#Erythrocytosis

[cyanocoraxx]

unhinged gabriel headcanon: being on testosterone can make you produce Too Much Blood so 1) he can lose some in battle and be OK and 2) V1 thinks its selfish that he doesn't share all that blood with it ))): 3) gabv1el real because blood

[skindyedblue]

Results came back from the bone marrow biopsy and PET scan. No cancer. There's other issues that are causing problems, but no cancer. Christ.

[genderkoolaid]

A common concern about gender-affirming hormone therapy for transmasculine people is the risk of red blood cell volume changes and erythrocytosis, a high concentration of red blood cells, with the use of prescribed testosterone. However, Mount Sinai researchers have found that testosterone treatment may be safer than previously reported, with results published today in The Journal of Clinical Endocrinology and Metabolism. Mount Sinai researchers from the Division of Endocrinology and Center for Transgender Medicine and Surgery examined the relationship between the use of testosterone as part of gender-affirming hormone therapy (GAHT) for transmasculine individuals and changes in hematocrit, a test that measures how much of a person's blood is made up of red blood cells. The study of a large North American cohort is the largest on this subject to date. [...] Researchers found that higher testosterone levels were associated with higher hematocrit levels, however, the magnitude of change in hematocrit was small and unlikely to be clinically meaningful. Only 8.4 percent of transmasculine individuals in the study had a hematocrit greater than 50 percent, and less than 1 percent had a hematocrit greater than 54 percent, the level at which treatment for erythrocytosis is recommended, often through the use of phlebotomy (bloodletting). These numbers are lower than those previously reported in smaller studies, and the finding of such a small degree of change in hematocrit and a lower risk of erythrocytosis should provide more assurance to those prescribing and using testosterone as GAHT.

Good news for everyone on T!

[lumienyx]

bloodless much?

I see @spacebarbarianweird's excellent point on Tav being unable to give Astarion blood that often since it would deteriorate their health.

But also listen.

One thing I love about DND sorcery is metamagic. At its most basic, it's ' twisting and adapting your spells to suit your needs.' Sure there are the canonical effects, but thinking outside game mechanics—technically as a sorcerer you can tinker with spells however you damn well please.

Which is what my Tav does when he makes a scroll that replenishes his blood faster than is humanly (or, well, half-elvenly) possible.

Astarion ends up drinking the extra blood, leaving Tav with just enough for him to function normally and go about his day as usual (something to be definitely included in touch too much ehehe)

Which means:

A totally valid canonical reason for Tav letting Astarion drink from him daily, sometimes several times a day, i.e. Astarion never has to go without a sentient creature's blood ever again and is always well fed

I'd assume the first times Tav attempts this don't go over that well and that makes his blood cells multiply a bit too fast. He ends up going over to Shadowheart, thoroughly embarrassed and asking for a complex healing session for the Serious Condition he really could not have ended up with that quickly, having to painstakingly explain to her what the hells even happened (spoiler: she is Not Impressed. “You’re seriously making me waste a day’s worth of energy fixing you up because you wanted to become an infinite blood bank for your thirsty vampire lover?”)

Alternatively, and this fits EVEN BETTER (thanks to @satanicspinosaurus for pointing it out), the excess number of red blood cells is called erythrocytosis, which is what Tav would accidentally end up with as he experiments. And one of the primary treatments for this is LITERALLY phlebotomy, i.e. removing blood. So Tav explaining the whole situation to Astarion would probably go somewhat like this...

“Uh, Astarion?” “Yes, my sweet—” Astarion frowns after taking one glance at Tav’s face. “What is it? You look a bit feverish. Is something the matter?” Tav bites his lip, feeling his cheeks grow warm as he speaks, “Well. Yes. And no? Kind of.” “Eloquent.” Tav heaves a deep sigh. “Anyway. Shadowheart sent me. She can’t heal this… disease I have—or, well, she can, but she actually said the best treatment is something you can do for me. And we need to get to it fast, otherwise I’ll die, so. Here.” Tav extends his wrist, bared and ready to be drunk from. Astarion only blinks at him, zero understanding in his eyes and now quite a bit more concern. “You’re going to have to be a bit more specific, love," he says. "Why exactly did our resident healer send you to get healed by me? Especially since this is serious? My talents lie in stealth, trickery, and necromancy as of late—and you still look very much alive.” “Blood,” Tav grits through his teeth, looking anywhere but Astarion’s face. “You need to drink my blood. A lot of it. I completely fucked up the strength of a spell.” “What spell,” Astarion demands, “would lead to you needing to lose blood?” “I wanted to create one that would increase the amount of blood I have by speeding up the body’s natural blood replenishment speed,” Tav explains to the clouds he’s distinctly observing. Anywhere but Astarion’s face. “And well. I ended up with far more of it than I need. It’s my first attempt, all right?” He forces his head to turn to look Astarion at last, who’s still staring at him blankly, with slightly parted lips. Probably thinking Tav is a massive idiot. “You can drink just about a quarter of my blood at this point," Tav offers weakly. "With no consequence.” Astarion doesn’t react at first. At all. Simply stands there before Tav, looking at him long and hard as if waiting for more words that never come, as the weight of embarrassment blocks all of Tav’s attempts at further explaining himself. “Well, darling,” Astarion finally says, taking the couple of steps that separate them—and suddenly, Tav feels Astarion’s hands on him, locking him in an embrace he’s happy to be captive in. Tav melts into it, mesmerized by the hungry look in those red eyes, as always comforted by the coolness of Astarion’s skin as he leans in to place a kiss on Tav’s neck. “How could I say no to such a delicious treat?”

Astarion gets his treat every day from now on. He is very happy with the arrangement

The result of Tav’s experiments is a Scroll of Blood Replenishment that I imagine Tav would stylize to look quite cool, red parchment and all. But since he would be making those scrolls on the daily, I guess the red would be a bit overkill to do that often and it ends up looking like any other scroll, much to Tav's dismay, but he needs to keep things efficient for his lover

In time, Tav learns to cast the spell sans scroll (does Gale help him out with it? sorcerer-wizard buddies ftw??) So, Astarion can just slide up to him, pull a Puss in Boots look, and Tav would just have to whisper a few words, his body instantly providing a filling meal for Astarion whenever and wherever they are

And I just think that’s neat, thanks for coming to my BloodTed Talk.

~~~

requests open

tag list (comment or dm to be added)

@spacebarbarianweird @satanicspinosaurus, @tallymonster, @tragedybunny

[wiredaughter]

Outbreak

××

allison cameron×robert chase ☆ zombie apocalypse ☆ 1008 words ☆ ao3

@augustwritingchallenge day 4: zombie apocalypse @aug-kissed week 1: blow a kiss

Doctor Allison Cameron squints at the whiteboard in House's office. Extending ecchymosis, low grade fever, rash. It doesn't entirely seem like a case but House is, if to be believed, consulting with the federal government; which makes it a case. Of course, he's not around to explain why the patient is at PPTH instead of some blacksite if that's the truth. She exits the room, it's not her job to know why anymore.

The ER pulls her from her job trajectory considerations easily, there seems to have been a highway wreck involving at least six vehicles and she spends the morning up to her elbows on life altering injuries and advanced life support. She doesn't think about the diagnostics team again until she chats with Foreman in the lift to the cafeteria and learns the patient went after a phlebotomist with teeth and nails, making House wonder whether they should add aggressiveness to the list or the patient is just a bit of a prick.

She thinks about it, vaguely, during her lunch with Chase but ultimately doesn't bring it up until they're walking back to their respective stations. Good choice too, going by his general disinterest in the matter.

‘It's irregular, is all, to have the patient here, don't you think?

There's resignation mixed with admiration in the look her boyfriend gives her, and a hint of selfdeprecation in his smile. ‘How is a government consult meant to compel me more than a gun to his head, again?’

Cameron shrugs, stops to kiss him quickly. ‘It just seemed interesting. I’ll see you later.’

As she walks away, she turns in time to see him blowing her a kiss. Yes, her life's changed ever since resigning from the diagnostics department and it hasn't always been easy, but she's excited to let someone in again. Doesn't mean everything's got to change, she thinks, back in House’s office, this time with most of the team assembled. There's more symptoms now, hyperpyrexia, necrosis, erythrocytosis, battle sign. Transmissible = BITES is underlined several times. They've quarantined the floor the patient is being held in, and have anyone who's been in direct contact with him in isolation.

‘Polycythemia vera,’ she suggests, more to get the ball rolling than as a real answer, being that she hasn't seen the patient at all.

‘No hypertension,’ Kutner objects. ‘It's dropping steadily, actually.’

‘How's his spleen?’

‘We're waiting on the test, but palpation suggested no abnormalities.’

‘How about a different neoplasm. Essential thrombocythaemia?’ Thirteen checks the file. ‘Plateletes were high too.’

‘It could fit, but there's no cyanosis…’

She trails off when House looks ready to rule on it, but the door opens before he can, to reveal a harassed looking Chase, still on OR scrubs holding his pager up. ‘You can't page me, House, you're not my boss.’

Instead of answering, House raises a brow as he feels for something on his desk. On cue, Chase's pager goes off. Cameron exchanges a look with Foreman, who looks ready to go back to the differential. Following their cue, Chase looks at the board, almost involuntarily, frowns at what's written there. ‘If you have to page me, can it be for something other than Resident Evil roleplay?’

‘That's your diagnosis?’ House sounds exasperated. ‘Our patient is a zombie?’

‘It's how it always starts, the outbreak. Fever, necrosis, head trauma… Biting.’

‘Thank you, for illustrating exactly why I fired you.’

Chase gives Cameron a look that questions her willingness to listen to this before setting his pager down on House's desk and making for the door. Later, she mouths, and he gives a short nod before exiting. He's back before anyone can comment, wide eyed oh shit expression replacing his previous eyeroll in progress. ‘Tell me Taub is in on the joke?’

‘He went in for an NCV, I told you there's no jo-'

House's words get drowned by gunfire. Cameron moves to where Chase stands, pulling him out of the most direct line from the door to House, guessing whatever this is it's probably House-related. Again. The uniformed men that barge in after a blood splattered Taub don't shoot at anyone, though. The leader pulls down his mask.

‘Doctor House?’ It's not really a question, as he continues speaking directly at him without giving him the chance to direct his attention anywhere else. ‘Your assistance is required on site now, until the situation is handled. This your team?’

House nods, eyes burning holes through Chase’s head like he's jinxed him somehow. The man, who still hasn't introduced himself, talks into his comm to coordinate an extraction as his men exit. Cameron takes the chance to peek out the door, to see twitching, bloodied bodies strewn across the floor. She steps back, horrified, to take Chase's hand. The words zombie outbreak play on her head in his voice.

‘So,’ House leans forward on his cane, holding Chase’s pager up looking entirely too satisfied for someone who just dismissed what seems to be the working theory. ‘In the team, or out?'

Chase squeezes her hand, gives House an unimpressed look and snatches it back. ‘Unless you know someone else with over sixty hours in Deadly Silence, in.’

‘I have 100% completion in Deadly Silence’ Cameron lets her calf slide against Chase's in the chopper after an incredibly short briefing by phone, her words made private by the noise around them.

‘Your government is actually bioengineering zombies and your move is proving my expendability?’ He holds his chest in an exaggerated fashion, pressing their knees together.

‘Competition breeds progress.’ Her tone is too affectionate for her words to have any meaning.

Chase leans in, like he's going to kiss her but thinks better of it, considering their surroundings and the ongoing ‘situation’ that spans half the continental states if the information hasn't changed since they took off. Instead, he settles for an air-kiss. Not her, not now. She pulls him by his improbable tie, locking their lips for what might be the last time if the zombies are really at the gates.

[coochiequeens]

This article is from last year but since I posted about detransitioners earlier this week I think this is relevant

Testosterone Therapy in a Transgender Male Patient as a cause of Acute Ischemic Stroke (P2-5.011)

Christina Tan, Lauren Kim Sing, Ron Danziger, Alex Aw, Chae Kim, Stephen Avila, Vilakshan Alambyan, Angud Mehdi, Michael Gezalian, Maranatha Ayodele, and Shahed ToossiAuthors Info & Affiliations

April 25, 2023 issue

Objective:

To share an intriguing case of a young transgender male patient receiving testosterone therapy who developed locked-in syndrome due to an acute ischemic stroke and to highlight potential risk factors for stroke in the LGBTQI+ community

Background:

There are many studies identifying risk factors for stroke in racially and ethnically diverse populations. However, there is little existing data for stroke risk factors in the LGBTQI+ community. Prior research has shown testosterone therapy in cis-gender men with initially low levels of testosterone increases the risk of stroke, especially in the first 2 years of use1. While testosterone therapy has been shown to increase the risk of venous thrombosis, its role in arterial thrombosis is unclear2. A proposed mechanism for thrombosis with testosterone replacement includes erythrocytosis, but the potential contribution of an independent pro-coagulant effect is yet to be determined3.

Design/Methods:

Literature review and case report.

Results:

An otherwise healthy 23-year-old transgender male on one year of testosterone therapy presented in an obtunded state. Examination revealed complete quadriplegia with sparing of vertical eye movements, consistent with locked-in syndrome. Imaging revealed complete occlusion of the basilar artery with distal reconstitution at the superior cerebellar arteries, and a large bilateral ischemic infarct of the pons. Computed tomography angiography did not demonstrate other large vessel disease or structural vascular abnormalities. Unfortunately, the patient was out of the time window for any acute stroke interventions. A hypercoagulable workup was performed but results were unrevealing and hematocrit was normal. Further investigation with transthoracic echocardiogram, transesophageal echocardiogram, and telemetry were negative for thrombus, patent foramen ovale, and atrial fibrillation.

Conclusions:

Acute ischemic stroke may be an under recognized complication of testosterone therapy in transgender males independent of degree of erythrocytosis. Further research is needed to establish a safety profile of testosterone therapy in this understudied population.

Disclosure: Dr. Tan has nothing to disclose. Mrs. Kim Sing has nothing to disclose. Dr. Danziger has nothing to disclose. Mr. AW has nothing to disclose. Dr. Kim has nothing to disclose. Dr. Avila has nothing to disclose. Dr. Alambyan has stock in Teleflex. Dr. Alambyan has stock in Natera. Dr. Alambyan has stock in Labcorp. Dr. Alambyan has stock in Veracyte. Dr. Alambyan has stock in Vicarious Surgical. Dr. Alambyan has stock in Unity Biotechnology. Dr. Alambyan has stock in Scynexis. Dr. Alambyan has stock in Stryker. Dr. Alambyan has stock in Eli Lilly. Dr. Alambyan has stock in DaVita. Dr. Alambyan has stock in Invitae. Dr. Alambyan has stock in Pfizer. Dr. Alambyan has stock in Bristol-Myers Squibb. Dr. Alambyan has stock in Johnson and Johnson. Dr. Alambyan has stock in Merck. Dr. Alambyan has stock in Medtronic. Dr. Alambyan has stock in AbbVie. The institution of Dr. Alambyan has received research support from Albert Einstein Healthcare Network. Dr. Mehdi has nothing to disclose. Dr. Gezalian has nothing to disclose. Dr. Ayodele has nothing to disclose. Dr. Toossi has nothing to disclose.

[mcatmemoranda]

Hormone therapy is not required for all transgender patients, but those who receive treatment generally report improved quality of life, higher self-esteem, and decreased anxiety. Feminizing and masculinizing hormone therapies, including the use of estrogen and/or androgen therapies such as testosterone, are partially irreversible. Thus, it is important to make a reasonable, educated decision and use informed consent prior to treatment. Patients who receive masculinizing therapy are at increased risk for erythrocytosis and those who receive feminizing hormone therapy often experience reduced muscle mass and fat redistribution

[leedsomics]

Single-cell transcriptomics reveal synergistic and antagonistic effects of T21 and GATA1s on hematopoiesis

Trisomy 21 (T21), or Down syndrome (DS), is associated with baseline macrocytic erythrocytosis, thrombocytopenia, and neutrophilia, and transient abnormal myelopoiesis (TAM) and myeloid leukemia of DS (ML-DS). TAM and ML-DS blasts both arise from an aberrant megakaryocyte-erythroid progenitor and exclusively express GATA1s, the truncated isoform of GATA1, while germline GATA1s mutations in a non-T21 context lead to congenital cytopenias without a leukemic predisposition. This suggests that T21 and GATA1s perturb hematopoiesis independently and synergistically, but this interaction has been challenging to study in part due to limited human cell and murine models. To dissect the developmental impacts of GATA1s on hematopoiesis in euploid and T21 cells, we performed a single-cell RNA-sequencing timecourse on hematopoietic progenitors (HPCs) derived from isogenic human induced pluripotent stem cells differing only by chromosome 21 and/or GATA1 status. These HPCs were surprisingly heterogeneous and displayed spontaneous lineage skew apparently dictated by T21 and/or GATA1s. In euploid cells, GATA1s nearly eliminated erythropoiesis, impaired MK maturation, and promoted an immature myelopoiesis, while in T21 cells, GATA1s appeared to compete with the enhanced erythropoiesis and suppressed megakaryopoiesis driven by T21 to give rise to immature erythrocytes, MKs, and myeloid cells. T21 and GATA1s both disrupted temporal regulation of lineage-specific transcriptional programs and specifically perturbed cell cycle genes. These findings in an isogenic system can thus be attributed specifically to T21 and GATA1s and suggest that these genetic changes together enhance HPC proliferation at the expense of maturation, consistent with a pro-leukemic phenotype. http://dlvr.it/T7PwJ0

[drforambhuta]

I. Polycythemia Diagnosis:

A. Clinical Assessment:

• The diagnostic process for polycythemia commences with a thorough examination of medical history and physical condition to detect signs indicative of erythrocytosis, assess potential risk factors (e.g., smoking habits, family history of thrombosis), and uncover underlying causes.

• Special attention should be given to symptoms of hyperviscosity syndrome (e.g., headaches, dizziness), skin manifestations (e.g., erythromelalgia), and signs of organ enlargement (e.g., splenomegaly, hepatomegaly).

B. Laboratory Tests:

• Laboratory investigations are crucial for diagnosing polycythemia and understanding its underlying mechanisms. Essential tests include a complete blood count (CBC) with differential, examination of peripheral blood smear, and measurement of serum erythropoietin levels.

• Additional tests, such as JAK2 mutation analysis, bone marrow biopsy, and molecular testing for other mutations associated with myeloproliferative neoplasms (e.g., CALR, MPL), may be necessary to confirm the diagnosis of PV and rule out alternative causes.

C. Imaging Techniques:

• Imaging methods like ultrasound, computed tomography (CT), or magnetic resonance imaging (MRI) may be used to evaluate organ enlargement (e.g., splenomegaly, hepatomegaly) and identify potential underlying factors for secondary polycythemia (e.g., renal tumors).

II. Polycythemia Treatment:

Management of polycythemia aims to alleviate symptoms, lower the risk of thrombotic complications, and prevent disease progression. Treatment approaches may vary depending on the underlying cause and severity, often involving a combination of strategies:

A. Phlebotomy (Venesection):

• Phlebotomy is the primary treatment for PV, involving the removal of excess blood to achieve target hematocrit levels (<45% in men, <42% in women).

• Regular phlebotomy sessions usually start at diagnosis and are adjusted based on individual response and disease activity.

B. Cytoreductive Therapy:

• Drugs like hydroxyurea, interferon-alpha, and ruxolitinib may be used in PV patients who do not respond to or cannot tolerate phlebotomy.

• These drugs work by suppressing abnormal hematopoietic proliferation and reducing the risk of blood clotting, with hydroxyurea being the most commonly used and studied cytoreductive drug in PV.

C. Antiplatelet Therapy:

• Aspirin and other antiplatelet drugs are often prescribed to PV patients with a history of blood clots or other high-risk factors to lower the risk of arterial thrombosis.

• Aspirin is usually started at low doses (e.g., 81 mg daily) and may be combined with cytoreductive therapy for better thromboprophylaxis.

D. Treating Underlying Conditions:

• Management of secondary polycythemia focuses on addressing the root cause to relieve hypoxia-induced erythropoiesis and prevent disease progression.

• Interventions may include oxygen therapy for patients with chronic respiratory problems, correction of hemoglobin disorders or other genetic issues, and surgical removal of erythropoietin-secreting tumors.

E. Lifestyle Changes:

• Lifestyle adjustments such as quitting smoking, maintaining a healthy weight, regular physical activity, and proper hydration are vital for improving clinical outcomes and reducing cardiovascular risks in polycythemia patients.

Doctors suggest undergoing regular health checkups for the early diagnosis and treatment of polycythemia. You can choose to undergo a regular full body health checkup at Jaslok Hospital Mumbai, which is one of India's best hospitals for the early detection and management of blood disorders.

[rebeccavoszphlebotomycareers]

Phlebotomy & Erythrocytosis Phlebotomy is the practice of bleeding a client. This was performed in primitive times since of medical lack of knowledge. Phlebotomy is the practice of bleeding a client. This was performed in primitive times since of medical lack of knowledge. Numerous bodybuilders get this done due to the fact that they are…

[mirandamckenni1]

Liked on YouTube: Czy można stworzyć dobrego Wiedźmina? || https://www.youtube.com/watch?v=EtuJ61y5wLI || Kup moją nową książkę! 📚📚📚 7 CZĄSTECZEK 📚📚📚 wejdź na https://siedem.alt.pl 👉 Patronite ► https://ift.tt/CdYxJsj 📚 Moja pierwsza książka ► https://ift.tt/05sUdjH 📚 Książka dla dzieci ► https://ift.tt/wMiDFvq 📚 E-book ► https://ift.tt/OGD6nNl 🎧 Mix audio ► http://ratstudios.pl/ Czy wszyscy zmienimy się w kraby? === Rozdziały: 0:00 Czym jest dobry Wiedźmin 1:51 Kocie oczy 3:55 Mięśnie 5:27 Kości 6:28 Wytrzymałość 8:38 Pospane 9:10 Trucizny, choroby i Ozzy 17:13 Młodość k... młodość 19:10 Dzieci - nie 20:13 To można czy nie? === Źródła (wybrane): R. Walker i in. - Epigenetic age analysis of children who seem to evade aging J. Zmajkovic i in. - A Gain-of-Function Mutation in EPO in Familial Erythrocytosis Y. He i in. - The Transcriptional Repressor DEC2 Regulates Sleep Length in Mammals N. Martinez-Gil I in. - Genetic Analysis in a Familial Case With High Bone Mineral Density Suggests Additive Effects at Two Loci H. Jafari-Ghakfarohi i in. - "Small supernumerary marker chromosomes and their correlation with specific syndromes" L. Korniszewski - Dziecko z zespołem wad wrodzonych. Diagnostyka dysmorfologiczna. E. Mutschler I in. - Farmakologia i toksykologia L. Boyden i in. - High Bone Density Due to a Mutation in LDL-Receptor–Related Protein 5 A. Tsatsakis I in. - "The dose response principle from philosophy to modern toxicology: The impact of ancient philosophy and medicine in modern toxicology science https://ift.tt/ifwFWdr By PLoS genetics - Found online at https://ift.tt/ZbTU0uM, the journal is open source so the images are also, work is by US government agency. Transferred from en.wikipedia by User:Moez., CC BY 2.5, https://ift.tt/EsjNyLK

[timesofpharma]

Polycythemia Vera

Polycythemia Vera (PA)/ Erythrocytosis: What is Polycythemia Vera? Why uncontrolled red blood cells are produced in polycythemia Vera? Polycythemia Vera is a blood disorder, where in the red blood cells formation is abnormally higher. Polycythemia Vera is a rare blood cancer, It is caused due to mutation in the gene Janus kinase-2 (JAK2), due to which a neoplastic growth of hematopoietic…

[meetmebythe1ake]

Cringe! *does my T shot*

You: risks dyslipidemia, acne, high blood pressure, cardiovascular disease, erythrocytosis, sleep apnea, weight gain, etc to be something you’ll never be

Me: unaffected 😎

This is a self own girly

[peertechz]

Chronic myeloid leukemia mimicking primary myelofibrosis: A case report

Bone marrow fibrosis leading to dry tap aspiration and often associated with blast crisis has previously been reported in both Chronic myeloid leukemia and Primary myelofibrosis. The similarities between these two conditions in terms of clinical presentation and morphology can really create a diagnostic dilemma. Here we present a case of Chronic myeloid leukemia in fibrosis and blast crisis in a 32 year old lady which closely resembled Primary myelofibrosis in transformation. All myeloproliferative neoplasms can undergo blast transformation. In this case, the detection of Philadelphia chromosome helped to distinguish Chronic myeloid leukemia from other myeloproliferative neoplasms. Myeloproliferative Neoplasm (MPN) results from unchecked proliferation of the cellular elements in the bone marrow characterized by panmyelosis and accompanied by erythrocytosis, granulocytosis, and/or thrombocytosis in the peripheral blood. Although trilineage cell involvement is characteristic of MPN, a single cell line is more prominently affected. The primary defect in MPN is in the pleuripotent hematopoietic stem cell. The Philadelphia chromosome containing BCR-ABL1 fusion gene is found in all hematopoietic cells in patients with Chronic Myeloid Leukemia (CML), while Janus Kinase (JAK2) gene was found to be mutated in almost all cases of Polycythemia vera and some cases of Essential thrombocythemia and Primary Myelofibrosis (PMF). CML is the most common MPN, accounting for 15-20% of all leukemia cases. It can occur at any age, but the incidence increases dramatically among those who are 55 years of age and older. CML can occur in young adults more so than other MPNs. Although rare, CML can also occur in childhood. The natural course of the disease occurs in three phases: chronic, accelerated and blast crisis. Most patients with CML are diagnosed in chronic phase [1]. As in CML, all other MPNs carry significant risk of terminating in acute leukemia. This transition may result from chromosomal instability in the original mutant stem cell or as the result of leukemogenic chemotherapy and radiotherapy for the original myeloproliferative neoplasm. Sometimes, it is very difficult to distinguish the different MPNs especially those in blast crisis and fibrosis. The treatment of CML involves targeted therapy namely, Imatinib mesylate, which is a tyrosine kinase inhibitor. Also, JAK1/2 inhibitors administered in PMF patients show clinical improvement [2]. So, it is Important to distinguish every MPNs even in their blastic phase as they have different treatment modalities in terms of targeted therapy depending on the underlying genetic abnormality.

https://www.peertechzpublications.com/articles/AHCRR-6-129.php

[bloodcanceruncensored]

Help on the horizon for Polycythemia Vera with rusfertide (PTG-300) as a possible option to reduce erythrocytosis in some patients?

Help on the horizon for Polycythemia Vera with rusfertide (PTG-300) as a possible option to reduce erythrocytosis in some patients?

This sounds like something we need to keep our finger on. Looks like a huge breakthrough and we will be looking forward to the 2021 EHA Annual Congress and other publications. At this point, it seems like a good idea to ask your hematologist what this might mean for…

[statlab-facts-blog]

Hematocrit

Women:36-49%

Men:44.2-53%

Note:Microhematocrit from capillary puncture values are slightly higher.

Hematocrit measures the Red Blood Cell mass by seperating the plasma from the blood cells. It is expressed as a percentage by volume of packed RBCs in the whole blood.

Decreased HCT

Anemia

Acute and chronic blood loss

Chronic disease

Hemolytic reaction

HCT less than 20% can lead to cardiac failure and death.

Increased HCT

Erythrocytosis

Polycythemia

Shock

HCT more than 60% can lead to spontaneous clotting.

ARUP Source