Occult Hepatitis B Virus Infection With Increased Virus DNA Levels in a Chronic Hemodialysis Patient

Dear Editor, Controlling hepatitis B virus (HBV) infection is a serious issue in dialysis hospitals. Occult HBV infection (OBI) is defined as the presence of HBV genome in the serum or liver tissue without detectable hepatitis B surface antigen (HBsAg). A previous study reported OBI prevalence in Japanese chronic hemodialysis (HD) patients to be 0.3% (1). The patients in that study tested negative for anti‐ hepatitis B surface antibody (HBsAb) and positive for anti‐hepatitis B core antibody (anti‐HBc), and HBV DNA was detected in their sera with a quantitative sensitivity of 2.1 log copies/mL (20 IU/mL). Herein, we report an OBI patient with increased serum HBV DNA levels who was undergoing HD.

Dear Editor, Controlling hepatitis B virus (HBV) infection is a serious issue in dialysis hospitals. Occult HBV infection (OBI) is defined as the presence of HBV genome in the serum or liver tissue without detectable hepatitis B surface antigen (HBsAg). A previous study reported OBI prevalence in Japanese chronic hemodialysis (HD) patients to be 0.3% (1).
The patients in that study tested negative for antihepatitis B surface antibody (HBsAb) and positive for anti-hepatitis B core antibody (anti-HBc), and HBV DNA was detected in their sera with a quantitative sensitivity of 2.1 log copies/mL (20 IU/mL). Herein, we report an OBI patient with increased serum HBV DNA levels who was undergoing HD.

CASE REPORT
An 86-year-old female started undergoing HD 6 years ago for end-stage kidney disease caused by nephrosclerosis. She had been diagnosed with colon and lung cancers at 65 and 84 years of age, respectively, both of which were completely resected. She required no chemotherapy or radiotherapy and had never received a blood transfusion. She was transferred to our hospital 4 years ago. She tested negative for HBsAg (<0.05 IU/mL), HBsAb (<10.0 mIU/mL), anti-hepatitis C virus antibody, and antihuman immunodeficiency virus antibody but positive for anti-HBc at low levels (10.2 S/CO). Aspartate aminotransferase and alanine aminotransferase levels were 13 and 6 U/L, respectively. Computed tomography scan and ultrasonography images revealed normal findings. Using real-time polymerase chain reaction (PCR), we assessed the serum HBV DNA levels of all patients in our hospital who exhibited positivity for HBsAg, HBsAb, or anti-HBc for strict infection control. In the HBsAg-negative patient group, only our current patient was detected with HBV DNA at a level of 2.6 log copies/mL (68 IU/mL); thus, she was diagnosed with OBI. She continued HD without any symptoms or abnormal laboratory tests for 6 months after OBI diagnosis. To prevent nosocomial horizontal HBV transmission, we fixed her bed and console and conducted routine examinations for viral infections.

DISCUSSION
The serological pattern of OBI includes cases of acute HBV infection in the window period and HBV reactivation during immunosuppressive therapy, which can lead to severe hepatitis. Because our patient had never exhibited hepatitis findings, we assumed that she had been infected previously. In general, after HBsAg disappearance, HBsAb persists for life and confers long-term immunity. To our knowledge, all reported HD patients with OBI tested negative for HBsAb (1)(2)(3), and most of them exhibited an isolated anti-HBc pattern. We speculated that impaired immune function in chronic HD patients contributes to HBsAb negativity, thereby allowing HBV to replicate.
Routine blood vessel punctures and extracorporeal circulation are risk factors for horizontal transmission. The degree of transmission risk depends on the virus DNA level in the infected patient. Although OBI in chronic HD patients exhibited low HBV DNA levels, they could increase over 2.1 log copies/mL (20 IU/mL). HD patients are recommended to undergo HBV DNA screening for infection control (4). Limiting the patients exhibiting an isolated anti-HBc pattern may be considered reasonable. The potential presence of OBI patients undergoing dialysis should be recognized. Dear Editor, Generalized pustular psoriasis (GPP) is characterized by a sudden fever, edema, erythema with pustules. A majority of GPP without a history of psoriasis vulgaris is caused by a deficiency of interleukin (IL)-36 receptor antagonist (DITRA) (1).
Granulocyte and monocyte adsorption apheresis (GMA) is an extracorporeal apheresis that removes activated granulocytes and monocytes using a column packed with cellulose acetate beads (2). The efficacy of GMA therapy in DITRA has been reported in only a few recent cases (1,3,4). We present the successful therapy with GMA for a GPP patient caused by DITRA, associated with a decrease in serum IL-6.
A 79-year-old woman exhibited edema, erythema with numerous small pustules on her trunk and extremities (Fig. 1a), and a fever (>39°C). Laboratory findings were as follows: leukocyte count, 13,700 /μL; C-reactive protein (CRP), 7.27 mg/dL; albumin, 3.5 g/dL; IL-6, 292 pg/mL (normal <12.5). A skin biopsy from erythema with a pustule revealed an intraepidermal pustule filled with neutrophils (Fig. 1c). Written informed consent was obtained from the patient for genetic analysis of the IL36RN gene, and the work was approved by institutional ethical committee. It revealed a homozygous mutation of c.115 + 6 T > C (p.Arg10ArgfsX1) in IL36RN, which is one of the GPP-causing founder mutations in the Japanese (1). From these