This case emphasizes the sudden unexplainable deterioration of com-pensated liver cirrhosis in the presence of cryptococcal infection, causingthe rapid demise of patient. Cirrhotics should also be considered as severelyimmunocompromised and be searched for the evidence of an opportunicinfection, e.g. cryptococcal infection, in the case of sudden deterioration oftheir compensated condition. This will be extremely crucial in liver trans-plant setting.

586

Abdominal pain and weightloss due to? gastric polypsTC Chauhan, MD; M Cerulli, MD FACG; I Ho, MD FACG V. Amin,MD. The Brooklyn Hospital Center, Brooklyn NY 11201

Background: Failure to evaluate patient as a whole and attributing symp-toms to a trivial incidental finding often leads to undesirable outcome forour patients.Case Report: As a Primary Care Physician, I saw a 56 years lady forweight loss. She has abdominal discomfort for past six months and haddwindled from 130 to 86 pounds. Her exam was significant for cachexiaand left supraclavicular node.

She was already seen by a Gastroenterlogist and had EGD, Colonoscopyand Abdominal CT done. She had multiple gastric polyps, all Hyperplasticon biopsy. She even had Laproscopic Cholecystectomy without improve-ment in her symptoms. She was referred to University center for treatmentof gastric polyps. After multiple EGDs, she had About 30 polyps removed,all Hyperplastic. Her dyspepsia was attributed to her obsessive nature. Twothings tipped me off-her weight loss and palpable supraclavicular node. Iarranged for her to have an ERCP done by another Gastroentrologist. Shewas found to have “Double Duct sign” and positive cytology due toinoperable pancreatic cancer.Teaching Points: 1. Do not attribute weight loss to psychogenic illnessuntill thorough workup is done. 2. Gastric Polyps are NOT known cause ofabdominal pain. 3. Do not recommend Cholecystectomy without justifica-tion to cure abdominal pain. 4. Appropriate clinical evaluation shouldalways precede any endoscopic work. 5. When evaluating patient with lossof weight with CT, Specify that you want thin cuts to visualize pancreatictumors, if any.Reference: Pg 780, Gastrointestinal Diseases, Sleishenger, 5 th E.

587

Hepatotoxity due to yet another herbalTC Chauhan, MD; M Cerulli, MD FACG; J. Geders, MD FACG: I.Ho,. MD FACG; V. Notar-Francesco, MD FACG; W. Sohn, MD M.Reddy, MD. The Brooklyn Hospital Center, Brooklyn NY 11201.

Background: Herbal preparations are known to have unpredictable andOften harmful effect on liver. This is the first reported case of liver toxicityfrom Chinese rice tea.Case Report: A 40 year old lady from Sri Lanka, presented with jaundice.Medical history was positive for only IDDM. She denied OTC or herbs. Onexam, she had few scratch marks, but no organomegaly. Her admissionlaboratory work (shown in the table) was very suggestive of obstruction.An abdominal CT was normal.

Liver biopsy was reported as–“Intrahepatic centrilobular cholestasis withdiscreet microvescicular steatosis and reactive, occasionally bineucleatedhepatocytes. Portal spaces are expanded by inflammatory edema Withpolymorph, few eosinophils and lymphocytic infiltrate.”

Test Admission Day 2 Day 6 Day 20

T.Bili 9.2 14.2 9.0 2.0D.Bili 7.4 11.2 7.4 1.3AST 219 103 73 17ALT 408 269 141 26ALP 435 448 327 161PT 15 18 17 13

Her liver enzymes started to normalize while she was in hospital. Whenshe was told that her liver was damaged by some medicine or chemical, sheconfessed that she had been using Chinese rice tea until her admission. Itcontains kelp and it is claimed to improve diabetes. She promised not to usethe herb again. During her follow up at week 3, her LFTs returned to nearnormalTeaching Point: Many medicines and herbs are known to have hepato-toxicity, but there was no reported case with Chinese Rice Tea. Theclinician must be aware that any herbal preparation may have hepatotox-icity and detail and direct questions must be asked as the patient may notbe aware of it.

588

Postpartal abdominal distentionTC Chauhan, MD; M Cerulli, MD FACG; I Ho, MD FACG L Liang,MD FACG. The Brooklyn Hospital Center, Brooklyn NY 11201.

Clinical Information: A 19 year old Hispanic female was seen in con-sultation by GI team to evaluate her abdominal discomfort and distention.She was 6 weeks post C-section. She had no nausea or vomiting, but mildcramps in abdomen. Due to symptoms of URI, her PMD started her onCephelexin 500 po QID for 10 days. During the third month of herpregnancy she experienced hairless and skin rash.

On exam, she had pedal edema and, fluid thrill and shifting dullness.Abdominal x-ray showed distended bowel loops and ground glass appear-ance. Significant labs-Albumin 2.4, LFTs and PT/PTT-normal, C.Diff�,ESR-20, At 5th month-C3 was 27 and C4 � 1.5 (both normal)

WHAT IS YOUR DIAGNOSIS?

1. Hypoalbuminemia leading to ascites2. Antibiotic associated C. Diff with colonic distention and ascites3. Primary peritonitis secondary to c-section, now masked by antibiotics4. Urinary ascites secondary to ureteric injury during c-section5. Ascites with CHF in post-partal myocarditis v/s myocarditis in SLE6. Serositis due SLE7. Exacerbation of SLE causing nephrotic syndrome/nephritis

WHAT TESTS WOULD YOU LIKE TO ORDER INITIALY?Abdominal US only confirmed ascites, ascitic tap showed abl-1.9, amylase-13, BUN zero. Colonoscopy showed petechial lesions, Biopsy confirmedvasculitis. 24-hour urinary protein was normal, C3 was 42.4 and C4 was4.4.

Teaching Points: 1. C. Diff colitis is not associated with ascites, but allother conditions mentioned above needs to be considered in differentialdiagnosis. 2. Post-partal flare of SLE should be considered due to historyof hair loss and that was her diagnosis. 3. It responds well to Prednisone andPlaquinil.

589

Fatal acute post-transfusional hepatitis C in a cirrhoticAhmad Cheema, M.D.1, Kapil Mehta, M.D.1, Abdul Nadir, M.D.1 and David Van Thiel, M.D.1*. 1Gastroenterology and Hepatology, LoyolaUniversity Medical Center, Maywood, Illinois, United States.

Purpose: Post-transfusion hepatitis has diminished to less than 5% in thelast decade because of better screening. Usually, acute HCV is asymptom-atic. Herein, we report a case of HCV that was acquired from transfusionin a cirrhotic awaiting liver transplantation in 2000.Results: This 55-year-old white male was admitted to the hospital withpainless jaundice. A diagnosis of alcohol-induced cirrhosis had been es-tablished previously with a liver biopsy and absence of other liver markersincluding HBcAb (total), HCV-Ab (Elisa III), HCV-RNA, HBV-DNA,ANA and a normal iron saturation. He denied using any new medications,including OTCs and recreational drugs. His physical exam was significant

S186 Abstracts AJG – Vol. 96, No. 9, Suppl., 2001

for obvious jaundice and mild peripheral edema, without any ascites,asterixis, or hepato-splenomegaly. Laboratory evaluation revealed an ALTof 1109 u/l, AST of 1460 u/l, Alk Phos of 258 u/l and T-bili of 14.6 mg/dl.He had received 3 units of pRBCs, 10 weeks earlier, after an episode ofesophageal variceal bleeding. Work up of jaundice, including an abdominalCT scan and an ERCP, was negative. Liver biopsy showed severe panlobular hepatitis with a lymphocyte predominant inflammatory infiltrate.Retesting for HCV-Ab and HCV-RNA was positive with viral load greaterthan 850,000 RNA copies/ml. IFN-� was begun within one week ofdiagnosis. During 7 weeks of therapy, virologic parameters improved withnear normalization of liver enzymes but clinical deterioration ensued, withonset of encephalopathy, severe ascites, neutropenia, and bacterial perito-nitis with VRE infection. He became hemodynamically unstable, devel-oped renal failure and died one week later: 2 months after the first increasein liver enzymes.Conclusions: This case highlights that even with improved HCV screen-ing, occasional transmission of HCV is possible. This happened probablyas a result of intermittent viremia that caused no detection of HCV at thetime of testing of the transfused blood. This caused a fatality in thisreported case.

590

Dermatomyositis: esophageal involvement and association withesophagitisMichael Y. Chen, M.D.*, David J. Ott, M.D., F.A.C.G. Department ofRadiology, Wake Forest University School Medicine, Winston-Salem,NC 27157.

Dermatomyositis is a collagen vascular disorder that may affect multipleorgan systems, including the esophagus. Esophageal dysmotility andesophagitis related to infection or reflux disease are the most commonmanifestations. We present a 51 year-old man with skin lesions and muscleweakness as a result of dermatomyositis; he was being treated with oralsteroids and presented with dysphagia. Barium esophagram and esophagealendoscopy both revealed a diffuse esophagitis, which was due to candidainfection. In this exhibit, the clinical history is reviewed more thoroughlyand the radiographic and endoscopic findings are discussed and illustrated.The clinical and pathologic features of dermatomyositis are also reviewedwith an emphasis on the esophageal involvement that may be seen in thisdisease.

591

‘Dropped’ gallstones: imaging appearances and clinical importanceMichael Y. Chen, M.D.*, David J. Ott, M.D., F.A.C.G. Department ofRadiology, Wake Forest University School Medicine, Winston-Salem,NC 27157.

During cholecystectomy, gallstones may migrate from the gallbladderunintentionally and remain in the peritoneal cavity, being called ‘dropped’gallstones. Although an uncommon occurrence, the prevalence of this eventand its clinical importance are uncertain. We present a 27 year-old femalewith sickle cell anemia who had a laparoscopic cholecystectomy for gall-stones. During the operative procedure, several pigmented gallstones‘dropped’ from a hole in the infundibulum of the gallbladder; however, allwere felt to be removed with a stone forceps. Following cholecystectomy,the patient presented with abdominal pain which likely was related to asickle cell crisis. Abdominal imaging with plain radiographs, ultrasound,and CT examination showed the presence of calcified densities which hadthe appearance of gallstones. In this exhibit, we present the clinical historyof this patient more thoroughly and also illustrate the findings of theimaging modalities used. The clinical impact and potential importance of‘dropped’ gallstones are reviewed.

592

Splenic vein thrombosis associated with hyperhomocysteinemiaPeter Chen1, Kim-Wing Ng1*, So-Wan Tan1, Chaw-Fung Jiang1, Kuo-Hsin Chen2 and Shwe-Winn Chen3. 1Division of Gastroenterology, Deptof Medicine, Far Eastern Memorial Hospital, Taipei, Taiwan; 2Dept ofSurgery, Far Eastern Memorial Hospital, Taipei, Taiwan; and 3Dept ofMedicine, Yo-Ming Hospital, Chung-Li, Taiwan.

Purpose: Splenic vein thrombosis (SVT) results in gastric varices whichmay rupture and lead to clinically significant upper gastrointestinal hem-orrhage. We report a case of SVT without apparent cause. The onlyassociation was hyperhomocysteinemia. Hyperhomocysteinemia have beenreported to be associated with arterial and venous thromboembolic disor-ders.Case Report: A 40-years-old male presented to FEMH with passage oftarry stool. He had history of AMI 6 years ago. Renal insufficiency wasnoted since then. No history of alcoholism, liver disease or pancreatitisbefore. Abdominal examination revealed enlarged spleen. Abnormal labdata included Hb 4.9 g/dl, Hct 14.9%, PT 14.0 sec (control 12.1 sec), BUN97 mg/dl, Cr 3.1 mg/dl and uric acid 10.3 mg/dl. EGD revealed chronicDU. Abdominal USG showed marked splenomegaly and chronic renalparenchymal disease. Abdominal CT and MRI confirmed SVT, but liverand pancreas appeared normal. Proetin C, protein S, anti- thrombin III andanti-phospholipid antibodies were within normal limits. Splenectomy wassuggested but patient refused. 8 months later, the patient was readmitted forpassage of tarry stool and vomiting of fresh blood. EGD revealed isolatedfundal varices in addition to DU. Plasma homocysteine was 19.02 mmol/L(4.45–12.42 mmol/L). Splenectomy and devascularization was performedthe next day. Operative findings confirmed SVT and congestive spleno-megaly with normal liver and pancreas. The patient developed AMI on 6thpost-op day and died on 7th post-op day.Conclusions: 1. SVT should be considered in differential diagnosis ofsplenomegaly with and without isolated gastric varices. 2. Hyperhomocys-teinemia may be considered in differential diagnosis of unexplained SVT.

593

Spontaneous intra-abdominal hemorrhage due to intra-abdominalvarices ruptureKim-Wing Ng1*, So-Wan Tan1, Peter Chen1, Chaw-Fung Jiang1 andKuo-Hsin Chen2. 1Division of Gastroenterology, Dept of Medicine, FarEastern Memorial Hospital, Taipei, Taiwan; and 2Dept of Surgery, FarEastern Memorial Hospital, Taipei, Taiwan.

Purpose: 5% of patients with cirrhotic ascites presented with spontaneousbloody ascites. One-third of these patients is due to leakage from hepaticlymph or small blood vessel. Two-third bleeds abruptly with hemodynamicinstability. One of the causes in the latter cases was rupture of intra-abdominal varices. We report a case of liver cirrhois with spontaneousrupture of intra-abdominal varices.Case Report: A 45-years-old male, a chronic alcoholic, presented toFEMH with right flank pain. He had history of liver cirrhosis for more than10 years. He was positive foe HBsAg and HCV Ab He had undergonedevascularization and splenectomy 10 years ago because of EV bleeding.On admission, the patient was lethargic with BP 84/53 mmHg, PR 124/min,RR 40/min. His conjunctiva was pale with iceteric sclera. Abdomen wasdistended but non-tender with hypoactive bowel sounds. Hb was 6.0 g/dl,Hct 19.1%, platelet 96 � 103/ mL, PT 25.4 sec/11.9 sec and APTT 56.3sec/28.5 sec. Abdominal CT showed liver cirrhosis, post-splenectomy,ascites and left pleural effusion. After fluid resuscitation, including bloodtransfusion, abdominal tapping was performed. 50 cc of non-coagulableblood was obtained. Exploratory lapatomy was performed on 10th hospitalhour. 9850 cc of bloody ascites was found. Prominent intra-abdominalvarices with 2 bleeders was found in abominal wall. Suture ligation ofbleeding varices was performed. The patient died on 39th hospital hour.Conclusions: Intra-abdominal varices was first recognized by Ellis in1958. 24 cases of spontaneous bleeding of intra-abdominal varices have

S187AJG – September, Suppl., 2001 Abstracts