Craniopharyngioma laboratory tests: Difference between revisions

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===Metyrapone test===
===Metyrapone test===
*The rationale for the administration of metyrapone is that it blocks 11-beta-hydroxylase (CYP11B1), the enzyme that catalyzes the conversion of 11-deoxycortisol to cortisol, resulting in a reduction in cortisol secretion.
*The rationale for the administration of metyrapone is that it blocks 11-beta-hydroxylase (CYP11B1), the enzyme that catalyzes the conversion of 11-deoxycortisol to cortisol, resulting in a reduction in cortisol secretion.<ref name="pmid17630614">{{cite journal |vauthors=Garrè ML, Cama A |title=Craniopharyngioma: modern concepts in pathogenesis and treatment |journal=Curr. Opin. Pediatr. |volume=19 |issue=4 |pages=471–9 |date=August 2007 |pmid=17630614 |doi=10.1097/MOP.0b013e3282495a22 |url=}}</ref> 
*The ensuing fall in serum cortisol should, if the hypothalamic-pituitary-adrenal axis is normal, cause an increase in ACTH secretion and therefore an increase in adrenal steroidogenesis up to and including 11-deoxycortisol.
*The ensuing fall in serum cortisol should, if the hypothalamic-pituitary-adrenal axis is normal, cause an increase in ACTH secretion and therefore an increase in adrenal steroidogenesis up to and including 11-deoxycortisol.<ref>Rx of Craniopharyngioma. Cancer gov. http://www.cancer.gov/types/brain/hp/child-cranio-treatment-pdq#link/_40_toc</ref>


===Cosyntropin stimulation test===
===Cosyntropin stimulation test===
*The rationale for the administration of cosyntropin (ACTH) is that the adrenal glands atrophy when they have not been stimulated for a prolonged period; as a result, they do not secrete cortisol normally in response to a bolus dose of ACTH.<ref name="pmid1260697">{{cite journal |vauthors=Petito CK, DeGirolami U, Earle KM |title=Craniopharyngiomas: a clinical and pathological review |journal=Cancer |volume=37 |issue=4 |pages=1944–52 |date=April 1976 |pmid=1260697 |doi= |url=}}</ref>
*The rationale for the administration of cosyntropin (ACTH) is that the adrenal glands atrophy when they have not been stimulated for a prolonged period; as a result, they do not secrete cortisol normally in response to a bolus dose of ACTH.<ref name="pmid1260697">{{cite journal |vauthors=Petito CK, DeGirolami U, Earle KM |title=Craniopharyngiomas: a clinical and pathological review |journal=Cancer |volume=37 |issue=4 |pages=1944–52 |date=April 1976 |pmid=1260697 |doi= |url=}}</ref>
*The test is usually performed by administering 0.25 mg (25 units) of cosyntropin (synthetic ACTH 1-24) intramuscularly or intravenously and measuring serum cortisol 60 minutes later.  
*The test is usually performed by administering 0.25 mg (25 units) of cosyntropin (synthetic ACTH 1-24) intramuscularly or intravenously and measuring serum cortisol 60 minutes later. <ref>Rx of Craniopharyngioma. Cancer gov. http://www.cancer.gov/types/brain/hp/child-cranio-treatment-pdq#link/_40_toc</ref>
*The [[Chemotherapy|chemotherapy drugs]] [[Paclitaxel]] and [[Carboplatin]] have shown a clinical significance in increasing the survival rate.<ref name="pmid1260697">{{cite journal |vauthors=Petito CK, DeGirolami U, Earle KM |title=Craniopharyngiomas: a clinical and pathological review |journal=Cancer |volume=37 |issue=4 |pages=1944–52 |date=April 1976 |pmid=1260697 |doi= |url=}}</ref>
*A serum cortisol concentration of ≥18 mcg/dL (497 nmol/L) is considered a normal response.<ref name="pmid1260697">{{cite journal |vauthors=Petito CK, DeGirolami U, Earle KM |title=Craniopharyngiomas: a clinical and pathological review |journal=Cancer |volume=37 |issue=4 |pages=1944–52 |date=April 1976 |pmid=1260697 |doi= |url=}}</ref>  
*A serum cortisol concentration of ≥18 mcg/dL (497 nmol/L) is considered a normal response.<ref name="pmid1260697">{{cite journal |vauthors=Petito CK, DeGirolami U, Earle KM |title=Craniopharyngiomas: a clinical and pathological review |journal=Cancer |volume=37 |issue=4 |pages=1944–52 |date=April 1976 |pmid=1260697 |doi= |url=}}</ref>  


Line 27: Line 28:
*The rationale for this test is that hypoglycemia induced by insulin administration is a sufficient stress to stimulate ACTH and therefore cortisol secretion.  
*The rationale for this test is that hypoglycemia induced by insulin administration is a sufficient stress to stimulate ACTH and therefore cortisol secretion.  
*The test is performed by administering 0.1 unit of insulin per kg of body weight and measuring serum glucose and cortisol before and 15, 30, 60, 90, and 120 minutes after the injection. <ref name="pmid6818504">{{cite journal |vauthors=Rush JA, Younge BR, Campbell RJ, MacCarty CS |title=Optic glioma. Long-term follow-up of 85 histopathologically verified cases |journal=Ophthalmology |volume=89 |issue=11 |pages=1213–9 |date=November 1982 |pmid=6818504 |doi= |url=}}</ref>
*The test is performed by administering 0.1 unit of insulin per kg of body weight and measuring serum glucose and cortisol before and 15, 30, 60, 90, and 120 minutes after the injection. <ref name="pmid6818504">{{cite journal |vauthors=Rush JA, Younge BR, Campbell RJ, MacCarty CS |title=Optic glioma. Long-term follow-up of 85 histopathologically verified cases |journal=Ophthalmology |volume=89 |issue=11 |pages=1213–9 |date=November 1982 |pmid=6818504 |doi= |url=}}</ref>
*In normal subjects, serum cortisol increases to ≥18 mcg/dL (498 nmol/L) if the serum glucose falls to <50 mg/dL (2.8 mmol/L).
*In normal subjects, serum cortisol increases to ≥18 mcg/dL (498 nmol/L) if the serum glucose falls to <50 mg/dL (2.8 mmol/L).<ref name="pmid7885544">{{cite journal |vauthors=Weiner HL, Wisoff JH, Rosenberg ME, Kupersmith MJ, Cohen H, Zagzag D, Shiminski-Maher T, Flamm ES, Epstein FJ, Miller DC |title=Craniopharyngiomas: a clinicopathological analysis of factors predictive of recurrence and functional outcome |journal=Neurosurgery |volume=35 |issue=6 |pages=1001–10; discussion 1010–1 |date=December 1994 |pmid=7885544 |doi= |url=}}</ref>
===Serum insulin-like growth factor-1 (IGF-1)===
===Serum insulin-like growth factor-1 (IGF-1)===
*A serum IGF-1 concentration lower than the age-specific lower limit of normal in a patient who has organic pituitary disease confirms the diagnosis of growth hormone deficiency.<ref name="pmid6818504">{{cite journal |vauthors=Rush JA, Younge BR, Campbell RJ, MacCarty CS |title=Optic glioma. Long-term follow-up of 85 histopathologically verified cases |journal=Ophthalmology |volume=89 |issue=11 |pages=1213–9 |date=November 1982 |pmid=6818504 |doi= |url=}}</ref>
*A serum IGF-1 concentration lower than the age-specific lower limit of normal in a patient who has organic pituitary disease confirms the diagnosis of growth hormone deficiency.<ref name="pmid6818504">{{cite journal |vauthors=Rush JA, Younge BR, Campbell RJ, MacCarty CS |title=Optic glioma. Long-term follow-up of 85 histopathologically verified cases |journal=Ophthalmology |volume=89 |issue=11 |pages=1213–9 |date=November 1982 |pmid=6818504 |doi= |url=}}</ref>

Revision as of 16:02, 14 February 2019

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Marjan Khan M.B.B.S.[2]

Overview

Patients with craniopharyngioma may have abnormal pituitary hormone levels, which is suggestive of disruption of hormone production due to pressure effects on the pituitary gland. The hypothalamic-pituitary axis hormones, namely growth hormone, thyroid hormone, luteinising and follicle stimulating hormone should be measured together with cortisol levels and an assessment of serum and urine osmolality. In addition, an estimate of bone age and, for young females, ovarian ultrasonography is useful. Ideally, any abnormalities should be corrected pre-operatively but, at the very least, low cortisol levels and diabetes insipidus should be treated prior to a surgical procedure.

Laboratory Findings

The following hormones should be checked in patients who are being suspected of having craniopharyngioma.[1][2]

    • Serum Growth hormone
    • Serum Leutinizing hormone
    • Serum Follicle stimulating hormone
    • Serum Prolactin
    • Serum Thyroid stimulating hormone
    • Serum ACTH
    • Morning serum cortisol

Metyrapone test

  • The rationale for the administration of metyrapone is that it blocks 11-beta-hydroxylase (CYP11B1), the enzyme that catalyzes the conversion of 11-deoxycortisol to cortisol, resulting in a reduction in cortisol secretion.[3]
  • The ensuing fall in serum cortisol should, if the hypothalamic-pituitary-adrenal axis is normal, cause an increase in ACTH secretion and therefore an increase in adrenal steroidogenesis up to and including 11-deoxycortisol.[4]

Cosyntropin stimulation test

  • The rationale for the administration of cosyntropin (ACTH) is that the adrenal glands atrophy when they have not been stimulated for a prolonged period; as a result, they do not secrete cortisol normally in response to a bolus dose of ACTH.[1]
  • The test is usually performed by administering 0.25 mg (25 units) of cosyntropin (synthetic ACTH 1-24) intramuscularly or intravenously and measuring serum cortisol 60 minutes later. [5]
  • The chemotherapy drugs Paclitaxel and Carboplatin have shown a clinical significance in increasing the survival rate.[1]
  • A serum cortisol concentration of ≥18 mcg/dL (497 nmol/L) is considered a normal response.[1]

Insulin-induced hypoglycemia test

  • The rationale for this test is that hypoglycemia induced by insulin administration is a sufficient stress to stimulate ACTH and therefore cortisol secretion.
  • The test is performed by administering 0.1 unit of insulin per kg of body weight and measuring serum glucose and cortisol before and 15, 30, 60, 90, and 120 minutes after the injection. [2]
  • In normal subjects, serum cortisol increases to ≥18 mcg/dL (498 nmol/L) if the serum glucose falls to <50 mg/dL (2.8 mmol/L).[6]

Serum insulin-like growth factor-1 (IGF-1)

  • A serum IGF-1 concentration lower than the age-specific lower limit of normal in a patient who has organic pituitary disease confirms the diagnosis of growth hormone deficiency.[2]

Provocative tests of growth hormone secretion

  • insulin-induced hypoglycemia or the combination of arginine and growth hormone-releasing hormone (GHRH) is a potent stimulus of growth hormone release. [7]
  • Subnormal increases in the serum growth hormone concentration (<5.1 ng/mL for the former and <4.1 ng/mL for the latter) in a patient who has organic pituitary disease confirms the diagnosis of growth hormone deficiency.[7]

References

  1. 1.0 1.1 1.2 1.3 Petito CK, DeGirolami U, Earle KM (April 1976). "Craniopharyngiomas: a clinical and pathological review". Cancer. 37 (4): 1944–52. PMID 1260697.
  2. 2.0 2.1 2.2 Rush JA, Younge BR, Campbell RJ, MacCarty CS (November 1982). "Optic glioma. Long-term follow-up of 85 histopathologically verified cases". Ophthalmology. 89 (11): 1213–9. PMID 6818504.
  3. Garrè ML, Cama A (August 2007). "Craniopharyngioma: modern concepts in pathogenesis and treatment". Curr. Opin. Pediatr. 19 (4): 471–9. doi:10.1097/MOP.0b013e3282495a22. PMID 17630614.
  4. Rx of Craniopharyngioma. Cancer gov. http://www.cancer.gov/types/brain/hp/child-cranio-treatment-pdq#link/_40_toc
  5. Rx of Craniopharyngioma. Cancer gov. http://www.cancer.gov/types/brain/hp/child-cranio-treatment-pdq#link/_40_toc
  6. Weiner HL, Wisoff JH, Rosenberg ME, Kupersmith MJ, Cohen H, Zagzag D, Shiminski-Maher T, Flamm ES, Epstein FJ, Miller DC (December 1994). "Craniopharyngiomas: a clinicopathological analysis of factors predictive of recurrence and functional outcome". Neurosurgery. 35 (6): 1001–10, discussion 1010–1. PMID 7885544.
  7. 7.0 7.1 Bunin GR, Surawicz TS, Witman PA, Preston-Martin S, Davis F, Bruner JM (October 1998). "The descriptive epidemiology of craniopharyngioma". J. Neurosurg. 89 (4): 547–51. doi:10.3171/jns.1998.89.4.0547. PMID 9761047.


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