 |
|
||||
| Home | Login | |||||
| About | Editorial board | Articles
|
NSI Publications
|
Search | Instructions | Online Submission | Subscribe | Videos | Etcetera | Contact |
|
||||||||||||||||||||
|
|
|
Anaplastic astrocytoma and pituitary macroadenoma within the same patient: A rare case of intracranial collision tumor
Correspondence Address: Source of Support: None, Conflict of Interest: None DOI: 10.4103/0028-3886.232341
Sir, The synchronous development of two primary brain tumors of distinct cell origin in proximity or in contact with each other is extremely rare. Coexistence of endodermal and neuroectodermal tumors, as was seen in our patient, is quite uncommon. Our patient presented with a pituitary macroadenoma coexisting with an anaplastic astrocytoma that could not be diagnosed with any other known tumor syndrome, making it a unique case of collision tumor. Although brain tumors are being diagnosed in an increasing number of patients due to the availability of computed tomography and magnetic resonance imaging (MRI), the simultaneous existence of primary brain tumors with different pathologies has been described in not more than 0.9% of all primary brain tumors; however, the majority of the cases were seen after radiotherapy or were associated with familial tumor syndromes.[1],[2] Furthermore, it is known that, in phacomatosis syndromes, mesodermal and neuroectodermal tumors can be seen together, and occurrence of an ependymoma, chromophobe pituitary adenoma, and astrocytoma in these patients have been reported elsewhere.[3],[4],[5] This is a rare case wherein two intracranial tumors were seen, one of an endodermal and another of neuroectodermal origin, in the same patient who did not suffer from any known germ line mutation. A 36-year old male patient was admitted with complaints of severe headache and diplopia. He also had a history of two episodes of focal convulsions involving the left upper limb and lower limb. No related familial history was discovered. On admission, his general examination was normal. No neurocutaneous markers were seen. Neurological examination revealed left temporal hemianopia and ptosis of the right eye. Visual acuity was 6/6 in both the eyes. The fundus examination was normal. Rest of the neurological examination was normal. Gadolinium-enhanced cranial MRI showed two different lesions in two different locations. One was an ill-defined mass lesion measuring 4 × 2.5 × 2.3 cm in the subcortical region of the right frontal lobe with perifocal edema. The lesion was heterogeneously hypointense on T1-weighted images (WI), and hyperintense on T2WI and fluid-attenuated inversion recovery (FLAIR) images [Figure 1]. It showed a mild patchy enhancement on post-contrast study [Figure 2]. On MR spectroscopy, there was an increase in the choline/creatine ratio (4.9) and a marked increase in the N-acetyl aspartate (NAA) and creatine peaks. The second mass lesion was noted in the sellar and suprasellar region. It was hyperintense on T1WI, heterogeneously hyperintense on T2WI and FLAIR images, and showed peripheral enhancement on postcontrast study [Figure 3]a and [Figure 3]b. Superolaterally, it was stretching bilateral optic nerves and optic chiasma, and laterally abutting the cavernous portion of bilateral internal carotid arteries, with well-maintained flow voids. Preoperative laboratory analysis showed that none of the pituitary hormones were excessively secreted. Medication with dexamethasone (24 mg daily) was started.
Treatment was planned in a single transcranial approach, with combined removal of the frontal lesion and subsequent removal of the sellar-suprasellar tumor through a right fronto-temporo-sphenoidal (modified pterional) craniotomy. The frontal lesion was grayish, hard, nodular with cystic components; and, gross total tumor removal was achieved. The sellar-suprasellar tumor was subsequently removed through the same approach. It was soft, suckable and grayish with some necrotic areas within; and, gross total tumor removal was done. Postoperatively, the patient was cooperative and oriented with no new neurological deficits. Histological examination of the right frontal tumor revealed cells with abundant eosinophilic cytoplasm, eccentric round nuclei with coarse chromatin, and occasional mitoses. No necrosis or microvascular and endothelial proliferation was seen. On immunohistochemistry, tumor cells were positive for glial fibrillary acidic protein (GFAP) and focally positive for synoptophysin. Occasionally, cells were positive for p53, whereas they were negative for AE1/AE3, chromogranin, thyroid transcription factor 1 (TTF1), epithelial membrane antigen (EMA), isocitrate dehydrogenase IDH1R132H. The MIB-1 labelling index was 6–8% in the areas with the highest proliferation. The histopathologic diagnosis was anaplastic astrocytoma, grade III (WHO, 2007). The sellar-suprasellar tumor consisted of monomorphic cells with eosinophilic granular cytoplasm and round nuclei. The tumor also had areas of coagulative necrosis with surrounding hemorrhage. The histopathological diagnosis was pituitary adenoma with apoplexy. Dexamethasone therapy was tapered and the patient was referred to the endocrinological department for hormone replacement therapy. Postoperative MRI showed no residual tumor in either of the locations [Figure 4]a, [Figure 4]b, [Figure 4]c. The patient was discharged on day 8 with recommendation of adjuvant radio-chemotherapy.
A collision tumor is described as a combination of two tumors with discrete histology occurring simultaneously and in proximity to each other at the same location. Such intracranial occurrences are rare with few reported cases in the literature [Table 1].
The mechanism responsible for this entity remains unclear; however, some hypotheses have been proposed. The observation that a significant number of reported cases had their tumor localization in juxtaposition raises the possibility that one tumor may act as an irritating agent for the local proliferation and growth of the other.[6] Surgical trauma, ionizing radiation, and genetic factors may influence tumor development.[7] This theory was suggested in the cases where the tumors were adjacent to each other. However, it may not explain why this collision occurred in our rare case, making the pathogenesis more complex and multifactorial. Most cases in the literature reported a collision of a glioma and a meningioma.[7],[8],[9],[10],[11],[12] A glioma may develop due to neoplastic transformation of the reactive glial cells surrounding a meningioma.[10] This process may be mediated by locally acting oncogenic factors. The most suspected substance is platelet-derived growth factor subunit alpha-R (PDGF-alpha-R), which is the main receptor in astrocytoma.[13] The astrocytoma growth is probably stimulated by PDGF in an autocrine mechanism. It is possible to develop a meningioma as a secondary malignant neoplasm due to the transformation of the arachnoidal cells in response to the growth of a subjacent glioma or after radiation therapy.[7] Glioblastomas account for 15–20% of all intracranial and 50% of all glial tumors. Pituitary tumors are detected in nearly 3% of all autopsy cases and approximately in 10% of cranial MRI scans. Coexistence of endodermal and neuroectodermal tumors, as seen in our patient, is quite uncommon. In phacomatosis syndromes, such as neurofibromatosis type 1, mesodermal and neuroectodermal tumors are reported to occur in the same patient simultaneously. In this disease, there are common features in chromosome 1, 6, 16, 22 mutations, which play an important role in tumorigenesis. There are no well-established similarities between pituitary adenomas and anaplastic astrocytomas that may be detectable by means of gene mutations. Our patient did not have a history of exposure to chemical substances, oncoviral infections, alcohol, smoking, trauma, or radiation that may also be responsible for multiple tumor occurrence. However, it has been stated that in rare cases, brain tumors might increase the frequency of transforming cells by an irritant effect on the surrounding tissue, which might result in new tumor development. Nevertheless, in our case, both tumors were considerably remote from each other, so that a direct interaction appears to be unlikely. Gyori and Gregg have reported a case of an invasive pituitary adenoma in coexistence with an infiltrative temporal lobe glioma in 1992.[3] In another patient with suspected Turcot's syndrome, a glioblastoma and a pituitary adenoma occurring together with a colorectal carcinoma were reported in 2012.[2] In our patient, there were no signs of an accompanying tumor syndrome. Coexistence of intracranial tumors of different histological lineage should be reported more frequently;[32] however, they are very rarely reported in the pertinent literature. Our patient presented with a pituitary adenoma coexisting with an anaplastic astrocytoma, a condition that could not be diagnosed as being a part of any other known tumor syndrome, making it a unique case in the relevant literature. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.
[Figure 1], [Figure 2], [Figure 3], [Figure 4]
[Table 1]
|
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
|||||
