देहरादून। उत्तराखंड के हरिद्वार में नए सरकारी मेडिकल कॉलेज की स्थापना को केंद्र सरकार द्वारा 100 एमबीबीएस सीटों के साथ स्वीकृति मिल गई है। यह मेडिकल कॉलेज प्रदेश में चिकित्सा शिक्षा को और सशक्त करेगा और राज्य की जनता को उच्चस्तरीय चिकित्सा सुविधाएं उपलब्ध कराएगा।
स्वास्थ्य विभाग के अनुसार, उत्तराखंड सरकार ने 2024-2025 शैक्षणिक सत्र के लिए 100 एमबीबीएस सीटों के साथ इस नए मेडिकल कॉलेज की स्थापना के लिए प्रस्ताव भेजा था। इसके बाद, नेशनल मेडिकल कमीशन (NMC) की पहली अपील में कॉलेज को कुछ खामियों के आधार पर अस्वीकृति मिली थी। हालांकि, दूसरी अपील में केंद्र सरकार ने इन खामियों की समीक्षा की और नए दस्तावेज़ों और प्रस्तुतियों के आधार पर मेडिकल कॉलेज को मंजूरी दे दी है।
केंद्र सरकार ने बताया कि कॉलेज में वर्तमान में 39 फैकल्टी सदस्य (13 प्रोफेसर, 7 एसोसिएट प्रोफेसर, 19 असिस्टेंट प्रोफेसर) और 26 सीनियर रेजिडेंट्स/ट्यूटर कार्यरत हैं। राज्य सरकार ने यह आश्वासन भी दिया है कि शैक्षणिक सत्र 2024-2025 शुरू होने से पहले सभी आवश्यक फैकल्टी और बुनियादी ढांचे को पूरा कर लिया जाएगा। इसके साथ ही, अस्पताल में पहले से चल रही सेवाओं के साथ-साथ ओपीडी और अन्य चिकित्सा सुविधाएं भी बढ़ाई जाएंगी, जिससे मरीजों को बेहतर उपचार मिलेगा।
मंत्री डॉ. धन सिंह रावत ने कहा कि हरिद्वार में इस मेडिकल कॉलेज की स्थापना से उत्तराखंड में चिकित्सा शिक्षा और स्वास्थ्य सेवाओं में एक बड़ा सुधार होगा। राज्य के मेडिकल कॉलेजों में बढ़ती सीटों के साथ, स्थानीय छात्रों को यहीं पर उच्चस्तरीय चिकित्सा शिक्षा प्राप्त करने का अवसर मिलेगा और प्रदेश में स्वास्थ्य सेवाओं का भी विस्तार होगा।
इस पहल से हरिद्वार और इसके आसपास के क्षेत्रों में चिकित्सा सुविधाओं की पहुंच और गुणवत्ता में उल्लेखनीय सुधार होगा, जिससे क्षेत्र के निवासियों को समय पर और सटीक चिकित्सा सेवाएं मिलेंगी। राज्य सरकार इस मेडिकल कॉलेज के माध्यम से ग्रामीण और दूरदराज के इलाकों में स्वास्थ्य सेवाओं की बेहतर उपलब्धता सुनिश्चित करेगी।
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Bestimmte Mutationen im Bereich der a- beziehungsweise b-Ketten des Hämoglobins können zu Hochaffinitäts-Hämoglobinen führen, die Sauerstoff im peripheren Gewebe in verringertem Maße freisetzen. So liegt bei einem O2-Partialdruck von 20 mm Hg im Kapillarbereich 35 % Oxyhämoglobin vor, wohingegen zum Beispiel beim Hochaffinitäts-Hämoglobin Johnstown noch 60 % oxygeniert sind (Grafik 1). Die dadurch verursachte Verringerung der Sauerstoffabgabe im peripheren Gewebe führt zu einer kompensatorischen Erhöhung der Hämoglobin-Konzentration. Daneben kann auch eine Erniedrigung des intraerythrozytären 2,3-Bisphosphoglyceratspiegels durch 2,3-Bisposphoglyceratmutase-Mangel zu einer erhöhten Sauerstoffaffinität des Hämoglobins führen.
Während bei der Schlafapnoe im Allgemeinen keine Erythropoietin-Erhöhung beobachtet wird, ist dies bei der COPD bei einem Absinken des Sauerstoffpartial-drucks unter 67 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 quick eleven Jahre (Oktober 2008 – Juli 2019) in Behandlung waren, untersucht, und davon ca.
Durch eine homozygote Mutation des VHL-Gens entsteht ein VHL-Protein mit reduzierter Aktivität, sodass die a-Ketten auch bei Normoxämie nicht abgebaut werden. Die dadurch hervorgerufene Erhöhung der Erythropoietin-Ausschüttung führt zu einem deutlichen Anstieg des Hämoglobinwertes. Dies weist auf andere Ursachen, wie zum Beispiel die beobachtete vermehrte Produktion des vaskulären endothelialen Wachstumsfaktors (VEGF), die ebenfalls durch HIF reguliert wird, hin (3). Angeborene Erythropoietin(EPO)-Rezeptor-Mutationen führen zu einer Verkürzung des intrazellulären Anteils des Rezeptorproteins (2). Dadurch können negative Regulatoren nicht mehr binden, sodass es zu einer konstitutiven Aktivierung des Rezeptors kommt. Im Gegensatz zur PV haben die Betroffenen kein erhöhtes Risiko für Thrombosen und Blutungen, was dafür spricht, dass die Erythrozytose nicht alleine dafür verantwortlich ist. Während die Menopause mit dem Ausbleiben der Regelblutung offensichtlich wird, fehlt ein solches Kardinalereignis beim Mann.
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.
Die konventionelle Zytogenetik ist bei der Diagnosestellung empfohlen, das Materials kann jedoch eventuell für spätere Testung asserviert werden. Aufgrund des im Allgemeinen indolenten Verlaufs der PV gehört eine erweiterte molekulare Untersuchung derzeit nicht zur Routine einer Abklärung. Dies ist jedoch in den Fällen mit grenzwertigem Erscheinungsbild, bei denen die Unterscheidung zu anderen MPN schwierig ist, oder bei denen der Verdacht auf ein Fortschreiten der Krankheit besteht, angezeigt. Die erweiterte Charakterisierung erfolgt mittels Subsequent Era Sequencing (NGS). Diese Untersuchung ist jedoch in der Regel mit höheren Kosten verbunden und bedarf einer Zustimmung der Krankenkasse mit einer Kostengutsprache. Die Betroffenen weisen quick immer eine Mutation im Gen JAK2 auf – dies, so sollte sich später herausstellen, warfare bei dem Patient nicht der Fall. Wegen des erhöhten Thromboserisikos für die Patientin und den Fetus (erhöhte Spontanabortrate, Plazentarinfarkt/-insuffizienz) ist aber eine intensive interdisziplinäre Betreuung erforderlich, die in gut 50 % zu Lebendgeburten führen kann.
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.
DHT entsteht beim Abbau von brennesselwurzel freies testosteron (https://dobrerzezarabiaj.eu/en/employer/kann-mann-offene-testosteron-ampullen/) 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.
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 Kind 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.
Diese sekundären Polyzythämien sind eine physiologische Antwort auf die entstehende Gewebehypoxie. Informieren Sie sich täglich (montags bis freitags) per E-Mail über das aktuelle Geschehen aus der Gesundheitspolitik und der Medizin. Bestellen Sie den kostenfreien E-newsletter des Deutschen Ärzteblattes.