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The occurrence of hepatobiliary disease with or without jaundice during pregnancy provides both the hepatologist and obstetrician with an interesting and urgent diagnostic challenge. Advances in our understanding and management of liver disorders unique to pregnancy and hepatobiliary disease in general have resulted in a significant improvement in the outcome for both mother and fetus. Certain disorders such as acute fatty liver of pregnancy and hepatic haemorrhage associated with toxaemia should be considered medical emergencies and delay in diagnosis of these conditions will probably adversely affect maternal and fetal outcome. A careful clinical history, physical examination, appropriate laboratory tests and radiological investigations should allow a diagnosis within 24-48 hours of presentation. Liver biopsy is rarely required. A careful history may provide important information. Does the patient have pre-existent liver disease? Has there been contact with hepatitis, intravenous drug abuse or any other factor predisposing to acute viral hepatitis? Does the patient have a family history of pruritus and/or jaundice to suggest intrahepatic cholestasis of pregnancy? Is the patient's alcohol consumption excessive? Has the patient received any hepatotoxic medications? Has there been abdominal pain and/or fever to suggest gallstones, hepatic bleeding or acute fatty liver of pregnancy? Laboratory investigations may give valuable diagnostic clues. Marked aminotransferase elevation would suggest acute viral or 'ischaemic' hepatitis. Haematological features of microangiopathic haemolysis would point towards toxaemia or AFLP. Hepatitis A and B serological tests may be helpful in viral liver disease. Radiological investigations may be indicated depending on the clinical context. Abdominal ultrasonography may be useful in the diagnosis of gallstones, biliary obstruction, liver tumours or intrahepatic bleeding. Fatty infiltration of the liver may be diagnosed by ultrasonography but computed tomography (CT) of the abdomen is probably more reliable for a diagnosis of acute fatty liver of pregnancy as it allows measurement of liver density which is typically reduced by fatty infiltration. CT scanning is also probably more valuable than ultrasound in assessing the extent of capsular rupture and haemorrhage into the liver and peritoneal cavity.
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PMID:Jaundice in pregnancy. 265 65

A 39-year-old Japanese man with a splenic hamartoma who underwent surgery, is reported herein. The patient had a volvulus of the transverse colon and acute Type A hepatitis. His symptoms included fever, abdominal pain and icterus and the serum chemistry showed liver dysfunction and an elevation of hepatitis A antibody levels. Barium enema revealed a volvulus of the transverse colon. Ultrasonogram showed a hypoechoic mass and angiogram showed evidence of stretching of the intrasplenic vessels in the arterial phase and a hypovascular mass lesion in the venous phase. Macroscopically, the tumor was a well-defined, whitish-yellow, hard nodule. Microscopically, the tumor was composed of fibrous scar tissue containing scattered red pulp tissues and the histologic diagnosis was a splenic hamartoma of the fibrous type. The patient's postoperative recovery was uneventful. The clinical features of splenic hamartoma are reviewed in this report and the differential diagnosis is also discussed.
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PMID:Splenic hamartoma: report of a case and review of the literature. 267 8

During normal pregnancy, serum transaminase levels remain within normal limits. An elevated level observed in a pregnant woman always signals a disease process, most often of hepatic origin, but in certain cases, of muscular origin. During the last three months of pregnancy and in the immediate post partum period a large number of liver diseases can cause elevated transaminase levels, depending upon the clinical presentation. In everyday practice, a complete liver battery together with specialized consultation is required for all pregnant women with raised transaminase levels. Toxaemia gravis may be evident in patients with severely raised blood pressure, especially if seizures occur. Epigastric or subcostal pain should suggest hepatic involvement. Hypertension may however be absent and epigastric or left shoulder pain may be the only clinical signs. Acute liver steatosis is 20 to 50 times more rare than toxaemia and may cause nausea and vomiting. Certain non-specific signs such as asthenia, anorexia, polyalgia, abdominal pain, diarrhoea and fever, together with pruritus should suggest acute hepatitis. A 25-fold increase in transaminase level is commonly encountered. The risk of fulminating hepatitis is less than 1/1000 but should always be entertained. All drugs should be stopped and careful research for recent xenobiotic contamination (drugs, infusions, alphamethyldopa, etc.) should be undertaken. Viral hepatitis requires serovaccination of the newborn at birth. Herpetic hepatitis is rare but requires rapid diagnosis (liver biopsy) and treatment with acyclovir in addition to cesarean section and treatment of the newborn at birth. Rare cases of hepatitis E may occur after a stay in North Africa, the Middle-East, Southeast Asia or Mexico. Chronic cases with or without temporary pruritus suggest infectious hepatitis B or C although, in chronic hepatitis C, serum transaminase levels often return to normal during pregnancy. Rare cases of asymptomatic elevations of serum transaminase levels can reveal subclinical chronic hepatitis.
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PMID:[Significance of elevated transaminase levels at the end of pregnancy]. 802 21

A 27-yr-old Jamaican male presented with a 2-month history of jaundice, pruritus, intermittent diarrhea, and right upper quadrant abdominal pain. Over the next month, his abdominal pain and diarrhea improved, but his jaundice and pruritus worsened. He was afebrile and profoundly jaundice, with a benign abdominal examination. Medical workup included a normal abdominal ultrasound, iron studies, ceruloplasm, and serum electrophoresis. Negative viral (Epstein-Barr virus, cytomegalovirus, mononucleosis, hepatitis A, B, C) studies, ANA, AMA, ASMA, RPR were noted. He denied any alcohol, drug, or toxin exposure. Liver tests revealed total bilirubin of 25.6 mg/dl, direct bilirubin of 13.9 mg/dl, alkaline phosphatase 278 IU/L, AST 45 IU/L, and ALT 71 IU/L. Liver biopsy demonstrated centrilobular zonal necrosis and cholestasis most consistent with a toxic reaction. The patient was again interviewed regarding potential toxins, and he admitted to the ingestion of ackee fruit, a native Jamaican fruit that is illegal in the United States. Shortly after he had ceased intake of the fruit, his symptoms resolved and his liver function tests returned to normal. We present a case of chronic ackee fruit ingestion that led to cholestatic jaundice, vomiting, and abdominal pain.
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PMID:Cholestatic jaundice due to ackee fruit poisoning. 807 44

The 1988-1989 hepatitis A epidemic in the Palms section of Ocoee, Florida, followed sewage overflows and involved 39 cases and a fetal death. Of the 18 index cases (i.e., the first hepatitis illness in a household), each had a history of contact with sewage-contaminated stormwater and no other known contact with the infection. Illnesses varied from mild to severe; 20 people reported that diarrhea, abdominal pain, varying degrees of ascites, and other symptoms continued for 2 y after the initial illness. Health injuries up to 20 y of lost life, measured by CEA-Clinical Epidemiological AnalysisSM, were found. Public records of rainfall and sewage flows provide evidence of massive stormwater entry into the utility system, which periodically appears to have flushed sewage from the utility lift station into residential areas.
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PMID:Hepatitis A epidemics from utility sewage in Ocoee, Florida. 847 3

Giant hepatocytes are commonly found in several neonatal and infantile liver diseases, but are rarely found in adult liver disease. A 42 year old white woman presented with a five month history of paraesthesia and numbness of both the upper and lower limbs and with vague abdominal pain. Abnormal liver function was noted on routine screening. Ultrasound scan of the abdomen showed gallstones; barium enema, ERCP and computed tomography scan were all normal. IgG antibodies to double stranded DNA were present at a titre of 40 units. Anti-cardiolipin antibodies, anti-mitochondrial antibodies and rheumatoid factor were not detected. Serology for hepatitis A, B, C, and paramyxoviruses was negative, as was the Paul Bunnell test. A clinical diagnosis of systemic lupus erythematosus (SLE) with an axonal sensory polyneuropathy was made, the latter confirmed on biopsy of the sural nerve. Giant cells were noted on liver biopsy. The patient was treated with corticosteroids; liver function had improved after two years of follow up. When extensive giant cell transformation is noted on liver biopsy, particularly when neuropathy is also a feature, the possibility of an association with SLE should be considered.
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PMID:Giant cell hepatitis associated with systemic lupus erythematosus. 865 94

Since the initial report by Warren and Marshall in 1984, Helicobacter pylori has assumed an increasingly important role in the pathogenesis of peptic ulcer disease and gastric carcinoma in all ages. A recent National Institutes of Health Consensus Development conference acknowledges the relationship between H. pylori infection and peptic ulcer disease and recommends that the medical community treat H. pylori infection in all patients with Helicobacter pylori and peptic ulcer. Although the same organism, the response to Helicobacter pylori infection in childhood differs somewhat from that seen in adults. The paediatric patient mounts a different inflammatory response, has different macroscopic appearances and has a markedly diminished peptic ulcer disease frequency compared with their adult counterparts. The appearances of antral nodularity appear to be characteristic of Helicobacter pylori infections. The appearances, however, are unrelated to symptoms and the underlying cause for this nodularity remains obscure. Younger children with peptic ulcer diseases are more likely to be Helicobacter pylori negative. This may suggest an increased susceptibility to gastric acid or possibly a very transient Helicobacter pylori infection rather than the well described lifelong infection without treatment. It is well known that the epidemiology of Helicobacter pylori would suggest that the incidence of infection increases with age. There is also geographical variations with the incidence being higher in countries of a third world background. These epidemiological observations fly in the face of all other infections where the major period of acquisition is in childhood. There has been recent evidence to suggest that in fact the incidence in childhood is decreasing in developed countries which could support the observation that there is a decreasing positive serology with successive decades in some countries. It is felt that the most likely mode of transmission to Helicobacter pylori is faecal to oral or oral to oral route. These are similar modes of transmission to Hepatitis A infections. It is obvious that most infections in childhood remain asymptomatic. It is also clear that there is no relationship between chronic recurrent abdominal pain of childhood syndrome and the presence of Helicobacter pylori infections. It remains to be seen as to who should be treated, what with and when. All of these issues will be discussed in the paper.
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PMID:Current treatment of Helicobacter pylori infection and peptic ulcer disease. 923 May 34

A 3-year-old boy, who underwent multiple anaesthetics including halothane in a short period of time, developed 3 days after the last operation abdominal pain, jaundice and fever. Laboratory tests showed hepatic failure, with cytolysis, cholestasis and eosinophilia. Tests for hepatitis A, B, C, CMV and EBV were negative. No other causes of postoperative jaundice were identified. Despite symptomatic treatment, the child died 5 days after the last anaesthetic. Post mortem liver biopsy showed massive hepatic necrosis. The authors discuss factors increasing the risk for halothane-hepatitis, especially multiple exposures.
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PMID:[Fatal hepatitis in a young child: probable role of halothane]. 975 Jun 9

Association of hepatitis viruses with acute pancreatitis in the setting of nonfulminant viral hepatitis is rare. We report six cases of nonfulminant viral hepatitis complicated by acute pancreatitis, including the first documented case of hepatitis E virus (HEV) associated acute pancreatitis. The other five patients had acute viral hepatitis caused by hepatitis A infection. Besides features of viral hepatitis, the presence of typical abdominal pain, high serum amylase, and ultrasound or CT scan features suggested the diagnosis of acute pancreatitis. This complication generally developed in the initial phase of the hepatitic illness. All of the patients had mild to moderate pancreatitis that recovered uneventfully with conservative treatment.
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PMID:Acute pancreatitis associated with viral hepatitis: a report of six cases with review of literature. 1044 66

We describe a 23-year-old male patient who presented with epigastric abdominal pain, 8 days following vaccination with inactivated hepatitis A virus (Haverix(R)). Clinical and laboratory data confirmed the diagnosis of pancreatitis. Repeat polymerase chain reaction (PCR) for hepatitis A replication was negative. A comprehensive evaluation ruled out other etiologies for pancreatitis. IgM Hepatitis A antibodies did not develop even after 3 months. Pancreatitis following Hepatitis A is a well-known complication of the viremia, but the exact mechanism is controversial. We suggest that the pancreatitis may have been a cellular immunlogical reaction to one of the antigens of hepatitis A virus vaccine, or it might have been caused by the release of mediators of anaphylaxis such as histamine and leucotriens, induced by HAV antigens, resulting in pancreatitis without development of humoral immunization.
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PMID:Pancreatitis following hepatitis A vaccination. 1080 26


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