Case 1 - Click here for Text and References
Submitted by: Rish K. Pai
Clinical Summary:
The patient is a 20 year old male who was working as a missionary in Cambodia until a few weeks ago. While in Cambodia he developed low grade fevers associated with nausea, mild jaundice and occasional vomiting. He also developed a maculopapular rash on his torso and extremities. He was started on an unknown antibiotic and admitted to Royal Rattanak Hospital in Cambodia. He subsequently underwent a ultrasound of the gallbladder which revealed stones. He underwent a cholecystectomy that demonstrated multiple gallstones as well as a stone in the common bile duct. He was presumed to have ascending cholangitis and started in IV antibiotics. However, he continued to be febrile and had persistent elevations in his white blood cell count. A subsequent T-tube cholangiogram was normal. All hepatitis serologies, blood cultures, and stool studies (including ova and parasites) were all negative. He was discharged but was soon re-admitted due to persistent fevers and jaundice. He was then transferred to Bangkok Hospital Medical center. On admission in Bangkok he had a markedly elevated alkaline phosphatase at 1358 IU/L with only mildly elevated transaminases. ESR and CRP were elevated at 95 and 220 resepectively. An ERCP was performed and was normal. He had an extensive infectious disease work-up which was negative. His rash became worse during admission and cracked lips and conjunctivitis. He was subsequently transferred to the United States for further care. Upon admission in the US, LFTs were cholestatic with marked elevations in alkaline phosphatase and bilirubin. Another ERCP was performed which was normal. Biopsies were also taken from the stomach and duodenum. A liver biopsy was also performed in order to determine the etiology of the patient's liver disease.
Striking portal expansion.
Mixed infiltrate of neutrophils and eosinophils with ductular reaction.
Occasional neutrophils infiltrate the bile duct lumens.
Trichrome showing portal expansion
While the portal tracts are expanded, this is mostly due to edema rather than true fibrosis
Case 2 - Click here for Text and References
Submitted by: Grace E. Kim
Clinical Summary:
This seven year old boy presented with pruritus, poor growth, and abdominal pain and distension. His AST was 138 U/L, ALT 130 U/L, and GGT 19 U/L. The scanned slide is of his most recent liver biopsy. He was born at full term, and at two months of age was noted to have jaundice and scleral icterus with elevated transaminases and had a liver biopsy.
Vaguely nodular liver at low power.
Trichrome stain highlights many of the nodules are partially and focally completely surrounded by fibrosis.
Small lobular aggregate of mature lymphocytes and foci of cholestasis. Pseudoacinar structures are also seen.
Small ducts paired with similar sized artery within a fibrous band, but no significant ductular reaction.
Lobular sinusoidal fibrosis on trichrome stain.
Case 3 - Click here for Text and References
Submitted by: Henry D. Appelman
Clinical Summary:
This is the saga of a 55 or 45 or 65 year old slender man or woman who suffered from heartburn, dyspepsia and flatulence. After a few months of this agony, he/she consulted a family medicine doctor. As part of the flatulence work-up, all kinds of biochemical and hematologic tests were performed. The results included the following: AST 88, ALT 89, Alkaline phosphatase 90, and bilirubin, albumin, prothrombin time and partial thromboplastin time all normal as were the blood counts. The patient was treated empirically with proton pump inhibitors which partly relieved the symptoms. Additional clinical information included lack of exposure to virtually everything, use of NSAIDs for occasional back pain, daily multivitamins for general health, hemorrhoid cream for hemorrhoids and 2 shots of single malt scotch daily for fun Because of the original elevated aminotransferases, a repeat chemical liver profile was performed 6 months later with almost identical results. Additional iron and copper studies were normal. Since this was now a case of chronic low level parenchymal enzyme elevations, also known to the hepatology insiders as “transaminitis”, the patient was referred to a hepatologist who reviewed the clinical and laboratory data and ordered tests for hepatitis viruses and autoimmune markers. Everything was normal except for an ANA that was positive at 1:80. “Aha”, said the hepatologist to him/her-self, “this is a typical case of autoimmune hepatitis. It is time to get a liver biopsy to stage this disease”. So, the patient was sent to a radiologist, since only radiologists performed liver biopsies in this hospital. Of course the hepatologist did not tell the radiologist anything about the patient. The radiologist used a skinny needle and got about a 1 cm long core of liver, which was placed in formalin and sent to the pathology department with this fabulous clinical history: “abnormal LFTs”. The radiologist assumed that this was the proper history, since it was the history for virtually every other liver biopsy he/she had been asked to perform over the previous 20 years. The pathologist looked at the H and E and a bunch of other stains, including trichrome, iron, copper, reticulin, and PAS with and without diastase. The findings on the H and E sections are the only ones included, since the other stains were useless. The pathologist’s diagnosis was “mild chronic hepatitis” with a lot of other things. The case was billed as 88307 for the H and E and 5 88313s for the useless special stains. The hepatologist called the pathologist and asked if this was autoimmune hepatitis. The pathologist said that it might be. The hepatologist asked that the case be sent to a consultant which ticked off the pathologist who sent the case to the consultant with no clinical history other than for the “abnormal LFTs”. All the changes in the biopsy are included in the following images.
enlarged, pale hepatocytes with mild variation in cell and nuclear size and some binucleation
a touch of steatosis
low-grade pericentral sinusoidal dilatation without hepatocyte cord atrophy and a tiny lobular lymphocytic inflammatory focus, an hepatic zit
a slightly larger but still tiny lobular inflammatory focus or zit
a very mildly inflammed portal tract, mostly with lymphocytes and with a few eosinophils, plasma cells and macrophages
a single necrotic hepatocyte or DLC (short for dead liver cell)
a tiny cluster of macrophages full of necrotic liver cell debris, a tombstone
a minimicrogranuloma, 8 Kuppfer cells holding membranes
Case 4 - Click here for Text and References
Submitted by: Michael S. Torbenson
Clinical Summary:
A 17 year old young man presents with abdominal pain. There is no past medical history and the patient is taking no medications. Equivocal gynecomastia is present on physical exam. Imaging studies showed a single 9 cm right lobe liver tumor with intratumoral calcifications. Lymph nodes in the liver hilum are enlarged and suspicious for metastatic disease
Pertinent Laboratory Data:
ALT/AST: both minimally elevated. Alkaline phosphatase: 389 IU/ml Serum alpha-fetoprotein (AFP): normal Des-gamma carboxyprothrombin (DCP) : moderately elevated

