ABSTRACT
We herein report a case of a 31-year-old Japanese man who simultaneously had a positive influenza A virus antigen test result and Vogt-Koyanagi-Harada disease (VKHD), demonstrated by both diffuse multiple early hyperfluorescent points on fluorescein fundus photography and serous retinal detachments on optical coherence tomography. He had meningitis. It was difficult to determine whether the main cause of meningitis was influenza A or VKHD. After initial treatment with peramivir for influenza A and then methylprednisolone pulse with subsequent corticosteroid therapy for VKHD, his symptoms improved gradually. These findings suggest that influenza A virus infection contributes to the onset or exacerbation of VKHD.
Subject(s)
Influenza, Human/complications , Retinal Detachment/etiology , Uveomeningoencephalitic Syndrome/virology , Acids, Carbocyclic , Adult , Antiviral Agents/therapeutic use , Cyclopentanes/therapeutic use , Glucocorticoids/therapeutic use , Guanidines/therapeutic use , Humans , Influenza A virus , Influenza, Human/diagnosis , Influenza, Human/therapy , Male , Methylprednisolone/administration & dosage , Tomography, Optical Coherence , Uveomeningoencephalitic Syndrome/diagnosis , Uveomeningoencephalitic Syndrome/therapyABSTRACT
PURPOSE: To describe a case of virus-associated hemophagocytic syndrome with ocular changes resembling Vogt-Koyanagi-Harada disease prior to the systemic changes. METHODS: A 51-year-old man presented with a sudden decline in vision. The patient was examined by fluorescein angiography, bone marrow biopsy, abdominal ultrasound, ocular examinations, and laboratory examinations. RESULTS: Fluorescein angiography revealed uveitis resembling Vogt-Koyanagi-Harada disease. Bone marrow biopsy specimen demonstrated histiocytic hyperplasia and some hemophagocytes. Abdominal ultrasound findings indicated hepato-splenomegaly. And ocular examinations revealed hematocytopenia and hypoproteinemia. CONCLUSION: The ocular changes resembling Vogt-Koyanagi-Harada disease observed in this study could be a kind of manifestation of virus-associated hemophagocytic syndrome in retina.
Subject(s)
Lymphohistiocytosis, Hemophagocytic/diagnosis , Uveomeningoencephalitic Syndrome/diagnosis , Antiviral Agents/therapeutic use , Cytomegalovirus Infections/diagnosis , Cytomegalovirus Infections/drug therapy , Dexamethasone/therapeutic use , Drug Therapy, Combination , Fatal Outcome , Fluorescein Angiography , Ganciclovir/therapeutic use , Hepatomegaly/diagnosis , Hepatomegaly/drug therapy , Hepatomegaly/virology , Humans , Lymphohistiocytosis, Hemophagocytic/drug therapy , Lymphohistiocytosis, Hemophagocytic/virology , Male , Middle Aged , Ofloxacin/therapeutic use , Splenomegaly/diagnosis , Splenomegaly/drug therapy , Splenomegaly/virology , Ultrasonography , Uveomeningoencephalitic Syndrome/diagnostic imaging , Uveomeningoencephalitic Syndrome/drug therapy , Uveomeningoencephalitic Syndrome/virology , Visual Acuity/drug effectsABSTRACT
AIM: To determine whether T lymphocytes of patients with Vogt-Koyanagi-Harada (VKH) disease cross-react with peptides of melanocytes and with exogenous antigens. METHODS: Cross-reactivity with melanocyte peptides, tyrosinase (tyrosinase(450-462): SYLQDSDPDSFQD) and the mimic virus peptide, i.e., cytomegalovirus envelope glycoprotein H (CMV-egH(290-302): SYLKDSDFLDAAL) was examined by a lymphocyte proliferation assay or cytokine production. The seroprevalence of various viruses was examined by a complement fixation test. To examine if the virus infections in VKH patients were latent, we measured genomic DNA of the virus using real-time polymerase chain reaction (PCR). RESULT: Some of the T cells established from VKH recognized melanocyte peptides including the tyrosinase peptide as well as the CMV-egH(290-302) peptide, which had a high amino acid homology to the tyrosinase peptide. Cytomegalovirus (CMV) peptide-specific T cells showed a significant proliferation not only to CMV-egH(290-302) but also to tyrosinase(450-462). The seroprevalence of CMV was significantly higher in VKH patients. In addition, all tested samples of VKH patients were negative for CMV-DNA. CONCLUSIONS: These results indicate that CMV infection may stimulate the production of T cells that cross-react with tyrosinase by a mechanism of molecular mimicry. These events may be responsible for the onset of VKH disease.
Subject(s)
Monophenol Monooxygenase/immunology , Peptide Fragments/immunology , T-Lymphocytes/immunology , Uveomeningoencephalitic Syndrome/immunology , Viral Envelope Proteins/immunology , Antigen-Presenting Cells/immunology , Complement Fixation Tests , Cross Reactions , Cytokines/biosynthesis , Cytomegalovirus/genetics , DNA, Viral/analysis , Genome, Viral , Herpesvirus 3, Human/genetics , Herpesvirus 4, Human/genetics , Humans , Lymphocyte Activation , Molecular Mimicry , Reverse Transcriptase Polymerase Chain Reaction , Seroepidemiologic Studies , Simplexvirus/genetics , Uveomeningoencephalitic Syndrome/virologyABSTRACT
PURPOSE: The role of Epstein-Barr virus (EBV) reactivation in the pathogenesis of Vogt-Koyanagi-Harada (VKH) disease was examined. MATERIAL AND METHODS: Using B lymphocytes obtained from 8 patients with VKH disease and 10 patients with other types of uveitis, immortarized lymphoblast lines were established and infected with EBV. The degree of EBV activation in each lymphoblast line, in the presence and absence of various stimuli, was assessed by measuring the expression of 3 different antigens involved in replication by immunofluorescent staining and western blot analysis. Quantification of EBV DNA in cell culture supernatants was done by polymerase chain reaction. RESULT: Cell lines established from VKH patients expressed more viral antigens that those established from patients with other types of uveitis. There were greater amounts of EBV DNA in the VKH cell lines. CONCLUSION: B lymphocytes from VKH patients may be more susceptible to EBV activation, and the reactivation of EBV may be involved in the pathogenesis of VKH.
