9 research outputs found
Is it necessary to delay antiviral therapy for 3-6 months to anticipate HBeAg seroconversion in patients with HBeAg-positive chronic hepatitis B in endemic areas of HBV genotype C?
Background/AimsSpontaneous HBeAg seroconversion occurs frequently in the immune reactive phase in HBeAg-positive chronic hepatitis B (CHB). Therefore, observation for 3-6 months before commencing antiviral therapy is recommended in patients with alanine aminotransferase (ALT) levels that exceed twice the upper limit of normal (ULN). However, HBeAg seroconversion occurs infrequently in patients infected with hepatitis B virus (HBV) genotype C. The aim of the present study was to determine whether the waiting policy is necessary in endemic areas of HBV genotype C infection.MethodsNinety patients with HBeAg-positive CHB were followed prospectively without administering antiviral therapy for 6 months. Antiviral therapy was initiated promptly at any time if there was any evidence of biochemical (i.e., acute exacerbation of HBV infection or aggravation of jaundice) or symptomatic deterioration. After 6 months of observation, antiviral therapy was initiated according to the patient's ALT and HBV DNA levels.ResultsOnly one patient (1.1%) achieved spontaneous HBeAg seroconversion. Biochemical and symptomatic deterioration occurred before 6 months in 17 patients (18.9%) and 5 patients, respectively. High ALT and HBV DNA levels were both independent risk factors for biochemical deterioration. Of 15 patients with HBV DNA ≥5.1×107 IU/mL and ALT ≥5×ULN, biochemical deterioration occurred in 7 (46.7%), including 1 patient receiving liver transplantation due to liver failure.ConclusionsSpontaneous HBeAg seroconversion in patients with HBeAg-positive CHB is rare within 6 months. Biochemical deterioration was common and may lead to liver failure. Immediate antiviral therapy should be considered, especially in patients with high ALT and HBV DNA levels in endemic areas of genotype C infection
Diffuse Large B-Cell Lymphoma Manifesting as Miliary Nodules in the Lung: A Case Report
Malignant lymphoma has various pulmonary manifestations on chest CT, including nodules, masses,
areas of consolidation, and ground-glass opacity. These presentations can pose a diagnostic challenge,
as they mimic other disease patterns. Herein, we report a case of diffuse large B-cell lymphoma
(DLBCL) manifesting as miliary nodules in a 67-year-old male initially presenting with dyspnea and fever.
Radiologic findings included diffuse, bilateral, multiple tiny nodules consistent with metastasis,
miliary tuberculosis, and fungal infection. However, further investigations, including laboratory tests,
imaging, and biopsies, led to the diagnosis of DLBCL involving the lungs. Herein we reported a rare
case of lymphoma involvement of the lung presenting as miliary nodules. Accurate diagnosis relies on
a comprehensive evaluation of the clinical history, physical features, laboratory test results, and imaging
findings
Angioinvasive Mucormycosis Mimicking Mass and Pulmonary Thromboembolism in a Patient with Myelodysplastic Syndrome: A Case Report
Mucormycosis encompasses a range of fungal infections that can impact various organs. Although
pulmonary mucormycosis is relatively rare, it poses a significant threat, particularly to
individuals with compromised immune systems. Pulmonary mucormycosis presents with various
radiological manifestations. Notably, the involvement of the angioinvasive pulmonary artery
in pulmonary mucormycosis cases has seldom been documented. In this report, we
showcase the radiological characteristics of angioinvasive mucormycosis, which can mimic
pulmonary thromboembolism or a pulmonary artery tumor, in a patient diagnosed with myelodysplastic
syndrome
Systemic Lupus Erythematosus and Lung Involvement: A Comprehensive Review.
Systemic lupus erythematosus (SLE) is a complex autoimmune disease with multiorgan manifestations, including pleuropulmonary involvement (20-90%). The precise mechanism of pleuropulmonary involvement in SLE is not well-understood; however, systemic type 1 interferons, circulating immune complexes, and neutrophils seem to play essential roles. There are eight types of pleuropulmonary involvement: lupus pleuritis, pleural effusion, acute lupus pneumonitis, shrinking lung syndrome, interstitial lung disease, diffuse alveolar hemorrhage (DAH), pulmonary arterial hypertension, and pulmonary embolism. DAH has a high mortality rate (68-75%). The diagnostic tools for pleuropulmonary involvement in SLE include chest X-ray (CXR), computed tomography (CT), pulmonary function tests (PFT), bronchoalveolar lavage, biopsy, technetium-99m hexamethylprophylene amine oxime perfusion scan, and (18)F-fluorodeoxyglucose positron emission tomography. An approach for detecting pleuropulmonary involvement in SLE includes high-resolution CT, CXR, and PFT. Little is known about specific therapies for pleuropulmonary involvement in SLE. However, immunosuppressive therapies such as corticosteroids and cyclophosphamide are generally used. Rituximab has also been successfully used in three of the eight pleuropulmonary involvement forms: lupus pleuritis, acute lupus pneumonitis, and shrinking lung syndrome. Pleuropulmonary manifestations are part of the clinical criteria for SLE diagnosis. However, no review article has focused on the involvement of pleuropulmonary disease in SLE. Therefore, this article summarizes the literature on the epidemiology, pathogenesis, diagnosis, and management of pleuropulmonary involvement in SLE