Metastic Carcinoma: Unusual Cause of Focal Brain Lesions in HIV
The most common causes of focal brain lesions (FBLs) in patients with HIV infection are cerebral toxoplasmosis, primary central nervous system lymphoma (PCNSL), and progressive multifocal leukoencephalopathy. Neoplasms other than PCNSL are uncommon. We report a rare case of metastatic carcinoma causing an FBL in a patient with HIV infection. The diagnostic workup and further management of FBLs in HIV are outlined in this review. The standard approach includes a lumbar puncture and cerebrospinal fluid (CSF) analysis for cytology and Epstein-Barr virus (EBV) DNA testing by polymerase chain reaction. Empiric therapy for PCNSL is justifiable for patients with positive CSF EBV-DNA test results and a positive single-photon emission computed tomography (SPECT) scan, especially if there has been no response to antitoxoplasmosis therapy. Brain biopsy may be indicated, however, in select cases that do not meet these criteria in order to identify potentially treatable infections and PCNSL.
A 50-year-old woman with a history of HIV infection was hospitalized with persistent temporal and occipital headaches of 1 week's duration. There was no history of other neurologic symptoms, weight loss, fever, or night sweats. CT of the brain showed high-density lesions in the left temporal lobe and the right posterior occipital lobe associated with vasogenic edema, which were enhanced following injection of intravenous contrast and produced mass effect on the ventricular system (Figure 1). Thallium 201 single-photon emission CT (SPECT) showed increased uptake in the left temporal lobe and the right posterior lobe (Figure 2). MRI of the brain with gadolinium confirmed 2 cerebral lesions with surrounding edema (Figure 3).
(Enlarge Image)
CT scan of the brain. Left, A high-density lesion with associated vasogenic edema involving the right occipital lobe enhanced with contrast. The vasogenic edema can be seen to extend into the splenium of the corpus callosum. Right, A second high-density lesion with surrounding vasogenic edema enhanced with contrast. The lesion can be seen to have a very thin wall.
(Enlarge Image)
Brain thallium 201 single-photon emission CT scan showing increased uptake in the left temporoparietal lobe and in the right posterior occipital lobe.
(Enlarge Image)
MRI scan of the brain. T1-weighted images showing lesions in the right occipital lobe and left temporal lobe. Both lesions were noted to be hemorrhagic and necrotic.
HIV-1 infection had been diagnosed in the patient 1 1/2 years before presentation, with a CD4 cell count of 4/µL and an HIV RNA level of 350,635 copies/mL. Her medical history also included thrush, hepatitis B, genital herpes, Pneumocystis jiroveci (formerly Pneumocystis carinii) pneumonia, Mycobacterium kansasii infection, and cervical intraepithelial neoplasia. Her medications at presentation included lamivudine, zidovudine, nelfinavir, and dapsone, and she admitted that she had been nonadherent to them. There was a 15-year "pack-a-day" smoking history, but she denied alcohol abuse or injection drug use.
Physical examination revealed no lymphadenopathy, hepatosplenomegaly, or focal neurologic deficits. Serum IgG Toxoplasma titers and Cryptococcus antigen testing were negative. Her CD4 cell count was 75/µL, and her HIV RNA level was 21,577 copies/mL. Her CD4 cell count had never risen above 113/µL since the initial HIV diagnosis.
The patient was empirically treated with antitoxoplasmosis therapy, including pyrimethamine (100 mg/d) and sulfadiazine (1 g every 6 hours). A repeated CT scan of the brain after 2 weeks revealed an increase in the size of the cerebral lesions and increased edema. Lumbar puncture revealed a normal cell count and normal protein and glucose levels; negative cytologic results; negative results for Epstein-Barr virus (EBV) DNA; and negative cultures for bacteria, mycobacteria, and fungi. Stereotactic brain biopsy revealed normal brain parenchyma with slight gliosis. A second biopsy revealed adenocarcinoma, with immunohistochemical stains negative for estrogen and progesterone receptors, thyroid transcription factor, and cytokeratin (CK) 20 and positive for CK 7, consistent with adenocarcinoma.
CT of the chest, abdomen, and pelvis revealed a multinodular goiter, a 7-mm hypodense pleural nodule in the posterior right thorax, 2 right subcrural masses measuring approximately 1.5 x 1.6 cm and 2.3 x 1.0 cm, atelectasis, and a small left pleural effusion. Although CT findings suggested that the patient's lung was the potential primary site of her metastatic disease, it should be noted that this pleural-based mass, measuring 3.5 x 2.5 cm, was present on a CT scan 6 months earlier, and the mass was now smaller by approximately 2 cm. The subcrural masses were unchanged in size from the earlier examination. She received whole-brain irradiation but died approximately 2 months after presentation.
The most common causes of focal brain lesions (FBLs) in patients with HIV infection are cerebral toxoplasmosis, primary central nervous system lymphoma (PCNSL), and progressive multifocal leukoencephalopathy. Neoplasms other than PCNSL are uncommon. We report a rare case of metastatic carcinoma causing an FBL in a patient with HIV infection. The diagnostic workup and further management of FBLs in HIV are outlined in this review. The standard approach includes a lumbar puncture and cerebrospinal fluid (CSF) analysis for cytology and Epstein-Barr virus (EBV) DNA testing by polymerase chain reaction. Empiric therapy for PCNSL is justifiable for patients with positive CSF EBV-DNA test results and a positive single-photon emission computed tomography (SPECT) scan, especially if there has been no response to antitoxoplasmosis therapy. Brain biopsy may be indicated, however, in select cases that do not meet these criteria in order to identify potentially treatable infections and PCNSL.
A 50-year-old woman with a history of HIV infection was hospitalized with persistent temporal and occipital headaches of 1 week's duration. There was no history of other neurologic symptoms, weight loss, fever, or night sweats. CT of the brain showed high-density lesions in the left temporal lobe and the right posterior occipital lobe associated with vasogenic edema, which were enhanced following injection of intravenous contrast and produced mass effect on the ventricular system (Figure 1). Thallium 201 single-photon emission CT (SPECT) showed increased uptake in the left temporal lobe and the right posterior lobe (Figure 2). MRI of the brain with gadolinium confirmed 2 cerebral lesions with surrounding edema (Figure 3).
(Enlarge Image)
CT scan of the brain. Left, A high-density lesion with associated vasogenic edema involving the right occipital lobe enhanced with contrast. The vasogenic edema can be seen to extend into the splenium of the corpus callosum. Right, A second high-density lesion with surrounding vasogenic edema enhanced with contrast. The lesion can be seen to have a very thin wall.
(Enlarge Image)
Brain thallium 201 single-photon emission CT scan showing increased uptake in the left temporoparietal lobe and in the right posterior occipital lobe.
(Enlarge Image)
MRI scan of the brain. T1-weighted images showing lesions in the right occipital lobe and left temporal lobe. Both lesions were noted to be hemorrhagic and necrotic.
HIV-1 infection had been diagnosed in the patient 1 1/2 years before presentation, with a CD4 cell count of 4/µL and an HIV RNA level of 350,635 copies/mL. Her medical history also included thrush, hepatitis B, genital herpes, Pneumocystis jiroveci (formerly Pneumocystis carinii) pneumonia, Mycobacterium kansasii infection, and cervical intraepithelial neoplasia. Her medications at presentation included lamivudine, zidovudine, nelfinavir, and dapsone, and she admitted that she had been nonadherent to them. There was a 15-year "pack-a-day" smoking history, but she denied alcohol abuse or injection drug use.
Physical examination revealed no lymphadenopathy, hepatosplenomegaly, or focal neurologic deficits. Serum IgG Toxoplasma titers and Cryptococcus antigen testing were negative. Her CD4 cell count was 75/µL, and her HIV RNA level was 21,577 copies/mL. Her CD4 cell count had never risen above 113/µL since the initial HIV diagnosis.
The patient was empirically treated with antitoxoplasmosis therapy, including pyrimethamine (100 mg/d) and sulfadiazine (1 g every 6 hours). A repeated CT scan of the brain after 2 weeks revealed an increase in the size of the cerebral lesions and increased edema. Lumbar puncture revealed a normal cell count and normal protein and glucose levels; negative cytologic results; negative results for Epstein-Barr virus (EBV) DNA; and negative cultures for bacteria, mycobacteria, and fungi. Stereotactic brain biopsy revealed normal brain parenchyma with slight gliosis. A second biopsy revealed adenocarcinoma, with immunohistochemical stains negative for estrogen and progesterone receptors, thyroid transcription factor, and cytokeratin (CK) 20 and positive for CK 7, consistent with adenocarcinoma.
CT of the chest, abdomen, and pelvis revealed a multinodular goiter, a 7-mm hypodense pleural nodule in the posterior right thorax, 2 right subcrural masses measuring approximately 1.5 x 1.6 cm and 2.3 x 1.0 cm, atelectasis, and a small left pleural effusion. Although CT findings suggested that the patient's lung was the potential primary site of her metastatic disease, it should be noted that this pleural-based mass, measuring 3.5 x 2.5 cm, was present on a CT scan 6 months earlier, and the mass was now smaller by approximately 2 cm. The subcrural masses were unchanged in size from the earlier examination. She received whole-brain irradiation but died approximately 2 months after presentation.
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