∂à“ß¢¬“¬∑àÕπÈ”¥’ à«π∑’Ë¡’°“√μ’∫μ—π‰¥âÕ’°¥â«¬ ª√– ‘∑∏‘¿“æ„π°“√°”®—¥π‘Ë« Ÿß¢÷Èπ∂÷ß√âÕ¬≈– 88 ∂â“„Àâ°“√√—°…“À≈“¬ «‘∏’√à«¡°—π ‰¥â·°à °“√∂à“ß¢¬“¬∑àÕπÈ”¥’·≈–„ à∑àÕ√–∫“¬ (T-tube) √à«¡°—∫ choledochoscopy ·≈– electrohydraulic lithotripsy66 ¿“¬À≈—ß®“°°”®—¥π‘Ë«À¡¥Õ¬à“ß ¡∫Ÿ√≥å·≈â«¬—ß “¡“√∂‡°‘¥π‘Ë«¢÷Èπ‰¥â„À¡à ∂÷ß√âÕ¬≈– 30 ‚¥¬√–¬–‡«≈“„π°“√‡°‘¥‰¡à·πàπÕπ ·μà®–æ∫‰¥â¡“°„πºŸâªÉ«¬∑’Ë¡’°“√ μ’∫μ—π¢Õß∑àÕπÈ”¥’„πμ—∫√à«¡¥â«¬67-68 ¬“ ursodeoxycholic acid (UDCA) ‡ªìπ¬“∑’Ë„™â‡æ◊ËÕ‡ªìπ°“√≈¥°“√ ‡°‘¥π‘Ë«´È” ‚¥¬¬—ß‰¡à∑√“∫°≈‰°°“√ÕÕ°ƒ∑∏‘Ï™—¥‡®π ·μà‡™◊ËÕ«à“‰¥âº≈¥’‚¥¬‡©æ“–∂â“

72 ®ÿ≈ “√ ¡“§¡·æ∑¬å√–∫∫∑“ß‡¥‘πÕ“À“√·Ààßª√–‡∑»‰∑¬, æƒ…¿“§¡- ‘ßÀ“§¡ 2559 ‡ªìπ°≈ÿà¡π‘Ë«™π‘¥‚§‡≈ ‡μÕ√Õ≈69 ¢âÕ¡Ÿ≈°“√»÷°…“„π —μ«å∑¥≈Õß·≈–„π§πæ∫«à“ UDCA (20 mg/kg/day) “¡“√∂‡æ‘Ë¡°“√‰À≈¢ÕßπÈ”¥’ ∑”„ÀâπÈ”¥’¡’§«“¡Àπ◊¥πâÕ¬ ≈ß “¡“√∂ªÑÕß°—π°“√‡°‘¥π‘Ë« ·≈–≈¥¢π“¥π‘Ë«‰¥â70-72 πÕ°®“°π’È UDCA ¬—ß‡ªìπ ¬“¡“μ√∞“π∑’Ë¡’ª√– ‘∑∏‘¿“æ„π°“√√—°…“¿“«–πÈ”¥’§—Ëß‡√◊ÈÕ√—ß ‡™àπ primary biliary cirrhosis, intrahepatic cholestasis of pregnancy ·≈– progressive familial intrahepatic cholestasis Õ¬à“ß‰√°Áμ“¡¬—ß‰¡à¡’¢âÕ¡≈°“√»÷°…“·∫∫Ÿ randomized controlled ¬◊π¬—π∂÷ßª√– ‘∑∏‘¿“æ¢Õß UDCA „π°“√ªÑÕß°—π°“√¥”‡π‘π‚√§¢Õß primary sclerosing cholangitis (PSC) ·≈– secondary sclerosing cholangitis ®“°¿“«–Õ◊ËπÊ √«¡∑—Èß RPC °“√„™â§≈◊Ëπ°√–·∑° ≈“¬π‘Ë« (extracorporeal shock-wave lithotripsy, ESWL) Kim ·≈–§≥–73 æ∫«à“°“√„™â ESWL √à«¡°—∫°“√π”π‘Ë«ÕÕ°ºà“π∑“ßº‘«Àπ—ß (percutaneous stone extraction) ‰¥â√—∫º≈ ”‡√Á®Õ¬à“ß¥’„πºŸâªÉ«¬ 16 √“¬ ®“° ∑—ÈßÀ¡¥ 18 √“¬ „π™à«ß‡«≈“‡°‘π°«à“ 3 ‡¥◊Õπ ‚¥¬¡’§à“‡©≈’Ë¬„π°“√∑” ESWL 4 §√—Èß73 Electrohydraulic shock-wave lithotripsy ·≈– NdYAG laser lithotripsy “¡“√∂„™â„π°√≥’∑’Ëπ‘Ë«¡’¢π“¥„À≠à¡“° ·≈–‰¡à “¡“√∂π”ÕÕ°¥â«¬«‘∏’ PTC ·∫∫ª°μ‘ °“√»÷°…“¢Õß Chen ·≈–§≥–74 π”π‘Ë«ÕÕ°À¡¥¥â«¬°“√„™â electrohydraulic shock-wave lithotripsy 6 √“¬ ·≈– NdYAG 1 √“¬ æ∫¿“«–·∑√° ´âÕπ‡≈Á°πâÕ¬®“° electrohydraulic shock-wave 3 √“¬ (2 √“¬æ∫ transient

¿“æ∑’Ë 6 Hepaticocutaneous jejunostomy ·≈–≈—°…≥– stoma80

Recurrent Pyogenic Cholangitis 73 haemobilia ·≈– 1 √“¬¡’‰¢â Àπ“« —Ëπ) Õ“°“√¥’¢÷ÈπÀ≈—ß„Àâ°“√√—°…“μ“¡Õ“°“√ à«π°“√√—°…“¥â«¬ NdYAG laser π—Èπ¡’√“§“·æß „™â‡«≈“π“π„π°“√∑”°“√√—°…“π“π ·≈–¡’§«“¡¬ÿàß¬“°„π°“√„™âß“π ®÷ß·π–π”„Àâ„™â°“√√—°…“¥â«¬ electrohydraulic shock-wave π—Èπ¡’ª√– ‘∑∏‘¿“æ ·≈–ª≈Õ¥¿—¬ 2.2 °“√ºà“μ—¥ ‡æ◊ËÕ°”®—¥ à«π∑’Ë¡’°“√μ‘¥‡™◊ÈÕ´È”Ê ∫√‘‡«≥∑àÕπÈ”¥’ à«π∑’Ë¡’°“√μ’∫μ—π ·≈– μ—¥μ—∫∑’ËΩÉÕ °“√»÷°…“¢π“¥„À≠à∑’Ë‡ª√’¬∫‡∑’¬∫°“√√—°…“¥â«¬°“√ºà“μ—¥°—∫°“√√—°…“ ¥â«¬«‘∏’°“√Õ◊Ëπ Ê ‰¡à¡’¢âÕ¡Ÿ≈¡“°π—° à«π„À≠à‡ªìπ°“√»÷°…“·∫∫¬âÕπÀ≈—ß„π‡Õ‡™’¬ æ∫«à“ °“√‡À≈◊Õ à«π¢Õß∑àÕ∑“ß‡¥‘ππÈ”¥’∑’Ë¡’°“√μ’∫μ—π „π°≈ÿà¡ºŸâªÉ«¬∑’Ë‰¥â√—∫°“√ √—°…“¥â«¬ percutaneous transhepatic cholangioscopic lithotomy ‚¥¬‰¡à ‰¥â∑”°“√ºà“μ—¥‡π◊ÈÕμ—∫ (hepatic resection) √à«¡¥â«¬ ®–¡’°“√°≈—∫‡ªìπ´È”¢Õßπ‘Ë« Ÿß ∂÷ß·¡â«à“®– “¡“√∂°”®—¥π‘Ë«ÕÕ°‰¥â∑—ÈßÀ¡¥°Áμ“¡ ‡¡◊ËÕ‡∑’¬∫°—∫°“√√—°…“¥â«¬ °“√ºà“μ—¥‡π◊ÈÕμ—∫°≈’∫´â“¬ (left lobectomy) √à«¡°—∫°“√ºà“μ—¥√–∫“¬πÈ”¥’ (biliary drainage)76-78 ·≈–„π‡√◊ËÕß§≥¿“æ™’«‘μÿ ‚√§μ—∫·¢Áß™π‘¥∑μ‘¬¿ÿ ¡‘Ÿ (secondary biliary cirrhosis) ¡–‡√Áß∑àÕπÈ”¥’ ·≈–Õ—μ√“°“√‡ ’¬™’«‘μ„π°≈ÿà¡∑’Ë‰¥â√—∫°“√√—°…“¥â«¬ °“√ºà“μ—¥°Á¥’°«à“‡™àπ‡¥’¬«°—π68, 78-79 °“√ºà“μ—¥√–∫“¬πÈ”¥’ (biliary drainage) ‡™àπ choledochoduodeno- stomy, Roux-en-Y choledochojejunostomy À√◊Õ sphincteroplasty Õ“®®– ‰¡à “¡“√∂√–∫“¬πÈ”¥’ÕÕ°‰¥â‡æ’¬ßæÕ ‡π◊ËÕß®“°¡’°“√μ’∫μ—π¢Õß∑àÕπÈ”¥’‡À≈◊ÕÕ¬Ÿà ®÷ß ·π–π”∑” biliary enteric anastomosis ‡™àπ hepaticojejunostomy85 ·≈–®“° °“√»÷°…“¬âÕπÀ≈—ß 10 ªï ·π–π”°“√√–∫“¬πÈ”¥’¥â«¬«‘∏’ hepaticojejunostomy ‡ªìπÕ—π¥—∫·√° ·≈–„Àâ∑”°“√√—°…“¥â«¬°“√ºà“μ—¥μ—∫ (hepatectomy) „π°√≥’ ∑’Ë¡’¿“«–·∑√°´âÕπ¢Õß RPC80 æ∫«à“ºŸâªÉ«¬∑’Ë‰¥â√—∫°“√√—°…“¥â«¬°“√ºà“μ—¥®–¡’§ÿ≥¿“æ™’«‘μ∑’Ë¥’ Õ—μ√“°“√ ‡°‘¥‚√§μ—∫·¢Áß®“°‚√§∑“ß‡¥‘ππÈ”¥’™π‘¥∑ÿμ‘¬¿Ÿ¡‘μË” (secondary biliary cirrhosis) ‚√§¡–‡√Áß∑àÕπÈ”¥’μË” ·≈–Õ—μ√“°“√μ“¬μË”°«à“‡¡◊ËÕ‡∑’¬∫°—∫«‘∏’Õ◊ËπÊ 68, 78-79 πÕ°®“°π’È¬—ß¡’√“¬ß“π°“√ª≈Ÿ°∂à“¬μ—∫ ‡æ◊ËÕ√—°…“¿“«–μ—∫·¢Áß®“° RPC81-82

74 ®ÿ≈ “√ ¡“§¡·æ∑¬å√–∫∫∑“ß‡¥‘πÕ“À“√·Ààßª√–‡∑»‰∑¬, æƒ…¿“§¡- ‘ßÀ“§¡ 2559 °“√æ¬“°√≥å‚√§ “‡Àμÿ¢Õß°“√‡ ’¬™’«‘μ à«π„À≠à„πºŸâªÉ«¬ RPC ‰¥â·°à °“√μ‘¥‡™◊ÈÕ ¿“«–μ—∫ «“¬ À√◊Õ¿“«–·∑√°´âÕπ®“°μ—∫·¢Áß·≈–§«“¡¥—π„πÀ≈Õ¥‡≈◊Õ¥æÕ√å∑—≈ ßŸ 68 ‡ªìπμâπ πÕ°®“°π’ÈºŸâªÉ«¬¬—ß¡’§«“¡‡ ’Ë¬ßμàÕ°“√‡°‘¥‚√§¡–‡√Áß¢Õß∑àÕπÈ”¥’‰¥â√âÕ¬≈– 3-5 ºŸâªÉ«¬ RPC ∑’Ë¡’Õ“°“√·¬à≈ß√«¥‡√Á« ‡™àπ πÈ”Àπ—°≈¥≈ß¡“° ‡À≈◊Õß¡“° ¢÷Èπ√«¥‡√Á« À√◊Õ¡’§«“¡º‘¥ª°μ‘„π°“√∑”ß“π¢Õßμ—∫∑’Ë‰¡à¡’‡ÀμÿÕ◊ËπÕ∏‘∫“¬ §«√®– ß —¬‚√§¡–‡√Áß∑àÕπÈ”¥’´÷Ëß‡°‘¥„π RPC ‚¥¬∑—Ë«‰ª¡—°®–‡°‘¥‚√§¡–‡√Áß∑àÕπÈ”¥’¢÷Èπ„π °≈’∫μ—∫∑’Ë¡’°“√ΩÉÕ °“√»÷°…“‡æ◊ËÕ‡ª√’¬∫‡∑’¬∫º≈°“√√—°…“√–À«à“ßºŸâªÉ«¬‚√§¡–‡√Áß∑àÕπÈ”¥’∑’Ë ‡°‘¥æ√âÕ¡°—∫π‘Ë«„π∑àÕπÈ”¥’ °—∫ºâªÉ«¬‚√§¡–‡√Áß∑àÕπÈ”¥’∑’Ë‡°‘¥μ“¡À≈—ß‚√§π‘Ë«„π∑àÕπÈ”¥’Ÿ æ∫«à“°≈ÿà¡ºŸâªÉ«¬‚√§¡–‡√Áß∑àÕπÈ”¥’∑’Ë‡°‘¥æ√âÕ¡°—∫‚√§π‘Ë«„π∑àÕπÈ”¥’ ‰¥âº≈°“√√—°…“ ∑’Ë¥’°«à“ºŸâªÉ«¬‚√§¡–‡√Áß∑àÕπÈ”¥’∑’Ë‡°‘¥μ“¡À≈—ß‚√§π‘Ë«„π∑àÕπÈ”¥’83 °“√§—¥°√Õß‡æ◊ËÕ‡ΩÑ“√–«—ß¡–‡√Áß∑àÕπÈ”¥’„πºŸâªÉ«¬ RPC ¬—ß‰¡à¡’°“√»÷°…“ ‚¥¬μ√ß À√◊Õ§”·π–π”∑’Ë™—¥‡®π à«π°“√ àßμ√«®∑“ß‡´≈≈å«‘∑¬“ (cytology) ®“°°“√∑” ERCP ¡’§«“¡‰«μË”¡“°„π°“√«‘π‘®©—¬¡–‡√Áß∑àÕπÈ”¥’ ∑—Èßπ’ÈÕ“®æ‘®“√≥“„™â·π«∑“ß §—¥°√Õß¡–‡√Áß∑àÕπÈ”¥’‡™àπ‡¥’¬«°—∫§”·π–π”„πºâªÉ«¬Ÿ PSC ‚¥¬°“√μ√«® ultrasound ·≈– serum CA19-9 Õ¬à“ßπâÕ¬ªï≈–§√—Èß ·≈– àßμ√«®‡æ‘Ë¡‡μ‘¡¥â«¬ MRI/CT +/- MRCP „π√“¬∑’Ë ß —¬84 ‡Õ° “√Õâ“ßÕ‘ß 1. Digby KH. Common-duct stones of liver origin. Br J Surg. 1930;17:578-91. 2. Cook J, Hou PC, Ho HC, McFADZEAN AJ. Recurrent pyogenic cholangitis. Br J Surg. 1954;42:188-203. 3. Glenn F, Moody FG. Intrahepatic calculi. Ann Surg. 1961;153:711-24. 4. Miyake H, Johnston CG. Gallstones: ethnological studies. Digestion. 1968;1:219- 28. 5. Nakayama F, Soloway RD, Nakama T, Miyazaki K, Ichimiya H, Sheen PC, et al.

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