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Duplication cyst. ÀÌ´Â ¾ö¹ÐÇÑ ÀǹÌÀÇ subepithelial cyst´Â ¾Æ´Õ´Ï´Ù. °ú°Å¿¡´Â malignancy¿Í °¨º°À» À§ÇÏ¿© ´ëºÎºÐ ¼ö¼úÀ» ÇÏ¿´À¸³ª ÃÖ±Ù¿¡´Â CT µîÀ¸·Î ÃßÀû°üÂû¸¸ ÇÏ´Â °æ¿ì°¡ ¸¹½À´Ï´Ù.
1³â »çÀÌ¿¡ »ó´çÈ÷ Ä¿Áø À§ »óÇÇÇÏÁ¾¾ç. »ó´çÈ÷ Ä¿Á³´õ¶óµµ Ưº°ÇÑ Ä¡·á´Â ÇÊ¿ä¾ø½À´Ï´Ù.
´Ù¹ß¼º ½ÊÀÌÁöÀå »óÇÇÇÏ Á¾¾ç. º°´Ù¸¥ ÀÓ»óÀû ÀÇÀÇ´Â ¾ø½À´Ï´Ù.
[¼Á¾¿Á ¼±»ý´ÔÀÇ ±â»ýÃæ°ú ³»½Ã°æ]
¼øõ °³¾÷°¡¿¡¼ È°µ¿ÁßÀÎ ¼Á¾¿Á ¼±»ý´Ô²²¼ ÀÌ¿ÕÀç ±³¼ö´ÔÀÌ ¹ßÇàÇÏ´Â °Ç°°ú »ý¸í 9¿ùÈ£¿¡ "±â»ýÃæ°ú ³»½Ã°æ"À» ±â°íÇϼ̽À´Ï´Ù. ¼Á¾¿Á ¼±»ý´Ô²²¼ Á¦°Ô PDF fileÀ» º¸³»¿À¼Ì½À´Ï´Ù. Èï¹Ì·Î¿î ³»¿ëÀÌ ¸¹¾Ò½À´Ï´Ù. Âü°íÇϽñ⠹ٶø´Ï´Ù.
2013³â 9¿ù 14ÀÏ Åä¿äÀÏ °ºÏ»ï¼ºº´¿ø¿¡¼ ±â´É¼ºÁúȯÇÐȸ ½ÉÆ÷Áö¾öÀÌ ¿·È½À´Ï´Ù. ÁÁÀº ÁÖÁ¦°¡ ¸¹¾Ò°í Åä·Ðµµ È°¹ßÇÏ¿´½À´Ï´Ù. Èï¹Ì·Î¿î Áõ·Ê Çϳª¿Í ÃÖ¸í±Ô ±³¼ö´ÔÀÇ Æ¯°À» ¿ä¾àÇÏ¿© ¼Ò°³ÇÕ´Ï´Ù.
[Áõ·Ê: Gastric band over-inflation¿¡ ÀÇÇØ ¹ß»ýÇÑ pseudoachalasia]
Áõ·Ê ¹ßÇ¥: 5³â Àü ºñ¸¸ Ä¡·á·Î gastric band (LapBand) ¼ö¼úÀ» ¹ÞÀº ȯÀÚÀÔ´Ï´Ù. ¼ö¼ú ÈÄ 1³â µ¿¾È 15 kg üÁßÀÌ °¨¼ÒÇÑ ÈÄ 3-4³â µ¿¾ÈÀº º¯È¾øÀÌ À¯ÁöµÇ¾ú½À´Ï´Ù. 1³â ÀüºÎÅÍ dysphagia°¡ ¹ß»ýÇÏ¸é¼ Ã¼ÁßÀÌ Ãß°¡·Î 20kg°¡ ºüÁ®¼ ³»¿øÇÏ¿´½À´Ï´Ù. ³»½Ã°æ, esophagography, esophageal manometry µîÀÇ Áø´ÜÀû °Ë»ç ÈÄ gastric bandÀÇ over-inflation¿¡ ÀÇÇÑ chronic concentric pouch dilatation°ú °ü·ÃµÈ pseudo-achalasia·Î Áø´ÜÇÏ¿´½À´Ï´Ù. Gastric band¿Í ¿¬°áµÈ ÇÇÇÏ port·ÎºÎÅÍ ÁÖ»ç±â·Î 4 cc Á¤µµ ¾×ü¸¦ aspirationÈÄ Áõ»óÀÌ È£ÀüµÇ¾ú½À´Ï´Ù.
Gastric band ¼ö¼ú: silicone band¸¦ proximal stomach¿¡ µÑ·¯ neo-stomachÀ̶ó°í ºÒ¸®´Â small pouch¸¦ ¸¸µë.
Esophagography¿¡¼ proximal stomachÀÌ È®ÀåµÇ¾î ÀÖ°í ±× ¾Æ·¡·Î ¹Ù·ýÀÌ Àß ³»·Á°¡Áö ¾ÊÀ½.
1) Áú¹®: 5³â Àü¿¡ gastric band¸¦ ÇÏ°í ¾à°£ üÁßÀÌ °¨¼ÒÇÑ »óÅ·ΠÀß À¯ÁöµÇ´Ù°¡ ¿Ö 1³â ÀüºÎÅÍ Áõ»óÀÌ ¹ß»ýÇÏ¿´À»±î?
¹ßÇ¥ÀÚ ´äº¯: ±âÁغ¸´Ù ¾à°£ tightÇÏ°Ô band°¡ Á¶¿©Áø °æ¿ì Á¡Â÷ÀûÀ¸·Î peristalsis°¡ °¨¼ÒµÇ¸é¼ ¸î ³â ÈÄ Áõ»óÀÌ ¹ß»ýÇÏ¿´À» °ÍÀÌ´Ù.
Floor ÀÇ°ß: Àß À¯ÁöµÇ´ø band°¡ 1³â Àü migrationµÇ¸é¼ Áõ»óÀÌ ¹ß»ýÇÑ °ÍÀÏ ¼ö ÀÖ°Ú´Ù.
2) Gastric band ÈÄ pseudo-achalasia°¡ ¹ß»ýÇÑ °ÍÀº ´ÙÀ½ ¼¼°¡Áö ÀÌÀ¯°¡ ÀÖÀ» °ÍÀ¸·Î ³íÀǵǾú½À´Ï´Ù.
[Ư° (ÃÖ¸í±Ô ±³¼ö´Ô): GI dysfunction in idiopathic Parkinson's disease]
ÃÖ¸í±Ô ±³¼ö´Ô ÆÀÀÇ ÆÄŲ½¼º´ °ü·Ã ¿¬±¸°ú ¸®ºä:
1) The prevalence and patterns of pharyngoesophageal dysmotility in patients with early stage Parkinson's disease. Mov Disord 2010;25(14):2361-8
These results suggest that the majority of patients with early-stage PD showed pharyngeal and esophageal dysfunction even before clinical manifestations of dysphagia, which may reflect selective involvement of either the brain stem or the esophageal myenteric plexus in early-stage PD.
2) Anorectal dysfunctions in Parkinson's disease. J Neurol Sci 2011;310(1-2):144-51
3) Anorectal manometric dysfunctions in newly diagnosed, early-stage Parkinson's disease. J Clin Neurol 2012;8(3):184-9
RESULTS: Anorectal manometry was abnormal in 12 of the 19 patients. These abnormalities were more common in patients with more severe anorectal symptoms, as measured using a self-reported scale. However, more than 40% of patients with no or minimal symptoms also exhibited manometric abnormalities.
CONCLUSIONS: These results suggest that anorectal dysmotility manifests in many early-stage PD patients, which this represent evidence for the involvement of neuronal structures in such nonmotor manifestations in PD.
ÃÖ¸í±Ô ±³¼ö´Ô²²¼ ¾ð±ÞÇϽŠHelicobacter¿Í ÆÄŲ½¼º´¿¡ ´ëÇÑ ¿¬±¸:
1) Helicobacter infection may play a causative role in the pathogenesis of PD by evoking autoimmunity against mitochondria, resulting in ENS damage. (Helicobacter hypothesis for idiopathic parkinsonism: before and beyond. Helicobacter 2008;13:309)
We challenge the concept of idiopathic parkinsonism (IP) as inevitably progressive neurodegeneration, proposing a natural history of sequential microbial insults with predisposing host response. Proof-of-principle that infection can contribute to IP was provided by case studies and a placebo-controlled efficacy study of Helicobacter eradication. "Malignant" IP appears converted to "benign", but marked deterioration accompanies failure. Similar benefit on brady/hypokinesia from eradicating "low-density" infection favors autoimmunity. Although a minority of UK probands are urea breath test positive for Helicobacter, the predicted probability of having the parkinsonian label depends on the serum H. pylori antibody profile, with clinically relevant gradients between this "discriminant index" and disease burden and progression. In IP, H. pylori antibodies discriminate for persistently abnormal bowel function, and specific abnormal duodenal enterocyte mitochondrial morphology is described in relation to H. pylori infection. Slow intestinal transit manifests as constipation from the prodrome. Diarrhea may flag secondary small-intestinal bacterial overgrowth. This, coupled with genetically determined intense inflammatory response, might explain evolution from brady/hypokinetic to rigidity-predominant parkinsonism.
2) A recent trial demonstrated that Hp eradication improved the clinical status of infected patients with PD and reduced motor fluctuations, possibly by eliminating Hp-induced interference with L-dopa absorption. (Helicobacter pylori infection and motor fluctuations in patients with Parkinson's disease. Lee WY. Mov Disord 2008;23:1696
HP infection could interfere with the absorption of L-dopa and provoke motor fluctuations. HP eradication can improve the motor fluctuations of HP infected patients with PD.
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