A 30 year old South-Asian female presented with 5 day history of high fever associated with severe myalgia, headache and yellowish discoloration of the skin. There was no history of contact with muddy water, alcohol consumption, or use of any drugs including antibiotics, anti-pyretics (acetaminophen) or antiemetics. Furthermore history of blood transfusion, sexual promiscuity or any other high risk behavior could not be elicited. She denied any pale stools or pruritus. At the time of admission, general examination revealed she was febrile and icteric but had no conjunctival hemorrhage, pallor, lymphadenopathy, rashes or scratch marks. The respiratory system was unremarkable and the abdominal examination did not elicit right hypochondrial tenderness, palpable gall bladder or abdominal guarding. The cardiovascular examination was normal and she had an initial blood pressure of 90 mmHg systole and 60 mmHg diastole, without a postural drop. She was conscious, alert, well oriented and nervous system examination was otherwise unremarkable.\nThe initial complete blood count revealed thrombocytopenia with a platelet count of 69 × 109/L (150–450), a normal white blood cell count (WBC) of 10.4 × 109/L (4–11) with a predominance of lymphocytes (55%) and a hemoglobin of 11.0 g/dL (11–17) . The blood picture mirrored the whole blood analysis and showed only thrombocytopenia, there was no neutrophil left shift or toxic granules and the red cell indices were normal. Liver functions showed a mildly elevated aspartate transaminase(AST) and alanine transaminase(ALT) which were 80 U/L(0–40) and 38 U/L (0–35 ) respectively with an elevated alkaline phosphatase(ALP) value of 450 U/L (100–360). Serum direct and total bilirubin levels were elevated at 6 mg/dL (0–0.3) and 9.1 mg/dL (0.3-1.9) respectively. Serum albumin was found to be reduced with a value of 2.3 g/dL (3.5 -5.5), with a normal international normalized ratio (INR). The renal functions were within normal reference range. The C- reactive protein (CRP) and erythrocyte sedimentation rate (ESR) were also within normal parameters. The following day the platelet count continued to drop and her jaundice deepened. A positive dengue non- structural protein1antigen test (NS1) and a positive dengue IgM antibody ELISA test on day 6 confirmed the clinical suspicion and diagnosis of dengue fever. Hepatitis B surface antigen, hepatitis C antibody, hepatitis A and E antibodies, Ebstein Barr Virus antibody and a retroviral screening were all negative. Leptospira microscopic agglutination test (Lepto MAT) titres were insignificant at 1:200 on day 6 and the titre value remained unchanged when the repeat test was performed on day 12 of the illness (a four -fold rise in titre or a high titre >1:800 is the gold standard for diagnosis). Blood cultures remained repeatedly negative.\nThe platelet count continued to drop rapidly in the following days reaching the lowest nadir value of 3 × 109/L (150–450) with rising alkaline phosphatase and bilirubin levels (Table ). On day 6 of the illness the patient became afebrile. As per the local guidelines and WHO dengue guidelines on management of critical phase of dengue hemorrhagic fever, she was maintained on a fluid regimen tailored to her body weight, with strict monitoring of the blood pressure, pulse pressure, heart rate and urine output.\nOn day 7 the patient became mildly tachypnoeic, and examination revealed reduced air entry in the right lung base which was stony dull to percussion and deep icterus, further abdominal examination elicited a small shifting dullness, signifying ascites. An ultrasound scan was done and confirmed a small right sided pleural effusion, an enlarged liver of 16 cm, without intra or extra hepatic bile duct dilatation, a thickened gall bladder wall of 7 mm in the absence of any gall stones and a sonographic Murphy’s sign could not be elicited. Mild ascites was also noted. The blood pressure and urine output were maintained. A packed cell volume was done and showed only a mild rise. The fluid regimen was continued as per guidance, giving adequate fluids to maintain blood pressure and urine output.\nOn day 9 of the illness, the patient’s clinical status and jaundice improved. Serial complete blood counts showed rising platelet counts. Similarly liver function tests revealed normalizing alkaline phosphatase and bilirubin levels. The patient was discharged on the 15th day of illness with normal cell counts and liver function parameters.\nA 46 year old previously well South-Asian female, presented with six days of high fever, myalgia and jaundice. She too denied any history of contact with muddy water, recent drug usage, blood transfusion or any high risk behavior. On examination, she appeared ill, febrile to touch and deeply jaundiced. Abdominal examination revealed a mildly tender and firm hepatomegaly. The gallbladder was not palpable nor was there guarding or a positive Murphy’s sign. The respiratory system examination revealed reduced air entry on auscultation and stony dullness to percussion in the base of the right lung. The cardiovascular examination was unremarkable, with a blood pressure of 100mmHg systole and 70 mmHg without a postural drop. The nervous system examination was normal.\nWhole blood analysis on presentation demonstrated thrombocytopenia with a platelet count of 10 × 109/L (150–450) and a lymphocytic predominant (51%) white cell count of 7.8 × 109/L (4–11) with a haemoglobin value of 11.6 g/dl with a packed cell volume of 34%. The liver enzymes were elevated with the AST more than the ALT which were 242 U/L (0–40) and 120 U/L(0–35) respectively. The alkaline phosphatase was mildly elevated with a value of 400 U/L (100 – 360), with a high direct bilirubin fraction of 12 μmol/L (0–3.4) and total bilirubin of 23 μmol/L (5–21). Albumin was found mildly reduced at 31 g/L (36–48). The INR was normal. The renal functions were normal. The ultrasound scan of the abdomen and chest confirmed an enlarged liver, with a cranio-caudal length of 16 cm. The gallbladder wall was thickened and measured 6 mm, a negative sonographic Murphy’s sign was noted and no gall stones were visualized. Leakage was confirmed as there was mild ascites and a pleural effusion in the right hemithorax. The ESR was 19 mm for the first hour and the CRP was mildly elevated with a value of 7 mg/L (0.0 – 5.0). The dengue IgM antibody was positive. A Lepto MAT was performed twice on day 7 and day 11 of the illness, and showed a titre of 1:400 (a four -fold rise in titre or a high titre >1:800 is the gold standard for diagnosis) without further rise. A hepatitis screen was performed and was found negative. EBV antibody was also negative. This patient was similarly managed with a fluid regimen tailored to her body weight as per guidance, with strict monitoring of hemodynamic parameters and urine output.\nThe platelet count continued to drop reaching a nadir of 5 × 109/L (150–450) on day 8 of the illness, and subsequently began to rise. The alkaline phosphatase and bilirubin continued to rise till day 10 of the illness, after which the liver functions began to normalize (Table ). The patient was discharged on day 12 of the illness, being afebrile for 4 days with a platelet count of 128 × 109/L (150–450) and a near normal bilirubin level.
A 53-yr-old man from Golpayegan, Isfahan Province, central Iran, with past history of cholecystectomy referred with complaint of vague colicky epigastric pain begun 2 yr from presentation and had fluctuation during the time. The pain became severe and constant gradually, with the peak about 4 months ago, led him to seek medical attention. There was no relationship between food consumption, especially high fat-containing meals, and pain severity. At the beginning of the disease course, the pain had been relieved by anti-acids but eventually, none of the outpatient medications made him free of pain. He did not mention any urticarial reaction, jaundice, nausea, vomiting, night sweats or pruritus during these two years, but he had history of occasional fever without any specific pattern accompanied by chills within this period. He did not have anorexia, but had increased appetite instead; constipation was a cardinal symptom along with malaise. Significant weight loss (about 10 kg) occurred late in the course of his disease (i.e. the last 2 months).\nThe patient agreed to be presented in this report and a written consent was signed by him. He was formerly a farmer and husband-man and from one year before the onset of disease (i.e. 3 yr from now), he was a trucker and had history of traveling around the country and taking unsafe and insanitary food and water. He denied consumption of any illicit drugs, alcohol, and opium at all, but he used to smoke cigarettes. No special medication he was taking.\nOn physical examination, he was afebrile and moderately ill, with stable vital signs and normal sclera without icterus. There was no rash or signs of excoriation, no conjunctivitis, no lymphadenopathy, no gynecomastia and abdominal distention. There was not any abnormality in cardiovascular and lung examination. Right upper quadrant tenderness existed on abdominal palpation, without rebound tenderness and organomegaly. Musculoskeletal and neurologic examinations were normal. The results of initial laboratory investigations are presented in . The first colonoscopy survey was normal and initial evaluation by upper gastrointestinal endoscopy revealed mild antral gastritis. Abdominal ultrasonography revealed dilated CBD without any visible lesion at its end. A hypo-echo mass lesion suggesting pathologic lymph node was seen lateral to aortic bifurcation, at left side. Abdominal CT-scan suggested dilated intra- and extrahepatic biliary ducts and CBD with 10 mm diameter and also some large intestinal lymph nodes with compressive effect on adjacent structures.\nThe second upper gastrointestinal endoscopic survey had the same result as the first.\nDuring Endoscopic retrograde cholangiopancreatography (ERCP), dilated common bile duct (CBD) about 12 millimeter and large ampulla were seen. After sphincterotomy, multiple flat whitish parasites were incarcerated behind Oddi’s sphincter and within common bile duct, which extracted. There was no stone in CBD and ampulla did not contain any mass. Serologic exam, using ELISA method was performed by somatic antigen of Fasciola and yielded positive according to the reference laboratory cut-off.\nThe patient was treated with triclabendazole 250 mg, three tablets daily, for two executive days (six tablets totally) successfully and he pains relieved after ERCP and full course of treatment. He advised not to use unsanitary food and water. On follow up, he was well and did not mention any similar abdominal pain as before.