Keywords
collision tumor - meningioma - pituitary adenoma - sellar region - endoscopic transsphenoidal
Introduction
Collision tumor is an uncommon entity representing the coexistence of two histologically
distinct neoplasms in the same area without histological admixture or an intermediate
cell population zone.[1] The term “collision tumor” needs to be distinguished from two other similar terms—“mixed
tumor” and “coexisting tumor.” A mixed tumor represents two different neoplasms with
histologically admixed cell types.[1] Coexisting tumor represents two different neoplasms existing in two different locations
not abutting against each other. Meningioma and pituitary adenoma are two most common
tumors of the central nervous system. Collision tumor of these two tumors in absence
of previous radiation therapy is extremely uncommon. We report a rare case of “collision
tumor” of nonfunctioning pituitary adenoma and diaphragma sella meningioma in a 50-year-old
lady diagnosed on histological examination.
Illustrative Case
A 50-year-old lady without previous history of cranial irradiation was referred to
our institution following complaints of bifrontal headache and progressive diminision
of vision over 3 years' duration. On physical examination she had marked reduction
of visual acuity (6/18) and bitemporal hemianopia. Her blood hormonal levels of anterior
pituitary were normal; prolactin (PRL) 6.5 ng/mL (normal range <25 ng/mL), growth
hormone (GH) 0.1 ng/mL (normal range <10 ng/mL), insulin-like growth factor I (IGF-I)
84 ng/mL (normal range: 80–209 ng/mL), adrenocorticotropic hormone (ACTH) 18 pg/mL
(normal range: 10–60 pg/mL), cortisol 21 mcg/dL (normal range: 5–25 mcg/dL), thyroid-stimulating
hormone 2.4 UI/mL (normal range: 0.5–5 UI/mL), thyroxine 1.74 ng/dL (normal range:
0.8–1.8 ng/dL), follicle-stimulating hormone 3.5 mUI/mL (normal range: 2.7–21.5 mIU/mL),
luteinizing hormone 1.9 mUI/mL (normal range: 1.1–11.6 mIU/mL), and testosterone 4.1 ng/mL
(normal range: 2–70 ng/mL). Magnetic resonance imaging (MRI) of the sellar region
performed on 3.0 tesla unit (Siemens Lumina) showed an isointense sellar mass on T1-weighted
(T1W) imaging (3 cm × 3 cm × 2 cm) and isointense to hypointense mass on T2W imaging
with homogenous contrast enhancement. The sellar component was extending in the suprasellar
region causing chiasmatic compression. The suprasellar component was broad based and
was reaching till the tuberculum sella ([Fig. 1]). Based on hormonal tests and radiological imaging, diagnosis of nonfunctioning
pituitary adenoma was agreed upon. Endoscopic transsphenoidal resection of pituitary
adenoma was performed. Intraoperatively, the sellar component was soft while the suprasellar
component was firm with rich vascularity. Histological diagnosis confirmed the presence
of pituitary adenoma in collision with fibrous meningioma ([Fig. 2]). Close follow-up of 1 year revealed no tumor recurrence.
Fig. 1 Preoperative magnetic resonance imaging (MRI) of sellar mass demonstrates an isointense
mass on sagittal T1-weighted image (T1WI) (A), isointense to hypointense mass on sagittal T2WI (B) with intense homogenous enhancement on coronal (C) and sagittal contrast imaging (D) occupying the sellar suprasellar region.
Fig. 2 Low- and high-power (100×) hematoxylin and eosin (H&E)-stained micrograph demonstrates
nests of uniform cells with round nuclei, prominent nucleoli, and a faint cytoplasm
consistent with pituitary adenoma (A, B) on the left. Same section shows spindle cells containing elongated, fibrillary nuclei,
prominent nucleoli, and scant stroma arranged in a whorl-like pattern with psammoma
bodies consistent with meningioma on the right (A, B).
Discussion
Pituitary adenomas are one of the most common sellar suprasellar lesions accounting
for 10 to 15% of cases seen on cranial autopsy and 23% of cases seen on MRI.[2]
[3] Meningiomas are one of the most frequent primary intracranial neoplasms accounting
for 15 to 25% of all intracranial neoplasms.[3] Both sellar meningioma and pituitary adenoma show female preponderance and manifest
in adults.[2] Coexistence of pituitary adenoma and other sellar mass like craniopharyngioma, gangliocytoma,
schwannoma, and meningioma is extremely uncommon with very few studies published.[1]
[2] The term “collision tumor” needs to be distinguished from similar terms “coexistent/concomitant
tumor” and “mixed tumor.” “Coexistent/concomitant” tumors are two different tumors
at two separate locations.[4]
A “mixed tumor” represents neoplasm in which endocrine and nonendocrine components
are strictly admixed with no shared border. Finz et al have reported a case of mixed
pituitary adenoma/craniopharyngioma in a 75-year-old woman and has reviewed five other
papers of mixed pituitary adenoma/craniopharyngioma reported in English literature.[4] A “collision tumor” represents two histologically distinct primary neoplasms occurring
in the same anatomic position with a shared border. [5] The concurrent occurrence of collision tumor involving ganglioglioma and ependymoma
and glioblastoma and meningioma have been reported.[6]
[7]
Collision tumor involving meningioma and pituitary adenoma in the sellar region is
extremely uncommon. Very few articles regarding collision tumors composed of pituitary
adenoma and meningioma have been published.[1]
[2]
[5]
[8]
[9]
[10]
[11]
[12]
[13]
[Table 1] depicts all cases of collision tumors of pituitary adenoma and meningioma. Articles
with “mixed” or “coexistent” tumors of pituitary adenoma and meningioma have been
excluded from the review. Honegger et al have reported three patients with “coexistent”
pituitary adenoma and meningioma. In all three patients the pituitary adenoma and
meningioma coexisted; however, both these tumors were never in close approximation
to each other to strictly label them as collision tumors—the first patient had temporal
pole meningioma, the second a falcine meningioma, and the third parietal convexity
meningioma.[14] The type of pituitary adenoma in a collision tumor may vary from nonfunctioning
to functioning adenoma. Though prolactinomas represent the most common type of pituitary
adenomas in adults, GH-secreting pituitary adenoma is most commonly found in concurrence
with meningiomas as a component of collision tumor.[3]
[10] Meningioma when coexist are generally found in proximity to pituitary adenoma—suprasellar,
parasellar, and sphenoid wing location.[10]
Table 1
Literature review of “collision tumor” of pituitary adenoma with meningioma isointense
sellar mass on T1W imaging (3 cm × 3 cm × 2 cm), isointense to hypointense mass on
T2W imaging with homogenous contrast enhancement
|
No.
|
Author
|
Year
|
Age/sex
|
Presenting complaint
|
Collision type 1
|
Collision type 2
|
Radiological findings
|
Surgical approach
|
Intraoperative findings
|
Follow-up
|
|
1
|
Present case
|
2023
|
50/F
|
Visual impairment
|
Nonfunctioning pituitary adenoma
|
Meningioma
|
Sellar lesion was isointense on T1W, iso- to hypointense on T2W with homogenous enhancement.
Suprasellar component was broad based
|
Transsphenoidal
|
Sellar component was soft, suprasellar component was firm with rich vascularity
|
No recurrence 1 year
|
|
2
|
Zhao et al[1]
|
2017
|
58/F (Patient 1)
|
Acromegaly
|
GH-secreting adenoma
|
Meningioma
|
T1W-hyperintense
T2W-iso-hyperintense, heterogeneous enhancement
|
Transsphenoidal followed by craniotomy
|
Pituitary tumor was gray, soft, fragile, partly tough with rich blood supply.
Meningioma was dark red, rubbery, vascular
|
Not available
|
|
|
|
58/F
(Patient 2)
|
Acromegaly
|
GH-secreting adenoma
|
Meningioma
|
T1W-hyperintense
T2W-hyperintense
|
Transsphenoidal followed by craniotomy
|
Pituitary tumor was gray, soft, vascular. Meningioma was dark red, vascular
|
Not available
|
|
3
|
Karsy et al[2]
|
2015
|
70/F
|
Altered mental status, incontinence, mutism
|
Nonfunctioning pituitary adenoma
|
Meningioma
|
CT-isodense spherical mass
MRI T1W-homogenous enhancement
T2W- isointense mass
|
Transsphenoidal/VP shunt for hydrocephalus
|
Not available
|
Not available
|
|
4
|
Gezer et al[5]
|
2020
|
34/F
|
Cushing's disease
|
ACTH secreting pituitary adenoma
|
Meningioma
|
Solid mass with well-defined margin in anterior part of gland suggestive of meningioma
|
Extended transsphenoidal
|
Not available
|
No recurrence 11 months
|
|
5
|
de Vries et al[8]
|
2023
|
75/F
|
Hypopituitarism, bitemporal visual field deficits
|
Nonfunctioning pituitary adenoma
|
Meningioma
|
Sellar suprasellar lesion with dural tail, sphenoid sinus extension. Inhomogeneous
intensity of tumor
|
Transsphenoidal
|
Suprasellar tumor was firm and completely separated from the sellar tumor by diaphragm
sella
|
Not available
|
|
6
|
Ruiz-Juretschke et al[9]
|
2015
|
61/F
|
Progressive visual loss, bitemporal hemianopia
|
Nonfunctioning pituitary adenoma
|
Meningioma
|
Homogenously enhancing sellar–suprasellar tumor
|
Transsphenoidal followed by redo surgery
|
Sellar component was soft while the suprasellar component was firm
|
Not available
|
|
7
|
Prevedello et al[10]
|
2007
|
52/F
|
Headache, right temporal visual field loss
|
Nonfunctioning pituitary adenoma
|
Meningioma
|
Sellar lesion was enhancing homogenously with T1 shortening, Planum sphenoidal lesion
was broad based, enhancing homogenously
|
Extended transsphenoidal
|
Sellar tumor was soft, suckable.
Planum sphenoidal tumor was debulked followed by extracapsular dissection
|
Not available
|
|
8
|
Cannavò et al[11]
|
1993
|
47/F
|
Acromegaly
|
GH-secreting pituitary adenoma
|
Meningioma
|
Sellar lesion showed nonhomogeneous enhancement with peripheral bright signal rim,
retrosellar component showed bright homogenous enhancement
|
Transcranial
|
Not available
|
Not available
|
|
9
|
Zentner and Gilsbach[12]
|
1989
|
61/F
|
Headache, visual field loss
|
Nonfunctioning pituitary adenoma
|
Meningioma
|
CT demonstrated large sellar suprasellar hyperdense lesion
|
Transsphenoidal followed by craniotomy
|
Pituitary adenoma was soft and fragile, meningioma was more firm
|
Not available
|
|
10
|
Banik et al[13]
|
1984
|
56/F
|
Asymptomatic
MEN 1 syndrome
Adrenal collision tumor
|
Nonfunctioning pituitary adenoma
|
Meningioma
|
Not available
|
Diagnosed on postmortem
|
Not available
|
–
|
Abbreviations: ACTH, adrenocorticotropic hormone; CT, computed tomography; F, female;
GH, growth hormone; M, male; MRI, magnetic resonance imaging; T1W, T1-weighted; VP,
ventriculoperitoneal.
Note: The sellar component was extending in the suprasellar region causing chiasmatic
compression. The suprasellar component was broad based and was reaching till the tuberculum
sella.
Amirjamshidi et al have reported two cases of coexisting pituitary adenoma and suprasellar
meningioma. The authors believed these coexisting tumors to be coincidental and not
collision tumors. Hence, these cases were not included in the table.[3] Zentner and Gilsbach reported the first case of collision tumor of pituitary adenoma
and meningioma in in a 61-year-old lady which was resected transsphenoidally as early
as 1989.[12] In 1984, Banik et al reported collision tumor of pituitary adenoma and meningioma
and another adrenal gland collision tumor in a patient with MEN1 syndrome on postmortem
examination.[13] Karsy et al have reported the case study of a 70-year-old lady presenting with altered
mental status, mutism, and incontinence. Radiological diagnosis was of pituitary adenoma.
The tumor was resected through transsphenoidal route. Pathological examination of
the resected tumor revealed coexistent meningioma along with pituitary adenoma.[2] Zhao et al have reported two patients with collision tumors of GH-secreting adenoma
and meningioma.[1] The GH-secreting adenoma was resected through transsphenoidal route. Craniotomy
was performed to excise the residual tumor which was diagnosed to be a meningioma.[1] Gezer et al have reported a collision tumor of corticotroph-secreting pituitary
adenoma and meningioma in a 34-year-old Caucasian lady. MRI revealed only tuberculum
sella meningioma. Histopathological examination confirmed a corticotroph-secreting
adenoma infiltrated by meningioma.[5]
The diagnosis of collision tumor is most often based on histopathological examination.
Preoperative MRI may seldom be able to diagnose dual sellar pathology, that is, two
different histological entities of pituitary adenoma and meningioma as both the tumors
may exhibit similar imaging characteristics. [5]
[11] Ruiz-Juretschke et al have reported a patient with collision tumor of pituitary
adenoma and meningioma.[9] Preoperative MRI could not distinguish the two separate tumor components and the
diagnosis of collision tumor was reached on histopathological examination.[9] Prevedello et al, however, in their patient have reported identification of collision
tumor of pituitary adenoma and meningioma based on MRI.[10] In the present case, preoperative radiological diagnosis of collision tumor was
not made as the two different components of the tumor showed the same signal intensity
on all sequences on MRI. On reviewing the images retrospectively, the broad based
suprasellar component reaching till the tuberculum sella could have been diagnosed
as meningeal component of the collision tumor.
In the present case, the tumor was excised completely via endonasal transsphenoidal
approach. Intraoperatively, the soft sellar component and firm suprasellar component
with high vascularity could represent the pituitary adenoma and meningeal component
of the collision tumor. de Vries et al and Ruiz-Juretschke et al have also reported
total excision of such collision tumor by endoscopic transsphenoidal approach.[8]
[9] Zhao et al have proposed a second surgery performed transcranially to resect residual
tumor.[1] Prevedello et al have described the extended endonasal transsphenoidal approach
for extirpation of pituitary adenoma and meningioma, obviating the need for additional
craniotomy.[10]
One of the proposed hypotheses for coexistence of meningioma and pituitary adenoma
is radiation therapy to pituitary adenoma.[8]
[14] Meningiomas tend to occur after a latent period of 5 years of radiation and within
the pathway of irradiation.[14] Honegger et al have reported one such patient of meningioma coexisting following
irradiation of pituitary adenoma.[14] We did not find any such case in literature of collision tumor composed of pituitary
adenoma and meningioma occurring after radiation of pituitary adenoma. On the other
hand, coincidental meningioma occurring in patient with pituitary adenoma without
prior radiation therapy is extremely uncommon.[9] Meningiomas in such patients tend to occur in perisellar location at the planum
sphenoidale, tuberculum sella, and sphenoid wing.[9] It is postulated that pituitary adenomas are a causative factor in the development
of meningiomas. Meningiomas express hormone receptors on the tumor surface, implying
that their growth is under hormonal control. This is more likely in case of functioning
pituitary adenoma especially if the adenoma is GH-secreting adenoma. GH secreted causes
meningioma growth.[1]
[8] Seventy-five percent of meningiomas express GH and IGF1 receptors.[8] However, meningiomas are also found in association with nonsecreting, PRL–secreting,
and ACTH-secreting pituitary adenoma. Hence, it is assumed that the coexistence of
a meningioma with pituitary adenoma is a casual finding with no relationship between
the two tumors.[11] The formation of a collision tumor composed of pituitary adenoma and meningioma
is difficult to explain in nonfunctioning pituitary adenoma.[11] In the present case, the only possible explanation of coexistence of nonfunctioning
pituitary adenoma and meningioma is coincidental. Progress in molecular genetics and
further research will shed more light on tumorogenesis of collision tumors.
Conclusion
Collision tumor comprising of nonfunctioning pituitary adenoma and meningioma is extremely
rare. Preoperative MRI may not always be able to distinguish these histologically
distinct neoplasms. Hence, histopathological examination is necessary to establish
the diagnosis. Endoscopic transsphenoidal approach may suffice in excision of these
collision tumors. Close follow-up is necessary to detect tumor recurrence. Though
the association of these tumors can be coincidental, casual relationship between the
occurrence of collision tumors cannot be totally excluded.
