Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical case of one patient with fever of unknown origin, due to granulomatous hepatitis of tuberculous etiology was presented. The patient was a a 50-year-old woman, with 50 days illness characterized by chills, 39 degrees C fever and heavy diaphoresis. She had a record of seven malaria cases. She looked thin and pale at the initial physical examination. During the evolution, she developed pancytopenia, massive hepatosplenomegaly, jaundice, and anasarca. The patient underwent screening tests for infection, neoplasias, collagenosis, and granulomatous diseases. The laboratory tests showed transaminase-alkaline phosphatase dissociation, which led to the final diagnosis of tuberculosis, through the histological examination of the liver parenchyma. The specific treatment against tuberculosis caused remission of fever, ascites, and hepatomegaly and normalization of liver tests, with satisfactory clinical evolution.
 ...
PMID:[Granulomatous tuberculous hepatitis as cause of fever of unknown origin]. 1252 48

Acute C hepatitis, compared with hepatitis A or B, may sometimes be associated with extrahepatic manifestations of a haematologic nature. The first case of hepatitis associated with aplastic anemia was reported by Lorenz in 1955. We observed a patient who developed acute hepatitis, associated with febrile purpura: pancytopenia was present, but not aplasia. This association is frequent in Flavivirus-related infections, like Dengue and Yellow Fever, and principally affects children and young people. HCV belongs to the Flavivirus family and so in this case clinical signs may have developed as a consequence of HCV infection.
 ...
PMID:[Hepatitis C virus infection mimicking hemorrhagic fever: a case report] 1271 45

A 21-year-old man was admitted to our hospital for acute hepatitis of unknown cause. His liver function improved with rest, but worsened 2 months later. He developed a high fever and pancytopenia. The serum level of cytokines including TNF-alpha, IFN-gamma, IL-6, and M-CSF was elevated, and hemophagocytes were seen in bone marrow. These findings suggested a hemophagocytic syndrome-like state. With prednisolone, gamma-globulin, and G-CSF, the high fever disappeared and the patient's liver function gradually recovered. However, the severe pancytopenia persisted. The bone marrow became acellular with a small number of hemophagocytes, and hepatitis-associated aplastic anemia was diagnosed. After immunosuppressive therapy with ATG, CyA and G-CSF was started, and the patient showed hematopoietic reconstitution. The bone marrow CD4+/CD8+ lymphocyte ratio recovered to within the normal range, and the serum cytokines including TNF-alpha and IFN-gamma decreased. The increase in serum cytokines, particularly TNF-alpha and INF-gamma, as well as the presence of activated T cells associated with the preceding hemophagocytic syndrome-like state may have predisposed this patient to aplastic anemia.
 ...
PMID:[Hepatitis-associated aplastic anemia preceded by a hemophagocytic syndrome-like state]. 1463 47

A 54-year-old female experienced morning stiffness and arthralgia of the hands from November 2001 and consulted her local doctor in January 2002. Hematological data showed liver dysfunction and antinuclear antibody was positive. In February 2002, the patient was admitted to our hospital to investigate these abnormalities of liver function further. The features of arthritis, thrombocytopenia with elevated platelet-associated IgG, positive antinuclear antibody, and anti-DNA antibody lead to a diagnosis of systemic lupus erythematosus. Liver biopsy revealed infiltration of Glisson's capsule by plasma cells, compatible with autoimmune hepatitis. We performed hepatic venography to investigate severe pancytopenia, remarkable splenomegaly and esophageal varices. Wedged hepatic venous pressure was mildly elevated, and hepatic veins displayed sharp angles, smooth walls and development of anastomosis with each other. These findings suggested idiopathic portal hypertension. Cytopenia and liver dysfunction gradually improved on treatment with 40 mg/day prednisolone. Esophageal varices were disappeared, and splenomegaly had improved after 6 months. As autoimmune factors are considered to underlie the development of idiopathic portal hypertension with systemic lupus erythematosus, steroid administration represents a therapeutic option in this condition.
 ...
PMID:[Beneficial effect of glucocorticosteroids for esophageal varices due to idiopathic portal hypertension following systemic lupus erythematosus]. 1504 15

The haemophagocytic syndrome is defined as a proliferation of phagocytic macrophages in the bone marrow, lymph nodes and spleen. Clinically, it is characterised by fever and pancytopenia. We present here a case of haemophagocytic syndrome after liver transplantation in a 63-year-old man who had undergone transplantation for autoimmune hepatitis. One month after liver transplantation, he developed ascites, fever and progressive pancytopenia. Bone marrow biopsy showed proliferation of non-neoplastic histiocytes, demonstrating phagocytosis of haemopoietic cells. No infectious or neoplasm-associated disease was found. Several kinds of treatment were attempted, but the course was fatal. The haemophagocytic syndrome is uncommon after liver transplantation, but this diagnosis has to be kept in mind in cases of pancytopenia of unknown origin.
 ...
PMID:Haemophagocytic syndrome after liver transplantation in adults. 1505 81

We report a 22-year-old female who presented with pyrexia, pancytopenia and liver dysfunction. The patient showed mild liver dysfunction with low-grade fever and mild hepatosplenomegaly 6 years previously, and autoimmune hepatitis (AIH) was diagnosed based on the examination of the laboratory data and liver biopsy. On admission, both markers of Epstein-Barr virus (EBV) and in-situ hybridisation from a liver biopsy specimen indicated chronic active EBV infection (CAEBV). The patient was administered an immunosuppressive agent and antiviral drug added to steroid therapy, but ultimately died from liver failure and virus-associated haemophagocytosis 10 months after the definite diagnosis. Retrospective examination of the serum at the diagnosis of AIH revealed extremely high titres of antibody to EBV, and EBV-DNA was also detectable by polymerase chain reaction. These results suggest the possibility that the patient may already have suffered from CAEBV at the initial diagnosis. We presume that hepatic involvement of CAEBV should be considered as differential diagnosis in cases showing liver dysfunction with clinical and biochemical features observed in AIH.
 ...
PMID:Fatal chronic active Epstein-Barr virus infection mimicking autoimmune hepatitis. 1507 99

We report herein a 21-year-old hepatitis B virus (HBV) female carrier who developed persistent fever, lymphadenopathy and pancytopenia in September of 2000. Hemophagocytes were found in the bone marrow smears. Epstein-Barr virus (EBV) serology showed positive for VCA-IgG, IgM and EB-ER and negative for EBNA. The EBV genome was detected in the peripheral blood. The patient was diagnosed as having EBV-associated hemophagocytic syndrome (EBV-AHS) and received chemotherapy. Although she was treated with lamivudine three months after the initiation of chemotherapy, she developed severe hepatitis. She recovered from the hepatitis through a combination of plasma exchange, immunosuppressive and antiviral therapies. Because of the refractoriness of her EBV-AHS to chemotherapy, she received allogeneic peripheral blood stem cell transplantation (PBSCT) from her HLA-identical brother. Hepatitis B did not recur after the PBSCT under administration of lamivudine. The EBV genome in the peripheral blood disappeared soon after the PBSCT but it was revealed again after the initiation of prednisolone for the treatment of acute GVHD. A donor lymphocyte infusion (DLI) was given on day 169 and the EBV genome copy number in the peripheral blood gradually decreased and disappeared. Although the origin of the EBV-infected cells could not be determined as being from the host or donor, DLI was a useful treatment for the recurrence of EBV infection after allogeneic stem cell transplantation for EBV-AHS.
 ...
PMID:[Allogeneic peripheral blood stem cell transplantation for a hepatitis B virus carrier with Epstein-Barr virus associated with hemophagocytic syndrome]. 1519 50

Hepatitis-associated aplastic anemia is an uncommon variant seen in young, previously healthy individuals. The pancytopenia follows hepatitis by a few weeks and is usually severe and prolonged. Bone marrow transplantation remains the cornerstone of therapy. However, immunosuppressive therapy has been found to be effective. We report an 8-year-old girl who had non-A, B, C and E hepatitis-associated severe aplastic anemia. She became transfusion-independent and had consistent, albeit incomplete recovery after immunosuppressive therapy with antithymocyte globulin and cyclosporine.
 ...
PMID:Hepatitis-associated aplastic anemia: successful outcome following immunosuppressive therapy. 1620 14

We report a case of Langerhans' cell histiocytosis (LCH) occurring after a living donor liver transplantation (LDLT) for fulminant hepatitis. A 9-month-old girl underwent an LDLT for fulminant hepatitis of an unknown cause. The histology of the native liver did not show any findings of LCH. On postoperative day 42, her Epstein-Barr virus (EBV)-DNA and cytomegalovirus antigenemia were both found to be positive. As a result, she was treated with antiviral agents and a reduction of the immunosuppression dosage. On postoperative day 98, acute rejection occurred, and she was treated with FK506, methylprednisolone, and finally, anti-CD3 murine monoclonal antibody was added. Subsequently, the EBV was re-activated. Thereafter, skin eruptions, swelling of the systemic lymph nodes, and pancytopenia appeared on postoperative day 127. LCH was diagnosed based on the typical histological findings as LCH, CD1a, and S-100-positive cells in her skin and a lymph nodes biopsy. She was treated by chemotherapy. The symptoms disappeared a few weeks after the start of the chemotherapy, and a clinical remission of LCH was obtained. We could not detect any evidence of EBV infection in the tumor cells. In spite of the fact that her LCH lesions thereafter remained in remission, she died of hepatic failure at 22 months after undergoing the liver transplantation. In conclusion, we discuss the factors influencing the occurrence of LCH in our patient after LDLT, while also evaluating the relationship between LCH and the immunosuppressive therapy administered to this patient.
 ...
PMID:Langerhans' cell histiocytosis after living donor liver transplantation: report of a case. 1623 11

Influenza A virus is well known for its capability for genetic changes either through antigen drift or antigen shift. Antigen shift is derived from reassortment of gene segments between viruses, and may result in an antigenically novel virus that is capable of causing a worldwide pandemic. As we trace backwards through the history of influenza pandemics, a repeating pattern can be observed, namely, a limited wave in the first year followed by global spread in the following year. In the 20th century alone, there were three overwhelming pandemics, in 1918, 1957 and 1968, caused by H1N1 (Spanish flu), H2N2 (Asian flu) and H3N2 (Hong Kong flu), respectively. In 1957 and 1968, excess mortality was noted in infants, the elderly and persons with chronic diseases, similar to what occurred during interpandemic periods. In 1918, there was one distinct peak of excess death in young adults aged between 20 and 40 years old; leukopenia and hemorrhage were prominent features. Acute pulmonary edema and hemorrhagic pneumonia contributed to rapidly lethal outcome in young adults. Autopsies disclosed multiple-organ involvement, including pericarditis, myocarditis, hepatitis and splenomegaly. These findings are, in part, consistent with clinical manifestations of human infection with avian influenza A H5N1 virus, in which reactive hemophagocytic syndrome was a characteristic pathologic finding that accounted for pancytopenia, abnormal liver function and multiple organ failure. All the elements of an impending pandemic are in place. Unless effective measures are implemented, we will likely observe a pandemic in the coming seasons. Host immune response plays a crucial role in disease caused by newly emerged influenza virus, such as the 1918 pandemic strain and the recent avian H5N1 strain. Sustained activation of lymphocytes and macrophages after infection results in massive cytokine response, thus leading to severe systemic inflammation. Further investigations into how the virus interacts with the host's immune system will be helpful in guiding future therapeutic strategies in facing influenza pandemics.
 ...
PMID:Influenza pandemics: past, present and future. 1644 64


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>