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Editor,—Since the discovery by Koprowski and co-workers in 1979, raised serum concentrations of carbohydrate antigenic determinant, CA 19.9, has been used as an additional diagnostic test for adenocarcinoma of the upper gastrointestinal tract.1-3 According to Benamouzig et al,3 at the usual 37 U/ml cut off value, CA 19.9 had a sensitivity of 90% and a specificity of 45% for malignant biliary obstruction due to pancreatic or biliary neoplasm. For a more increased cut off value of 200 U/ml, its sensitivity was 65% and specificity was 91%. If higher cut off values are used, specificity rises so that at levels greater than 1000 U/ml, it approaches 100%.4 A very high concentration of serum CA 19.9 is therefore currently the “gold standard” marker for malignant biliary obstruction resulting from pancreatic cancer.4
Here, we report an exceptional high concentration of serum CA 19.9 in a patient with alcoholic liver disease. When the patient ceased drinking, the CA 19.9 serum concentration returned to normal within few months.
A 58 year man was admitted to our hospital because of jaundice and weight loss. He also complained of fatigue and pruritus of several weeks duration. His medical history was, except for psoriasis, unremarkable. However, he took acetylcysteine, eprazinohydrochloride, and prior to admission clarithromycin for a respiratory infection and obstructive lung disease. The patient smoked 15 cigarettes a day. For his ischiatic pain, he also took naloxonhydrochloride and tramadolhydrochloride. In addition he consumed approximately 10 pints of beer a day for many years and for the past two years also a quarter bottle of gin a day.
Physical examination showed jaundice, firm hepatomegaly and psoriatic skin lesions.
Laboratory investigations revealed increased concentrations of plasma bilirubin (total 6.26 mg/dl, conjugated 3.92 mg/dl, normal <1 mg/dl), alkaline phosphatase (1071 U/l, normal <240 U/l), aspartate aminotransferase (197 U/l, normal <20 U/l), alanine aminotransferase (101 U/l, normal <20 U/l), and γ-glutamyltranspeptidase (1700 U/l, normal <60 U/l). The patient also had raised concentrations of triglycerides (1398 mg/dl, normal <200 mg/dl) and cholesterol (667 mg/dl, normal <240 mg/dl). Serological markers for hepatitis A, B and C did not indicate a recent infection or active viral replication. Autoantibodies were negative. Serum CA 19.9 was extremely high at 10.981 U/ml (confirmed in a retrospective examination), while carcinoembryonic antigen (CEA; normal <5 μg/l) was 14.4 μg/l.
An ultrasonography and a computed tomography scan indicated hepatomegaly and fatty change without focal lesions or dilated biliary ducts. Endoscopic retrograde cholangiopancreaticography showed no abnormalities, in particular no signs of primary sclerosing cholangitis or other biliary and pancreatic duct abnormalities.
A liver biopsy revealed micro- and macrovesicular steatosis, periportal fibrosis, Mallory’s bodies, in addition to the presence of bilirubinostasis. Liver histology was very suggestive of alcoholic liver changes.
Although the use of medical drugs, especially clarithromycin, may contribute to this clinical syndrome, we believe that alcohol misuse was the most attributable factor. We therefore advised the patient to stop drinking. Once alcohol consumption ceased, there was a dramatic improvement in clinical and biochemical abnormalities. During a follow up visit three months after presentation, biochemistry values had almost returned to normal.The serum concentration of CA 19.9 had decreased to 96 U/ml.
We conclude, therefore, that an exceptionally high concentration of serum CA 19.9 may be found in patients with alcoholic liver disease.
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