Hepatitis E is the fifth known form of human viral hepatitis. Although not very common in our clinical practice, the incidence in Western countries is increasing. Infection with the hepatitis E virus (HEV) may be related to acute illness, liver failure, chronic hepatitis and cirrhosis. HEV itself is an RNA virus, with eight described genotypes (HEV 1–8), four of which more commonly affect humans and have, thus, been better studied. Besides liver manifestations, genotype 3 is also related to extra-hepatic manifestations, such as neurological, renal and rheumatological. Evolution to chronic disease occurs especially in patients who underwent transplantation, have hematological malignancies requiring chemotherapy, or have infection with the human immunodeficiency virus. The diagnosis may be difficult because of the low availability of tests and due to low sensibility and specificity. The acute form of illness does not have to be treated, but the chronic one does. We present here a literature review of hepatitis E and the relation between chronic hepatitis E and transplantation.
The disease and the case reported here are relevant especially because of their varied clinical presentation, possibility of being associated with other disorders affecting several organs and possible differential diagnoses. Congenital Hepatic Fibrosis is an autosomal recessive disease due to mutation in the PKHD1 gene, which encodes the fibrocystin/polyductine protein. It is a cholangiopathy, characterized by varying degrees of periportal fibrosis and irregular proliferation of bile ducts. Affected patients are typically diagnosed in childhood, but in some cases the disease may remain asymptomatic for many years. The exact prevalence and incidence of the disease are not known, but it is consider a rare disease, with a few hundred cases described worldwide. It can affect all ethnic groups and occur associated with various hereditary and non-hereditary disorders. The clinical presentation is quite variable, with melena and hematemesis being initial symptoms in 30%-70% of the cases. More rarely, they may present episodes of cholangitis. The disease has been classified into four types: portal hypertension, cholestasis / cholangitis, mixed and latent. Diagnosis begins with imaging tests, but the definition is made by the histopathological sample. So far, there is no specific therapy that can stop or reverse the pathological process. Currently, the therapeutic strategy is to treat the complications of the disease.
Splenosis, one type of manifestation of ectopic spleen tissue, 1,2 is a heterotopic autotransplantation of splenic tissue after abdominal trauma or surgical intervention (Figures 1). Hepatic splenosis is very rare, usually asymptomatic and cannot be distinguished from hepatic malignancies because of lack of significant radiological features. 2,3 Therefore, suspicion is an important step for diagnosis and invasive procedures are usually necessary to establish a definitive diagnosis. An important differentiation is made with hepatic adenomas, which are generally benign and, if smaller than 5 cm and asymptomatic, do not require surgical treatment, but if they are larger, they should be resected, due to the risk of hemorrhage or malign transformation. 4 This was the initial suspicion in the presented clinical case and, therefore, the patient underwent surgical resection. Splenosis is a benign entity, but with several differential diagnoses and need for clinical correlation and images for correct definition .4-8 In patients with cirrhosis the most important differential diagnosis is with hepatocellular carcinoma and invasive procedures may be necessary for the definition. 4,9 In this article we describe a clinical case of hepatic splenosis, its differential diagnoses and review of imaging methods for diagnostic definition. Case presentation Male, 47 years old, with an incidental finding of hepatic lesion, during investigation of nephrolithiasis. Previous history of splenectomy after abdominal trauma due to automobile accident 20 years ago. Hypertensive in use Olmesartan, denied other pathologies and surgeries. On physical examination: good general condition, anicteric, painless abdomen, without palpable masses. Laboratory tests: Hb 14g/dL (13,5-17,5), Hct 44,4% (39-55), Platelets 268,000/ mm3 (150.000-400.000), creatine 0,9mg/dL (1,5), INR 0,8, CEA 1,33 ng/mL (<3,0), CA 19-9 20U/mL (<37), AFP 1,5ng/dl (<7,22), albumin 4,19g/dL (3,4-4,8), AST 20U/L (17-55), ALT 18U/L (21-71), GGT 54U/L (15/73), AP 48U/L (38-126), total bilirrubin 0,57mg/ dL (0,2-1,3). MRI showed nodular hepatic lesion, 42x41x28mm, slight hyperintense in T2, with contrast enhancement and washout in late phase, in segment II, without dilatation of biliary tract (Figures 2). The initial diagnosis was hepatic adenoma. Proceeded with hepatic segmentectomy, with good evolution. The surgical specimen referred to pathological anatomy and revealed hepatic splenosis (Figures 1).
Background: Crohn’s disease (CD) and ulcerative colitis (UC) are chronic diseases that result from the deregulation of the mucosal immune system of the gastrointestinal tract. The use of biological therapies, including infliximab (IFX), is one of the strategies to treat both CD and UC. The IFX treatment is monitored by complementary tests, namely: fecal calprotectin (FC); C-reactive protein (CRP); and endoscopic and cross-sectional imaging. Besides, serum IFX evaluation and antibody detection are also used. Objective: To evaluate trough levels (TL) and antibodies in a population with inflammatory bowel (IBD) disease undergoing treatment with IFX, and the factors that might impact the treatment effectiveness. Methods: Retrospective, cross-sectional study with patients with IBD that were assessed for TL and antibody (ATI) levels in a southern Brazilian hospital, from June 2014 to July 2016. Results: The study assessed 55 patients (52.7% female) submitted to serum IFX and antibody evaluations (95 blood samples, 55 first test; 30 second test, and 10 as third testing. Forty-five (47.3%) cases were diagnosed with CD (81.8%), and ten with UC (18.2%). Serum levels were adequate in 30 samples (31.57%), subtherapeutic in 41 (43.15%), and supratherapeutic in 24 (25.26%). IFX dosages were optimized for 40 patients (42.10%), maintained for 31 (32.63%), and discontinued for 7 (7.60%). The intervals between infusions were shortened in 17.85% of the cases. In 55 tests (55.79%), the therapeutic approach was exclusively defined according to IFX and/or serum antibody levels. The assessment of patients one year later indicated that: the approach was maintained with IFX for thirty-eight patients (69.09%); the class of biological agent was changed for eight (14.54%); changes using the same class of biological agent occurred for two patients (3.63%); the medication was discontinued and not replaced for three patients (5.45%), and four patients (7.27%) were lost to follow-up. Conclusion: There were no differences in TL between groups with or without immunosuppressants, serum albumin (ALB), erythrocyte sedimentation rate (ESR), FC, CRP, and endoscopic and imaging examinations. Current therapeutic approach could be maintained for almost 70% of patients. Thus, serum and antibody levels are a useful tool in the follow-up of patients undergoing maintenance therapy and after treatment induction in patients with inflammatory bowel disease.
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