sd , a 45-year - old caucasian male , was referred for evaluation for liver 
 transplantation because 
 of end - stage liver disease caused by hepatitis b. he had 
 been well until six months prior to his initial visit , when he started losing 
 weight and developed severe fatigue . during the six - month period , he had lost 
 25 kilograms .
his past 
 medical history was significant for non - hodgkin 's lymphoma that was diagnosed 
 eleven years ago .
he was treated with 8 cycles of chop chemotherapy and had 
 been in remission since then . on examination , the patient appeared mildly icteric .
the abdomen was 
 soft with some tenderness in the right upper quadrant and ascites .
complete 
 blood count showed a leukocyte count of 2500 cells / mm , hemoglobin 
 of 9.8 gm / dl , and platelet count of 29 000 cells / mm .
his liver 
 function tests were abnormal with a total bilirubin of 5 mg / dl ( normal , 0.21.2 mg / dl ) , alt : 
 361 u / l ( normal , 1763 u / l ) , ast : 750 iu / l ( normal , 1540 u / l ) , total 
 protein : 15.4 g / dl ( normal , 6.17.9 g / dl ) , albumin : 2.9 g / dl ( normal , 3.94.8 g / dl ) , and an 
 inr of 1.9 .
serological tests for viral hepatitis were as follows : hepatitis b 
 surface antigen positive ( hbsag ) , hepatitis b surface antibody negative 
 ( antihbs ) , hbe antigen negative , hbe antibody positive , igm antibody to 
 hepatitis b core antigen positive , igg antibody to hepatitis b core antigen 
 positive , and hbv dna 4 150 000 iu / ml ( by pcr ) .
ct 
 scan and ultrasound examination of the abdomen showed a small liver with 
 moderate ascites , splenomegaly , patent portal , and hepatic veins .
the striking elevation in his globulin fraction ( 12.5 g / dl ) 
 was further worked up .
serum protein electrophoresis showed the presence of a 
 large monoclonal protein spike ( m protein ) in the gamma region which on 
 immunofixation electrophoresis ( ife ) was identified to be iga - kappa type ( see figure 1 ) .
the iga levels were increased at 6730 mg / dl ( reference range 70400 mg / dl ) and 
 the igg and igm levels were decreased at 466 mg / dl ( reference range 7001600 mg / dl ) and 
 25.6 mg / dl ( reference range 40320 mg / dl ) , 
 respectively .
a bone 
 marrow biopsy on two separate occasions showed normocellular bone marrow with 
 less than 2 percent population of plasma cells .
full body positron emission tomography ( pet ) scan and ct scan were 
 performed , and no focus suspicious for lymphoma or myeloma or infection was 
 identified .
whole body mri was unremarkable . on retrospective review , the 
 patient had an elevated total protein ( 12 g / dl ) approximately six months prior 
 to initial visit . within the 
 next few weeks , the patient continued to deteriorate , and he developed 
 worsening ascites with hyponatremia .
it was clear that the patient had 
 progressive liver disease from chronic hepatitis b with a relatively high meld 
 score of 23 , and he would benefit from a liver transplantation .
our dilemma 
 before proceeding with liver transplantation was whether he had an underlying 
 hematological malignancy that was causing the monoclonal gammopathy .
we were also concerned 
 about potential vascular complications after liver transplant given his 
 increased viscosity .
however , due to his deterioration and absence of any 
 clear - cut evidence of malignancy , it was decided to place the patient on the 
 liver transplant wait list .
anti - hbv 
 therapy was initiated with a combination of entecavir ( 0.5 mg / day ) and 
 tenofovir ( 300 mg / day ) to decrease his hbv dna to the lowest possible level 
 before transplantation .
however , he was on this antiviral therapy for less than 
 a month as he received a deceased donor liver transplant ten days after 
 listing . in the period between listing and liver transplantation , his bilirubin 
 continued to trend up from 3.3 mg / dl to 4.6 mg / dl , and his total protein level 
 fluctuated between 12.5 g / dl and 13.5 g / dl .
, he received two doses of rabbit antithymocyte globulin at 1.5 mg / kg during the time of transplant and on postoperative day 2 .
subsequently , the 
 mycophenolate mofetil was withdrawn , and he is currently on tacrolimus 
 monotherapy with trough levels between 35 mg / ml . he 
 continues to receive hepatitis b immunoglobulin infusion every month along with 
 entecavir ( 0.5 mg / day ) , and his hepatitis b antibody titre has been kept above 
 300 miu / ml . he is currently 9 months posttransplant , his total protein levels 
 range 4 - 5 g / dl , and he has had no detectable m protein spike .
the temporal relation 
 of the liver transplant with disappearance of hepatitis b surface antigen and 
 normalization of the monoclonal spike implicates hepatitis b as the 
 possible cause of the m protein spike .
there is very little data and uncertainty regarding the incidence and natural history of 
 m proteins in a person with hepatitis b. it has been suggested that the immunological response elicited against hepatitis 
 b virus in the host rather than the direct cytopathic effect of the virus may 
 be the basis for the pathogenesis of hepatic and nonhepatic manifestations .
hepatitis b 
 virus seems particularly well suited to initiate a chronic immune disease 
 because of its tendency to persist in spite of a good immune response .
this may cause clonal expansion of the 
 immunoglobulin secreting cells and may explain the above phenomenon
. 
 alternately , the m protein spike could represent increased serum 
 immunoconglutinin titres .
it has been previously suggested that elevated serum 
 immunoconglutinin titers in patients with acute and chronic hepatitis b virus 
 infection may represent a physiological autoimmune response to hbsag / anti - hbs 
 immune complexes .
although our patient did not have the anti - hbs antibody , 
 it has been suggested that in the light of massive antigenemia present in 
 chronic hbsag carriers , it is possible that anti - hbs exists in the form of 
 hbsag / anti - hbs immune complexes .
this would make it difficult to detect 
 anti - hbs in serum samples by conventional serological methods .
the primary issue was whether 
 he was eligible for liver transplantation in the presence of an increasing m 
 protein .
the fact that he had lymphoma 10 years ago complicated this 
 evaluation . additionally , an association between hepatitis b infection 
 and non - hodgkin 's lymphoma has been previously described .
however , he had had regular follow - ups every six months 
 after remission of lymphoma , and also his malignancy workup prior to transplant 
 was negative .
moreover , the m protein spike was noticed only 6 months prior to 
 transplant and this coincided with the elevation of his liver function tests . 
 surprisingly , his igm antibody to hepatitis b core antigen was positive , as was 
 his total core antibody .
he did have active hepatitis and this can be deduced 
 by the fact that he had an alt level that was 10 times the upper limits of 
 normal ; his explanted liver showed significant inflammatory activity .
it was felt 
 that most likely he had a flare of his chronic hbv , which might have triggered 
 the elevation in m protein .
because 
 of his elevated m protein and an urgent need for liver transplantation , we 
 decided to initiate dual therapy with a nucleoside ( entecavir ) and nucleotide 
 ( tenofovir ) analogue to decrease his hbv dna .
however , he was on therapy less than a month before a suitable organ 
 became available .
we decided to accept the organ because of high meld score 
 rather than to wait for hbv dna disappearance .
since we were planning to 
 continue therapy posttransplant along with hbig ( target anti - hbs titers > 500 iu / ml first three months and levels of > 300 iu / ml after three months ) , 
 we believed that the risk of recurrence of hbv was very small .
unfortunately in 
 the time period before the transplant and after initiation of antiviral therapy , 
 we failed to follow his iga levels and hbv dna levels .
however , his protein levels remained 
 unchanged suggesting that there may have been very little change in his 
 gammopathy , and this is not surprising given the fact that nucleos(t)ide 
 therapy seldom leads to hbsag clearance in that time frame .
after 
 liver transplantation and with clearance of the hepatitis b surface antigen , 
 the m protein levels became normal .
one and the most likely reason is the 
 removal of antigen source with native hepatectomy .
his hepatitis b surface 
 antigen , m protein , and total protein levels remain within normal limits 1 year 
 after transplantation .
the second possibility is the impact of thymocyte , given 
 at the time of transplant , on plasma cells .
antithymocyte globulin has been 
 used in treatment of plasma cell dyscrasias   due to its activity against 
 several plasma cell antigens .
this is less likely in our patient because 
 thymocyte globulin was used only as induction therapy at the time of 
 transplantation .
the elimination half time of thymoglobulin is 2 - 3 days and is 
 unlikely that its effect on plasma cell is sustained for a year . in 
 conclusion , this case demonstrates that monoclonal gammopathy can be associated 
 with chronic hepatitis b infection and can be eliminated after successful 
 transplantation .
 monoclonal gammopathy of undetermined significance ( mgus ) has been most commonly associated with diseases like multiple myeloma , waldenstrom 's macroglobulinemia , primary systemic amyloidosis , hiv , and other lymphoproliferative disorders . 
 there has been an isolated report of mgus in patients coinfected with hiv and hepatitis b , as the work by amara et al . in 2006 .   here 
 , we report a case of iga - kappa light chain gammopathy secondary to hepatitis b infection , which resolved after liver transplantation . to our knowledge 
 , this is the first reported case of m protein spike seen in the context of hepatitis b infection only . 