Magnet Compression Anastomosis for Bilioenteric Anastomotic Stricture after Removal of a Choledochal Cyst: A Case Report / 대한소화기내시경학회지

Magnet compression anastomosis is a nonsurgical method that uses two magnets to treat bilio-biliary and bilio-enteric anastomotic strictures after a living donor transplantation. The compression pressure of the two magnets induces ischemic necrosis at the anastomostic stricture and creates a fistula at the stricture site. A choledochal cyst is an uncommon congenital anomaly characterized by dilatation of the biliary tree and can cause obstructive jaundice, cholangitis, biliary stones, and cholangiocelluar carcinoma. Treatment for choledochal cyst is essentially surgical including total excision of the cyst with hepaticoenterostomy, but there can be complications such as postoperative intrahepatic stones and recurrent cholangitis due to a stricture at the site of the anastomosis. Endoscopic and fluoroscopy-guided radiologic interventions can be applied to resolve the anastomotic stricture, and re-operation is possible as the method of last resort. We report here a first case, trial magnet compression anastomosis in Korea of a bilioenteric anastomotic stricture after excision of a choledochal cyst and hepaticojejunostomy.

Case of Colonic Polyps with Abdominal Splenosis Mimicking Carcinomatosis / 대한내과학회지

Splenosis is an ectopic implantation of splenic tissue after splenic injury or splenectomy. These splenic implants may be located throughout the abdominal cavity and may be misdiagnosed as a malignancy or tumorous condition. Here, we report a case of splenosis that was initially diagnosed as carcinomatosis from colon cancer in a patient with colon polyps that had undergone explo-laparotomy.

Portal Vein Thrombosis Associated with Antiphospholipid Syndrome / 대한류마티스학회지

Antiphospholipid syndrome is a disorder characterized by the presence of antiphospholipid antibodies, recurrent arterial and/or venous thromboembolism, and spontaneous abortion. Deep vein thrombosis, pulmonary thromboembolism, and cerebral infarction are major thrombotic event, but portal vein thrombosis, especially in young age male, is rarely reported. A 27-year- old man, without prior thrombotic event, presented with severe abdominal pain for 4 days. Extensive portal vein thrombosis was noted on abdominal CT scan and MR angiography. Lupus anticoagulant was suspected and was confirmed according to the guidelines of the International Society on Thrombosis and Hemostasis and the patient was diagnosed as having primary antiphospholipid syndrome associated with portal vein thrombosis. Intravenous heparin infusion was initiated and switched to warfarin upon discharge. Now the patients is being followed in outpatient clinic and treated with warfarin without any evidence suggesting the recurrence of thrombotic event.

Uremic Encephalopathy Associated with Bilateral Basal Ganglia and Cerebellar Lesion in a Non-diabetic Hemodialysis Patient / 대한신장학회잡지

Involvement of central nervous system is a well- known compication in uremic patients. However, development of acute extrapyramidal symptoms with bilateral basal ganglia involvement (acute basal ganglia syndrome), especially in non-diabetic hemodialysis patient is very rare. We report a case of acute basal ganglia syndrome in a non-diabetic hemodialysis patient. A 45-year-old man with autosomal dominant polycystic kidney disease (ADPKD) on chronic hemodialysis treatment for the last 4 years was admitted due to generalized myalgia. On admission, the patient was found to have rhabdomyolysis and intractable metabolic acidosis. Nine days after admission, he suddenly developed dysarthria, lateralizing ataxia, and bradykinesia. Brain MRI demonstrated low and high signals in bilateral basal ganglia and cerebellar vermis in T1-weighted and T2-weighted images, respectively. Intensified hemodialysis treatment combined with general supportive therapy resolved the severe metabolic acidosis and the neurologic manifestations gradually improved. Follow up brain CT scan taken 3 months later showed decreased size of initial low attenuation lesions in bilateral basal ganglia and cerebellar vermis. Although no definite pathophysiology is yet established, severe metabolic disorder is believed to play an important role in development of acute basal ganglia syndrome. Correction of metabolic acidosis and hypoglycemia in our patient lead to improvement in neurologic manifestations and organic brain lesions. Our case suggests that severe metabolic acidosis and hypoglycemia in uremic patient may act as risk factors for acute basal ganglia syndrome even in non-diabetic patient.