Special thanks to my GI attending, Dr. Jessica Tracht, for this helpful information.
(pictures/examples will be uploaded shortly)
This basically means there is active hepatitis.
You must see significant interface activity! This means that inflammation from the portal tract spills over the "limiting plate" and involves/damages the adjacent hepatocytes.
If fibrosis occurs it will be portal-based fibrosis.
ALT and AST will be elevated.
Significant interface activity
Increased portal inflammation.
Increased plasma cells.
Acidophil body formation (dead hepatocytes in the lobules).
Inflammation and hepatocyte damage going all the way to zone 3 (central veins) = panlobular hepatitis.
Helpful stains for medical liver:
Differential diagnosis for Hepatitic pattern of injury
VAD (viral, autoimmune, drug induced liver injury (DILI)! Always use this differential in your write up especially if it is unclear clinically what is going on. I usually put the differential I favor first. Below are some common features that may help you favor a particular etiology:
Favor Viral etiology
Predominantly lymphocytic infiltrate.
Lymphoid aggregate formation.
Positive viral serologies.
Note: HCV requires its own special write up that will be outlined elsewhere.
Favor Autoimmune etiology
Increased plasma cells.
Hepatocyte disarray at the interface.
Hepatocyte dropout or necrosis is more likely seen in AIH, and should be stated in the diagnostic line with a percentage.
Positive serology: ASMA, IgG >2,000, positive F-actin or other autoimmune markers.
Note: Some drugs can cause an autoimmune-like pattern.
Favor Drug-induced etiology
Clinical history of recent new medication use with elevated liver enzymes.
Very hard to completely rule this out.
Livertox.nih.gov is great resource for what medications can cause liver injury and what type of injury they case.
Note: Drugs can also biliary, steatotic, and cholestatic patterns of injury. They can also mimic autoimmune hepatitis.
Example Sign out
Liver, native, core biopsy:
-Panlobular hepatitis, at least moderate, with rare foci of dropout.
-Mild centrizonal fibrosis.
PATHOLOGIST'S COMMENT: The specimen consists of two adequate core liver biopsies. The portal tracts contain moderate to marked chronic inflammation consisting primarily of lymphocytes with rare plasma cells and eosinophils with evidence of interface activity. The interlobular bile ducts are intact but appear injured due to the surrounding inflammation. There is inflammation present throughout the lobules including foci of central perivenulitis with focal hepatocyte dropout. Since some of the portal tracts seem to be in close proximity, there was likely prior focal parenchymal collapse. There are numerous ceroid-laden macrophages throughout, consistent with prior injury. A trichrome stain is difficult to stage in the presence of hepatocyte dropout and collapse, but shows mild centrizonal sinusoidal fibrosis. An iron stain is negative. A PAS-D stain shows no PAS positive globules.
The patient’s history of negative viral and autoimmune serologies is noted. The differential diagnosis includes autoimmune, drug, or viral related etiologies. With negative viral serologies this most likely represents autoimmune hepatitis or an autoimmune pattern of drug induced liver injury (DILI). While autoimmune hepatitis remains a possibility, the inflammatory infiltrate does not have a predominance of plasma cells and the autoimmune serologies are negative, therefore autoimmune hepatitis-like DILI must be excluded.
Continue reading about the other patterns of pathology in medical liver...