Cases reported "Necrosis"

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1/74. Case report: lamivudine therapy for submassive hepatic necrosis due to reactivation of hepatitis B following chemotherapy.

    This report describes the case of a 53-year-old woman who developed severe hepatitis following chemotherapy for breast carcinoma. The patient was hepatitis B surface antigen positive, e antigen negative and e antibody positive and had high levels of hepatitis b virus-dna. liver biopsy revealed submassive hepatic necrosis, consistent with reactivation of hepatitis B. Treatment with lamivudine resulted in rapid loss of hepatitis b virus-dna, resolution of hepatitis and clinical recovery.
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2/74. Resolution of chronic delta hepatitis after 12 years of interferon alfa therapy.

    Chronic delta hepatitis is an uncommon but severe form of chronic viral hepatitis for which there is currently no satisfactory therapy. A patient with chronic delta hepatitis was treated with interferon alfa, 5 million units daily for 12 years. Serial serum samples were tested for routine liver tests and selected samples for quantitative levels of hepatitis B surface antigen (HBsAg) and hepatitis delta virus rna. liver biopsies were performed before, during, and after an initial 1-year course of therapy and again after 3 and 10 years of continuous therapy. With initiation of interferon therapy, serum aminotransferase levels decreased to normal range, became abnormal again when the dose was reduced, and increased to pretreatment levels when therapy was stopped. With reinstitution and prolonged therapy, aminotransferase levels became persistently normal; after several years, both hepatitis delta virus rna and serum HBsAg became undetectable. liver biopsy, which initially revealed cirrhosis, showed gradual improvement in inflammatory and fibrosis scores and, after 10 years, no abnormalities or fibrosis. Therapy was stopped, and the patient remained free of evidence of infection. In conclusion, long-term therapy with interferon alfa in high doses led to resolution of chronic delta hepatitis, disappearance of hepatitis delta and B virus markers, and improvement in fibrosis.
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3/74. Graft failure in human donor corneas due to transmission of herpes simplex virus.

    AIM: To report the clinical consequences of contamination of human donor corneas by herpes simplex virus (HSV) in organ culture. methods: Two patients without previous history of ocular HSV infection underwent penetrating keratoplasty (PK), one for keratoconus and the other for fuchs' endothelial dystrophy. One patient suffered primary graft failure while the other developed a persistent epithelial defect, ultimately resulting in graft failure. Viral culture of swabs taken from both corneas during the early postoperative period was undertaken. The failed donor corneas were examined histopathologically by immunohistochemistry (IHC) for HSV-1 antigens, transmission electron microscopy (TEM), and by polymerase chain reaction (PCR) for HSV dna. Both failed corneas were replaced within 6 weeks of the initial surgery. The records of the fellow donor corneas were also examined for evidence of infection. RESULTS: HSV was cultured from both corneas during the early postoperative period. histology of both donor corneas demonstrated a thickened corneal stroma with widespread necrosis of keratocytes and loss of endothelial cells. IHC showed keratocytes positive with antibodies to HSV-1 antigens. TEM demonstrated HSV-like viral particles within degenerating keratocytes. PCR performed on the failed corneal grafts was positive for HSV-1 dna, whereas PCR performed on the excised host corneal buttons was negative in both patients. Records of the fellow donor corneas showed that one cornea was successfully transplanted into another recipient after 18 days in organ culture, whilst the other was discarded because of extensive endothelial cell necrosis noted after 15 days in organ culture. CONCLUSION: HSV within a donor cornea may cause endothelial destruction in organ culture and both primary graft failure and ulcerative keratitis after transplantation. Endothelial necrosis of a donor cornea in culture also raises the possibility of HSV infection within the fellow cornea.
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4/74. infection with jc virus and possible dysplastic ganglion-like transformation of the cerebral cortical neurons in a case of progressive multifocal leukoencephalopathy.

    infection of the cerebral cortical neurons with jc virus (JCV) with possible dysplastic ganglion-like alteration of the infected neurons found in a case of progressive multifocal leukoencephalopathy (PML) is described. The patient was a 21-year-old man with common variable immunodeficiency who died of PML after a 9-month clinical course. At autopsy, the white matter of the cerebrum, brainstem, cerebellum, and spinal cord exhibited extensive demyelination and necrosis. Numerous inclusion-bearing oligodendrocytes and bizarre astrocytes were found. In the occipital and temporal cortex, thick band-like aggregates of dysplastic ganglion-like cells (DGLCs) were found. These DGLCs showed immunohistochemical properties of neurons, and nuclei of some DGLCs were immunoreactive for large T antigen of SV40/JCV and p53, but not for capsid protein JCV VP1. in situ hybridization for mRNA of JCV large T antigen revealed positive signals in the nuclei of some DGLCs. These results indicate that JCV infected neurons and it is suggested that binding of the large T antigen with cellular proteins could have resulted in the dysplastic, ganglion cell-like change of the infected neurons, although the possibility that the aggregates of DGLCs represent a pre-existent malformative lesion of the cortex cannot be excluded completely.
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5/74. Clinical expression of 'silent' hepatitis b virus infection in a patient with visceral leishmaniasis.

    A 69-year-old male was hospitalized in January 1999 because of visceral leishmaniasis. He had also suffered from anti-hepatitis c virus (HCV)-positive chronic hepatitis for years. All serum hepatitis b virus (HBV) antigens and antibodies were negative except for anti-HBc. The patient was treated with amphotericin b cholesteryl sulfate (2 mg/kg twice a day for 7 days, iv). fever disappeared on the 3rd day of treatment, the clinical condition improved rapidly and the patient recovered. In May 1999 the patient developed icteric HBsAg-negative acute hepatitis (aspartate aminotransferase 722 U/l; alanine aminotransferase 988 U/l). Anti-HBc IgM was positive and HBV-dna was detected in serum by PCR. Anti-HAV IgM was negative. A serum sample obtained on presentation and stored at -80 degrees C was retrospectively tested and found positive for HBV-dna. In July 1999, complete remission of acute hepatitis and seroconversion to anti-HBs was observed. We suppose that a moderate depression of the immune system, probably associated with leishmaniasis, may have enhanced HBV replication in the patient who had an HBsAg-negative 'silent' HBV infection. Restoration of the immune system after successful antiprotozoan therapy might have induced cell-mediated necrosis of the HBV-infected hepatocytes and seroconversion to anti-HBs.
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6/74. Submassive liver necrosis in a hepatitis B carrier with Cushing's syndrome.

    Reactivation of hepatitis b virus (HBV) replication in hepatitis B surface antigen (HBsAg)-positive patients is associated with immunosuppressive therapy. However, the interactions between endogenous glucocorticoid in Cushing's syndrome and HBV-related hepatitis remain unclear. Here, we describe the management of a 32-year-old male HBV carrier with Cushing's syndrome caused by an adrenal cortical adenoma, who developed severe hepatitis B. Repeated episodes of septicemia resulting from hypercortisolemia-related immunosuppression further compromised his hepatic condition. adrenalectomy could not be performed due to coagulopathy. lamivudine was not available at that time in taiwan, and this patient died of hepatic failure and sepsis. At autopsy, his liver showed submassive necrosis with small regenerative nodules. The hepatocytes were positive for HBsAg (membrane and cytoplasmic) and hepatitis B core antigen (nuclear and cytoplasmic). Screening for HBsAg is of crucial significance for immunocompromised individuals. Once positive HBsAg is detected in immunosuppressed patients, liver function and viral status should be closely monitored to enable earlier diagnosis and prompt treatment with the newer nucleoside analogues that actively fight HBV.
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7/74. Chronic disseminated intravascular coagulation and childhood-onset skin necrosis resulting from homozygosity for a protein C Gla domain mutation, Arg15Trp.

    A toddler of Haitian descent presented with an 18-month history of chronic consumption coagulopathy, followed by catastrophic skin necrosis. protein c deficiency (1% to 3% of control) was noted by functional assay; chromogenic assay and antigen levels were 30% of control. plasma infusion abrogated the disseminated intravascular coagulation-like state. The authors identified a homozygous mutation, C1432T, resulting in a missense, Arg15Trp, in the gamma-carboxyglutamate domain of the protein. Chronic consumption coagulopathy without purpura fulminans or venous thrombosis is a rare presentation of defective protein C pathway. The result of this mutation is a mixed type I (low antigen) and type II (low function) phenotype.
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8/74. Lymph node infarction. An immunohistochemical study of 11 cases.

    CONTEXT: The etiology of lymph node infarction may be difficult or impossible to determine by histologic examination. Lymph node infarction is followed by malignant lymphoma in some but not all patients. The role of immunohistochemistry in the evaluation of lymph node infarction is not well defined. Although it is widely believed that necrotic tissue is not suitable for immunohistochemical study, this view may be inaccurate. OBJECTIVE: To determine whether lymphoid antigens are preserved in infarcted lymph nodes and to determine the utility of immunohistochemical staining in the evaluation of lymph node infarction. DESIGN: Retrospective immunohistochemical study of infarcted lymph nodes using archival formalin-fixed, paraffin-embedded tissue. SETTING: Academic medical center. patients: Eleven adult patients with lymph node infarction retrieved from pathology files. MAIN OUTCOMES MEASURES: Results of immunohistochemistry, diagnosis of lymphoma. RESULTS: Preservation of lymphoid antigens was observed in 4 of 6 cases of lymph node infarction associated with malignant lymphoma, including 3 of 5 cases of diffuse large B-cell lymphoma and 1 case of peripheral T-cell lymphoma. Nonspecific staining was not encountered. In 1 case, in which an infarcted lymph node showed a benign pattern of lymphoid antigen expression, lymphoma has not developed after 5 years. CONCLUSION: Lymphoid antigens are frequently preserved in cases of lymph node infarction, and immunohistochemical study of infarcted lymph nodes may provide clinically useful information.
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9/74. Subcutaneous panniculitis-like T-cell lymphoma: presentation of 2 cases and observations.

    Subcutaneous panniculitis-like T-cell lymphoma is a rare tumor of primary cutaneous origin representing far < 1% of all non-Hodgkin's lymphomas. The disease typically follows a distinctive, indolent course of recurrent, self-healing subcutaneous nodules. These nodules mimic lipomas clinically, while histologically resembling a panniculitis. Alternatively, a rapidly progressive course might be seen with subcutaneous nodules accompanied by constitutional symptoms and, in some cases, the development of a potentially fatal hemophagocytic syndrome with significant cytopenia. This tumor is widely regarded as a tumor of CD8 cytotoxic T cells with the presence of cytotoxic proteins, T-cell-restricted intracellular antigen, and granzyme B commonly demonstrated. A number of modalities have been reported in the treatment of this tumor, with varying degrees of success. In this report, we present 2 cases of subcutaneous panniculitis-like T-cell lymphoma with variable clinical courses. We also review the literature of this unusual lymphoma.
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10/74. carcinosarcoma of the stomach.

    In the gastrointestinal tract, carcinosarcomas are most frequently seen in the esophagus. carcinosarcoma in the stomach is a rare tumor. We report a carcinosarcoma of the antrum of stomach. The tumor was polypoid and exophytic in appearance and located in the antrum. Immunohistochemical studies showed positivity for cytokeratin, epithelial membrane antigen and cytoplasmic carcinoembryonic antigen in the epithelial component. Positive staining with vimentin, desmin and focal smooth muscle actin and negative staining with chromogranin were observed in spindle cells. Nuclear positive staining was observed with p53 and Ki-67 in both glandular and spindle atypical cells.
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