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Acute liver failure caused by diffuse hepatic melanoma infiltration
Journal of Hepatology 37 (2002) 540–541 www.elsevier.com/locate/jhep
Letter to the Editor
Acute liver failure caused by diffuse hepatic melanoma infiltration To the Editor: Malignant hepatic infiltration is a very rare cause of acute liver failure (ALF). Among 4020 admissions of ALF at the Liver Failure Unit of King’s College Hospital of London in the United Kingdom during the period 1978–1995, only 18 cases were identified as attributable to hepatic malignant infiltration [1]. Nevertheless, none of them were originated from a development of a melanoma. The incidence of melanoma is consistently rising over the last years and affects the liver in 20–32% of the patients in advanced stage [2]. However, in these conditions a significant liver dysfunction is very uncommon. Only a few cases of ALF caused by melanoma have been reported [3–5]. The majority of the patients show nodular infiltration in the liver, but massive diffuse liver metastasis is very rare and difficult to identify. We report a case of ALF due to diffuse liver infiltration by advanced melanoma. A 48-year-old man was admitted to our Liver Unit for evaluation of jaundice, nausea and vomiting with general malaise in the previous 2 weeks. Previously he had been
healthy and no epidemiological features of hepatitis were found in his history. He was treated for a supraciliar melanoma 18 months earlier and the pathological findings were Clark stage II, with less than 1 mm of depth and tumor-free resection margins. At admission, the patient was alert with normal vital signs, and no skin lesions were found. He had clear signs of jaundice and the abdomen was soft without pain. The liver was palpable 5 cm below the right side margin. No signs of encephalopathy were found. The laboratory data obtained after admission showed normal hemogram, aspartate aminotransferase 515 U/l (normal , 45Þ, alanine aminotransferase 493 U/l (normal , 45Þ, g-glutamyl transferase 1122 U/l (normal , 50Þ, alkaline phosphatase 503 U/l (normal , 120Þ, lactate dehydrogenase 643 U/l (normal , 480Þ, and total bilirubin 10.3 mg/dl (normal , 1:2Þ. Prothrombin activity reached 45% and partial thromboplastin time was 50.2 s (normal , 30Þ. Viral serological and autoimmune markers were negative. The rest of the biochemical parameters were normal. The ultrasound study observed hepatomegaly with homoge-
Fig. 1. The abnormal polygonal cells showed positive cytoplasm staining for HMB-45 cellular marker detected by immunohistochemistry. Original magnification £ 200. 0168-8278/02/$20.00 q 2002 European Association for the Study of the Liver. Published by Elsevier Science B.V. All rights reserved. PII: S01 68- 8278(02)0021 9-2
J.L. Montero et al. / Journal of Hepatology 37 (2002) 540–541
neous normal echogenicity without focal lesions and ascites. An abdominal computed tomographic scan was performed without endovenous contrast and showed hepatomegaly without focal lesions, splenomegaly, ascites and bilateral pleural effusion. A liver biopsy stained with hematoxylin– eosin indicated an extensive necrosis with the presence of massive diffuse infiltration of brown polygonal cells with melanin granular inclusions in sinusoids. These abnormal cells were identified as melanocytes by their positive staining for HMB-45 cellular marker by immunohistochemistry (Fig. 1). The liver function tests worsened in the next days (serum bilirubin rose to 18 mg/dl and the prothrombin activity decreased to 22%) despite standard liver failure therapy. The patient suffered progressive encephalopathy to grade IV and severe renal dysfunction, and died 10 days later. This case of ALF by hepatic malignant infiltration from melanoma origin represents a very rare cause of ALF. Most of them are identified in postmortem studies, as the biopsy is very difficult to perform in the context of the severe coagulopathy present during ALF. In these patients, liver biopsy may be obtained by transjugular route to avoid the risk of hemorrhage. Moreover, this method is also useful to determine the degree of portal hypertension, providing additional knowledge on the mechanism of ascites formation. Lymphomas and leukemia mostly cause ALF secondary to malignant infiltration. As previously mentioned, a few cases of ALF by melanoma are reported in the literature, and only one with diffuse melanoma infiltration of the liver [3–5]. In
541
the present report, the induction of ALF by diffuse hepatic melanoma infiltration has been fully demonstrated in the biopsy by histological studies. Jose´ L. Montero 1, Jordi Muntane´ 1, Silvia de las Heras 1, Rosa Ortega 2, Enrique Fraga 1, Manuel De la Mata 1 1 Unidad Clı´nica Aparato Digestivo, Hospital Universitario Reina Sofı´a, Avenida Menendez Pidal s/n, 14004 Co´rdoba, Spain, 2Servicio Anatomı´a Patolo´gica, Hospital Universitario Reina Sofı´a, Co´rdoba, Spain
References [1] Rowbotham D, Wendon J, Williams R. Acute liver failure secondary to hepatic infiltration: a single center experience of 18 cases. Gut 1998;42:576–580. [2] Te HS, Schiano TD, Kahaleh M, Lissoos TW, Baker AL, Hart J, et al. Fulminant hepatic failure secondary to malignant melanoma: case report and review of the literature. Am J Gastroenterol 1999;94:262– 266. [3] Lesur G, Bergemer AM, Metges JP, Barre O, Dupuy P, Le Parc JM. Le foie me´ tastatique; une cause rare d’insuffisancee hepatoce´ llulaire. Ann Gastroenterol Hepatol 1992;28:217–220. [4] Bouloux PM, Scott RJ, Goligher JE, Kindell C. Fulminant hepatic failure secondary to diffuse liver infiltration by melanoma. J R Soc Med 1986;79:302–303. [5] Muehlenberg K, Wardelmann E. Akutes leberversagen bei metastasierenden melanom. Leber Magen Darm 1992;22:192–194.
Letter to the Editor
Acute liver failure caused by diffuse hepatic melanoma infiltration To the Editor: Malignant hepatic infiltration is a very rare cause of acute liver failure (ALF). Among 4020 admissions of ALF at the Liver Failure Unit of King’s College Hospital of London in the United Kingdom during the period 1978–1995, only 18 cases were identified as attributable to hepatic malignant infiltration [1]. Nevertheless, none of them were originated from a development of a melanoma. The incidence of melanoma is consistently rising over the last years and affects the liver in 20–32% of the patients in advanced stage [2]. However, in these conditions a significant liver dysfunction is very uncommon. Only a few cases of ALF caused by melanoma have been reported [3–5]. The majority of the patients show nodular infiltration in the liver, but massive diffuse liver metastasis is very rare and difficult to identify. We report a case of ALF due to diffuse liver infiltration by advanced melanoma. A 48-year-old man was admitted to our Liver Unit for evaluation of jaundice, nausea and vomiting with general malaise in the previous 2 weeks. Previously he had been
healthy and no epidemiological features of hepatitis were found in his history. He was treated for a supraciliar melanoma 18 months earlier and the pathological findings were Clark stage II, with less than 1 mm of depth and tumor-free resection margins. At admission, the patient was alert with normal vital signs, and no skin lesions were found. He had clear signs of jaundice and the abdomen was soft without pain. The liver was palpable 5 cm below the right side margin. No signs of encephalopathy were found. The laboratory data obtained after admission showed normal hemogram, aspartate aminotransferase 515 U/l (normal , 45Þ, alanine aminotransferase 493 U/l (normal , 45Þ, g-glutamyl transferase 1122 U/l (normal , 50Þ, alkaline phosphatase 503 U/l (normal , 120Þ, lactate dehydrogenase 643 U/l (normal , 480Þ, and total bilirubin 10.3 mg/dl (normal , 1:2Þ. Prothrombin activity reached 45% and partial thromboplastin time was 50.2 s (normal , 30Þ. Viral serological and autoimmune markers were negative. The rest of the biochemical parameters were normal. The ultrasound study observed hepatomegaly with homoge-
Fig. 1. The abnormal polygonal cells showed positive cytoplasm staining for HMB-45 cellular marker detected by immunohistochemistry. Original magnification £ 200. 0168-8278/02/$20.00 q 2002 European Association for the Study of the Liver. Published by Elsevier Science B.V. All rights reserved. PII: S01 68- 8278(02)0021 9-2
J.L. Montero et al. / Journal of Hepatology 37 (2002) 540–541
neous normal echogenicity without focal lesions and ascites. An abdominal computed tomographic scan was performed without endovenous contrast and showed hepatomegaly without focal lesions, splenomegaly, ascites and bilateral pleural effusion. A liver biopsy stained with hematoxylin– eosin indicated an extensive necrosis with the presence of massive diffuse infiltration of brown polygonal cells with melanin granular inclusions in sinusoids. These abnormal cells were identified as melanocytes by their positive staining for HMB-45 cellular marker by immunohistochemistry (Fig. 1). The liver function tests worsened in the next days (serum bilirubin rose to 18 mg/dl and the prothrombin activity decreased to 22%) despite standard liver failure therapy. The patient suffered progressive encephalopathy to grade IV and severe renal dysfunction, and died 10 days later. This case of ALF by hepatic malignant infiltration from melanoma origin represents a very rare cause of ALF. Most of them are identified in postmortem studies, as the biopsy is very difficult to perform in the context of the severe coagulopathy present during ALF. In these patients, liver biopsy may be obtained by transjugular route to avoid the risk of hemorrhage. Moreover, this method is also useful to determine the degree of portal hypertension, providing additional knowledge on the mechanism of ascites formation. Lymphomas and leukemia mostly cause ALF secondary to malignant infiltration. As previously mentioned, a few cases of ALF by melanoma are reported in the literature, and only one with diffuse melanoma infiltration of the liver [3–5]. In
541
the present report, the induction of ALF by diffuse hepatic melanoma infiltration has been fully demonstrated in the biopsy by histological studies. Jose´ L. Montero 1, Jordi Muntane´ 1, Silvia de las Heras 1, Rosa Ortega 2, Enrique Fraga 1, Manuel De la Mata 1 1 Unidad Clı´nica Aparato Digestivo, Hospital Universitario Reina Sofı´a, Avenida Menendez Pidal s/n, 14004 Co´rdoba, Spain, 2Servicio Anatomı´a Patolo´gica, Hospital Universitario Reina Sofı´a, Co´rdoba, Spain
References [1] Rowbotham D, Wendon J, Williams R. Acute liver failure secondary to hepatic infiltration: a single center experience of 18 cases. Gut 1998;42:576–580. [2] Te HS, Schiano TD, Kahaleh M, Lissoos TW, Baker AL, Hart J, et al. Fulminant hepatic failure secondary to malignant melanoma: case report and review of the literature. Am J Gastroenterol 1999;94:262– 266. [3] Lesur G, Bergemer AM, Metges JP, Barre O, Dupuy P, Le Parc JM. Le foie me´ tastatique; une cause rare d’insuffisancee hepatoce´ llulaire. Ann Gastroenterol Hepatol 1992;28:217–220. [4] Bouloux PM, Scott RJ, Goligher JE, Kindell C. Fulminant hepatic failure secondary to diffuse liver infiltration by melanoma. J R Soc Med 1986;79:302–303. [5] Muehlenberg K, Wardelmann E. Akutes leberversagen bei metastasierenden melanom. Leber Magen Darm 1992;22:192–194.