This case was reported in a literature article and described the occurrence of death NOS in a male patient who received Hepatitis B vaccine. The patient's past medical history included acute hepatitis B, kidney transplant, transplant rejection and transplant rejection. Previously administered products included Lamivudine/zidovudine, lopinavir/ritonavir, tenofovir and antithymocyte globulin. Concurrent medical conditions included haemodialysis, HIV infection and end stage renal disease. Concomitant products included darunavir, ritonavir, raltegravir, etravirine, mycophenolate, tacrolimus, prednisone and antithymocyte globulin. In February 2013, the patient received the 1st dose of Hepatitis B vaccine. On 23rd April 2013, 61 days after receiving Hepatitis B vaccine, the patient experienced hepatitis B reactivation (serious criteria GSK medically significant). In December 2013, the patient experienced death NOS (serious criteria death and GSK medically significant). On an unknown date, the outcome of the death NOS was fatal and the outcome of the hepatitis B reactivation was unknown. The reported cause of death was unknown cause of death. It was unknown if the reporter considered the death NOS to be related to Hepatitis B vaccine. The reporter considered the hepatitis B reactivation to be related to Hepatitis B vaccine. Additional information was provided. This case was reported in a literature article and described the occurrence of hepatitis B virus (HBV) reactivation in a male aged 40-year or above who was vaccinated with unspecified HBV vaccine (manufacturer unknown). This case corresponds to source patient in this literature article. The patient was a part of the study that reviewed HBV serologic results of all facility haemodialysis patients and the HBsAg testing procedures at a commercial laboratory. The patient was under haemodialysis treatment. The patient was the source case in the literature article. No information on patient's family or concomitant medication was provided. In 1989, the patient was diagnosed with acute HBV infection. Later, in 1997, the patient was diagnosed with human immunodeficiency virus (HIV) infection with secondary end-stage renal disease. Subsequently, long-term haemodialysis therapy was initiated in 1997. The patient had received antiretroviral therapy1 for HIV infection (Lamivudine/zidovudine, lopinavir/ritonavir, and beginning in 2005 HBV-suppressive including tenofovir (dosages unknown for all), which had been discontinued during preparation for kidney transplantation in November 2011. Between 2002 and 2011, the anti-HBc and anti-HBs was positive whereas HBsAg was negative. The antiretroviral therapy2 included darunavir (800 mg/d), ritonavir (100 mg/d), raltegravir (400 mg twice daily), and etravirine (200 mg twice daily). Immunosuppressive regimen included mycophenolate, tacrolimus, and prednisone; antithymocyte globulin in January 2012. During early 2012, the patient experienced acute transplant rejection and received antithymocyte globulin. In May 2012, after transplant failure, the patient returned to outpatient haemodialysis therapy and was documented as HBsAg negative. The anti-HBc and anti-HBs was positive and negative respectively. In August 2012, the anti-HBs were found positive. In October 2012, acute transplant rejection was again diagnosed and prednisone initiated at 30 mg/day; tapered dosing of 2.5-5 mg every other day during February 2013 was prescribed. The HBsAg was found negative when performed at laboratory A (the laboratory used by the facility for urgent testing). In January 2013, the patient was reported to be anti-HBs negative by routine testing initiated though standing orders at the facility. This result, interpreted as possible waning immunity, prompted HBsAg testing in February 2013. On 21February 2013, the patient's first HBsAg test result A was initially reported as positive.  The preneutralisation value was 354 HBsAg. A reduction in HBsAg value did not occur during the confirmatory neutralisation step, though the sample may not have been adequately diluted per test kit instructions. However, after a confirmatory neutralization step, the presence of HBsAg was not confirmed and the final result was reported as HBsAg negative. On an unspecified date in February 2013, after a subsequent negative HBsAg test result at Laboratory A with a different source patient sample, the patient received 1 dose of unspecified HBV vaccine (administration route and site unspecified; batch number not provided). On an unspecified date, in March 2013, peak alanine transaminase (ALT) level was 33 (Units: IU/L). During May 2012 to March 2013, the patient shared the same station 3 times weekly for 10 months with the index patient of the same literature article, who was dialysed immediately after the patient. Between 24 April 2013 and 30 April 2013, the patient was reported to be HBsAg positive at Laboratory B (the laboratory used by the facility for routine testing), and dialysing in isolation was started. The ALT level was 155 IU/L. Due to the HBsAg positive result, additional HBV serologic tests were conducted at Laboratory A and were available in early May 2013; HBsAg was not detected, despite a positive test result for hepatitis B e antigen (HBeAg) and high viral titre, a discrepancy not identified by facility staff despite their practice of reviewing all laboratory results upon receipt and again at weekly rounds. Between 1 May 2013 and 8 May 2013, HBsAg was negative (the preneutralisation value was 519 HBsAg. A reduction in HBsAg value did not occur during the confirmatory neutralisation step, though the sample may not have been adequately diluted per test kit instructions and anti-HBc, anti-HBs and HBeAg were positive). The HBV DNA was 5.4 x 10E7 IU/mL and ALT was 170. Between 22 May 2013 and 27 May 2013, the patient was reported to be HBsAg with anti-HBs as positive and ALT as 80. In June 2013, the lab tests revealed HBsAg, anti-HBc, anti-HBs and HBeAg as positive whereas anti-Hbe and IgM anti-HBc as negative. ALT was noted as 52. Samples obtained during July 2013 from the patient revealed HBV viral loads greater than 1.1 x 10E8 IU/mL. Subsequently, the patient was diagnosed with HBV reactivation. The patient resumed haemodialysis therapy in isolation. The patient's HBV genotype was A. (In this study, laboratory A failed to strictly adhere to the HBsAg test manufacturer's guidelines for adequate dilution of patient serum samples during the confirmatory neutralization step. Therefore, the patient's sample might not have been adequately diluted in February and May 2013, resulting in potentially false-negative HBsAg results). The patient's HBV whole genome sequences analysis indicated 99.9% genetic homology with the index patient of the same literature article. In December 2013, the patient died. HBV infection was not listed as a contributing cause. It was unknown if the autopsy was performed. The cause of death was unknown. This case has been considered serious due to death NOS. The authors did not comment on the relationship between HBV reactivation and unspecified HBV vaccine. The authors stated "The patient's high viral titers and increased infectivity were likely related to severe immunosuppression and cessation of HBV-suppressive antiretroviral therapy". The authors concluded that  "In conclusion, HBV transmission occurred after an HIV-positive hemodialysis patient with transplant-related immunosuppression experienced HBV reverse seroconversion and reactivation. Providers should be aware of this possibility, especially among severely immunosuppressed patients, and maintain stringent infection control". This is 1 of the 2 valid cases reported in the same literature article.