BACKGROUND: Hepatitis B rarely leads to demyelinating neuropathy, despite peripheral neuropathy being the first symptom of hepatitis B infection.
METHODS: A 64-year-old man presented with sensorimotor symptoms in multiple peripheral nerves. Serological testing showed that these symptoms were due to hepatitis B. After undergoing treatment involving intravenous immunoglobulin and an antiviral agent, there was a notable improvement in his symptoms.
CONCLUSIONS: Although hepatitis B virus (HBV) infection is known to affect hepatocytes, it is crucial to recognize the range of additional manifestations linked to this infection. The connection between long-term HBV infection and demyelinating neuropathy has seldom been documented; hence, prompt diagnostic and treatment are essential. The patient\'s positive reaction to immunoglobulin seems to be associated with production of the antigen-antibody immune complex.

Hepatitis B virus (HBV) infection is a major global health problem. It can cause chronic infection and put people at high risk of death from cirrhosis and liver cancer. This study aims to present a case of chronic hepatitis B flare in a very young adult patient. An 18-year-old previously healthy female presented with jaundice developing in one week, following the previous complaints of nausea, vomiting, abdominal pain, loss of appetite, and tiredness for about three months. The patient had no risk factors for getting HBV infection, but her HBsAg-positive mother was probably an inactive HBV carrier. The hepatitis B serological testing revealed HBsAg positivity, anti-HBs seronegativity, HBeAg positivity, anti-HBe seronegativity, anti-HBc IgM seronegativity, and high levels of HBV DNA detected > 1.70 × 108 IU/mL. There was a sharp increase in serum ALT to ≥ 5-fold ULN. The abdominal ultrasonography revealed a hepatitis feature, unremarkable portal venous flow, and an extrahepatic biliary system. The liver transient elastography revealed 15.6 kPa of liver stiffness, which was in accordance with the F3-F4 fibrosis stage. These features were typical of a hepatitis B flare, the HBeAg-positive chronic hepatitis B, previously known as the immune reactive phase. A long-term nucleos(t)ide analog therapy was programmed with Tenofovir alafenamide 25 mg daily.

BACKGROUND: Patients with chronic inflammatory disorders are at a higher risk of developing aggressive Merkel cell carcinoma (MCC). Diabetes is a common chronic inflammatory disease that is possibly associated with MCC; however, there are still no reports on the association between hepatitis B virus (HBV) infection and MCC. Whether there is an association between these three diseases and the specific mechanisms behind their effects is worth further research in the future.
METHODS: We herein report a rare case of MCC with extracutaneous and nodal invasion in an Asian individual with type 2 diabetes mellitus and chronic HBV infection, but no immunosuppression or other malignancies. Such cases are uncommon and have rarely been reported in the literature. A 56-year-old Asian male presented with a significant mass on his right cheek and underwent extensive resection combined with parotidectomy, neck lymphadenectomy, and split-thickness skin grafting. Based on the histopathological findings, a diagnosis of MCC involving the adipose tissue, muscle, nerve, and parotid gland with lymphovascular invasion was made. Subsequently, he received radiotherapy with no adverse reactions.
CONCLUSIONS: MCC is a rare, aggressive skin cancer with frequent local recurrence, nodal invasion, and metastasis, which usually arises in older people of the white race. Patients with chronic inflammatory disorders are at a higher risk of developing aggressive MCC. The diagnosis can be confirmed with histology and immunohistochemistry. For localized MCC, surgery is the preferred treatment option. However, for advanced MCC, radiotherapy and chemotherapy have proven to be effective. In cases where chemotherapy is not effective or in the advanced stages of MCC, immune therapy plays an important role in treatment. As with any rare disease, the management of MCC remains an enormous challenge for clinicians; thus, follow-up should be individualized and future progress needs multidisciplinary collaborative efforts. Furthermore, physicians should include MCC in their list of possible diagnoses when they come across painless, rapidly growing lesions, particularly in patients with chronic HBV infection or diabetes, as these patients are more susceptible to the development of this condition and it tends to be more aggressive in them.

Visceral leishmaniasis is an opportunistic infection in immunocompromised patients. Herein, we report a case of an adult male patient with a persistent fever of unknown origin, along with chronic hepatitis B. The patient underwent bone marrow aspiration twice, which revealed hemophagocytosis. Abdomen enhanced CT revealed splenomegaly with a persistent strengthening of multiple nodules, and hemangiomas were diagnosed. A subsequent 18-fluoro-deoxyglucose (18F-FDG) PET/CT scan, which was implemented to search for the reason for the fever, showed diffuse splenic disease uptake, and splenic lymphoma was considered as the diagnosis. His clinical symptoms improved after receiving hemophagocytic lymphohistiocytosis (HLH) chemotherapy. However, the patient was readmitted for fever again only 2 months later. Splenectomy surgery is performed to confirm the diagnosis and classification of lymphoma. Visceral leishmaniasis was eventually diagnosed in a spleen specimen and the third bone marrow biopsy. He received treatment with lipid amphotericin B and remained recurrence-free for 1 year. In this paper, we aim to provide detailed information that will help further our understanding of the clinical symptoms and radiographic findings of visceral leishmaniasis.

UNASSIGNED: Hepatitis B virus (HBV) transmission in hemodialysis units has become a rare event since implementation of hemodialysis-specific infection control guidelines: performing hemodialysis for hepatitis B surface antigen (HBsAg)-positive patients in an HBV isolation room, vaccinating HBV-susceptible (HBV surface antibody and HBsAg negative) patients, and monthly HBsAg testing in HBV-susceptible patients. Mutations in HBsAg can result in false-negative HBsAg results, leading to failure to identify HBsAg seroconversion from negative to positive. We describe 4 unique cases of HBsAg seroconversion caused by mutant HBV infection or reactivation in hemodialysis patients.
UNASSIGNED: Following identification of a possible HBsAg seroconversion and mutant HBV infection, public health investigations were launched to conduct further HBV testing of case patients and potentially exposed patients. A case patient was defined as a hemodialysis patient with suspected mutant HBV infection because of false-negative HBsAg testing results. Confirmed case patients had HBV DNA sequences demonstrating S-gene mutations.
UNASSIGNED: Case patients and patients potentially exposed to the case patient in the respective hemodialysis units in multiple US states.
UNASSIGNED: 4 cases of mutant HBV infection in hemodialysis patients were identified; 3 cases were confirmed using molecular sequencing. Failure of some HBsAg testing platforms to detect HBV mutations led to delays in applying HBV isolation procedures. Testing of potentially exposed patients did not identify secondary transmissions.
UNASSIGNED: Lack of access to information on past HBsAg testing platforms and results led to challenges in ascertaining when HBsAg seroconversion occurred and identifying and testing all potentially exposed patients.
UNASSIGNED: Mutant HBV infections should be suspected in patients who test HBsAg negative and concurrently test positive for HBV DNA at high levels. Dialysis providers should consider using HBsAg assays that can also detect mutant HBV strains for routine HBV testing.

BACKGROUND: Antineutrophil cytoplasmic antibodies comprise a family of autoantibodies that are often used as biomarkers for certain forms of small-vessel vasculitis; however, chronic infections tend to induce the production of antineutrophil cytoplasmic antibodies. Infective endocarditis and hepatitis B virus infection have been reported to exhibit antineutrophil cytoplasmic antibody positivity and to mimic antineutrophil cytoplasmic antibody-associated vasculitis, which may lead to misdiagnosis and inappropriate treatment.
METHODS: We report a case of a 46-year-old Han Chinese man with untreated chronic hepatitis B virus infection who featured proteinase-3 antineutrophil cytoplasmic antibody positivity while hospitalized with infective endocarditis. Cardiac ultrasound echocardiography disclosed mitral and aortic regurgitation with vegetation. On the 15th hospital day, the patient underwent mitral and aortic valve replacement and was then treated with antibiotics for more than 1 month. On the 57th hospital day, the patient was discharged. His urinary abnormalities and renal function were gradually recovering. Four months after being discharged, his proteinase-3 antineutrophil cytoplasmic antibody levels had returned to the normal range.
CONCLUSIONS: The findings in this study update and expand current understanding of antineutrophil cytoplasmic antibody positivity in patients with both infective endocarditis and hepatitis B virus. Treatment (including surgery, antibiotics, corticosteroids and/or cyclophosphamide, antiviral agents, and even plasma exchange) is challenging when several diseases are combined. Renal biopsy is suggested if the patient\'s condition allows. Antineutrophil cytoplasmic antibody testing should be repeated after therapy, because some cases might require more aggressive treatment.

Richter\'s syndrome, the development of high-grade non-Hodgkin lymphoma in patients with chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL), may be triggered by viral infections (eg, Epstein-Barr virus infection). Herein, we report an unusual case of CD5-negative CLL/SLL patient with gastrointestinal mantle cell lymphoma (MCL) and hepatitis B virus infection. CLL/SLL was diagnosed based on lymph node immunohistochemistry and bone marrow pathology. This patient was treated with seven cycles of multi-agent chemotherapy. During treatment, the hepatitis B viruses were activated. Then, after 20 months of antiviral treatment with entecavir, he developed abdominal discomfort and abdominal lymphadenopathy and was diagnosed with MCL based on intestinal biopsy. This work indicates that the hepatitis B virus in patients with CLL/SLL may accelerate the progress or transformation to MCL.

OBJECTIVE: Little information is available about the impact of Chinese herbal medicine (CHM) treatment on acute exacerbation of hepatitis. This study aimed to assess the risk of acute exacerbation of hepatitis and subsequent cirrhosis and hepatoma in HBV patients with and without CHM use.
METHODS: This population-based case-control study used data from the Taiwan Longitudinal Health Insurance Database from 2000 to 2013. Newly diagnosed HBV patients had acute exacerbation of hepatitis and subsequent cirrhosis and hepatoma as the case group, while another patients had no acute exacerbation of hepatitis and cirrhosis and hepatoma as the control group. To correct the differences in sociodemographic factors and Western medication use between the two groups, propensity score matching was used at a 1:1 ratio, and resulted in a comparison of 1306 and 805 patients per group, respectively.
METHODS: Occurrence of acute exacerbation of hepatitis and subsequent cirrhosis and hepatoma.
RESULTS: Overall rate of acute exacerbation of hepatitis and subsequent cirrhosis and hepatoma was 7.9% and 4.8%, respectively. Patients receiving CHM had a significantly lower risk of acute exacerbation of hepatitis (adjusted odds ratio [aOR] =0.20, 95% confidence interval [95%CI]: 0.13-0.31) and subsequent cirrhosis and hepatoma (aOR = 0.29, 95%CI: 0.18-0.49) than those not receiving CHM after adjusting for relevant covariates. However, no dose-dependent relationship was exhibited for either incidence of acute exacerbation of hepatitis and cirrhosis and hepatoma.
CONCLUSIONS: These findings highlight that the use of CHM was associated with a significantly reduced risk of acute exacerbation of hepatitis and subsequent cirrhosis and hepatoma in patients with HBV. Future research could further explore the benefit of CHM therapies for treatment of acute hepatitis exacerbation.

BACKGROUND: Despite the introduction of universal hepatitis B immunization programs worldwide, outbreaks of acute infection still occur in unimmunized individuals. A timely diagnosis of hepatitis B is necessary to ensure adequate clinical care and public health interventions that will reduce transmission. Yet, interpretation of hepatitis B serological markers can be complex. We present a case of hepatitis B with atypical markers, including delayed appearance of hepatitis B core antibody.
METHODS: A 62-year-old white woman was identified as a sexual contact of a male individual with acute hepatitis B virus infection. She had a history of recurrent low-grade non-Hodgkin lymphoma and had recently received immunosuppressive therapy. At baseline she had a negative serology and received three double doses (40 μg) of Engerix-B vaccine (hepatitis B vaccine) with a 0-month, 1-month, and 6-month schedule. One month following the last dose, hepatitis B surface antigen was positive in the absence of hepatitis B core antibody. The only sign of infection was a slight elevation of alanine aminotransferase enzymes a few months after first sexual contacts with the male individual. Hepatitis B virus infection was later confirmed despite the absence of hepatitis B core antibody. The development of hepatitis B core antibody was finally noted more than 6 months after the first positive hepatitis B surface antigen and more than 12 months after elevation of alanine aminotransferase enzymes. Immunosuppression including rituximab treatment was the most likely explanation for this serological profile. On her last medical assessment, she had not developed HBeAg seroconversion despite lower hepatitis B virus deoxyribonucleic acid levels with tenofovir treatment.
CONCLUSIONS: When confronted with positive hepatitis B surface antigen in the absence of hepatitis B core antibody, consideration should be given to the possibility of both acute and persistent infection particularly in the setting of immunosuppression so that appropriate clinical management and public health interventions can take place. Given the increasing use of biologicals such as anti-tumor necrosis factor therapies either alone or with other immunosuppressive agents, this phenomenon may be encountered more frequently.