Misleading 18 FDG-PET/CT finding caused by chronic HIV infection in a patient with gastric carcinoma: a case report

Introduction

Kaposi sarcoma, non-Hodgkin lymphoma, and cervical cancer commonly occur in association with chronic HIV infection. ¹ The risk of cancer associated with other viruses (such as Epstein Barr, hepatitis B and C) also increases due to immunosuppression and chronic inflammation in patients with HIV infection (such as hepatocellular, anal cancer, Hodgkin lymphoma). Anti-retroviral treatments increase the life span of patients and reduce the incidence of AIDS-associated malignancy at early ages. ² Despite the success of anti-retroviral treatment on the progression towards AIDS and AIDS-associated malignancies, the incidence of non-AIDS malignancies remains high in the HIV-positive population and is among the leading causes of death. ³ Little is known about gastric cancer among HIV-infected patients, ⁴ but as for all cancers in HIV-infected patients, the outcome seems to be poorer. ⁵

Case

A 49-year-old male patient presented with stomach pain, anemia, and weight loss. Upper GIT endoscopy revealed an ulcerated mass with malignant appearance in the gastric corpus. Adenocarcinoma was diagnosed by endoscopic biopsy. A ¹⁸FDG-PET/CT scan requested for staging purposes showed FDG uptake of 53-mm diameter in the gastric corpus (SUV: 10.2) and multiple lymph nodes measuring 21-mm in diameter in axillary (SUV: 4.6), mediastinal and paratracheal areas (SUV: 3.6), 15-mm peripancreatic (SUV: 2.4), 17-mm bilateral inguinal (SUV: 2.6), and 12-mm bilateral external-internal iliac lymph nodes (SUV: 3.3) (Figures 1(a), (c), (e) and 2(a)). A biopsy of the lymph node with the highest SUV was performed. Due to reactive findings on histological examination and no signs of malignancy, the patient was started on chemotherapy with neoadjuvant epirubicin, cisplatin, and capecitabine with the diagnosis of locally advanced and/or metastatic gastric carcinoma. The first course of chemotherapy was administered after testing for hepatitis and HIV antibodies, although the patient did not report a history of infection. Serologic tests revealed HIV positivity, and anti-retroviral therapy (emtricitabine/tenofovir and efavirenz) was initiated. CD4 cell count was not performed. However, HCV-RNA detection was positive. A ¹⁸FDG-PET/CT obtained after three courses of chemotherapy showed diffuse regression in the lymph nodes and FDG uptake. There was regression in the gastric corpus, 16 mm in diameter in jugular, axillary (SUV: 3.1), 2 mm mediastinal, paratracheal (SUV: 2.0), 11 mm peripancreatic, paraaortic (SUV: 1.9), and 11 mm iliac lymph nodes (SUV: 1.6) (Figures 1(b), (d), (f) and 2(b)). However, the SUV of the primary tumor located in the gastric corpus remained unchanged. This response pattern suggested response of the lymph nodes to anti-retroviral therapy rather than response to chemotherapy. Unresponsiveness of the primary tumor raised the possibility to perform surgery due to the presence of a localized disease. The patient underwent a total gastrectomy, and no lymph node involvement was detected. The patient was diagnosed to have a pT3 N0 poorly-differentiated intestinal adenocarcinoma and was administered chemoradiotherapy. A 24-month survival was achieved in this patient. OPEN IN VIEWER

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Figure 2.

Fused coronary axis showing a hypermetabolic activity of the lymph nodes of gastric cancer before (a) and after (b) the induction of antiretroviral treatment and chemotherapy (¹⁸FDG-PET/CT images).

Discussion

The incidence of carcinoma in patients with chronic HIV infection is high due to immunosuppression, and early onset of anti-retroviral treatment prolongs survival and decreases the rate of cancer development.^6,7 Decreased CD4 cell count levels, co-infection with other viruses, smoking and alcohol consumption, and advanced age are risk factors associated with poor prognosis. ⁶

HIV-infected memory CD4 T cells show localization in the lymphoid tissues. The replication of HIV virus in these tissues causes local inflammation and loss of CD4 T cells. PET-CT is able to detect this inflammation and is correlated to HIV RNA viral load. ⁸ The finding of hypermetabolic lymph nodes may initially cause the cancer stage to be perceived as advanced. When the performed lymph node biopsy is reactive, this should alert the clinician to search for a viral infection at the same time.

Anti-neoplastic agents and anti-viral treatments are frequently used concurrently in HIV-associated cancers. The intracellular half-lives of nucleotide reverse-transcriptase inhibitors are long. Their concomitant use with chemotherapeutic agents (bexarotene, docetaxel, cyclophosphamide, irinotecan, vinblastine) increases the risk of anemia, neutropenia, peripheral neuropathy, and cardiovascular disease. ⁹

If the patient has a known HIV infection and is receiving anti-retroviral therapy, chemotherapeutic drugs may achieve maximum cure. ¹⁰ In some patients who were diagnosed with HIV infection and cancer simultaneously, the administration of anti-viral treatments after chemotherapeutic agents provides better tolerance of chemotherapy. Anti-retroviral treatments may even be discontinued in case of drug interactions. There is no absolute consensus on current treatments. ⁹

Conclusion

PET/CT scans in cancer staging of patients with chronic HIV infection may show advanced stage disease. Spread of the primary tumor to unusual sites should be a warning sign for possible presence of concurrent diseases, and histopathologic examination of these sites must be performed. However, this did not change the course of treatment in this case, where the HIV infection was diagnosed by serology. Changes in FDG uptake after initiation of chemotherapy and anti-viral therapy in patients with malignancy and concurrent HIV infection may be a predictor of response to therapy and good survival.