(Chongqing Liver Diseases Research and Treatment Center，National Key Department of Medicine，the Second College of Clinical Medicinethe Second Affiliated Hospital of Chongqing Medical Univercity，Chongqing 400010)

[Abstract] Introduction Thyrotoxicosis hepatitis is common.It is difficult in therapy，especially thyroid crisis with severe hepatitis，propylthiouracil-induced hepatic disfunction and even hepatic failure or severe hepatitis or fulminant hepatitis is come to light，as is methimazole. If propylthiouracil or methimazole controls hyperthroidism，liver disfunction would be deteriorated，and even patient die. If we only treat hepatitis，hyperthroidism couldn't be controled，the patient would also be worsen. Methods 131I therapy for oral cures hyperthyroidism，meanwhils liver dysfunction can return to normal. Results Thyrotoxic crisis was under control，and liver function hadgradual return. Conclusion 131I can be recognized as the safer，more convenient and effective and feasible treatment than ATD for thyrotoxicosis hepatitis.There were no harmful side effects or complications. It should be widelyapply clinically.

[Key Words] Hyperthyroidsm;Hepatitis;131I

Thyrotoxicosis hepatitis is common.It is difficult in therapy，especially thyroid crisis with severe hepatitis， propylthiouracil -induced hepatic disfunction and even hepatic failure or severe hepatitis or fulminant hepatitis is come to light[1-4]，as is methimazo- le[5-6].

If propylthiouracil or methimazole controls hyperthroidism，liver disfunction would be deteriorated， and even patient die.If we only treat hepatitis，hyperthroidism couldn't be controled，the patient would also be worsen. 131I therapy cures hyperthyroidism，meanwhils evere liver dysfunction can return to normal. We successfully treat the case of thyroid storm accompanying severe hepatitis with 131I therapy， this is the first report of this kind in the literature. Now，we report it.

1Case Presentation

1.1Before131ITherapy

A 60-year-old male，a retired worker visited the office complaining of feeling unwell for the past two months asthenia，obvious weakness，mild abdominal distention， bad appetite，one thirds quondam quantity of food，weight decreased 15kg，severe skin scleral jaundice and tea coloured flamboyantly urine，severediarrhea(over 20~30/d) and restlessness and mild pruritus， but no nausea，vomiting，abdomal pain，argillaceous feces，lumbago and fever.His vital signs were normal. He was afebrile. His physical examination was normal except for severe skin and scleral jaundice，He had thyromegaly and hepatomegaly flexibly，and not splenomegaly. Abdomal were soft without tenderness and rebound tenderness. There was sign of ascites. The urine was tea coloured and frothed upon shaking. A dipstick showed a large amount of bilirubin.History failed to show risk factors for hepatitis A，B，or C，E(no piercing，tattooing，or needle sharing)，and for blood transfusion，surgical trauma，operation，and for quantitive alcohol;there was no history of liver injury drugs cardiopathy，cardiopathy，hypertensive disease;and there washistoryofleptospirosis cured.

The investigations were: immunoglobulin M(IgM)included nRNP， Sm， SSA， SSB， Sc1-70， Jo-1，AMA-M2，LKM-1，SLA/LP were negative;the markers of viral A，C，E were negative;The hepatitis B surface，E antigen results were negative，The hepatitis B center antbody was positive(0.54Ncu/mL); a blood count showed hemoglobin 113g/L，red blood cell 3.59×1012/L，leukocyte 5.67×109/L，granulocyte 4.29×109/L(75.6%)， plastocyte 76×09/L;cultivation of feces with no harmful microorganism;blood plasm alanine andaspartateaminotransferase49IU/L(N:0~40) and 63 IU/L(N:5~34) respectively ，alkaline phosphatase 217 IU/L(N:15-112)，bilirubin 523μmol/L (N:2.3～20.4) direct bilirubin 468.6 μmol/L(N:0.0～20.4)，and gamma-glutamyl transpeptidase 47IU/L(N:5～54)， prothrombin time， PT 14second; blood plasma FT38.6pmol/L(N:3.53～4.45)， FrT4 44.6pmol/L(N:11.45～23.17)，TSH 0.02mU/L(N:0.35～5.5) and albumen(ALB)26.6g/L. Abdominal ultrasonography and MRI+ECP showed hepatomegaly，normal bile ducts and tumefacient liver andmild peritoneal fluid;thyroid iodine uptake ratio was 54%;Thyroid was proved hyperthyroidism by radio.

On the basis of these data and Burch， sprinciple[1]， the patient was diagnosed as thyroid storm accompanying severe hepatitis[7].

1.2 After 131ITherapy

131I(6mCi)for oral use controls hyperthroidism，the patient retained to normal after disinfection therapy for 73 days and careful medical integrative therapy for 44 days.The retesting results were:blood plasm alanine and aspartate aminotransferase 48IU/L and 55IU/L respectively，alkaline phosphatase 203IU/L，bilirubin 54.7μmol/Ldirect bilirubin 49μmol/L，and gamma-glutamyl transpeptidase 122IU/L，prothrombin time，PT 14 second;blood plasm FT3 4.20pmol/L，F(xiàn)rT4 8.38pmol/L，TSH 2.09mU/L and albumen33.5g/L.

The patient is survival， 131I is the key role of the successful cure of the patient，careful medical integrative therapy is undeniably important.

2 Conclusion

On the basis of these data，we successfully treat the case of thyroid storm accompanying severe hepatitis with 131I therapy，this is the first report of this kind in the literature. 131I is the key role to the successful cure of the patient，careful medical integrative therapy is undeniably important. 131I is safer，more convenient and effective feasible treatment than ATD for thyrotoxicosis hepatitis. There were no harmful side effects or complications. It should be widely applied clinically，and even thyroid storm accompanying severe hepati.

[Reference]

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[3] Kirkland JL. Propylthiouracil-induced hepatic failure and encephalopathy in a child[J]. DICP， 1990，24(5):470-471.

[4] Hayashida CY，Duarte AJ，Sato AE. Neonatal hepatitis and lymphocyte sensitizationbyplacentaltransferofpropylthiouracil[J]. J Endocrinol Invest， 1990，13(11):937-941

[5] Diaz Gomez MI， Godoy HM， Castro JA. Further studies on dimethylnitrosamine metabolism，activation and its ability to cause liver injury[J]. Arch Toxicol， 1981，47(3):159-68.

[6] Raviolo P，Rizzetto M，Tabone M，et al. Intrahepatic cholestasis in hyperthyroidism[J].Recenti Prog Med， 1991，82(6):319-323.

(收稿日期:2009-02-27)