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Human Monoclonal Antibodies and Immune Modulation in Viral Hepatitis, Schistosomiasis, and HTLV Infection
Published in Thomas F. Kresina, Immune Modulating Agents, 2020
Thomas F. Kresina, Garry A. Neil, Steven K. H. Foung
Viral hepatitis is a systemic infection in which hepatic cell necrosis and inflammation result in a constellation of hepatic sequelae. The multiple viral agents have distinct immunoserological characteristics, specific epidemiological attributes, and separate causes. No single histopathological lesion in the liver is diagnostic for viral hepatitis. However, there are common inflammatory characteristics apparent in viral hepatitis. Acute portal hepatitis is characterized by edema and an inflammatory infiltrate comprising lymphocytes and histiocytes that enlarge portal tracts. In hepatitis C infection, focal bile duct lesions are common and in chronic infection can result in degenerative changes, including necrosis and periductular fibrosis. Necrosis of periportal hepatocytes and merger of portal and lobular inflammation are characteristic of “piecemeal necrosis” and can occur in either acute or chronic active hepatitis. A further characteristic of viral hepatitis is lobular disarray where spotty necrosis occurs and the inflammatory cells accumulate in areas of hepatocyte necrosis [47]. Thus, infection with hepatitis B virus or hepatitis C virus without subsequent resolution or cure results in hepatic inflammation that progresses to chronic hepatitis, cirrhosis, and primary liver cancer [48].
Organ-specific autoimmune diseases
Published in Gabriel Virella, Medical Immunology, 2019
Gabriel Virella, George C. Tsokos
Diagnosis of CAH is usually established by liver biopsy. Typically, the biopsy will reveal a picture of “piecemeal necrosis,” characterized by marked mononuclear cell infiltration of the periportal spaces and/or paraseptal mesenchymal-parenchymal junctions, often expanding into the lobules. Plasma cells are often prominent in the infiltrate. There is also evidence of hepatocyte necrosis at the periphery of the lobules, with evidence of regeneration and fibrosis. It is believed that this picture reflects an immune attack of the infiltrating lymphocytes directed against the periportal and paraseptal lymphocytes. In one-quarter to one-half of the patients (depending on the study), evidence of postnecrotic cirrhosis is detected; and in some patients, the evolution toward cirrhosis is progressive.
Metronidazole
Published in M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson, Kucers’ The Use of Antibiotics, 2017
Fulminant hepatitis has been described in association with metronidazole rechallenge in a 24-year-old woman, resulting in coma and subsequent death. Two years prior to this presentation she had been treated with metronidazole, which was also complicated by hepatitis, and following this insult, her transaminase levels improved but remained abnormal. At autopsy her liver showed fulminant necrosis (Bjornsson et al., 2002). Another 36-year-old woman developed deranged liver function tests following 5 days of metronidazole treatment. A liver biopsy confirmed acute hepatitis. This patient was then treated with two further courses of ornidazole. After each course of ornidazole, she developed biochemical evidence of hepatitis in association with nausea, vomiting, and jaundice. Her liver function tests failed to return to normal. On each occasion, a liver biopsy was performed that showed chronic hepatitis with piecemeal necrosis (Ersoz et al., 2001).
The effect of dexmedetomidine on liver injury secondary to lower extremity ischemia-reperfusion in a diabetic rat model
Published in Clinical and Experimental Hypertension, 2021
Seyfi Kartal, Ahmet Şen, Levent Tümkaya, Basar Erdivanlı, Tolga Mercantepe, Adnan Yılmaz
Group C showed typical Remark cords in normal appearing hepatocytes (Figure 2a–b). DM group showed focal necrotic hepatocytes with diffuse vacuoles and diffuse vascular congestions (Figure 2c–d). IR group showed extensive piecemeal necrosis, bridging necrosis, vascular congestions and moderate levels of leukocyte infiltration (Figure 2e–f). DEX group showed few necrotic hepatocytes among typical hepatocytes. Also, the degree of vascular congestion was less compared to DM and IR groups (Figure 2g–h).
Glycyrrhizin and Omega-3 fatty acids have hepatoprotective roles through toll-like receptor-4
Published in Egyptian Journal of Basic and Applied Sciences, 2019
Nada F. Abo El-Magd, Amro El-Karef, Mamdouh M. El-Shishtawy, Laila A. Eissa
Examination of TAA group showed moderate to severe necroinflammatory activity with average scores of (14.5) which characterized by marked piecemeal necrosis, zone 3 necrosis, multiple portal central bridging necrosis, frequent apoptosis, focal inflammation in addition to moderate and marked portal inflammation. TAA also significantly increased the amount of collagen deposition in liver tissue stained with Masson’s trichrome (Figures 8 and 9).
The Effect of Calcium Dobesilate on Liver Damage in Experimental Obstructive Jaundice
Published in Journal of Investigative Surgery, 2019
Yilmaz Unal, Salih Tuncal, Koray Kosmaz, Berkay Kucuk, Kemal Kismet, Turgut CAVUSOGLU, Pinar Celepli, Mehmet Senes, Selin Yildiz, Sema Hucumenoglu
The typical changes in histopathology are shown in Figure 1. In the control group, the sinusoidal structure was disrupted and focal inflammation, piece-meal necrosis, and confluent necrosis were evident. When compared with this group, the proliferation of bile duct in portal areas was found to have decreased and focal inflammation and necrosis were fewer in the CaDob group.