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Comments(5)
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The mutations that define the subclade N-M46[Phylogenetics 2] are M46/Tat and
P105. It appears that Flück and coworkers (2025) have selectively learn our article and seems that have been they who interpreted
our conclusions in a biased and subjective trend.
The function of biological gender and ethnicity is indeed established in sport
efficiency. Their criticism lies on the reality that confounding factors corresponding to ethnicity and organic gender weren’t considered in our evaluation and
in accordance with them, this was the weakest point
in our evaluation.
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References:
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comment https://Precise.co.za says
May 19, 2025 at 2:37 amDHT entsteht beim Abbau von Testosteron und ist das biologisch wirksamere
Hormon. Es kann zu dem sogenannten erblich bedingten Haarausfall (der androgenetischen Alopezie) führen, worunter
etwa die Hälfte aller Männer ab einem bestimmten Alter in unterschiedlicher Ausprägung leidet.
Grund hierfür ist die erhöhte Empfindlichkeit der
Haarwurzeln gegenüber Dihydrotestosteron, die eine verstärkte Schädigung und
Schwächung der Haarfollikel bedingt.
Der Prozess der Andropause und ihre hormonellen Veränderungen verläuft langsamer
– quasi schleichend – und wird daher häufig nicht erkannt.
Bei unbehandeltem Prostatakrebs sollte auf eine Testosteronsubstitution verzichtet
werden. Auch bei den extrem seltenen Fällen von männlichem
Brustkrebs sollte keine testosteron propionat fettverbrennung (https://Precise.co.za)behandlung
erfolgen. Neben Erythropoetin ist auch Cortisol ein Erythropoese-stimulierendes
Hormon. Erhöhte Cortisolspiegel als Ausdruck eines Cushing-Syndroms oder eines Morbus Cushing können somit ebenfalls eine Polyglobulie verursachen.
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 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.
Allerdings muss die Therapie wegen grippeähnlicher Symptome, Haarausfall und/oder psychiatrischer
Störungen häufig abgebrochen werden (22). Werden die JAK2-spezifischen Mutationen nicht nachgewiesen und ist der EPO-Spiegel regular oder erhöht,
ist eine PV unwahrscheinlich. In diesem Fall sollte nach Tumoren, die
zu einer EPO-Erhöhung führen können, gesucht und
eine primäre Polyzythämie ausgeschlossen werden. Ist die JAK2V617F-Mutation nicht vorhanden und der EPO-Spiegel erniedrigt, sollte danach das Exon 12 auf Mutationen untersucht werden.
Er tritt bei über 60 % der Patienten auf und wird durch Wasser unterschiedlicher Qualität und Temperatur hervorgerufen, teilweise bereits durch
starkes Schwitzen oder Händewaschen. Am besten ist der aquagene Pruritus durch
eine konsequente Therapie der PV (Aderlässe oder zytoreduktive
Therapie) beherrschbar. Bei anhaltendem Pruritus empfehlen die Autoren die
Zugabe von Bicarbonat beziehungsweise Stärke zum Badewasser, wobei unklar ist, wie
die Wirkung zustande kommt. Bei Nichtansprechen stehen Antihistaminika,
Serotoninwiederaufnahmehemmer (zum Beispiel Fluoxetin, Paroxetin) oder die topische Applikation einer Capsaicincreme zur Verfügung.
Bei hartnäckig refraktärem Pruritus bietet sich die Phototherapie
an. Für sie konnte allerdings die Kanzerogenität bisher
nicht ausgeschlossen werden (10). Im Jahre 2005 wurde
unabhängig voneinander von 5 Forschergruppen die JAK2V617F-Mutation in Exon 14 des JAK2-Gens entdeckt (14).
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 adverse Polyzythämie, welche eine heterogene Gruppe von Entitäten umfasst.
Produziert der Körper nicht genügend Testosteron, kann eine Substitutionstherapie mit natürlichem
Testosteron erfolgen.
Aus dieser Beobachtung heraus resultierte die Angst, dass
die Substitution mit Testosteron das Wachstum einer bisher nicht erkannten Prostatakrebserkrankung beschleunigen könne.
Weder wurde vermehrt Prostatakrebs unter einer Testosteronsubstitutionstherapie diagnostiziert, noch besteht bei Männern mit hohen Testosteronspiegeln eine erhöhte Tumorinzidenz.
Hohes Testosteron wird häufig mit vermehrtem Haarausfall in Verbindung gebracht.
Ein Zusammenhang, der in dieser monokausalen Form nicht besteht.Eine hormonelle Ursache für verstärkten Haarausfall kann allerdings eine Erhöhung des Hormons Dihydrotestosteron (DHT) sein.
Die PV ist eine hämatologische, klonale Erkrankung, welche zu der Gruppe der myeloproliferativen Neoplasien (MPN) gehört.
Die PV-Patienten haben ein deutlich erhöhtes Risiko für venöse
und arterielle thromboembolische (auch lebensbedrohliche) Ereignisse.
Zudem besteht bei ihnen ein Risiko für die Entwicklung einer Myelofibrose, einer Type der MPN mit einer
ungünstigeren Prognose. In seltenen Fällen kann die Erkrankung auch
in eine akute myeloische Leukämie (AML) fortschreiten. Gemäss der Klassifikation der Tumorerkrankungen der Weltgesundheitsorganisation (WHO) sowie dem
Internationalen Consensus der Klassifikation (ICC) der MPN aus dem Jahr 2022 gibt
es klare diagnostische Kriterien für die PV (Tab. 1). Prostatakrebszellen sind in der Lage, das Hormon Testosteron für ihr
eigenes Wachstum zu nutzen. Durch Hormonentzug kann es vorübergehend zu einem Stillstand des Tumorwachstums kommen.