Craniopharyngioma laboratory tests: Difference between revisions

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==Overview==
==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.
Patients with craniopharyngioma may have abnormal [[Pituitary gland|pituitary hormone levels]], which is suggestive of disruption of [[Hormone|hormone production]] due to [[Pressure|pressure effects]] on the [[pituitary gland]]. Th[[Hypothalamic-pituitary-thyroid axis|e hypothalamic-pituitary axis]] hormones, namely [[Growth hormone 1|growth hormone]], [[Thyroid hormone|thyroid hormone,]] [[Luteinizing hormone|luteinising]] and [[follicle stimulating hormone]] should be measured together with [[Cortisol|cortisol levels]] and an assessment of [[Osmolality|serum and urine osmolality]]. In addition, an estimate of [[bone age]] and, for young females, [[Ovary|ovarian]] [[Medical ultrasonography|ultrasonography]] is useful. Ideally, any abnormalities should be corrected [[Surgery|pre-operatively]] but, at the very least, low [[Cortisol|cortisol levels]] and [[diabetes insipidus]] should be treated prior to a [[Surgery|surgical procedure.]]


==Laboratory Findings==
==Laboratory Findings==
The following hormones should be checked in patients who are being suspected of having craniopharyngioma.
The following hormones should be checked in patients who are being suspected of having craniopharyngioma.<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><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>
 
**[[Growth hormone 1|Serum Growth hormone]]
**Serum Growth hormone
**[[Luteinizing hormone|Serum Leutinizing hormone]]
**Serum Leutinizing hormone
**[[Follicle-stimulating hormone|Serum Follicle stimulating hormone]]
**Serum Follicle stimulating hormone
**[[Prolactin|Serum Prolactin]]
**Serum Prolactin
**[[Thyroid-stimulating hormone|Serum Thyroid stimulating hormone]]
**Serum Thyroid stimulating hormone
**[[Adrenocorticotropic hormone|Serum ACTH]]
**Serum ACTH
**[[Cortisol|Morning serum cortisol]]
**Morning serum cortisol


===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.
*[[Metyrapone]] blocks [[Hydroxylase|11-beta-hydroxylase]] , the [[enzyme]] that [[Catalysis|catalyzes]] the conversion of [[Deoxycortisol|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.
*Fall in [[Cortisol|serum cortisol]] is observed if the [[Hypothalamic pituitary adrenal axis|hypothalamic-pituitary-adrenal axis]] is normal.
*Increase in [[Adrenocorticotropic hormone|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.
*[[Cosyntropin]] ([[Adrenocorticotropic hormone|ACTH]]) stimulates [[Adrenal gland|adrenal glands]] when they have not been stimulated for a prolonged period.<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]] ([[Adrenocorticotropic hormone|synthetic ACTH]]) [[Intramuscular injection|intramuscularly]] or [[Intravenous therapy|intravenously]].
*A serum cortisol concentration of ≥18 mcg/dL (497 nmol/L) is considered a normal response.
*[[Cortisol|Serum cortisol]] 60 minutes later after administration of [[cosyntropin]]. <ref>Rx of Craniopharyngioma. Cancer gov. http://www.cancer.gov/types/brain/hp/child-cranio-treatment-pdq#link/_40_toc</ref>
*A [[Cortisol|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>


===Insulin-induced hypoglycemia test===
===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.  
*[[Insulin]] administration is a sufficient stress to stimulate [[Adrenocorticotropic hormone|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.  
*The test is performed by administering 0.1 unit of [[insulin]] per kg of body weight and measuring [[Blood sugar|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 [[Cortisol|serum cortisol]] increases to ≥18 mcg/dL (498 nmol/L) if the [[Blood sugar|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.
*A [[Insulin-like growth factor-I|serum IGF-1]] concentration lower than the age-specific lower limit of normal in a patient who has [[Pituitary disease|organic pituitary disease]] confirms the diagnosis of [[Growth hormone deficiency|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>
===Provocative tests of growth hormone secretion===
===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.  
*[[Hypoglycemia|Insulin-induced hypoglycemia]] or the combination of [[arginine]] and [[growth hormone-releasing hormone]] (GHRH) is a potent stimulus of [[Growth hormone|growth hormone release]]. <ref name="pmid9761047">{{cite journal |vauthors=Bunin GR, Surawicz TS, Witman PA, Preston-Martin S, Davis F, Bruner JM |title=The descriptive epidemiology of craniopharyngioma |journal=J. Neurosurg. |volume=89 |issue=4 |pages=547–51 |date=October 1998 |pmid=9761047 |doi=10.3171/jns.1998.89.4.0547 |url=}}</ref>
*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.
*Subnormal increases in the serum [[growth hormone]] concentration in a patient who has [[Pituitary disease|organic pituitary disease]] confirms the diagnosis of [[Growth hormone deficiency|growth hormone deficiency.]]<ref name="pmid9761047">{{cite journal |vauthors=Bunin GR, Surawicz TS, Witman PA, Preston-Martin S, Davis F, Bruner JM |title=The descriptive epidemiology of craniopharyngioma |journal=J. Neurosurg. |volume=89 |issue=4 |pages=547–51 |date=October 1998 |pmid=9761047 |doi=10.3171/jns.1998.89.4.0547 |url=}}</ref>


==References==
==References==

Latest revision as of 16:48, 26 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]

Metyrapone test

Cosyntropin stimulation test

Insulin-induced hypoglycemia test

  • 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)

Provocative tests of growth hormone secretion

References

  1. 1.0 1.1 1.2 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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