Department of Neurosurgery, Kumamoto University Medical School (MM, JK, HN, YU) and Kumamoto City Hospital (SY), Kumamoto, Japan Neurosurgery 30; 624-627, 1992 ABSTRACT: A 13-year-old boy with an anaplastic meningioma at the site of the jugular foramen had an increased serum level of aklaline phosphatase (ALPase) (liver form) in the serum before surgery. Immediately after excision of the tumor, the serum ALPase level decreased dramatically. Histochemical and immunohistochemical examinations revealed ALPase activity (liver form) in the neoplastic cells. This case would be the third with clinical evidence that the increased level of serum ALPase is of neoplastic cell origin from the meningioma. The implications of ALPase in brain tumors are discussed. KEY WORDS: Alkaline phosphatase; Jugular foramen; Meningioma INTRODUCTION The occurrence of intracranial meningioma in children under the age of 15 years is rare. Mendiratta et al. (13) reported data on 38 meningiomas among 2620 intracranial tumors (1.5%) in children under age 15. Wakai et al. (23) described the distribution of 18 cases of meningioma in children monitored for 55 years; 50% of the lesions were located in the parasagittal region, falx and convexity, whereas 2 (11%) were in the posterior fossa. Meningiomas at the site of the jugular foramen were noted in 3 children (1,12,19). Alkaline phosphatase (ALPase) is a well-known plasma membrane marker enzyme distributed in the serum and in some organs such as liver, bone, kidney, intestine, and placenta (2). Cytochemical studies of ALPase in the normal brain and in brain tumors such as meningioma, craniopharyngioma, and glioma have been described (5,9,11,16,21,22). We add to two previously reported ones (8,15) a third patient with a high level of ALPase in the serum before surgical intervention for a tumor that was found to be of meningioma cell origin and that was located in the posterior fossa. CASE REPORT A 13-year-old boy was admitted to our hospital complaining of occipital headache of 1-month duration. A mass in the posterior fossa was seen on the computed tomographic scan taken at a local clinic. At the time of admission, he had occipital headache and slight papilledema. All other
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AUTHOR(S): Murakami, Masaji, M.D.; Yoshioka, Susumu, M.D.; Kuratsu, Jun-ichi, M.D.; Nakamura, Hideo, M.D.; Ushio, Yukitaka, M.D.
neurological findings were noncontributory. The computed tomographic scan showed a homogeneously enhanced round mass in the left posterior fossa with moderate peripheral edema. There was no evidence of bone involvement on the computed tomographic scan or on skull tomography of the posterior fossa. Magnetic resonance imaging demonstrated a low-signal intensity on the T1weighted image and an iso- to high-signal intensity on the T2-weighted image. A sagittal scan with gadolinium-diethylenetriamine pentaacetic acid (GdDTPA) revealed a well-enhanced round mass with attachment to the dura and extending into the jugular foramen (Fig. 1). An angiogram revealed a moderately vascular tumor supplied by the left ascending pharyngeal artery (Fig. 2). Laboratory data at the time of admission revealed the following values: total protein, 7.8 (6.5-8.1) g/dl; serum albumin, 2.7 (4.1-5.1) g/dl; total bilirubin, 0.2 (0.31.2) mg/dl; glutamic-oxaloacetic transferase, 87 (8-32) µ/L; glutamic-pyruvic transferase, 170 (6-38) µ/L; lactate dehydrogenase, 284 (236-427) µ/L; ALP 531 (42-123) µ/L; leukocyte alkaline phosphatase, 199 (36-72) µ/L; γ-guanosine 5'-triphosphatase, 206 (10-70) µ/L. The value of ALPase was extremely high, and the isoenzyme pattern of the increased ALPase showed 82% of type II, 14% of Type I, and 4% of Type III. The main form of the increased serum ALPase seen on electrophoretic study was that of the liver (Fig. 3). A left unilateral suboccipital craniectomy and total removal of the tumor with excision of the left jugular vein were done. The tumor was moderately vascular, reddish, elastic, and 3.0 × 2.8 cm in diameter and was attached firmly to the dura near the jugular foramen. Histological study revealed that the tumor was mainly composed of meningothelial cells in a whorl formation, and in some parts, small cells with chromatin-rich nuclei and mitoses were frequent (Fig. 4). The tumor was diagnosed as an anaplastic meningioma. For adjuvant therapy, 50 Gy of local irradiation was given postoperatively. The postoperative level of ALPase in the serum was dramatically reduced over the value of serum ALPase just after total removal of the tumor and was normalized within 3 weeks (Fig. 5). The postoperative course was uncomplicated, and the patient remains well 7 months after the surgery. Histochemical and immunohistochemical examinations were made of the tumor. Thin-sectioned frozen tissues (5 µm) were used. In the histochemical study, naphthol-AS-MX phosphate was used as the substrate and the tissues were visualized by fast red (4) . In the immunohistochemical study, rabbit antiserum against the human liver form of ALPase was used (unpublished observation), and the avidin-biotin complex (ABC kit; Vector Laboratories, Inc., Burlingame, CA) method was applied. Red granular staining was observed within the cytoplasma and also on the plasma membrane in 60 to 70% of the neoplastic cells. The staining was strongly inhibited by 1 mmol/L levamisole. The brown staining in the immunohistochemical study was observed within the cytoplasm and on the plasma membrane in 20 to 30% of the neoplastic cells (Fig. 6).
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Neurosurgery 1992-98 April 1992, Volume 30, Number 4 624 High Serum Alkaline Phosphatase Level of Meningioma Cell Origin: Case Report and Review of the Literature Case Report
Function of ALPase It has been suggested that ALPase reduces cellular adhesion and stickiness or increases in the hepatoma cell membrane before infiltrative growth of the hepatoma to the surrounding tissues (3,14). Little is known of the functional significance of ALPase activity in brain and brain tumors. In the brain, this enzyme may have a role in activation and inactivation of enzymes through dephosphorylation and the membrane location of ALPase may be of significance in functions of the blood-brain barrier. In some brain tumors, a correlation between malignancy and ALPase activity has been postulated. In gliomas, ALPase activity increases in the luminal plasma membrane of endothelial cells with advancement of the malignancy (11). In meningiomas, ALPase was noted on endothelial and meningioma cells. ALPase activity is restricted to the basolateral membrane of the endothelial cells, and with advancement of the malignancy, ALPase activity disappears in the endothelial cells (16). In tissues from our patient, light microscopy revealed ALPase activity on the endothelial as well as the meningioma cells; however, distribution of the enzyme within the endothelial cells was unclear.
Clinical implications of ALPase At one time it was thought that only germinoma elevates the level of ALPase in serum or cerebrospinal fluid in cases of intracranial tumors (17) . Tumors outside of the central nervous system such as osteogenic sarcoma, bronchogenic carcinoma, and hepatoma give rise to increased levels of some isoenzymes of ALPase in the serum (6). Elevated levels of ALPase in the serum of meningioma patients have been reported by Kepes et al. (8) and Mignot et al. (15). Thus, the case presented here would be the third reported case documenting the clinical evidence that the increased level of serum ALPase was probably of meningioma cell origin, and therefore, the serum ALPase level may prove to be a sensitive indicator of a recurrence of this tumor. ACKNOWLEDGMENTS We thank Drs. Yosuke Mihara, Akira Takada, and Kenjiro Matsuno for critical comments on the manuscript and Miss Ikuko Kawasaki for technical assistance. Received for publication, June 25, 1991; accepted, final form, October 4, 1991. Reprint requests: Masaji Murakami, M.D., Department of Neurosurgery, Kumamoto University Medical School, 1-1-1 Honjo, Kumamoto 860, Japan. REFERENCES: (1-23) 1.
Liver form of ALPase in meningioma The main form of serum ALPase in children is the bone form (Type III). In our patient, 80 to 90% of the elevated levels of ALPase in the serum was the liver form. In addition, the elevated levels of ALPase in the serum seemed to have originated from the meningioma cells on the basis of the following: 1) the level of ALPase in the serum began to decrease just after the surgical removal of the meningioma and was normalized within 3 weeks; 2) the isozyme of the increased level of serum ALPase (Type II, liver form) was consistent with the isoform of ALPase determined by histochemical and immunohistochemical examinations. The discrepancy between the staining patterns on histochemical and immunohistochemical studies is thought to relate to inhibition of the staining for ALPase by the specific inhibitor, levamisol, thereby indicating that the ALPase is the liver-bone-kidney form (7,20). In addition, the immunohistochemical study done with an anti-human liver form ALPase antibody revealed the ALPase to be the liver form. For this reason, the brown staining in the immunohistochemical study was seen on a smaller number of the tumor cells than that seen in the histochemical study. Other
2.
3. 4.
5. 6.
7.
Arita K, Uozumi T, Oba S, Saito Y, Oki S, Suzuki M, Harada Y: A case of jugular foramen meningioma in a child. No Shinkei Geka 17:87-92, 1989 (in Japanese). Bahr M, Wilkinson JH: Urea as a selective inhibitor of human tissue alkaline phosphatase. Clin Chim Acta 17:367-370, 1967. Berwick L, Coman DR: Some chemical factors in cellular adhesion and stickness. Cancer Res 22; 982-987, 1962. Burstone MS: Histochemical comparison of naphthol AS-phosphates for the demonstration of phosphatases. J Natl Cancer Inst 20:601-615, 1958. Feigin I, Wolf A: The alkaline phosphomonoesterase activity of brain tumors. AMA Arch Pathol 67:670-678, 1959. Fishman WH, Inglis NI, Stolbach LL, Krant MJ: A serum alkaline phosphatase isoenzyme of human neoplastic cell origin. Cancer Res 28:150-154, 1968. Goldstein DJ, Harris H: Mammalian brain alkaline phosphatase; expression of liver/bone/kidney locus. Comparison of fetal and adult activities. J Neurochem 36:53-57,
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Distribution of ALPase in brain and brain tumors In 1942, Landow et al. (9) described the distribution of ALPase in the central nervous system. In the normal brain, ALPase activity appears to be mainly restricted to endothelial cells, choroid plexus, arachnoid cells, and astrocytic processes in the developing rat cerebral cortex (18). In brain tumors, ALPase activity was found mainly in meningioma, craniopharyngioma, and glioma (5,9,10,11,16,21,22).
investigators reported that the biochemical properties of tissue extraction of ALPase from five meningiomas are consistent with those of the major form of ALPase (liver form), on the basis of the electrophoretic motility, the effect of urea, or heat treatment (20).
Redistribution of this article permitted only in accordance with the publisher’s copyright provisions.
DISCUSSION
10. 11.
12.
13. 14.
15.
16.
17.
18.
19.
20.
21. 22. 23.
Downloaded from https://academic.oup.com/neurosurgery/article-abstract/30/4/624/2753025 by Washington University, Law School Library user on 15 February 2019
9.
1981. Kepes JJ, MacGee EE, Vergara G, Sil R: Malignant meningioma with extensive pulmonary metastases. J Kans Med Soc 72:312 316, 1971. Landow H, Kabat EA, Newman W: Distribution of alkaline phosphatase in normal and in neoplastic tissues of the nervous system. Arch Neurol Psychiatry 48:518-530, 1942. Lolova I, Ivanova A: A histochemical study of meningiomas. Acta Neuropathol (Berl) 20:110121, 1972. Maeda T: Alkaline phosphatase activity in human gliomas as revealed by light and electron microscopy. No To Shinkei 39:527533, 1987 (in Japanese). Maniglia AJ, Page LK: Posterior cranial fossa and temporal bone meningioma in a child, appearing as a neck mass. Otolaryngol Head Neck Surg 87:578-583, 1979. Mendiratta SS, Rosenblum JA, Strobos RJ: Congenital meningioma. Neurology (Minneap) 17:914-918, 1967. Miedema E, Kouse PF Jr: Effect of predonisolone and contact phenomena or the alkaline phosphatase activity of Hep-2 cells. Biochem Biophys Res Commun 26:704-711, 1967. Mignot B, Hauw JJ, Pasquier P, DeSigalony JP II, Bricaire F: Perturbations biologiques reversibles evoluant parallelement à un meningiome recidivant et avec metastases. Sem Hop Paris 54:1231-1237, 1978. Ogashiwa M, Nishiyama F, Fukai K, Takeuchi K, Hirano H: Cytochemical study of Mg2+ATPase and ALPase activity in human meningiomas. No To Shinkei 42:497-503, 1990 (in Japanese). Remakrishnan S, Manifold IH, Ward AM, Forster DMC: CSF placental alkaline phosphatase as marker in cranial dysgerminoma. Lancet 2:225, 1989. Rowan RA, Maxwell DS: An ultrastructural study of vascular proliferation and vascular alkaline phosphatase activity in the developing cerebral cortex of the rat. Am J Anat 160:257-265, 1981. Tada W, Nagasawa M, Suzuki M, Harada Y, Oda K, Oki S: Infantile meningioma extended from the posterior cranial fossa into the parapharyngeal space. Otolaryngol-Head Neck Surg (Tokyo) 60:113-117, 1988. Takahara N, Herz F, Singer RM, Hirano A, Koss LG: Induction of alkaline phosphatase activities in cultured human intracranial tumor cells. Cancer Res 42:563-568, 1982. Timperley WR, Turner P, Davies S: Alkaline phosphatase in craniopharyngiomas. J Pathol 103:257-262, 1971. Timperley WR, Warnes TW: Alkaline phosphatase in meningiomas. Cancer 26:100103, 1970. Wakai S, Ochiai C, Takakura K, Keiji Sano:
Redistribution of this article permitted only in accordance with the publisher’s copyright provisions.
8.
Redistribution of this article permitted only in accordance with the publisher’s copyright provisions.
Figure 2. The angiogram shows a moderate vascular tumor stain, supplied by the left ascending pharyngeal artery.
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Figure 1. The sagittal view with Gd-DTPA enhancement shows a well-enhanced mass extending into the jugular foramen. A, axial view; B, sagittal view.
Redistribution of this article permitted only in accordance with the publisher’s copyright provisions.
Figure 4. Light microscopy shows the tumor to be mainly composed of meningothelial cells with a whorl formation (A). In some parts, small cells with chromatin-rich nuclei and mitoses are frequent (B).
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Figure 3. The electrophoretic pattern of the serum ALPase shows that the major part of the increased serum ALPase is liver form.
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Figure 5. Serum ALPase dramatically decreased just after total removal of the tumor and was normalized within 3 weeks.
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Figure 6. Histochemically, the red granular staining was present not only within the cytoplasm but also on the plasma membrane of the neoplastic cells (A). Immunohistochemically, the brown staining was evident in a smaller number of tumor cells than that seen in the histochemical study (B).
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AUTHOR(S): Murakami, Masaji, M.D.; Yoshioka, Susumu, M.D.; Kuratsu, Jun-ichi, M.D.; Nakamura, Hideo, M.D.; Ushio, Yukitaka, M.D.
neurological findings were noncontributory. The computed tomographic scan showed a homogeneously enhanced round mass in the left posterior fossa with moderate peripheral edema. There was no evidence of bone involvement on the computed tomographic scan or on skull tomography of the posterior fossa. Magnetic resonance imaging demonstrated a low-signal intensity on the T1weighted image and an iso- to high-signal intensity on the T2-weighted image. A sagittal scan with gadolinium-diethylenetriamine pentaacetic acid (GdDTPA) revealed a well-enhanced round mass with attachment to the dura and extending into the jugular foramen (Fig. 1). An angiogram revealed a moderately vascular tumor supplied by the left ascending pharyngeal artery (Fig. 2). Laboratory data at the time of admission revealed the following values: total protein, 7.8 (6.5-8.1) g/dl; serum albumin, 2.7 (4.1-5.1) g/dl; total bilirubin, 0.2 (0.31.2) mg/dl; glutamic-oxaloacetic transferase, 87 (8-32) µ/L; glutamic-pyruvic transferase, 170 (6-38) µ/L; lactate dehydrogenase, 284 (236-427) µ/L; ALP 531 (42-123) µ/L; leukocyte alkaline phosphatase, 199 (36-72) µ/L; γ-guanosine 5'-triphosphatase, 206 (10-70) µ/L. The value of ALPase was extremely high, and the isoenzyme pattern of the increased ALPase showed 82% of type II, 14% of Type I, and 4% of Type III. The main form of the increased serum ALPase seen on electrophoretic study was that of the liver (Fig. 3). A left unilateral suboccipital craniectomy and total removal of the tumor with excision of the left jugular vein were done. The tumor was moderately vascular, reddish, elastic, and 3.0 × 2.8 cm in diameter and was attached firmly to the dura near the jugular foramen. Histological study revealed that the tumor was mainly composed of meningothelial cells in a whorl formation, and in some parts, small cells with chromatin-rich nuclei and mitoses were frequent (Fig. 4). The tumor was diagnosed as an anaplastic meningioma. For adjuvant therapy, 50 Gy of local irradiation was given postoperatively. The postoperative level of ALPase in the serum was dramatically reduced over the value of serum ALPase just after total removal of the tumor and was normalized within 3 weeks (Fig. 5). The postoperative course was uncomplicated, and the patient remains well 7 months after the surgery. Histochemical and immunohistochemical examinations were made of the tumor. Thin-sectioned frozen tissues (5 µm) were used. In the histochemical study, naphthol-AS-MX phosphate was used as the substrate and the tissues were visualized by fast red (4) . In the immunohistochemical study, rabbit antiserum against the human liver form of ALPase was used (unpublished observation), and the avidin-biotin complex (ABC kit; Vector Laboratories, Inc., Burlingame, CA) method was applied. Red granular staining was observed within the cytoplasma and also on the plasma membrane in 60 to 70% of the neoplastic cells. The staining was strongly inhibited by 1 mmol/L levamisole. The brown staining in the immunohistochemical study was observed within the cytoplasm and on the plasma membrane in 20 to 30% of the neoplastic cells (Fig. 6).
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Neurosurgery 1992-98 April 1992, Volume 30, Number 4 624 High Serum Alkaline Phosphatase Level of Meningioma Cell Origin: Case Report and Review of the Literature Case Report
Function of ALPase It has been suggested that ALPase reduces cellular adhesion and stickiness or increases in the hepatoma cell membrane before infiltrative growth of the hepatoma to the surrounding tissues (3,14). Little is known of the functional significance of ALPase activity in brain and brain tumors. In the brain, this enzyme may have a role in activation and inactivation of enzymes through dephosphorylation and the membrane location of ALPase may be of significance in functions of the blood-brain barrier. In some brain tumors, a correlation between malignancy and ALPase activity has been postulated. In gliomas, ALPase activity increases in the luminal plasma membrane of endothelial cells with advancement of the malignancy (11). In meningiomas, ALPase was noted on endothelial and meningioma cells. ALPase activity is restricted to the basolateral membrane of the endothelial cells, and with advancement of the malignancy, ALPase activity disappears in the endothelial cells (16). In tissues from our patient, light microscopy revealed ALPase activity on the endothelial as well as the meningioma cells; however, distribution of the enzyme within the endothelial cells was unclear.
Clinical implications of ALPase At one time it was thought that only germinoma elevates the level of ALPase in serum or cerebrospinal fluid in cases of intracranial tumors (17) . Tumors outside of the central nervous system such as osteogenic sarcoma, bronchogenic carcinoma, and hepatoma give rise to increased levels of some isoenzymes of ALPase in the serum (6). Elevated levels of ALPase in the serum of meningioma patients have been reported by Kepes et al. (8) and Mignot et al. (15). Thus, the case presented here would be the third reported case documenting the clinical evidence that the increased level of serum ALPase was probably of meningioma cell origin, and therefore, the serum ALPase level may prove to be a sensitive indicator of a recurrence of this tumor. ACKNOWLEDGMENTS We thank Drs. Yosuke Mihara, Akira Takada, and Kenjiro Matsuno for critical comments on the manuscript and Miss Ikuko Kawasaki for technical assistance. Received for publication, June 25, 1991; accepted, final form, October 4, 1991. Reprint requests: Masaji Murakami, M.D., Department of Neurosurgery, Kumamoto University Medical School, 1-1-1 Honjo, Kumamoto 860, Japan. REFERENCES: (1-23) 1.
Liver form of ALPase in meningioma The main form of serum ALPase in children is the bone form (Type III). In our patient, 80 to 90% of the elevated levels of ALPase in the serum was the liver form. In addition, the elevated levels of ALPase in the serum seemed to have originated from the meningioma cells on the basis of the following: 1) the level of ALPase in the serum began to decrease just after the surgical removal of the meningioma and was normalized within 3 weeks; 2) the isozyme of the increased level of serum ALPase (Type II, liver form) was consistent with the isoform of ALPase determined by histochemical and immunohistochemical examinations. The discrepancy between the staining patterns on histochemical and immunohistochemical studies is thought to relate to inhibition of the staining for ALPase by the specific inhibitor, levamisol, thereby indicating that the ALPase is the liver-bone-kidney form (7,20). In addition, the immunohistochemical study done with an anti-human liver form ALPase antibody revealed the ALPase to be the liver form. For this reason, the brown staining in the immunohistochemical study was seen on a smaller number of the tumor cells than that seen in the histochemical study. Other
2.
3. 4.
5. 6.
7.
Arita K, Uozumi T, Oba S, Saito Y, Oki S, Suzuki M, Harada Y: A case of jugular foramen meningioma in a child. No Shinkei Geka 17:87-92, 1989 (in Japanese). Bahr M, Wilkinson JH: Urea as a selective inhibitor of human tissue alkaline phosphatase. Clin Chim Acta 17:367-370, 1967. Berwick L, Coman DR: Some chemical factors in cellular adhesion and stickness. Cancer Res 22; 982-987, 1962. Burstone MS: Histochemical comparison of naphthol AS-phosphates for the demonstration of phosphatases. J Natl Cancer Inst 20:601-615, 1958. Feigin I, Wolf A: The alkaline phosphomonoesterase activity of brain tumors. AMA Arch Pathol 67:670-678, 1959. Fishman WH, Inglis NI, Stolbach LL, Krant MJ: A serum alkaline phosphatase isoenzyme of human neoplastic cell origin. Cancer Res 28:150-154, 1968. Goldstein DJ, Harris H: Mammalian brain alkaline phosphatase; expression of liver/bone/kidney locus. Comparison of fetal and adult activities. J Neurochem 36:53-57,
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Distribution of ALPase in brain and brain tumors In 1942, Landow et al. (9) described the distribution of ALPase in the central nervous system. In the normal brain, ALPase activity appears to be mainly restricted to endothelial cells, choroid plexus, arachnoid cells, and astrocytic processes in the developing rat cerebral cortex (18). In brain tumors, ALPase activity was found mainly in meningioma, craniopharyngioma, and glioma (5,9,10,11,16,21,22).
investigators reported that the biochemical properties of tissue extraction of ALPase from five meningiomas are consistent with those of the major form of ALPase (liver form), on the basis of the electrophoretic motility, the effect of urea, or heat treatment (20).
Redistribution of this article permitted only in accordance with the publisher’s copyright provisions.
DISCUSSION
10. 11.
12.
13. 14.
15.
16.
17.
18.
19.
20.
21. 22. 23.
Downloaded from https://academic.oup.com/neurosurgery/article-abstract/30/4/624/2753025 by Washington University, Law School Library user on 15 February 2019
9.
1981. Kepes JJ, MacGee EE, Vergara G, Sil R: Malignant meningioma with extensive pulmonary metastases. J Kans Med Soc 72:312 316, 1971. Landow H, Kabat EA, Newman W: Distribution of alkaline phosphatase in normal and in neoplastic tissues of the nervous system. Arch Neurol Psychiatry 48:518-530, 1942. Lolova I, Ivanova A: A histochemical study of meningiomas. Acta Neuropathol (Berl) 20:110121, 1972. Maeda T: Alkaline phosphatase activity in human gliomas as revealed by light and electron microscopy. No To Shinkei 39:527533, 1987 (in Japanese). Maniglia AJ, Page LK: Posterior cranial fossa and temporal bone meningioma in a child, appearing as a neck mass. Otolaryngol Head Neck Surg 87:578-583, 1979. Mendiratta SS, Rosenblum JA, Strobos RJ: Congenital meningioma. Neurology (Minneap) 17:914-918, 1967. Miedema E, Kouse PF Jr: Effect of predonisolone and contact phenomena or the alkaline phosphatase activity of Hep-2 cells. Biochem Biophys Res Commun 26:704-711, 1967. Mignot B, Hauw JJ, Pasquier P, DeSigalony JP II, Bricaire F: Perturbations biologiques reversibles evoluant parallelement à un meningiome recidivant et avec metastases. Sem Hop Paris 54:1231-1237, 1978. Ogashiwa M, Nishiyama F, Fukai K, Takeuchi K, Hirano H: Cytochemical study of Mg2+ATPase and ALPase activity in human meningiomas. No To Shinkei 42:497-503, 1990 (in Japanese). Remakrishnan S, Manifold IH, Ward AM, Forster DMC: CSF placental alkaline phosphatase as marker in cranial dysgerminoma. Lancet 2:225, 1989. Rowan RA, Maxwell DS: An ultrastructural study of vascular proliferation and vascular alkaline phosphatase activity in the developing cerebral cortex of the rat. Am J Anat 160:257-265, 1981. Tada W, Nagasawa M, Suzuki M, Harada Y, Oda K, Oki S: Infantile meningioma extended from the posterior cranial fossa into the parapharyngeal space. Otolaryngol-Head Neck Surg (Tokyo) 60:113-117, 1988. Takahara N, Herz F, Singer RM, Hirano A, Koss LG: Induction of alkaline phosphatase activities in cultured human intracranial tumor cells. Cancer Res 42:563-568, 1982. Timperley WR, Turner P, Davies S: Alkaline phosphatase in craniopharyngiomas. J Pathol 103:257-262, 1971. Timperley WR, Warnes TW: Alkaline phosphatase in meningiomas. Cancer 26:100103, 1970. Wakai S, Ochiai C, Takakura K, Keiji Sano:
Redistribution of this article permitted only in accordance with the publisher’s copyright provisions.
8.
Redistribution of this article permitted only in accordance with the publisher’s copyright provisions.
Figure 2. The angiogram shows a moderate vascular tumor stain, supplied by the left ascending pharyngeal artery.
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Figure 1. The sagittal view with Gd-DTPA enhancement shows a well-enhanced mass extending into the jugular foramen. A, axial view; B, sagittal view.
Redistribution of this article permitted only in accordance with the publisher’s copyright provisions.
Figure 4. Light microscopy shows the tumor to be mainly composed of meningothelial cells with a whorl formation (A). In some parts, small cells with chromatin-rich nuclei and mitoses are frequent (B).
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Figure 3. The electrophoretic pattern of the serum ALPase shows that the major part of the increased serum ALPase is liver form.
Redistribution of this article permitted only in accordance with the publisher’s copyright provisions.
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Figure 5. Serum ALPase dramatically decreased just after total removal of the tumor and was normalized within 3 weeks.
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Figure 6. Histochemically, the red granular staining was present not only within the cytoplasm but also on the plasma membrane of the neoplastic cells (A). Immunohistochemically, the brown staining was evident in a smaller number of tumor cells than that seen in the histochemical study (B).
