INTERESTING IMAGE
High Liver FDG Uptake on PET/CT in Patient With Lymphoma Diagnosed With Hereditary Hemochromatosis Jose R. Infante, PhD, Manuel Moreno, MD, Juan I. Rayo, PhD, Justo Serrano, PhD, Maria L. Dominguez, MD, and Lucia Garcia, MD Abstract: Hereditary hemochromatosis is an autosomal recessive disorder of iron metabolism resulting in toxic accumulation of iron in vital organs. We present a 64-year-old white man with non-Hodgkin lymphoma treated with high-dose chemotherapy and stem cell transplant that was subsequently diagnosed with hereditary hemochromatosis. 18F-FDG PET/CTwas performed as routine follow-up and showed a pathological finding of homogeneous increased liver glucose metabolism. Increased FDG avidity in the liver suggested the presence of damage caused by hemochromatosis. Key Words: PET/CT, 18F-FDG, hemochromatosis, lymphoma (Clin Nucl Med 2015;40: 538–539)
Received for publication September 29, 2014; revision accepted November 17, 2014. From the Department of Nuclear Medicine, Infanta Cristina Hospital, Badajoz, Spain. Conflicts of interest and sources of funding: none declared. Reprints: Jose R. Infante, PhD, Servicio de Medicina Nuclear, Hospital U. Infanta Cristina, Ctra. de Portugal s/n, 06080-Badajoz, Spain. E-mail: [email protected]. Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved. ISSN: 0363-9762/15/4006–0538
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REFERENCES 1. Crownover BK, Covey CJ. Hereditary hemochromatosis. Am Fam Physician. 2013; 87:183–190. 2. Adams PC, Reboussin DM, Barton JC, et al. Hemochromatosis and iron-overload screening in a racially diverse population. N Engl J Med. 2005;352:1769–1778. 3. European Association for the Study of the Liver. EASL clinical practice guidelines for HFE hemochromatosis. J Hepatol. 2010;53:3–22. 4. Leitman SF. Hemochromatosis: the new blood donor. Hematology Am Soc Hematol Educ Program. 2013;2013:645–650. 5. Kew MC. Hepatic iron overload and hepatocellular carcinoma. Liver Cancer. 2014; 3:31–40. 6. Bacon BR, Adams PC, Kowdley KV, et al. Diagnosis and management of hemochromatosis: 2011 practice guideline by the American Association for the Study of Liver Diseases. Hepatology. 2011;54:328–343. 7. Lichtman SM, Attivissimo L, Goldman IS, et al. Secondary hemochromatosis as a long-term complication of the treatment of hematologic malignancies. Am J Hematol. 1999;61:262–264. 8. Ito K, Minamimoto R, Morooka M, et al. A case of secondary hemochromatosis with high uptake of liver in F-18 FDG PET/CT imaging. Clin Nucl Med. 2011; 36:606–608.
Clinical Nuclear Medicine • Volume 40, Number 6, June 2015 Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
Clinical Nuclear Medicine • Volume 40, Number 6, June 2015
Liver FDG Uptake in Hereditary Hemochromatosis
FIGURE 1. We present a 64-year-old white male patient with history of non-Hodgkin diffuse large B-cell lymphoma. He was treated with chemotherapy, radiotherapy, and stem cell transplant. Subsequent 18F-FDG PET/CT showed normal distribution (A). One month later, patient related abdominal pain and fever. Abdominal ultrasound revealed heterogeneous echo pattern throughout the liver without focal masses. Biochemical parameters of the blood showed high level of ferritin (1068 ng/mL; reference range, 10–120 ng/mL). Genetic study revealed homozygosity for the H63D mutation, confirming the diagnosis of hereditary hemochromatosis. Patient was treated with phlebotomy. Three months later, a new FDG PET/CT was conducted as a follow-up for his hematological malignancy. There was no clinical suspicion of tumor recurrence, and β2-microglobulin and lactate dehydrogenase showed normal values. Coronal (B) and axial PET/CT images (C) revealed high glucose metabolism in the liver with homogeneous pattern (SUVmax, 19.1) and not other pathological finding. After 5 months of follow-up, the patient remained lymphoma free. Increased FDG uptake was not due to tumor disease but to liver damage caused by increased iron deposits probably due to intense hematological therapy. Hereditary hemochromatosis is an autosomal recessive disorder in which iron regulation is disrupted; this remains the most common genetic disorder in white people, most commonly in populations of northern European origin.1,2 C282Y homozygotes account for 80% to 85% of patients, but there are 2 other regularly identified mutations, including H63D mutation.3 Family screening should be recommended for all first-degree relatives. Persons with hereditary hemochromatosis usually are asymptomatic. Symptomatic disease rarely presents in patients younger than 40 years.1 Principal clinical features include weakness, abdominal pain, and arthralgias. It is associated with malignancies, particularly hepatocellular carcinoma.4,5 Phlebotomy remains the mainstay of treatment to reduce total body iron levels and achieve normal ferritin levels.6 The long-term follow-up of patient with hematological malignancy should include analysis of iron status.7 To our knowledge, only 1 study has been reported previously about FDG PET/CT uptake of the liver in patients diagnosed with hemochromatosis.8
© 2015 Wolters Kluwer Health, Inc. All rights reserved. Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
www.nuclearmed.com
539
High Liver FDG Uptake on PET/CT in Patient With Lymphoma Diagnosed With Hereditary Hemochromatosis Jose R. Infante, PhD, Manuel Moreno, MD, Juan I. Rayo, PhD, Justo Serrano, PhD, Maria L. Dominguez, MD, and Lucia Garcia, MD Abstract: Hereditary hemochromatosis is an autosomal recessive disorder of iron metabolism resulting in toxic accumulation of iron in vital organs. We present a 64-year-old white man with non-Hodgkin lymphoma treated with high-dose chemotherapy and stem cell transplant that was subsequently diagnosed with hereditary hemochromatosis. 18F-FDG PET/CTwas performed as routine follow-up and showed a pathological finding of homogeneous increased liver glucose metabolism. Increased FDG avidity in the liver suggested the presence of damage caused by hemochromatosis. Key Words: PET/CT, 18F-FDG, hemochromatosis, lymphoma (Clin Nucl Med 2015;40: 538–539)
Received for publication September 29, 2014; revision accepted November 17, 2014. From the Department of Nuclear Medicine, Infanta Cristina Hospital, Badajoz, Spain. Conflicts of interest and sources of funding: none declared. Reprints: Jose R. Infante, PhD, Servicio de Medicina Nuclear, Hospital U. Infanta Cristina, Ctra. de Portugal s/n, 06080-Badajoz, Spain. E-mail: [email protected]. Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved. ISSN: 0363-9762/15/4006–0538
538
www.nuclearmed.com
REFERENCES 1. Crownover BK, Covey CJ. Hereditary hemochromatosis. Am Fam Physician. 2013; 87:183–190. 2. Adams PC, Reboussin DM, Barton JC, et al. Hemochromatosis and iron-overload screening in a racially diverse population. N Engl J Med. 2005;352:1769–1778. 3. European Association for the Study of the Liver. EASL clinical practice guidelines for HFE hemochromatosis. J Hepatol. 2010;53:3–22. 4. Leitman SF. Hemochromatosis: the new blood donor. Hematology Am Soc Hematol Educ Program. 2013;2013:645–650. 5. Kew MC. Hepatic iron overload and hepatocellular carcinoma. Liver Cancer. 2014; 3:31–40. 6. Bacon BR, Adams PC, Kowdley KV, et al. Diagnosis and management of hemochromatosis: 2011 practice guideline by the American Association for the Study of Liver Diseases. Hepatology. 2011;54:328–343. 7. Lichtman SM, Attivissimo L, Goldman IS, et al. Secondary hemochromatosis as a long-term complication of the treatment of hematologic malignancies. Am J Hematol. 1999;61:262–264. 8. Ito K, Minamimoto R, Morooka M, et al. A case of secondary hemochromatosis with high uptake of liver in F-18 FDG PET/CT imaging. Clin Nucl Med. 2011; 36:606–608.
Clinical Nuclear Medicine • Volume 40, Number 6, June 2015 Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
Clinical Nuclear Medicine • Volume 40, Number 6, June 2015
Liver FDG Uptake in Hereditary Hemochromatosis
FIGURE 1. We present a 64-year-old white male patient with history of non-Hodgkin diffuse large B-cell lymphoma. He was treated with chemotherapy, radiotherapy, and stem cell transplant. Subsequent 18F-FDG PET/CT showed normal distribution (A). One month later, patient related abdominal pain and fever. Abdominal ultrasound revealed heterogeneous echo pattern throughout the liver without focal masses. Biochemical parameters of the blood showed high level of ferritin (1068 ng/mL; reference range, 10–120 ng/mL). Genetic study revealed homozygosity for the H63D mutation, confirming the diagnosis of hereditary hemochromatosis. Patient was treated with phlebotomy. Three months later, a new FDG PET/CT was conducted as a follow-up for his hematological malignancy. There was no clinical suspicion of tumor recurrence, and β2-microglobulin and lactate dehydrogenase showed normal values. Coronal (B) and axial PET/CT images (C) revealed high glucose metabolism in the liver with homogeneous pattern (SUVmax, 19.1) and not other pathological finding. After 5 months of follow-up, the patient remained lymphoma free. Increased FDG uptake was not due to tumor disease but to liver damage caused by increased iron deposits probably due to intense hematological therapy. Hereditary hemochromatosis is an autosomal recessive disorder in which iron regulation is disrupted; this remains the most common genetic disorder in white people, most commonly in populations of northern European origin.1,2 C282Y homozygotes account for 80% to 85% of patients, but there are 2 other regularly identified mutations, including H63D mutation.3 Family screening should be recommended for all first-degree relatives. Persons with hereditary hemochromatosis usually are asymptomatic. Symptomatic disease rarely presents in patients younger than 40 years.1 Principal clinical features include weakness, abdominal pain, and arthralgias. It is associated with malignancies, particularly hepatocellular carcinoma.4,5 Phlebotomy remains the mainstay of treatment to reduce total body iron levels and achieve normal ferritin levels.6 The long-term follow-up of patient with hematological malignancy should include analysis of iron status.7 To our knowledge, only 1 study has been reported previously about FDG PET/CT uptake of the liver in patients diagnosed with hemochromatosis.8
© 2015 Wolters Kluwer Health, Inc. All rights reserved. Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
www.nuclearmed.com
539
