A 54-year-old woman Para 5 was admitted to the hospital because of increasing abdominal enlargment. She felt well until a year ago, when abdominal distention gradually developed.In abdominal ultrasongraphy a coarse, echogenic liver and ascites was detected, the spleen was enlarged and other intraabdominal organs were normal. Abdominal paracentesis was performed. Serum-ascites albumin gradient was greater than 1.1 gr/dl (high serum-ascites albumin gradient).Laboratory-tests for evaluating the etiology of cirrhosis revealed: HBs Ag: Neg , HBc Ab: Neg , Hcv Ab: Neg , Anti HBs: Pos.ASMA (anti smooth muscle antibody):NegANCA (anti neutrophilic cytoplasmic antibody):NegANA (anti nuclear antibody):NegAMA (anti mitochondrial antibody):NegSPEP (serum protein electrophoresis):Normal range The patient had no history of hepatotoxic drug usage.In upper GI endoscopy two columns grade II varicose veins were seen.Based on the history and para clinic evaluation cryptogenic cirrhosis was the most probable DIAGNOSIS.The patient underwent medical therapy with furosemide and spironolactone, and in regular follow up amount of ascites was under control.A month ago the amount of ascites increased and several therapeutic paracentesis were performed.Ascites analysis showed high serum-ascite albumin gradient and negative cytology for malignancy.Ultrasonography reported multiple focuses on peritoneal surface with seeding like appearance, cirrhotic liver, enlarged spleen and massive ascites, normal kidneys and uterus and ovaries. Tumour markers measurement revealed:CEA=0.3 (Normalrange=0 - 5ng/ml)aFP=0.4 (Normalrange=0 - 10IU/ml)CA 125=244 (Normalrange= 0 - 35 IU/ml)Abdominal and pelvic CT scan didn't show any tumoural lesion and no paraaortic lymphadenopathy. Trans vaginal sonography reported normal uterus and ovaries. Further tumour marker analysis revealed:Elevated serum level of CA 125to 414 IU/ml CV'CA 15- 3 = 27 (normal = up to 40 IU/ml)JLJCA 19- 9 = 25 (normal = up to 40 IU/ml)A week later level of CA 125 decreased to 262. Therefore we obtained fluctuating level of CA 125, normal CT scan and normal level of other tumour markers.We found in papers from other countries in the same situation that they performed laparotomy but they found nothing except cirrhosis (l).In some articles CA 125 presented as a marker of ascites in patients with liver cirrhosis (2). Some authors suggested that quantification of CA 125 in peritoneal fluid (PCAI25) and serum (SCA125) can differentiate between cancer cases and non cancer disease, and they found that ratio of PCA125 to SCA125 (PIS CA125) was significantly lower in non cancer patients than that in cancer ones. (lf the ratio is upper than five the risk of malignancy increased) (3). We quantified CA125 level simultaneously in peritoneal fluid and serum: PCA125 = 210, SCAl25 = 250, PIS CA125 = 0.84.The ratio of 0.84 was predictive of a benign disease. In an overview to our patient, we had one sonography that reported seeding like appearance in peritoneal surface, but in CT scan no lesion was detected. Fluctuating level (increase decrease) of CA125 and low PIS ratio, normal level of other tumour markers, made us to come to the final step oflaparoscopic examination and biopsy to determine whether it is malignant or benign.In laparoscopic examination no cancerous lesion or fibrin deposit or tuberculosis granolurna with normal omentum and cirrhotic liver detected.Multiple biopsies were taken from peritoan beside liver which reported normal (no: 159104).We came to this conclusion that in cirrhotic patient with ascites the elevated level of CA125 with normal level of other tumour markers and low PIS ratio and no malignant finding in imaging is suggestive of a benign process, as described in other articles.More studies on this matter should be performed in order to prevent the unnecessary laparatomies.

A 46 years old gentleman was admitted to hospital following a 10 months history of sever diarrhea. On examination, the patient appeared as mildly dehydrated though his vital sings were within normal limits. important result tests were:Bun=55 mg/dl Na=149 mEq/dl WBC=11.6*103/mlHemoglobin=16.2 g/dCr=3 mg/dl K=3.9 mEq/dl HCT=49.7% Plt=324*103 Tbo/ulNeutr=74%After ten days administration of IV fluid, BUN and createnine gradually became normal (Cr=1.1mg/dl, BUN=14mg/dl).There was no macroscopic or microscopic gastrointestinal pathology in upper and lower endoscopy. We took biopsies even from ileum terminal.We suspected endocrine tumors and pancreatic disorders, so we requested abdominal and pelvic CT scan (IV and oral contrast) and hormonal tests such as serum cortisole, metanephrin, normetanephrine, which were all normal. We therefore did an octrotide scan which was again normal.Because almost all organic etiologies of chronic diarrhea were excluded, we focused on neurological and psychological causes of chronic diarrhea. Therefore we consulted with neurologist & psychiatrist and they recommended brain CT scan and EEG which were normal. After complete interview, the psychiatrist diagnosed PTSD and depressive disorder NOS and prescribed imipramin 25 mg/day. After 10 days the chronic diarrhea improved.As we excluded all the organic causes, we concluded likely the patient had IBS with PTSD and depressive disorder NOS.

Introduction: Superior mesenteric syndrome is not a very common disease but it has a relatively simple pathophysiology. Being compressed by SMA from above to underlying structures of retro peritoneum like abdominal aorta, third part of duodenum is obstructed and causes the patient acute, or chronic and intermittent symptoms of obstruction.Case report: A 24 years old man with 4 years history of dysphagia to solid foods, complained of weight loss, semi liquid food dysphagia dysphonia and eyelid ptosis.In upper GI endoscopy; esophagus was normal, stomach was dilated and clues of food stasis were seen. Endoscopic Biopsies were normal. The patient underwent CT scanning in which stenosis of third part of the duodenum and dilatation of the proximal part to the stenosis are seen. After 3D reconstruction of CT scan images, it was noticed that the angle of origin of superior mesenteric artery from aorta was decreased.Conclusion: predisposing factor to superior mesenteric syndrome is excessive cachectia and since MNGIE syndrome appears with dysphagia, malnutrition and cachectia, the fat pad between aorta and superior mesenteric artery regresses and this can results in superior mesenteric artry syndrome.