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Eine seltene, aber bei Männern wichtige Differenzialdiagnose der Polyglobulie ist die testosteronbedingte Polyglobulie.
Die Therapie der primären Polyglobulie wird im Artikel Polycythaemia vera
besprochen. Bei sekundären Polyglobulien muss die Grunderkrankung behandelt werden.
DHT entsteht beim Abbau von Testosteron und ist das biologisch
wirksamere Hormon. Es kann zu dem sogenannten erblich bedingten Haar­ausfall
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Grund hierfür ist die erhöhte Empfindlichkeit der Haarwurzeln gegenüber Dihydrotes­tosteron,
die eine verstärkte Schädigung und Schwächung der Haarfollikel bedingt.


Ein niedriger P50-Wert (PO2 bei 50% Sättigung) in der Blutgasanalyse spiegelt eine hohe Hb-Sauerstoffaffinität wider (5).

Die JAK2-Mutationen können primär aus dem
peripheren Blut getestet werden. Seine Produktion – angeregt
durch das luteinisierende Hormon (LH) aus
der Hirnanhangdrüse – findet hauptsächlich in den Leydigschen Zwischenzellen der
Hoden statt.
Im hoden testosteron reaktivieren spielt Testosteron eine wesentliche Rolle bei der Spermatogenese.
Über diese androgene Wirkung hinaus werden Sexualverhalten und -aktivität
beim Mann beeinflusst. Dementsprechend vielgestaltig ist die klinische Ausprägung eines Testosteronmangels.
Die Substitutionsbehandlung mit Testosteronpräparaten ist in der Praxis fest etabliert.
Therapienutzen und Risiken müssen jedoch je nach Indikation sorgfältig abgewogen werden.
Während bei der Schlafapnoe im Allgemeinen keine Erythropoietin-Erhöhung beobachtet wird, ist dies bei
der COPD bei einem Absinken des Sauerstoffpartial-drucks unter sixty seven mmHg der Fall.
Von Ausdauersportlern wird dies im sogenannten Höhentraining ausgenutzt.
Prinzipiell treten die erworbenen Formen der JAK2-unmutierten Polyzythämie am häufigsten im klinischen Alltag auf.
In der Universitätsklinik der Hämatologie des Inselspitals Bern wurde eine
Studie durchgeführt, in welcher die Epidemiologie,
Ursachen und die Komplikationen der JAK2-unmutierten Polyzythämie analysiert wurden (1).
730’000, welche am Inselspital über fast
eleven Jahre (Oktober 2008 – Juli 2019) in Behandlung waren, untersucht, und davon ca.

Auf den Einsatz zytoreduktiver Medikamente mit leukämogenem Risikoprofil sollte insbesondere bei
jungen Patienten verzichtet werden. Das 20-Jahres-Risiko eines Übergangs
in eine postpolyzythämische Myelofibrose, das
heißt eine Verfaserung des Knochenmarks mit zunehmender Auswanderung der Hämatopoese in Milz und Leber, betrug
in der Studie 10 % (12). Da die angeborenen Polyzythämien und die sekundäre Polyzythämie bei zyanotischen kongenitalen Herzerkrankungen selten hämatologische Behandlung erfordern, wird im Folgenden nur die Therapie der PV dargestellt.
Ziel ist es, die PV-assoziierten potenziell lebensbedrohlichen thromboembolischen und Blutungskomplikationen sowie die auftretenden unspezifischen Symptome zu mindern.
Die kongenitalen Erythrozytosen benötigen aus
hämatologischer Sicht ebenfalls meistens keine spezifische Therapie und sind nicht mit erhöhtem
Risiko für Thrombosen oder Transformation in eine andere
Erkrankung verbunden. Die Ausnahme ist die Chuvah Erythrozytose (VHL-mutiert), da diese
für eine Thrombosetendenz bekannt ist. Mit der Zunahme der Testung für
die kongenitalen Erythrozytosen sowie einer besseren Datenlage, können hoffentlich zukünftig
die klaren Managementstrategien etabliert werden. Um die Mutation,
welche für die kongenitale Erythrozytose verantwortlich ist,
zu untersuchen, muss eine molekulare Testung durchgeführt werden. Diese kann vom peripherenBlut erfolgen und mit NGS
durchgeführt werden.
1’400 Patienten, welche die Hb/Hkt WHO Kriterien für PV erfüllt haben, identifiziert.
Mit der Entdeckung von JAK2-Treibermutationen im Jahr 2005
und breit verfügbaren Methoden zur Testung stellt die PV meist keine diagnostische
Schwierigkeit mehr dar. Eine diagnostische Herausforderung ist dagegen die JAK2-unmutierte d.h.
JAK-2 negative Polyzythämie, welche eine heterogene Gruppe von Entitäten umfasst.
Produziert der Körper nicht genügend Testosteron, kann eine Substitutions­therapie mit
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