Hypogonadism in Rhodesian sleeping sickness: evidence for acute and chronic dysfunction of the hypothalamic-pituitary-gonadal axis
To investigate acute and long-term effects of Rhodesian sleeping sickness on the function of the hypothalamic-pituitary-gonadal (HPG) axis in men. An observational, cross-sectional study. Primary health care centers under care of the National Sleeping Sickness Control Program in southeast Uganda. Fi...
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Veröffentlicht in: | Fertility and sterility 1996-01, Vol.65 (1), p.68-75 |
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creator | Petzke, Frank Heppner, Christina Mbulamberi, Dawson Winkelmann, Werner Chrousos, George P. Allolio, Bruno Reincke, Martin |
description | To investigate acute and long-term effects of Rhodesian sleeping sickness on the function of the hypothalamic-pituitary-gonadal (HPG) axis in men.
An observational, cross-sectional study.
Primary health care centers under care of the National Sleeping Sickness Control Program in southeast Uganda.
Fifty-two male patients with sleeping sickness at different stages of treatment and 11 clinically healthy male volunteers recruited from health care personnel.
Patients and controls were questioned about loss of libido and impotence. All received 100 μg GnRH IV. Blood was drawn before and 30 minutes after GnRH administration.
Frequency of loss of libido and impotence. Baseline T and sex hormone-binding globulin baseline and GnRH-stimulated serum LH and FSH concentrations.
Loss of libido and/or impotence were present in 39% of men with active disease before therapy, whereas 84% were biochemically hypogonadal. After cure, 45% of men still were symptomatic and 45% were biochemically hypogonadal. Compared with controls (806±59 pg/mL [conversion factor to SI unit, 0.03467]; mean±SEM), T concentrations were decreased substantially in patients before (249±48 ng/dL), during treatment (429±56 ng/dL), and after cure (431±58 ng/dL). Corresponding baseline LH concentrations were inappropriately low and the relative LH response to GnRH was reduced both before and during treatment (794%±131% versus 322%±68%). Follicle-stimulating hormone concentrations increased gradually up to 8.0±1.3 mIU/mL (conversion factor to SI unit, 1.00) at the end of treatment, returning to 4.2±0.6 mIU/mL after cure.
Rhodesian sleeping sickness causes acute and chronic HPG axis dysfunction. The clinical and biochemical picture suggest a combined central and peripheral hypogonadism. This is only in part reversible after cure and most likely due to direct parasitic infiltration and/or secondary inflammation causing necrosis and/or fibrosis at the pituitary and gonadal levels. |
doi_str_mv | 10.1016/S0015-0282(16)58029-7 |
format | Article |
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An observational, cross-sectional study.
Primary health care centers under care of the National Sleeping Sickness Control Program in southeast Uganda.
Fifty-two male patients with sleeping sickness at different stages of treatment and 11 clinically healthy male volunteers recruited from health care personnel.
Patients and controls were questioned about loss of libido and impotence. All received 100 μg GnRH IV. Blood was drawn before and 30 minutes after GnRH administration.
Frequency of loss of libido and impotence. Baseline T and sex hormone-binding globulin baseline and GnRH-stimulated serum LH and FSH concentrations.
Loss of libido and/or impotence were present in 39% of men with active disease before therapy, whereas 84% were biochemically hypogonadal. After cure, 45% of men still were symptomatic and 45% were biochemically hypogonadal. Compared with controls (806±59 pg/mL [conversion factor to SI unit, 0.03467]; mean±SEM), T concentrations were decreased substantially in patients before (249±48 ng/dL), during treatment (429±56 ng/dL), and after cure (431±58 ng/dL). Corresponding baseline LH concentrations were inappropriately low and the relative LH response to GnRH was reduced both before and during treatment (794%±131% versus 322%±68%). Follicle-stimulating hormone concentrations increased gradually up to 8.0±1.3 mIU/mL (conversion factor to SI unit, 1.00) at the end of treatment, returning to 4.2±0.6 mIU/mL after cure.
Rhodesian sleeping sickness causes acute and chronic HPG axis dysfunction. The clinical and biochemical picture suggest a combined central and peripheral hypogonadism. This is only in part reversible after cure and most likely due to direct parasitic infiltration and/or secondary inflammation causing necrosis and/or fibrosis at the pituitary and gonadal levels.</description><identifier>ISSN: 0015-0282</identifier><identifier>EISSN: 1556-5653</identifier><identifier>DOI: 10.1016/S0015-0282(16)58029-7</identifier><identifier>PMID: 8557157</identifier><identifier>CODEN: FESTAS</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Adult ; Animals ; Biological and medical sciences ; Cross-Sectional Studies ; Erectile Dysfunction - etiology ; Follicle Stimulating Hormone - blood ; FSH ; Human protozoal diseases ; Humans ; hypogonadism ; Hypogonadism - etiology ; hypothalamic-pituitary-gonadal axis ; Hypothalamo-Hypophyseal System - physiopathology ; Infectious diseases ; Luteinizing Hormone - blood ; Male ; Medical sciences ; Middle Aged ; Parasitic diseases ; Protozoal diseases ; Sex Hormone-Binding Globulin - analysis ; Testis - physiopathology ; testosterone ; Testosterone - blood ; Trypanosoma brucei rhodesiense ; Trypanosomiasis ; Trypanosomiasis, African - physiopathology</subject><ispartof>Fertility and sterility, 1996-01, Vol.65 (1), p.68-75</ispartof><rights>1996 American Society for Reproductive Medicine</rights><rights>1996 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c436t-f7ff7135c79c5a12e9fdbdf90ab4291843f627e79fa407b8a704dae4bb2e07d13</citedby><cites>FETCH-LOGICAL-c436t-f7ff7135c79c5a12e9fdbdf90ab4291843f627e79fa407b8a704dae4bb2e07d13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0015-0282(16)58029-7$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>315,781,785,3551,4025,27928,27929,27930,46000</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2982527$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8557157$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Petzke, Frank</creatorcontrib><creatorcontrib>Heppner, Christina</creatorcontrib><creatorcontrib>Mbulamberi, Dawson</creatorcontrib><creatorcontrib>Winkelmann, Werner</creatorcontrib><creatorcontrib>Chrousos, George P.</creatorcontrib><creatorcontrib>Allolio, Bruno</creatorcontrib><creatorcontrib>Reincke, Martin</creatorcontrib><title>Hypogonadism in Rhodesian sleeping sickness: evidence for acute and chronic dysfunction of the hypothalamic-pituitary-gonadal axis</title><title>Fertility and sterility</title><addtitle>Fertil Steril</addtitle><description>To investigate acute and long-term effects of Rhodesian sleeping sickness on the function of the hypothalamic-pituitary-gonadal (HPG) axis in men.
An observational, cross-sectional study.
Primary health care centers under care of the National Sleeping Sickness Control Program in southeast Uganda.
Fifty-two male patients with sleeping sickness at different stages of treatment and 11 clinically healthy male volunteers recruited from health care personnel.
Patients and controls were questioned about loss of libido and impotence. All received 100 μg GnRH IV. Blood was drawn before and 30 minutes after GnRH administration.
Frequency of loss of libido and impotence. Baseline T and sex hormone-binding globulin baseline and GnRH-stimulated serum LH and FSH concentrations.
Loss of libido and/or impotence were present in 39% of men with active disease before therapy, whereas 84% were biochemically hypogonadal. After cure, 45% of men still were symptomatic and 45% were biochemically hypogonadal. Compared with controls (806±59 pg/mL [conversion factor to SI unit, 0.03467]; mean±SEM), T concentrations were decreased substantially in patients before (249±48 ng/dL), during treatment (429±56 ng/dL), and after cure (431±58 ng/dL). Corresponding baseline LH concentrations were inappropriately low and the relative LH response to GnRH was reduced both before and during treatment (794%±131% versus 322%±68%). Follicle-stimulating hormone concentrations increased gradually up to 8.0±1.3 mIU/mL (conversion factor to SI unit, 1.00) at the end of treatment, returning to 4.2±0.6 mIU/mL after cure.
Rhodesian sleeping sickness causes acute and chronic HPG axis dysfunction. The clinical and biochemical picture suggest a combined central and peripheral hypogonadism. This is only in part reversible after cure and most likely due to direct parasitic infiltration and/or secondary inflammation causing necrosis and/or fibrosis at the pituitary and gonadal levels.</description><subject>Adult</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cross-Sectional Studies</subject><subject>Erectile Dysfunction - etiology</subject><subject>Follicle Stimulating Hormone - blood</subject><subject>FSH</subject><subject>Human protozoal diseases</subject><subject>Humans</subject><subject>hypogonadism</subject><subject>Hypogonadism - etiology</subject><subject>hypothalamic-pituitary-gonadal axis</subject><subject>Hypothalamo-Hypophyseal System - physiopathology</subject><subject>Infectious diseases</subject><subject>Luteinizing Hormone - blood</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Parasitic diseases</subject><subject>Protozoal diseases</subject><subject>Sex Hormone-Binding Globulin - analysis</subject><subject>Testis - physiopathology</subject><subject>testosterone</subject><subject>Testosterone - blood</subject><subject>Trypanosoma brucei rhodesiense</subject><subject>Trypanosomiasis</subject><subject>Trypanosomiasis, African - physiopathology</subject><issn>0015-0282</issn><issn>1556-5653</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkM-L1TAQx4Mo63P1T1jIQUQP1SRtmtaLyKKusCD44xzSZLIdbZOatIvv6l9u-97jXT0Nw3xm5suHkCvOXnPG6zffGOOyYKIRL3n9SjZMtIV6QHZcyrqQtSwfkt0ZeUye5PyTMVZzJS7IRSOl4lLtyN-b_RTvYjAO80gx0K99dJDRBJoHgAnDHc1ofwXI-S2Fe3QQLFAfEzV2mYGa4KjtUwxoqdtnvwQ7Yww0ejr3QPv1_NybwYxoiwnnBWeT9sXhoxmo-YP5KXnkzZDh2alekh8fP3y_viluv3z6fP3-trBVWc-FV94rXkqrWisNF9B61znfMtNVouVNVfpaKFCtNxVTXWMUq5yBqusEMOV4eUleHO9OKf5eIM96xGxhGEyAuGStVLv6qjZQHkGbYs4JvJ4SjmtszZne3OuDe72J1Wt3cK_Vund1erB0I7jz1kn2On9-mptszeCTCRbzGRNtI6TYsHdHDFYZ9whJZ4ubdYcJ7KxdxP8E-QcL_6O3</recordid><startdate>199601</startdate><enddate>199601</enddate><creator>Petzke, Frank</creator><creator>Heppner, Christina</creator><creator>Mbulamberi, Dawson</creator><creator>Winkelmann, Werner</creator><creator>Chrousos, George P.</creator><creator>Allolio, Bruno</creator><creator>Reincke, Martin</creator><general>Elsevier Inc</general><general>Elsevier Science</general><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>7X8</scope></search><sort><creationdate>199601</creationdate><title>Hypogonadism in Rhodesian sleeping sickness: evidence for acute and chronic dysfunction of the hypothalamic-pituitary-gonadal axis</title><author>Petzke, Frank ; Heppner, Christina ; Mbulamberi, Dawson ; Winkelmann, Werner ; Chrousos, George P. ; Allolio, Bruno ; Reincke, Martin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c436t-f7ff7135c79c5a12e9fdbdf90ab4291843f627e79fa407b8a704dae4bb2e07d13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>Adult</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cross-Sectional Studies</topic><topic>Erectile Dysfunction - etiology</topic><topic>Follicle Stimulating Hormone - blood</topic><topic>FSH</topic><topic>Human protozoal diseases</topic><topic>Humans</topic><topic>hypogonadism</topic><topic>Hypogonadism - etiology</topic><topic>hypothalamic-pituitary-gonadal axis</topic><topic>Hypothalamo-Hypophyseal System - physiopathology</topic><topic>Infectious diseases</topic><topic>Luteinizing Hormone - blood</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Parasitic diseases</topic><topic>Protozoal diseases</topic><topic>Sex Hormone-Binding Globulin - analysis</topic><topic>Testis - physiopathology</topic><topic>testosterone</topic><topic>Testosterone - blood</topic><topic>Trypanosoma brucei rhodesiense</topic><topic>Trypanosomiasis</topic><topic>Trypanosomiasis, African - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Petzke, Frank</creatorcontrib><creatorcontrib>Heppner, Christina</creatorcontrib><creatorcontrib>Mbulamberi, Dawson</creatorcontrib><creatorcontrib>Winkelmann, Werner</creatorcontrib><creatorcontrib>Chrousos, George P.</creatorcontrib><creatorcontrib>Allolio, Bruno</creatorcontrib><creatorcontrib>Reincke, Martin</creatorcontrib><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>MEDLINE - Academic</collection><jtitle>Fertility and sterility</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Petzke, Frank</au><au>Heppner, Christina</au><au>Mbulamberi, Dawson</au><au>Winkelmann, Werner</au><au>Chrousos, George P.</au><au>Allolio, Bruno</au><au>Reincke, Martin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hypogonadism in Rhodesian sleeping sickness: evidence for acute and chronic dysfunction of the hypothalamic-pituitary-gonadal axis</atitle><jtitle>Fertility and sterility</jtitle><addtitle>Fertil Steril</addtitle><date>1996-01</date><risdate>1996</risdate><volume>65</volume><issue>1</issue><spage>68</spage><epage>75</epage><pages>68-75</pages><issn>0015-0282</issn><eissn>1556-5653</eissn><coden>FESTAS</coden><abstract>To investigate acute and long-term effects of Rhodesian sleeping sickness on the function of the hypothalamic-pituitary-gonadal (HPG) axis in men.
An observational, cross-sectional study.
Primary health care centers under care of the National Sleeping Sickness Control Program in southeast Uganda.
Fifty-two male patients with sleeping sickness at different stages of treatment and 11 clinically healthy male volunteers recruited from health care personnel.
Patients and controls were questioned about loss of libido and impotence. All received 100 μg GnRH IV. Blood was drawn before and 30 minutes after GnRH administration.
Frequency of loss of libido and impotence. Baseline T and sex hormone-binding globulin baseline and GnRH-stimulated serum LH and FSH concentrations.
Loss of libido and/or impotence were present in 39% of men with active disease before therapy, whereas 84% were biochemically hypogonadal. After cure, 45% of men still were symptomatic and 45% were biochemically hypogonadal. Compared with controls (806±59 pg/mL [conversion factor to SI unit, 0.03467]; mean±SEM), T concentrations were decreased substantially in patients before (249±48 ng/dL), during treatment (429±56 ng/dL), and after cure (431±58 ng/dL). Corresponding baseline LH concentrations were inappropriately low and the relative LH response to GnRH was reduced both before and during treatment (794%±131% versus 322%±68%). Follicle-stimulating hormone concentrations increased gradually up to 8.0±1.3 mIU/mL (conversion factor to SI unit, 1.00) at the end of treatment, returning to 4.2±0.6 mIU/mL after cure.
Rhodesian sleeping sickness causes acute and chronic HPG axis dysfunction. The clinical and biochemical picture suggest a combined central and peripheral hypogonadism. This is only in part reversible after cure and most likely due to direct parasitic infiltration and/or secondary inflammation causing necrosis and/or fibrosis at the pituitary and gonadal levels.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>8557157</pmid><doi>10.1016/S0015-0282(16)58029-7</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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source | MEDLINE; Access via ScienceDirect (Elsevier); Alma/SFX Local Collection; EZB Electronic Journals Library |
subjects | Adult Animals Biological and medical sciences Cross-Sectional Studies Erectile Dysfunction - etiology Follicle Stimulating Hormone - blood FSH Human protozoal diseases Humans hypogonadism Hypogonadism - etiology hypothalamic-pituitary-gonadal axis Hypothalamo-Hypophyseal System - physiopathology Infectious diseases Luteinizing Hormone - blood Male Medical sciences Middle Aged Parasitic diseases Protozoal diseases Sex Hormone-Binding Globulin - analysis Testis - physiopathology testosterone Testosterone - blood Trypanosoma brucei rhodesiense Trypanosomiasis Trypanosomiasis, African - physiopathology |
title | Hypogonadism in Rhodesian sleeping sickness: evidence for acute and chronic dysfunction of the hypothalamic-pituitary-gonadal axis |
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