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Intrahepatic cholestasis in subclinical and overt hyperthyroidism: two case reports.

Soylu A, Taskale MG, Ciltas A, Kalayci M, Kumbasar AB - J Med Case Rep (2008)

Bottom Line: On the other hand, the use of anti-thyroid drugs has rarely been associated with toxic hepatitis and cholestatic jaundice.Here we present two cases of cholestasis that accompanied two distinct forms of clinical hyperthyroidism.The second case had developed intrahepatic cholestasis in the presence of subclinical hyperthyroidism, and improved with rifampicin treatment.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Gastroenterology, Dr Sadi Konuk Research Hospital, Istanbul, Turkey. aliyesoylu@superonline.com

ABSTRACT

Introduction: Non-specific abnormalities in liver function tests might accompany the clinical course of hyperthyroidism. Hyperthyroidism can cause the elevation of hepatic enzymes and bilirubin. Jaundice is rare in overt hyperthyroidism, especially in subclinical hyperthyroidism. On the other hand, the use of anti-thyroid drugs has rarely been associated with toxic hepatitis and cholestatic jaundice.

Case presentation: Here we present two cases of cholestasis that accompanied two distinct forms of clinical hyperthyroidism. The first patient had a clinical presentation of severe cholestasis in the absence of congestive failure related to hyperthyroidism. The second case had developed intrahepatic cholestasis in the presence of subclinical hyperthyroidism, and improved with rifampicin treatment.

Conclusion: Hyperthyroidism should be a consideration in non-specific liver dysfunction.

No MeSH data available.


Related in: MedlinePlus

Liver biopsy results consistent with intrahepatic cholestasis. Hematoxylin and eosin stain, magnification ×100.
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Figure 1: Liver biopsy results consistent with intrahepatic cholestasis. Hematoxylin and eosin stain, magnification ×100.

Mentions: A 67-year-old female patient was admitted to hospital with complaints of pruritus and jaundice. She had no history of liver disease, and had been diagnosed with hyperthyroidism three years previously. The patient had been on anti-thyroid medications for one year, and had not experienced any hepatic problems during this period. Anti-thyroid drug therapy had been discontinued two years previously because she had reached normal thyroid status both clinically and on laboratory tests. In her laboratory results two months previously, serum thyrotropin levels were suppressed (TSH less than 0.01 uIU/ml (N: 0.4–4)), and free thyroxine was within normal limits (FT4 1.15 ng/dl (N: 0.9–1.7)). Our assessment was that the patient had subclinical hyperthyroidism. Six weeks prior to her admission to our clinic, she had developed pruritus; she had no history of other pharmaceutical or herbal medication use, infections, abuse of alcohol or contact with toxic substances. Physical examination findings were normal except for jaundice and the skin manifestations of pruritus. At the time of admission, her laboratory results were: AST 38 IU/l (N: 5–34), ALT 41 IU/l (N: 0–55), GGT 203 IU/l (N: 9–64), ALP 358 IU/l (N: 40–150), LDH 182 IU/l (N: 125–243), total bilirubin 24.5 mg/dl (N: 0.2–1.3), direct bilirubin 17.5 mg/dl (N: 0.1–0.5), Ca 8.8 mg/dl (N: 8.4–10.2) and P 2.3–4.7 mg/dl. Markers of viral hepatitis (HBsAg, anti-HBc IgM, anti-HAV IgM, HCV, HIV, VDRL, CMV, EBV), brucella and autoimmune hepatitis (ANA, AMA, ASMA and LKM1) were all negative. Endoscopic retrograde cholangiopancreatography (ERCP) and other imaging techniques did not reveal any pathology. Follow-up thyroid hormone levels were FT3 3.8 ng/dl, FT4 1.34 ng/dl (N: 1.8–4.2) and TSH 0.08 uIU/ml, correlating with subclinical hyperthyroidism. The patient's serum was negative for thyroid autoantibodies. Thyroid USG revealed a multinodular goiter pattern. The thyroid biopsy revealed nodular hyperplasia. Liver biopsy results showed degeneration and regeneration of hepatocytes, pigment accumulation in the cytoplasm of some hepatocytes, dilatation of the sinusoids, bile plugs, a slight increase in Kupffer cells, rare mononuclear inflammatory cells and regular appearance of bile ductules. This was consistent with intrahepatic cholestasis (Figure 1).


Intrahepatic cholestasis in subclinical and overt hyperthyroidism: two case reports.

Soylu A, Taskale MG, Ciltas A, Kalayci M, Kumbasar AB - J Med Case Rep (2008)

Liver biopsy results consistent with intrahepatic cholestasis. Hematoxylin and eosin stain, magnification ×100.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2365967&req=5

Figure 1: Liver biopsy results consistent with intrahepatic cholestasis. Hematoxylin and eosin stain, magnification ×100.
Mentions: A 67-year-old female patient was admitted to hospital with complaints of pruritus and jaundice. She had no history of liver disease, and had been diagnosed with hyperthyroidism three years previously. The patient had been on anti-thyroid medications for one year, and had not experienced any hepatic problems during this period. Anti-thyroid drug therapy had been discontinued two years previously because she had reached normal thyroid status both clinically and on laboratory tests. In her laboratory results two months previously, serum thyrotropin levels were suppressed (TSH less than 0.01 uIU/ml (N: 0.4–4)), and free thyroxine was within normal limits (FT4 1.15 ng/dl (N: 0.9–1.7)). Our assessment was that the patient had subclinical hyperthyroidism. Six weeks prior to her admission to our clinic, she had developed pruritus; she had no history of other pharmaceutical or herbal medication use, infections, abuse of alcohol or contact with toxic substances. Physical examination findings were normal except for jaundice and the skin manifestations of pruritus. At the time of admission, her laboratory results were: AST 38 IU/l (N: 5–34), ALT 41 IU/l (N: 0–55), GGT 203 IU/l (N: 9–64), ALP 358 IU/l (N: 40–150), LDH 182 IU/l (N: 125–243), total bilirubin 24.5 mg/dl (N: 0.2–1.3), direct bilirubin 17.5 mg/dl (N: 0.1–0.5), Ca 8.8 mg/dl (N: 8.4–10.2) and P 2.3–4.7 mg/dl. Markers of viral hepatitis (HBsAg, anti-HBc IgM, anti-HAV IgM, HCV, HIV, VDRL, CMV, EBV), brucella and autoimmune hepatitis (ANA, AMA, ASMA and LKM1) were all negative. Endoscopic retrograde cholangiopancreatography (ERCP) and other imaging techniques did not reveal any pathology. Follow-up thyroid hormone levels were FT3 3.8 ng/dl, FT4 1.34 ng/dl (N: 1.8–4.2) and TSH 0.08 uIU/ml, correlating with subclinical hyperthyroidism. The patient's serum was negative for thyroid autoantibodies. Thyroid USG revealed a multinodular goiter pattern. The thyroid biopsy revealed nodular hyperplasia. Liver biopsy results showed degeneration and regeneration of hepatocytes, pigment accumulation in the cytoplasm of some hepatocytes, dilatation of the sinusoids, bile plugs, a slight increase in Kupffer cells, rare mononuclear inflammatory cells and regular appearance of bile ductules. This was consistent with intrahepatic cholestasis (Figure 1).

Bottom Line: On the other hand, the use of anti-thyroid drugs has rarely been associated with toxic hepatitis and cholestatic jaundice.Here we present two cases of cholestasis that accompanied two distinct forms of clinical hyperthyroidism.The second case had developed intrahepatic cholestasis in the presence of subclinical hyperthyroidism, and improved with rifampicin treatment.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Gastroenterology, Dr Sadi Konuk Research Hospital, Istanbul, Turkey. aliyesoylu@superonline.com

ABSTRACT

Introduction: Non-specific abnormalities in liver function tests might accompany the clinical course of hyperthyroidism. Hyperthyroidism can cause the elevation of hepatic enzymes and bilirubin. Jaundice is rare in overt hyperthyroidism, especially in subclinical hyperthyroidism. On the other hand, the use of anti-thyroid drugs has rarely been associated with toxic hepatitis and cholestatic jaundice.

Case presentation: Here we present two cases of cholestasis that accompanied two distinct forms of clinical hyperthyroidism. The first patient had a clinical presentation of severe cholestasis in the absence of congestive failure related to hyperthyroidism. The second case had developed intrahepatic cholestasis in the presence of subclinical hyperthyroidism, and improved with rifampicin treatment.

Conclusion: Hyperthyroidism should be a consideration in non-specific liver dysfunction.

No MeSH data available.


Related in: MedlinePlus