Neuroendocrine dysfunction in the acute phase of traumatic brain injury
Summary background Pituitary hormone abnormalities have been reported in up to 50% of survivors of traumatic brain injury (TBI) who were investigated several months or longer following the event. The frequency of pituitary dysfunction in the early post‐TBI period is unknown. aim To evaluate the pr...
Gespeichert in:
| Veröffentlicht in: | Clinical endocrinology (Oxford) 2004-05, Vol.60 (5), p.584-591 |
|---|---|
| Hauptverfasser: | , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 591 |
|---|---|
| container_issue | 5 |
| container_start_page | 584 |
| container_title | Clinical endocrinology (Oxford) |
| container_volume | 60 |
| creator | Agha, Amar Rogers, Bairbre Mylotte, Darren Taleb, Faisal Tormey, William Phillips, Jack Thompson, Christopher J. |
| description | Summary
background Pituitary hormone abnormalities have been reported in up to 50% of survivors of traumatic brain injury (TBI) who were investigated several months or longer following the event. The frequency of pituitary dysfunction in the early post‐TBI period is unknown.
aim To evaluate the prevalence of anterior and posterior pituitary dysfunction in the early phase following TBI.
subjects Fifty consecutive patients admitted to the neurosurgical unit with severe or moderate TBI [initial Glasgow Coma Scale (GCS) score 3–13], and 31 matched healthy control volunteers were studied.
methods The glucagon stimulation test (GST) was performed at a median of 12 days (range 7–20) following TBI. Baseline thyroid function, PRL, IGF‐1, gonadotrophins, testosterone or oestradiol, plasma sodium, plasma and urine osmolalities or the standard observed water deprivation test were performed. The control subjects underwent the GST for GH and cortisol responses; other parameters were compared to locally derived reference ranges.
results Control data indicated that peak serum GH of > 5 ng/ml and cortisol > 450 nmol/l following glucagon stimulation should be taken as normal. Nine TBI patients (18%) had GH response |
| doi_str_mv | 10.1111/j.1365-2265.2004.02023.x |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_71855442</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>71855442</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5263-1a3e316d00d14f5c11c530b7a05c345ae7b3cb9b5b833e08219093d12f0fd123</originalsourceid><addsrcrecordid>eNqNkMFu1DAQhq0K1G4Lr1BZleCWMLbjOHvggFZlC7Tbw1aC28hxHNVpNlnsWOy-PQm7KhUnfBiPNN8_Gn2EUAYpG9-HJmUilwnnuUw5QJYCBy7S3QmZPQ9ekRkIgATyPDsj5yE0ACALUKfkjEkGmczZjCxXNvredlVvvOssrfahjp0ZXN9R19Hh0VJt4mDp9lEHS_uaDl7HjR6coaXXbqKa6PdvyOtat8G-Pf4X5OHz9cPiJrm9X35ZfLpNjOS5SJgWVrC8AqhYVkvDmJECSqVBGpFJbVUpTDkvZVkIYaHgbA5zUTFeQz1WcUHeH9Zuff8z2jDgxgVj21Z3to8BFSukzLIJvPoHbProu_E0ZPOi4CqTaoSKA2R8H4K3NW6922i_RwY4icYGJ584-cRJNP4RjbsxenncH8uNrf4Gj2ZH4N0R0MHotva6My684JTkXEzcxwP3y7V2_98H4OJ6NXVjPjnkXRjs7jmv_RPmSiiJ31dL_LFar799Xa_xTvwGB0-m3g</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>198827457</pqid></control><display><type>article</type><title>Neuroendocrine dysfunction in the acute phase of traumatic brain injury</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><creator>Agha, Amar ; Rogers, Bairbre ; Mylotte, Darren ; Taleb, Faisal ; Tormey, William ; Phillips, Jack ; Thompson, Christopher J.</creator><creatorcontrib>Agha, Amar ; Rogers, Bairbre ; Mylotte, Darren ; Taleb, Faisal ; Tormey, William ; Phillips, Jack ; Thompson, Christopher J.</creatorcontrib><description>Summary
background Pituitary hormone abnormalities have been reported in up to 50% of survivors of traumatic brain injury (TBI) who were investigated several months or longer following the event. The frequency of pituitary dysfunction in the early post‐TBI period is unknown.
aim To evaluate the prevalence of anterior and posterior pituitary dysfunction in the early phase following TBI.
subjects Fifty consecutive patients admitted to the neurosurgical unit with severe or moderate TBI [initial Glasgow Coma Scale (GCS) score 3–13], and 31 matched healthy control volunteers were studied.
methods The glucagon stimulation test (GST) was performed at a median of 12 days (range 7–20) following TBI. Baseline thyroid function, PRL, IGF‐1, gonadotrophins, testosterone or oestradiol, plasma sodium, plasma and urine osmolalities or the standard observed water deprivation test were performed. The control subjects underwent the GST for GH and cortisol responses; other parameters were compared to locally derived reference ranges.
results Control data indicated that peak serum GH of > 5 ng/ml and cortisol > 450 nmol/l following glucagon stimulation should be taken as normal. Nine TBI patients (18%) had GH response < 5 ng/ml (12 mU/l). Eight patients (16%) had peak cortisol responses < 450 nmol/l. Compared to controls, basal cortisol values were significantly lower in patients with subnormal cortisol responses to glucagon and significantly higher in patients with normal cortisol responses (P < 0·05). GH and cortisol deficiencies were unrelated to patient age, BMI, initial GCS or IGF‐1 values (P > 0·05). Forty patients (80%) had gonadotrophin deficiency, with low sex steroid concentrations, which was unrelated to the presence of hyperprolactinaemia. In males there was a positive correlation between serum testosterone concentration and GCS (r = 0·32, P = 0·04). One patient had TSH deficiency. Hyperprolactinaemia was present in 26 patients (52%) and serum PRL levels correlated negatively with the GCS score (r =−0·36, P = 0·011). Thirteen patients (26%) had cranial diabetes insipidus (DI) and seven (14%) had syndrome of inappropriate ADH secretion.
conclusion Our data show that post‐traumatic neuroendocrine abnormalities occur early and with high frequency, which may have significant implications for recovery and rehabilitation of TBI patients.</description><identifier>ISSN: 0300-0664</identifier><identifier>EISSN: 1365-2265</identifier><identifier>DOI: 10.1111/j.1365-2265.2004.02023.x</identifier><identifier>PMID: 15104561</identifier><identifier>CODEN: CLECAP</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Science Ltd</publisher><subject>Acute Disease ; Adult ; Biological and medical sciences ; Brain Injuries - blood ; Brain Injuries - physiopathology ; Case-Control Studies ; Endocrinopathies ; Estradiol - blood ; Female ; Fundamental and applied biological sciences. Psychology ; Glucagon ; Human Growth Hormone - blood ; Humans ; Hydrocortisone - blood ; Insulin-Like Growth Factor I - analysis ; Logistic Models ; Male ; Medical sciences ; Middle Aged ; Pituitary Gland - physiopathology ; Pituitary Hormones - blood ; Testosterone - blood ; Vertebrates: endocrinology ; Water Deprivation</subject><ispartof>Clinical endocrinology (Oxford), 2004-05, Vol.60 (5), p.584-591</ispartof><rights>2004 INIST-CNRS</rights><rights>Copyright Blackwell Scientific Publications Ltd. May 2004</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5263-1a3e316d00d14f5c11c530b7a05c345ae7b3cb9b5b833e08219093d12f0fd123</citedby><cites>FETCH-LOGICAL-c5263-1a3e316d00d14f5c11c530b7a05c345ae7b3cb9b5b833e08219093d12f0fd123</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1365-2265.2004.02023.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1365-2265.2004.02023.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15752231$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15104561$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Agha, Amar</creatorcontrib><creatorcontrib>Rogers, Bairbre</creatorcontrib><creatorcontrib>Mylotte, Darren</creatorcontrib><creatorcontrib>Taleb, Faisal</creatorcontrib><creatorcontrib>Tormey, William</creatorcontrib><creatorcontrib>Phillips, Jack</creatorcontrib><creatorcontrib>Thompson, Christopher J.</creatorcontrib><title>Neuroendocrine dysfunction in the acute phase of traumatic brain injury</title><title>Clinical endocrinology (Oxford)</title><addtitle>Clin Endocrinol (Oxf)</addtitle><description>Summary
background Pituitary hormone abnormalities have been reported in up to 50% of survivors of traumatic brain injury (TBI) who were investigated several months or longer following the event. The frequency of pituitary dysfunction in the early post‐TBI period is unknown.
aim To evaluate the prevalence of anterior and posterior pituitary dysfunction in the early phase following TBI.
subjects Fifty consecutive patients admitted to the neurosurgical unit with severe or moderate TBI [initial Glasgow Coma Scale (GCS) score 3–13], and 31 matched healthy control volunteers were studied.
methods The glucagon stimulation test (GST) was performed at a median of 12 days (range 7–20) following TBI. Baseline thyroid function, PRL, IGF‐1, gonadotrophins, testosterone or oestradiol, plasma sodium, plasma and urine osmolalities or the standard observed water deprivation test were performed. The control subjects underwent the GST for GH and cortisol responses; other parameters were compared to locally derived reference ranges.
results Control data indicated that peak serum GH of > 5 ng/ml and cortisol > 450 nmol/l following glucagon stimulation should be taken as normal. Nine TBI patients (18%) had GH response < 5 ng/ml (12 mU/l). Eight patients (16%) had peak cortisol responses < 450 nmol/l. Compared to controls, basal cortisol values were significantly lower in patients with subnormal cortisol responses to glucagon and significantly higher in patients with normal cortisol responses (P < 0·05). GH and cortisol deficiencies were unrelated to patient age, BMI, initial GCS or IGF‐1 values (P > 0·05). Forty patients (80%) had gonadotrophin deficiency, with low sex steroid concentrations, which was unrelated to the presence of hyperprolactinaemia. In males there was a positive correlation between serum testosterone concentration and GCS (r = 0·32, P = 0·04). One patient had TSH deficiency. Hyperprolactinaemia was present in 26 patients (52%) and serum PRL levels correlated negatively with the GCS score (r =−0·36, P = 0·011). Thirteen patients (26%) had cranial diabetes insipidus (DI) and seven (14%) had syndrome of inappropriate ADH secretion.
conclusion Our data show that post‐traumatic neuroendocrine abnormalities occur early and with high frequency, which may have significant implications for recovery and rehabilitation of TBI patients.</description><subject>Acute Disease</subject><subject>Adult</subject><subject>Biological and medical sciences</subject><subject>Brain Injuries - blood</subject><subject>Brain Injuries - physiopathology</subject><subject>Case-Control Studies</subject><subject>Endocrinopathies</subject><subject>Estradiol - blood</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Glucagon</subject><subject>Human Growth Hormone - blood</subject><subject>Humans</subject><subject>Hydrocortisone - blood</subject><subject>Insulin-Like Growth Factor I - analysis</subject><subject>Logistic Models</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Pituitary Gland - physiopathology</subject><subject>Pituitary Hormones - blood</subject><subject>Testosterone - blood</subject><subject>Vertebrates: endocrinology</subject><subject>Water Deprivation</subject><issn>0300-0664</issn><issn>1365-2265</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkMFu1DAQhq0K1G4Lr1BZleCWMLbjOHvggFZlC7Tbw1aC28hxHNVpNlnsWOy-PQm7KhUnfBiPNN8_Gn2EUAYpG9-HJmUilwnnuUw5QJYCBy7S3QmZPQ9ekRkIgATyPDsj5yE0ACALUKfkjEkGmczZjCxXNvredlVvvOssrfahjp0ZXN9R19Hh0VJt4mDp9lEHS_uaDl7HjR6coaXXbqKa6PdvyOtat8G-Pf4X5OHz9cPiJrm9X35ZfLpNjOS5SJgWVrC8AqhYVkvDmJECSqVBGpFJbVUpTDkvZVkIYaHgbA5zUTFeQz1WcUHeH9Zuff8z2jDgxgVj21Z3to8BFSukzLIJvPoHbProu_E0ZPOi4CqTaoSKA2R8H4K3NW6922i_RwY4icYGJ584-cRJNP4RjbsxenncH8uNrf4Gj2ZH4N0R0MHotva6My684JTkXEzcxwP3y7V2_98H4OJ6NXVjPjnkXRjs7jmv_RPmSiiJ31dL_LFar799Xa_xTvwGB0-m3g</recordid><startdate>200405</startdate><enddate>200405</enddate><creator>Agha, Amar</creator><creator>Rogers, Bairbre</creator><creator>Mylotte, Darren</creator><creator>Taleb, Faisal</creator><creator>Tormey, William</creator><creator>Phillips, Jack</creator><creator>Thompson, Christopher J.</creator><general>Blackwell Science Ltd</general><general>Blackwell</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope></search><sort><creationdate>200405</creationdate><title>Neuroendocrine dysfunction in the acute phase of traumatic brain injury</title><author>Agha, Amar ; Rogers, Bairbre ; Mylotte, Darren ; Taleb, Faisal ; Tormey, William ; Phillips, Jack ; Thompson, Christopher J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5263-1a3e316d00d14f5c11c530b7a05c345ae7b3cb9b5b833e08219093d12f0fd123</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Acute Disease</topic><topic>Adult</topic><topic>Biological and medical sciences</topic><topic>Brain Injuries - blood</topic><topic>Brain Injuries - physiopathology</topic><topic>Case-Control Studies</topic><topic>Endocrinopathies</topic><topic>Estradiol - blood</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Glucagon</topic><topic>Human Growth Hormone - blood</topic><topic>Humans</topic><topic>Hydrocortisone - blood</topic><topic>Insulin-Like Growth Factor I - analysis</topic><topic>Logistic Models</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Pituitary Gland - physiopathology</topic><topic>Pituitary Hormones - blood</topic><topic>Testosterone - blood</topic><topic>Vertebrates: endocrinology</topic><topic>Water Deprivation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Agha, Amar</creatorcontrib><creatorcontrib>Rogers, Bairbre</creatorcontrib><creatorcontrib>Mylotte, Darren</creatorcontrib><creatorcontrib>Taleb, Faisal</creatorcontrib><creatorcontrib>Tormey, William</creatorcontrib><creatorcontrib>Phillips, Jack</creatorcontrib><creatorcontrib>Thompson, Christopher J.</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Clinical endocrinology (Oxford)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Agha, Amar</au><au>Rogers, Bairbre</au><au>Mylotte, Darren</au><au>Taleb, Faisal</au><au>Tormey, William</au><au>Phillips, Jack</au><au>Thompson, Christopher J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Neuroendocrine dysfunction in the acute phase of traumatic brain injury</atitle><jtitle>Clinical endocrinology (Oxford)</jtitle><addtitle>Clin Endocrinol (Oxf)</addtitle><date>2004-05</date><risdate>2004</risdate><volume>60</volume><issue>5</issue><spage>584</spage><epage>591</epage><pages>584-591</pages><issn>0300-0664</issn><eissn>1365-2265</eissn><coden>CLECAP</coden><abstract>Summary
background Pituitary hormone abnormalities have been reported in up to 50% of survivors of traumatic brain injury (TBI) who were investigated several months or longer following the event. The frequency of pituitary dysfunction in the early post‐TBI period is unknown.
aim To evaluate the prevalence of anterior and posterior pituitary dysfunction in the early phase following TBI.
subjects Fifty consecutive patients admitted to the neurosurgical unit with severe or moderate TBI [initial Glasgow Coma Scale (GCS) score 3–13], and 31 matched healthy control volunteers were studied.
methods The glucagon stimulation test (GST) was performed at a median of 12 days (range 7–20) following TBI. Baseline thyroid function, PRL, IGF‐1, gonadotrophins, testosterone or oestradiol, plasma sodium, plasma and urine osmolalities or the standard observed water deprivation test were performed. The control subjects underwent the GST for GH and cortisol responses; other parameters were compared to locally derived reference ranges.
results Control data indicated that peak serum GH of > 5 ng/ml and cortisol > 450 nmol/l following glucagon stimulation should be taken as normal. Nine TBI patients (18%) had GH response < 5 ng/ml (12 mU/l). Eight patients (16%) had peak cortisol responses < 450 nmol/l. Compared to controls, basal cortisol values were significantly lower in patients with subnormal cortisol responses to glucagon and significantly higher in patients with normal cortisol responses (P < 0·05). GH and cortisol deficiencies were unrelated to patient age, BMI, initial GCS or IGF‐1 values (P > 0·05). Forty patients (80%) had gonadotrophin deficiency, with low sex steroid concentrations, which was unrelated to the presence of hyperprolactinaemia. In males there was a positive correlation between serum testosterone concentration and GCS (r = 0·32, P = 0·04). One patient had TSH deficiency. Hyperprolactinaemia was present in 26 patients (52%) and serum PRL levels correlated negatively with the GCS score (r =−0·36, P = 0·011). Thirteen patients (26%) had cranial diabetes insipidus (DI) and seven (14%) had syndrome of inappropriate ADH secretion.
conclusion Our data show that post‐traumatic neuroendocrine abnormalities occur early and with high frequency, which may have significant implications for recovery and rehabilitation of TBI patients.</abstract><cop>Oxford, UK</cop><pub>Blackwell Science Ltd</pub><pmid>15104561</pmid><doi>10.1111/j.1365-2265.2004.02023.x</doi><tpages>8</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0300-0664 |
| ispartof | Clinical endocrinology (Oxford), 2004-05, Vol.60 (5), p.584-591 |
| issn | 0300-0664 1365-2265 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_71855442 |
| source | MEDLINE; Wiley Online Library Journals Frontfile Complete |
| subjects | Acute Disease Adult Biological and medical sciences Brain Injuries - blood Brain Injuries - physiopathology Case-Control Studies Endocrinopathies Estradiol - blood Female Fundamental and applied biological sciences. Psychology Glucagon Human Growth Hormone - blood Humans Hydrocortisone - blood Insulin-Like Growth Factor I - analysis Logistic Models Male Medical sciences Middle Aged Pituitary Gland - physiopathology Pituitary Hormones - blood Testosterone - blood Vertebrates: endocrinology Water Deprivation |
| title | Neuroendocrine dysfunction in the acute phase of traumatic brain injury |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-20T20%3A00%3A40IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Neuroendocrine%20dysfunction%20in%20the%20acute%20phase%20of%20traumatic%20brain%20injury&rft.jtitle=Clinical%20endocrinology%20(Oxford)&rft.au=Agha,%20Amar&rft.date=2004-05&rft.volume=60&rft.issue=5&rft.spage=584&rft.epage=591&rft.pages=584-591&rft.issn=0300-0664&rft.eissn=1365-2265&rft.coden=CLECAP&rft_id=info:doi/10.1111/j.1365-2265.2004.02023.x&rft_dat=%3Cproquest_cross%3E71855442%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=198827457&rft_id=info:pmid/15104561&rfr_iscdi=true |