Growth hormone deficiency causes: Difference between revisions

	Growth hormone deficiency Microchapters
Home
Patient Information
Overview
Historical Perspective
Classification
Pathophysiology
Causes
Differentiating Growth hormone deficiency from other Diseases
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications and Prognosis
Diagnosis
Diagnostic Criteria
History and Symptoms
Physical Examination
Laboratory Findings
X Ray
CT
MRI
Echocardiography or Ultrasound
Other Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Surgery
Primary Prevention
Secondary Prevention
Cost-Effectiveness of Therapy
Future or Investigational Therapies
Case Studies
Case #1
Growth hormone deficiency causes On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
American Roentgen Ray Society Images of Growth hormone deficiency causes All Images X-rays Echo & Ultrasound CT Images MRI
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA on Growth hormone deficiency causes
CDC on Growth hormone deficiency causes
Growth hormone deficiency causes in the news
Blogs on Growth hormone deficiency causes
Directions to Hospitals Treating Growth hormone deficiency
Risk calculators and risk factors for Growth hormone deficiency causes

VisualWikitext

Latest revision as of 14:07, 25 October 2017

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

Overview

Causes of growth hormone deficiency could be congenital or acquired. Congenital causes can be genetic or structural. The genetic causes are due to genetic mutations in POU1F1, PROP-1, and GH-1 genes while the structural causes include optic nerve hypoplasia, agenesis of corpus callosum, septo-optic dysplasia, empty sella syndrome, and holoprosencephaly. Acquired causes of growth hormone deficiency include brain surgery and radiation therapy for brain tumors, central nervous system infection, craniopharyngioma, and pituitary adenoma.

Causes

Congenital growth hormone deficiency:

Genetic causes

It is usually recognized by the presence of affected relatives and confirmed by molecular testing for the causative genes, which include POU1F1, PROP-1, and GH1:

The POU1F1 gene is responsible for pituitary-specific transcription of genes for GH, prolactin, thyrotropin, and the growth hormone-releasing hormone (GHRH) receptor.^[1]
PROP1 mutations result in failure to activate POU1F1/Pit1 gene expression and probably cause pituitary hypoplasia and familial multiple pituitary hormone deficiencies.^[2]
Gene deletions, frameshift mutations, and nonsense mutations of GH1 which codes for GH, have been described as causes of familial GHD.^[3]^[4]

Structural Causes

GHD is highly likely to be permanent in these patients
It is associated with midline craniofacial anomalies causing agenesis of the hypothalamic-pituitary stalk:^[5]
- Optic nerve hypoplasia
- Midline facial defects
- Agenesis of corpus callosum
- Arachnoid cyst
- Holoprosencephaly
- Septo-optic dysplasia
- Encephalocele
- Empty Sella syndrome
- Hydrocephalus

Acquired growth hormone deficiency

GHD following brain surgery and radiation therapy for brain tumors. Permanent GHD is highly likely to be permanent in infants or young children^[6]
Central nervous system infection^[5]
Pituitary adenoma^[7]
Craniopharyngioma
Rathke’s cleft cyst
Glioma/astrocytoma
Germinoma
Infiltrative/granulomatous disease:^[8]
Surgery of the pituitary or hypothalamus^[11]
Sheehan’s syndrome^[12]
Idiopathic

Laron syndrome

This is the most common known cause of genetically-mediated growth hormone insensitivity (GHI).^[13]
Growth hormone insensitivity is an absence of the effects of growth hormone despite a normal production of GH.
Laron syndrome is characterized by growth failure and normal levels of GH.
It is caused by mutations in the growth hormone receptor gene which affects the GH-binding of the receptor.
Its severity correlates to IGF-I and insulin-like growth factor-binding protein 3 (IGFBP-3) levels.

References

↑ Li S, Crenshaw EB, Rawson EJ, Simmons DM, Swanson LW, Rosenfeld MG (1990). "Dwarf locus mutants lacking three pituitary cell types result from mutations in the POU-domain gene pit-1". Nature. 347 (6293): 528–33. doi:10.1038/347528a0. PMID 1977085.
↑ Obermannova B, Pfaeffle R, Zygmunt-Gorska A, Starzyk J, Verkauskiene R, Smetanina N; et al. (2011). "Mutations and pituitary morphology in a series of 82 patients with PROP1 gene defects". Horm Res Paediatr. 76 (5): 348–54. doi:10.1159/000332693. PMID 22024773.
↑ Pellegrini-Bouiller I, Bélicar P, Barlier A, Gunz G, Charvet JP, Jaquet P; et al. (1996). "A new mutation of the gene encoding the transcription factor Pit-1 is responsible for combined pituitary hormone deficiency". J Clin Endocrinol Metab. 81 (8): 2790–6. doi:10.1210/jcem.81.8.8768831. PMID 8768831.
↑ Wu W, Cogan JD, Pfäffle RW, Dasen JS, Frisch H, O'Connell SM; et al. (1998). "Mutations in PROP1 cause familial combined pituitary hormone deficiency". Nat Genet. 18 (2): 147–9. doi:10.1038/ng0298-147. PMID 9462743.
↑ ^5.0 ^5.1 Molitch ME, Clemmons DR, Malozowski S, Merriam GR, Vance ML, Endocrine Society (2011). "Evaluation and treatment of adult growth hormone deficiency: an Endocrine Society clinical practice guideline". J Clin Endocrinol Metab. 96 (6): 1587–609. doi:10.1210/jc.2011-0179. PMID 21602453.
↑ Snyder PJ, Fowble BF, Schatz NJ, Savino PJ, Gennarelli TA (1986). "Hypopituitarism following radiation therapy of pituitary adenomas". Am J Med. 81 (3): 457–62. PMID 3092668.
↑ Jahangiri A, Wagner JR, Han SW, Tran MT, Miller LM, Chen R; et al. (2016). "Improved versus worsened endocrine function after transsphenoidal surgery for nonfunctional pituitary adenomas: rate, time course, and radiological analysis". J Neurosurg. 124 (3): 589–95. doi:10.3171/2015.1.JNS141543. PMID 26252454.
↑ Charbonnel B, Chupin M, Le Grand A, Guillon J (1981). "Pituitary function in idiopathic haemochromatosis: hormonal study in 36 male patients". Acta Endocrinol (Copenh). 98 (2): 178–83. PMID 6794282.
↑ Cheung CC, Ezzat S, Smyth HS, Asa SL (2001). "The spectrum and significance of primary hypophysitis". J Clin Endocrinol Metab. 86 (3): 1048–53. doi:10.1210/jcem.86.3.7265. PMID 11238484.
↑ Cheung CC, Ezzat S, Smyth HS, Asa SL (2001). "The spectrum and significance of primary hypophysitis". J Clin Endocrinol Metab. 86 (3): 1048–53. doi:10.1210/jcem.86.3.7265. PMID 11238484.
↑ Jahangiri A, Wagner JR, Han SW, Tran MT, Miller LM, Chen R; et al. (2016). "Improved versus worsened endocrine function after transsphenoidal surgery for nonfunctional pituitary adenomas: rate, time course, and radiological analysis". J Neurosurg. 124 (3): 589–95. doi:10.3171/2015.1.JNS141543. PMID 26252454.
↑ Barkan AL (1989). "Pituitary atrophy in patients with Sheehan's syndrome". Am J Med Sci. 298 (1): 38–40. PMID 2750772.
↑ Kurtoğlu S, Hatipoglu N (2016). "Growth hormone insensitivity: diagnostic and therapeutic approaches". J Endocrinol Invest. 39 (1): 19–28. doi:10.1007/s40618-015-0327-2. PMID 26062520.

Haleigh Williams, B.S. Template:WS

[pmid1977085-1] Li S, Crenshaw EB, Rawson EJ, Simmons DM, Swanson LW, Rosenfeld MG (1990). "Dwarf locus mutants lacking three pituitary cell types result from mutations in the POU-domain gene pit-1". Nature. 347 (6293): 528–33. doi:10.1038/347528a0. PMID 1977085.

[pmid22024773-2] Obermannova B, Pfaeffle R, Zygmunt-Gorska A, Starzyk J, Verkauskiene R, Smetanina N; et al. (2011). "Mutations and pituitary morphology in a series of 82 patients with PROP1 gene defects". Horm Res Paediatr. 76 (5): 348–54. doi:10.1159/000332693. PMID 22024773.

[pmid8768831-3] Pellegrini-Bouiller I, Bélicar P, Barlier A, Gunz G, Charvet JP, Jaquet P; et al. (1996). "A new mutation of the gene encoding the transcription factor Pit-1 is responsible for combined pituitary hormone deficiency". J Clin Endocrinol Metab. 81 (8): 2790–6. doi:10.1210/jcem.81.8.8768831. PMID 8768831.

[pmid9462743-4] Wu W, Cogan JD, Pfäffle RW, Dasen JS, Frisch H, O'Connell SM; et al. (1998). "Mutations in PROP1 cause familial combined pituitary hormone deficiency". Nat Genet. 18 (2): 147–9. doi:10.1038/ng0298-147. PMID 9462743.

[pmid216024532-5] 5.0 ^5.1 Molitch ME, Clemmons DR, Malozowski S, Merriam GR, Vance ML, Endocrine Society (2011). "Evaluation and treatment of adult growth hormone deficiency: an Endocrine Society clinical practice guideline". J Clin Endocrinol Metab. 96 (6): 1587–609. doi:10.1210/jc.2011-0179. PMID 21602453.

[pmid3092668-6] Snyder PJ, Fowble BF, Schatz NJ, Savino PJ, Gennarelli TA (1986). "Hypopituitarism following radiation therapy of pituitary adenomas". Am J Med. 81 (3): 457–62. PMID 3092668.

[pmid26252454-7] Jahangiri A, Wagner JR, Han SW, Tran MT, Miller LM, Chen R; et al. (2016). "Improved versus worsened endocrine function after transsphenoidal surgery for nonfunctional pituitary adenomas: rate, time course, and radiological analysis". J Neurosurg. 124 (3): 589–95. doi:10.3171/2015.1.JNS141543. PMID 26252454.

[pmid6794282-8] Charbonnel B, Chupin M, Le Grand A, Guillon J (1981). "Pituitary function in idiopathic haemochromatosis: hormonal study in 36 male patients". Acta Endocrinol (Copenh). 98 (2): 178–83. PMID 6794282.

[pmid112384842-9] Cheung CC, Ezzat S, Smyth HS, Asa SL (2001). "The spectrum and significance of primary hypophysitis". J Clin Endocrinol Metab. 86 (3): 1048–53. doi:10.1210/jcem.86.3.7265. PMID 11238484.

[pmid11238484-10] Cheung CC, Ezzat S, Smyth HS, Asa SL (2001). "The spectrum and significance of primary hypophysitis". J Clin Endocrinol Metab. 86 (3): 1048–53. doi:10.1210/jcem.86.3.7265. PMID 11238484.

[pmid262524542-11] Jahangiri A, Wagner JR, Han SW, Tran MT, Miller LM, Chen R; et al. (2016). "Improved versus worsened endocrine function after transsphenoidal surgery for nonfunctional pituitary adenomas: rate, time course, and radiological analysis". J Neurosurg. 124 (3): 589–95. doi:10.3171/2015.1.JNS141543. PMID 26252454.

[pmid2750772-12] Barkan AL (1989). "Pituitary atrophy in patients with Sheehan's syndrome". Am J Med Sci. 298 (1): 38–40. PMID 2750772.

[pmid26062520-13] Kurtoğlu S, Hatipoglu N (2016). "Growth hormone insensitivity: diagnostic and therapeutic approaches". J Endocrinol Invest. 39 (1): 19–28. doi:10.1007/s40618-015-0327-2. PMID 26062520.

[1]

[2]

[3]

[4]

[5]

[6]

[7]

[8]

[9]

[10]

[11]

[12]

[13]

@@ Line 1: / Line 1: @@
 __NOTOC__
 {{Growth hormone deficiency}}
-{{CMG}}
+{{CMG}}; {{AE}} {{MAD}}
 ==Overview==
+Causes of growth hormone deficiency could be congenital or acquired. Congenital causes can be genetic or structural.  The genetic causes are due to [[genetic mutations]] in ''POU1F1'', ''PROP-1'', and ''GH-1 genes'' while the structural causes include [[optic nerve hypoplasia]], [[Agenesis of the corpus callosum|agenesis of corpus callosum]], [[septo-optic dysplasia]], [[empty sella syndrome]], and [[holoprosencephaly]]. Acquired causes of growth hormone deficiency include [[brain surgery]] and [[radiation therapy]] for [[brain tumors]], [[central nervous system infection]], [[craniopharyngioma]], and [[pituitary adenoma]].
 ==Causes==
-There are many causes of GH deficiency. Some examples include:
+=== Congenital growth hormone deficiency: ===
-* [[mutation]]s of specific [[gene]]s (e.g., [[GHRHR]], GH1)
+==== Genetic causes ====
-* [[congenital malformation]]s involving the pituitary (e.g., [[septo-optic dysplasia]], posterior pituitary ectopia)
+It is usually recognized by the presence of affected relatives and confirmed by molecular testing for the causative genes, which include ''POU1F1'', ''PROP-1'', and ''GH1:''
-* damage to the pituitary from incracranial disease (e.g., [[hydrocephalus]]),
+* The ''POU1F1'' gene is responsible for [[Pituitary gland|pituitary]]-specific [[Transcription (genetics)|transcription of genes]] for [[Growth hormone|GH]], [[prolactin]], [[thyrotropin]], and the [[growth hormone-releasing hormone]] ([[GHRH]]) [[receptor]].<ref name="pmid1977085">{{cite journal| author=Li S, Crenshaw EB, Rawson EJ, Simmons DM, Swanson LW, Rosenfeld MG| title=Dwarf locus mutants lacking three pituitary cell types result from mutations in the POU-domain gene pit-1. | journal=Nature | year= 1990 | volume= 347 | issue= 6293 | pages= 528-33 | pmid=1977085 | doi=10.1038/347528a0 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1977085  }}</ref>
-* [[brain tumor|intracranial tumors]] in or near the [[sella turcica]], especially [[craniopharyngioma]],
+* ''[[PROP1]]'' [[mutations]] result in failure to activate ''POU1F1/Pit1'' [[gene expression]] and probably cause pituitary hypoplasia and [[familial]] multiple pituitary hormone deficiencies.<ref name="pmid22024773">{{cite journal| author=Obermannova B, Pfaeffle R, Zygmunt-Gorska A, Starzyk J, Verkauskiene R, Smetanina N et al.| title=Mutations and pituitary morphology in a series of 82 patients with PROP1 gene defects. | journal=Horm Res Paediatr | year= 2011 | volume= 76 | issue= 5 | pages= 348-54 | pmid=22024773 | doi=10.1159/000332693 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22024773  }}</ref>
-* damage to the pituitary from [[radiation therapy]] to the head for [[leukemia]] or [[brain tumor]]s,
+* [[Gene deletion|Gene deletions]], [[Frameshift mutation|frameshift mutations]], and [[nonsense mutations]] of ''GH1'' which codes for GH, have been described as causes of [[familial]] GHD.<ref name="pmid8768831">{{cite journal| author=Pellegrini-Bouiller I, Bélicar P, Barlier A, Gunz G, Charvet JP, Jaquet P et al.| title=A new mutation of the gene encoding the transcription factor Pit-1 is responsible for combined pituitary hormone deficiency. | journal=J Clin Endocrinol Metab | year= 1996 | volume= 81 | issue= 8 | pages= 2790-6 | pmid=8768831 | doi=10.1210/jcem.81.8.8768831 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8768831  }}</ref><ref name="pmid9462743">{{cite journal| author=Wu W, Cogan JD, Pfäffle RW, Dasen JS, Frisch H, O'Connell SM et al.| title=Mutations in PROP1 cause familial combined pituitary hormone deficiency. | journal=Nat Genet | year= 1998 | volume= 18 | issue= 2 | pages= 147-9 | pmid=9462743 | doi=10.1038/ng0298-147 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9462743  }}</ref>
-* surgery in the area of the pituitary,
-* [[autoimmunity|autoimmune]] [[inflammation]] (hypophysitis),
+==== '''Structural Causes''' ====
-* severe [[head trauma]],
+* GHD is highly likely to be permanent in these patients
-* ischemic or hemorrhagic infarction from low blood pressure ([[Sheehan syndrome]]) or hemorrhage [[pituitary apoplexy]].
+* It is associated with midline [[craniofacial]] anomalies causing agenesis of the [[Hypothalamic pituitary adrenal axis|hypothalamic-pituitary stalk]]:<ref name="pmid216024532">{{cite journal| author=Molitch ME, Clemmons DR, Malozowski S, Merriam GR, Vance ML, Endocrine Society| title=Evaluation and treatment of adult growth hormone deficiency: an Endocrine Society clinical practice guideline. | journal=J Clin Endocrinol Metab | year= 2011 | volume= 96 | issue= 6 | pages= 1587-609 | pmid=21602453 | doi=10.1210/jc.2011-0179 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21602453  }}</ref>
-Many cases of isolated growth hormone deficiency (IGHD) recognized in childhood are idiopathic. IGHD has been reported to affect about 1 in 4000 children, but IGHD is difficult to distinguish from other causes of shortness such as constitutional delay, and the true incidence is unsettled.
+**[[Optic nerve hypoplasia]]
-Severe prenatal deficiency of GH, as occurs in congenital hypopituitarism, has little effect on fetal growth. However, prenatal and congenital deficiency can reduce the size of a male's [[penis]], especially when gonadotropins are also deficient. Besides [[micropenis]], additional consequences of severe deficiency in the first days of life can include [[hypoglycemia]] and exaggerated [[jaundice]] (both direct and indirect hyperbilirubinemia). Female infants will lack the [[micropenis|microphallus]] of course but may suffer from hypoglycemia and jaundice.
+**Midline facial defects
-Even congenital GH deficiency does not usually impair length growth until after the first few months of life. From late in the first year until mid teens, poor growth and/or shortness is the hallmark of childhood GH deficiency. Growth is not as severely affected in GH deficiency as in untreated [[hypothyroidism]], but growth at about half the usual velocity for age is typical. It tends to be accompanied by delayed physical maturation so that [[bone age|bone maturation]] and [[puberty]] may be several years delayed. When severe GH deficiency is present from birth and never treated, adult heights can be as short as 48-58 inches (122-147 cm).
+**[[Agenesis of the corpus callosum|Agenesis of corpus callosum]]
-Severe GH deficiency in early childhood also results in slower [[muscle|muscular]] development, so that gross motor milestones such as standing, walking, and jumping may be delayed. [[Body composition]] (i.e., the relative amounts of [[bone]], muscle, and [[adipose tissue|fat]]) is affected in many children with severe deficiency, so that mild to moderate chubbiness is common (though GH deficiency alone rarely causes severe obesity). Some severely GH-deficient children have recognizable, cherubic facial features characterized by [[maxilla]]ry hypoplasia and forehead prominence (said to resemble a kewpie doll).
+**[[Arachnoid cyst]]
+**[[Holoprosencephaly]]
+**[[Septo-optic dysplasia]]
+**[[Encephalocele]]
+**[[Empty sella syndrome|Empty Sella syndrome]]
+**[[Hydrocephalus]]
+=== '''Acquired growth hormone deficiency''' ===
+* GHD following brain surgery and radiation therapy for [[brain tumors]]. Permanent GHD is highly likely to be permanent in infants or young children<ref name="pmid3092668">{{cite journal| author=Snyder PJ, Fowble BF, Schatz NJ, Savino PJ, Gennarelli TA| title=Hypopituitarism following radiation therapy of pituitary adenomas. | journal=Am J Med | year= 1986 | volume= 81 | issue= 3 | pages= 457-62 | pmid=3092668 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3092668  }}</ref>
+* [[Central nervous system infection]]<ref name="pmid216024532" />
+* [[Pituitary adenoma]]<ref name="pmid26252454">{{cite journal| author=Jahangiri A, Wagner JR, Han SW, Tran MT, Miller LM, Chen R et al.| title=Improved versus worsened endocrine function after transsphenoidal surgery for nonfunctional pituitary adenomas: rate, time course, and radiological analysis. | journal=J Neurosurg | year= 2016 | volume= 124 | issue= 3 | pages= 589-95 | pmid=26252454 | doi=10.3171/2015.1.JNS141543 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26252454  }}</ref>
+* [[Craniopharyngioma]]
+* [[Rathke’s pouch|Rathke’s]] cleft [[cyst]]
+* [[Glioma]]/[[astrocytoma]]
+* [[Germinoma]]
+* [[Infiltrative and Metabolic Diseases Affecting the Liver|Infiltrative]]/[[Granulomatous|granulomatous disease]]:<ref name="pmid6794282">{{cite journal| author=Charbonnel B, Chupin M, Le Grand A, Guillon J| title=Pituitary function in idiopathic haemochromatosis: hormonal study in 36 male patients. | journal=Acta Endocrinol (Copenh) | year= 1981 | volume= 98 | issue= 2 | pages= 178-83 | pmid=6794282 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6794282  }}</ref>
+**[[Langerhans cell histiocytosis]]
+**[[Sarcoidosis]]<ref name="pmid112384842">{{cite journal| author=Cheung CC, Ezzat S, Smyth HS, Asa SL| title=The spectrum and significance of primary hypophysitis. | journal=J Clin Endocrinol Metab | year= 2001 | volume= 86 | issue= 3 | pages= 1048-53 | pmid=11238484 | doi=10.1210/jcem.86.3.7265 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11238484  }}</ref>
+**[[Tuberculosis]]
+**[[Hypophysitis]]<ref name="pmid11238484">{{cite journal| author=Cheung CC, Ezzat S, Smyth HS, Asa SL| title=The spectrum and significance of primary hypophysitis. | journal=J Clin Endocrinol Metab | year= 2001 | volume= 86 | issue= 3 | pages= 1048-53 | pmid=11238484 | doi=10.1210/jcem.86.3.7265 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11238484  }}</ref>
+* Surgery of the [[Pituitary gland|pituitary]] or [[hypothalamus]]<ref name="pmid262524542">{{cite journal| author=Jahangiri A, Wagner JR, Han SW, Tran MT, Miller LM, Chen R et al.| title=Improved versus worsened endocrine function after transsphenoidal surgery for nonfunctional pituitary adenomas: rate, time course, and radiological analysis. | journal=J Neurosurg | year= 2016 | volume= 124 | issue= 3 | pages= 589-95 | pmid=26252454 | doi=10.3171/2015.1.JNS141543 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26252454  }}</ref>
+* [[Sheehan's syndrome|Sheehan’s syndrome]]<ref name="pmid2750772">{{cite journal| author=Barkan AL| title=Pituitary atrophy in patients with Sheehan's syndrome. | journal=Am J Med Sci | year= 1989 | volume= 298 | issue= 1 | pages= 38-40 | pmid=2750772 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2750772  }}</ref>
+* [[Idiopathic]]
-==References==
+==== '''[[Laron syndrome]]''' ====
-{{reflist|2}}
+* This is the most common known cause of genetically-mediated growth hormone insensitivity (GHI).<ref name="pmid26062520">{{cite journal| author=Kurtoğlu S, Hatipoglu N| title=Growth hormone insensitivity: diagnostic and therapeutic approaches. | journal=J Endocrinol Invest | year= 2016 | volume= 39 | issue= 1 | pages= 19-28 | pmid=26062520 | doi=10.1007/s40618-015-0327-2 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26062520  }}</ref>
+* [[Growth hormone insensitivity syndrome|Growth hormone insensitivity]] is an absence of the effects of [[growth hormone]] despite a normal production of [[Growth hormone|GH]].
+* [[Laron syndrome]] is characterized by [[growth failure]] and normal levels of [[Growth hormone|GH]].
+* It is caused by [[mutations]] in the growth hormone receptor gene which affects the GH-binding of the [[receptor]].
+* Its severity correlates to [[IGF-I]] and [[Insulin-like growth factor-binding protein 1|insulin-like growth factor-binding protein]] 3 ([[IGFBP-3]]) levels.
-{{WH}}
+== References ==
+{{Reflist|2}}
+{{HW}}
 {{WS}}
-[[Category:Disease]]
-[[Category:Endocrinology]]