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Autoimmune Hepatitis A Case Report and Literature Review.
Hong, AS, Desta, M, Hong, JM, Ohning, GV, Pillinger, MH, Saxena, A, Modjinou, DV
Bulletin of the Hospital for Joint Disease (2013). 2019;(2):146-152
Abstract
INTRODUCTION Autoimmune hepatitis (AIH) is a cause of chronic liver disease. It is usually suspected based on clinical presentation and laboratory findings, but the diagnosis relies on the presence of specific autoantibodies and characteristic histology. Other unexplained findings should always prompt investigation for coexisting syndromes. CASE PRESENTATION The patient is a 60-year-old Hispanic female with a history of mild asthma presented with exertional and pleuritic chest pain with weight loss, arthralgia, subjective fever, and night sweats for the last 3 months. Given the nonspecific nature of the presentation, further workup was pursued. Laboratory results indicated pancytopenia, elevated INR, and positive autoimmune panel including ANA, anti-chromatin, anti-histone, and rheumatoid factor as well as abnormal C3 and C4. Subsequent liver biopsy with interface hepatitis lead to a diagnosis of AIH with concurrent systemic lupus erythematosus suspected. CONCLUSION The diagnostic work up for AIH is multimodal and aims to differentiate other etiologies such as congestive hepatopathy, iron overload, viral hepatitis, and other autoimmune liver diseases. In this particular case, unusual clinical and laboratory findings led to diagnosis of the overlap syndrome. Treatment for both was necessary to prevent further progression of disease.
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2.
Literature review of liver injury induced by Tinospora crispa associated with two cases of acute fulminant hepatitis.
Huang, WT, Tu, CY, Wang, FY, Huang, ST
Complementary therapies in medicine. 2019;:286-291
Abstract
INTRODUCTION Species of Tinospora are used as herbal remedies for the treatment of various diseases with very few toxic effects having been reported. Tinospora cordifolia (TCF) has been reported to effectively prevent hepatotoxicity. However, there are an increasing number of cases revealing that Tinospora crispa (TCP) might have the negative effect of inducing hepatotoxicity. Because of the similar leaves, people may mistake TCP for TCF, and consume it with the purpose of protecting liver function. OBJECTIVE Find out the misusing level of TCP and TCF and which chemical compound in TCP might induce hepatotoxicity. METHODS We report two cases of acute fulminant hepatitis associated with chronic use of TCP. Given that the two herbs were misidentified in these two reports, we investigated the frequency of erroneous identification by using three keywords ("Guduchi", "Tinospora cordifolia", "Tinospora crispa") to search images from the Google Images database. To further clarify the influence of liver function between TCP and TCF, we searched PubMed (up to 29 July 2018) for relevant publications on clinical trials or case reports. RESULTS Based on web review, over 35 percent of websites failed to accurately identify these two herbs. The different effects on liver function between TCP and TCF were compared through literature review. It indicated that TCF exerted liver protection, TCP had a contrary effect, suggesting its cis-Clerodane-type furano-diterpenoids might be an important factor of inducing hepatotoxicity. CONCLUSIONS We concluded that people might cause hepatic injury or even death without correctly identifying these two Tinospora species.
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3.
[Wilson's disease - a case report].
Karwowska, K, Skrzypek, J, Chabik, G, Członkowska, A, Zaborowska, M, Wawrzyniak, S
Polski merkuriusz lekarski : organ Polskiego Towarzystwa Lekarskiego. 2016;(235):28-31
Abstract
Wilson's disease (WD) or hepatolenticular degeneration, is a rare autosomal recessive genetic disorder caused by mutations in the Wilson disease protein (ATP7B) gene. It is characterized by impaired copper metabolism leading to its accumulation in various tissues and organs, including the liver and central nervous system, this results in the development of characteristic liver disease and neuropsychiatric symptoms. Liver symptoms usually appear during first three decades of life, while psychiatric symptoms are observed in people who are in their twenties or older. WD is one of few genetic diseases that can be effectively treated with pharmacotherapy. However, some cases, especially diagnosed late in the course of the disease, may not respond well to treatment. Here we present a case of a 22-year-old male with neurological, psychiatric and liver disease symptoms as an example of diagnostic and therapeutic challenges in patients. Wilson's disease (WD) should be considered in all patients presenting with neurological, psychiatric and liver disease symptoms especially those of young age.
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4.
Hepatic fibrinogen storage disease: identification of two novel mutations (p.Asp316Asn, fibrinogen Pisa and p.Gly366Ser, fibrinogen Beograd) impacting on the fibrinogen γ-module.
Asselta, R, Robusto, M, Braidotti, P, Peyvandi, F, Nastasio, S, D'Antiga, L, Perisic, VN, Maggiore, G, Caccia, S, Duga, S
Journal of thrombosis and haemostasis : JTH. 2015;(8):1459-67
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Abstract
BACKGROUND Quantitative fibrinogen deficiencies (hypofibrinogenemia and afibrinogenemia) are rare congenital disorders characterized by low/unmeasurable plasma fibrinogen antigen levels. Their genetic basis is invariably represented by mutations within the fibrinogen genes (FGA, FGB and FGG coding for the Aα, Bβ and γ chains). Currently, only four mutations (p.Gly284Arg, p.Arg375Trp, delGVYYQ 346-350, p.Thr314Pro), all affecting the fibrinogen γ chain, have been reported to cause fibrinogen storage disease (FSD), a disorder characterized by protein aggregation, endoplasmic reticulum retention and hypofibrinogenemia. OBJECTIVES To investigate the genetic basis of FSD in two hypofibrinogenemic patients. METHODS The mutational screening of the fibrinogen genes was performed by direct DNA sequencing. The impact of identified mutations on fibrinogen structure was investigated by in-silico molecular modeling. Liver histology was evaluated by light microscopy, electron microscopy and immunocytochemistry. RESULTS Here, we describe two hypofibrinogenemic children with persistent abnormal liver function parameters. Direct sequencing of the coding portion of fibrinogen genes disclosed two novel FGG missense variants (p.Asp316Asn, fibrinogen Pisa; p.Gly366Ser, fibrinogen Beograd), both present in the heterozygous state and affecting residues located in the fibrinogen C-terminal γ-module. Liver sections derived from biopsies of the two patients were examined by immunocytochemical analyses, revealing hepatocyte cytoplasmic inclusions immunoreactive to anti-fibrinogen antibodies. CONCLUSIONS Our work strongly confirms the clustering of mutations causing FSD in the fibrinogen γ chain between residues 284 and 375. Based on an in-depth structural analysis of all FSD-causing mutations and on their resemblance to mutations leading to serpinopathies, we also comment on a possible mechanism explaining fibrinogen polymerization within hepatocytes.
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How much did you take? Reviewing acetaminophen toxicity.
Janssen, J, Singh-Saluja, S
Canadian family physician Medecin de famille canadien. 2015;(4):347-9
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Autoimmune hepatitis with giant-cell transformation.
Estradas, J, Pascual-Ramos, V, Martínez, B, Uribe, M, Torre, A
Annals of hepatology. 2009;(1):68-70
Abstract
BACKGROUND/AIMS: Giant-cell hepatitis (GCH), also known as postinfantile or syncytial giant cell hepatitis, is a frequent pattern of liver injury in the neonate, primarily seen in the first three months of life. Few cases in adults have been reported, some of them associated to autoimmune diseases such as autoimmune hepatitis. METHODS We present a case of autoimmune hepatitis with giant cell transformation in a 39 year old male with polyarthritis. We discuss his clinical presentation and course. We made a review of the literature of agents associated to this diagnosis, the mechanisms involved in the formation of giant hepatocytes, the histological findings, clinical course, treatment options and prognosis of this rare entity. RESULTS AND CONCLUSIONS In conclusion, the clinical course varies from normalization of hepatic histology to progression to cirrhosis and liver failure. The prognosis is dictated by the underlying liver disease and in the setting of autoimmune hepatitis the clinical course is usually severe with most of the patients progressing to cirrhosis. Prolonged treatment with corticosteroids and immunosuppressants is usually effective in rendering the cirrhosis inactive.
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Terbinafine hepatotoxicity. A case report and review of literature.
Zapata Garrido, AJ, Romo, AC, Padilla, FB
Annals of hepatology. 2003;(1):47-51
Abstract
We report a 53-year old Mexican female who developed liver dysfunction following a seven-day course of treatment with terbinafine for onychomycosis. She presented with jaundice and abdominal pain. Her serum bilirubin levels showed a peak value of 23.2 mg/dL seven weeks after discontinuing the medication. Infectious causes (hepatitis viruses A, B and C) were excluded. Imaging studies of the abdomen did not reveal any abnormalities. Serum iron and ceruloplasmin levels were normal. Autoantibodies were negative. A liver biopsy revealed necrosis and mononuclear infiltration of the parenchyma, mainly along the sinusoids and surrounding the portal spaces and biliary ducts. Eosinophil infiltration of the portal spaces was also noted. Treatment with ursodeoxycholic acid and ademethionine was started. Her liver tests normalized in the sixth months after stopping terbinafine.
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Liver involvement and abnormal iron variables in undiagnosed Addison's disease.
Rizvi, AA, Kerrick, JG
Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists. 2001;(3):184-8
Abstract
OBJECTIVE To describe a case of untreated Addison's disease manifesting as severe gastrointestinal symptoms, persistently increased liver enzymes, substantially increased ferritin, and hepatic iron deposition and to document changes in these variables after corticosteroid replacement. METHODS We thoroughly reviewed the clinical history and results of laboratory tests before and after treatment in a 23-year-old man during a period of 18 months. The relevant medical literature was also reviewed. RESULTS The study patient had frequent episodes of severe abdominal symptoms, hemodynamic instability, and electrolyte imbalance. He underwent extensive laboratory investigations and was prescribed various treatment regimens. Increased levels of serum transaminases, ferritin, and transferrin saturation led to a liver biopsy, which showed lymphocytic infiltration and increased iron deposition. Eventually, cosyntropin stimulation (250 microg) confirmed the presence of adrenal insufficiency, and these abnormalities resolved after institution of daily administration of glucocorticoids and mineralocorticoids. CONCLUSION Addison's disease can be a cause of unexplained hypertransaminasemia and profoundly increased ferritin levels. These changes are reversible but may lead to diagnostic confusion and delay in commencement of lifesaving corticosteroid therapy.
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Terbinafine-induced hepatic dysfunction.
Chambers, WM, Millar, A, Jain, S, Burroughs, AK
European journal of gastroenterology & hepatology. 2001;(9):1115-8
Abstract
A 41-year-old man developed severe hepatic dysfunction following a 3.5-week course of terbinafine (250 mg/day). He suffered marked pruritus, jaundice, malaise, anorexia and loin pain. Serum bilirubin rose to a peak value of 718 micromol/l with alkaline phosphatase at 569 U/l, alanine aminotransferase at 90 U/l, aspartate aminotransferase at 63 U/l and a prolonged prothrombin time of 21 s, unresponsive to vitamin K. Transjugular liver biopsy showed canalicular cholestasis consistent with a drug reaction. Symptoms resolved 11 months after drug cessation, with liver function tests returning to normal values after 15 months. This case represents the most severe cholestatic reaction reported to date, resulting in patient recovery without liver transplantation. A comprehensive literature review is provided.