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Liver, Biliary Tract and Pancreatic Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Liver biopsy: This may reveal a chronic active hepatitis or cirrhosis. Periodic acid–Schiff (PAS)-positive, diastase-resistant globules in the hepatocytes containing α1-antitrypsin are characteristic but not specific.
Thorax
Published in Dave Maudgil, Anthony Watkinson, The Essential Guide to the New FRCR Part 2A and Radiology Boards, 2017
Dave Maudgil, Anthony Watkinson
Lymphoid interstitial pneumonia is associated with the following conditions. True or false? Acquired immune deficiency syndrome (AIDS).Chronic active hepatitis.Salivary gland enlargement.Parenchymal cysts.Centrilobular nodules.
Infection and sexual health
Published in David M. Luesley, Mark D. Kilby, Obstetrics & Gynaecology, 2016
Hepatitis B is a hepadna virus (DNA). It is endemic worldwide with high carriage rates of up to 20 percent in high-risk areas, such as South and East Asia, Central and South America, Africa and Eastern Europe. In the UK, 0.01–0.04 percent of blood donors have evidence of hepatitis B infection. In 2010, there were 5805 cases notified in England and Wales. Transmission is sexual, parenteral and vertical. The incubation is 40–160 days. It is mainly asymptomatic in children and in 10–50 percent of adults and is especially likely in coexistent HIV infection. The prodrome and icteric phases are similar to hepatitis A. Fulminant hepatitis can occur in <1 percent. Chronic infection (greater than six months) occurs in 5–10 percent and is more likely in HIV patients. Chronic active hepatitis can proceed to cirrhosis and liver cancer. Concurrent infection with HIV or hepatitis C worsens the disease. It is important to screen for other STIs, to check liver function and to advise to avoid sexual intercourse.
Triclabendazole for the treatment of human fascioliasis and the threat of treatment failures
Published in Expert Review of Anti-infective Therapy, 2021
Luis Marcos, Vicente Maco, Angelica Terashima
The migration of the juvenile parasite through the liver parenchyma causes fever, eosinophilia, liver abscesses, serpiginous track-like lesions, and hemorrhages. The imaging of the liver by computed tomography (CT) may show in the acute infection nodular and fusiform, low-density lesions distributed diffusely in the subcapsular and peripheral areas, hypondense serpiginous lesions with centripetal direction, subcapsular hematoma, and Glisson’s capsule (contrast-enhanced) and necrotic granuloma [15,20,25]. When a biopsy of the liver is performed for other reasons (i.e. rule out malignancy), the pathology report may show chronic active hepatitis with acute necrosis and presence of eosinophils in portal spaces [15]. After 6 months of successful treatment, CT of the liver may show residual ovoid-shape, calcified, popcorn-like lesions scattered throughout the hepatic parenchyma [20]. Fascioliasis may also mimic a hepatic tumor requiring invasive surgical procedures [26]. Occasionally, the larva may migrate during the acute infection to extrahepatic locations such as brain, subcutaneous tissue, or lungs causing significant morbidity [27,28]. In diagnosis, serologic tests can detect antibodies within 2 weeks after infection. The serological test is an antibody-based ELISA (96% sensitivity) using the Fasciola excretory/secretory proteins of the adult parasite [29,30].
Pharmacotherapy options for managing hepatitis B in children
Published in Expert Opinion on Pharmacotherapy, 2021
Haruki Komatsu, Ayano Inui, Sachiyo Yoshio, Tomoo Fujisawa
In the past decade however, the emerging data have challenged the notion that the immune-tolerant phase is a quiescent disease phase. Children and adolescents in the immune-tolerant phase showed the existence of an HBV-specific response which is less compromised than that in adults with chronic active hepatitis B [127]. Clonal hepatocyte expansion and HBV DNA integration to chromosomes, which contribute to the development of cirrhosis and HCC, are detected in liver tissues form children at the immune-tolerant phase [15]. These findings suggest that early therapeutic intervention might be necessary for HBeAg-positive children with normal ALT in order to prevent cirrhosis and HCC. Moreover, NAs give us an opportunity to treat children at the immune-tolerant phase. Antiviral therapy alters the balance between host immunity and viral replication. Weak virus-specific immunity is strengthened by antiviral therapy [128]. Lamivudine treatment induced the restoration of HBV-specific CTL reactivity in HBeAg-positive patients with chronic active hepatitis [129,130]. The combination of lamivudine with conventional IFN elicited a vigorous HBV-specific T-cell response in vertically infected HBeAg-positive children with normal ALT [131].
Lupus hepatitis, more than just elevated liver enzymes
Published in Scandinavian Journal of Rheumatology, 2020
W Afzal, M Haghi, SA Hasni, KA Newman
To date, there is no standardized treatment for LH. In a retrospective study of 238 SLE patients with elevated liver enzymes, 14 patients had no reason for elevated liver enzymes other than SLE. Twelve patients with liver disease were treated with corticosteroids for possible SLE rather than LH (4), and the results were transformation from chronic active hepatitis to chronic persistent hepatitis (n = 1); initial improvement but subsequent development of liver cirrhosis and death (n = 1); improvement in liver enzymes but development of fibrosis on histology (n = 1); improvement in liver enzymes with no follow-up biopsies (n = 5); and no improvement of liver enzymes (n = 4), of whom two later died because of liver failure (4). Despite this mixed response of LH to corticosteroids, they were continued to be used in subsequent studies. In a retrospective study, four (3%) out of 131 SLE patients had liver involvement due to LH with positive anti-ribosomal P antibody (8), and prednisone effectively improved symptoms in the majority of patients. Azathioprine has been used as steroid-sparing agent to avoid relapse, especially in chronic active hepatitis or in those with high ALT at the time of diagnosis (6). Mycophenolate mofetil may be considered in LH refractory to tacrolimus, azathioprine, and cyclophosphamide (66). There is a general agreement that corticosteroids may lead to a lowering of liver enzymes in LH; however, corticosteroid-induced NAFLD, and LH relapse upon cessation of corticosteroids, remain concerns (6, 15). Figure 1 illustrates LH diagnosis and treatment.