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Primary erythrocytosis or autonomous production of excess erythrocytes most commonly occurs due to polycythemia vera (PV), a myeloproliferative neoplastic process that may be asymptomatic or may present with thrombosis, constitutional or vasomotor symptoms, or splenomegaly.

Secondary erythrocytosis, which is more common than PV, has a broad differential diagnosis that includes hypoxic lung disease, cyanotic congenital heart disease, medications (e.g., testosterone) and erythropoietin-producing malignant disorders.

Differentiating between PV and secondary erythrocytosis requires clinical evaluation and specialized investigations including measurement of the serum erythropoietin level and Janus kinase 2 mutation testing.

To reduce the risk of thrombosis, most patients with PV are treated with low-dose acetylsalicylic acid and phlebotomy to achieve a target hematocrit value of less than 0.45, whereas patients at high risk for thrombosis may receive cytoreductive therapy.

Treatment of secondary erythrocytosis should be directed at the underlying cause, and phlebotomy is not routinely recommended.

Erythrocytosis refers to an erythrocyte count above the sex-specific normal range and can be subclassified into relative erythrocytosis, caused by a reduction in plasma volume (hemoconcentration), or absolute erythrocytosis, caused by increased erythrocyte mass. Primary erythrocytosis refers to autonomous production of erythrocytes, typically from a myeloproliferative neoplasm (polycythemia vera [PV]). In contrast, secondary erythrocytosis is caused by a physiologically appropriate response to elevated serum erythropoietin levels.

Up to 4% of ambulatory men and 0.4% of ambulatory women in Canada have erythrocytosis, based on hemoglobin levels greater than 165 g/L or 160 g/L, respectively.1 Differentiating PV from other causes of erythrocytosis is critical because early recognition and treatment of PV can prevent many of its vasomotor and thrombotic complications. Polycythemia vera is rare, with an incidence and prevalence of 0.84 and 22 per 100 000, respectively.2,3 Although the prevalence of secondary erythrocytosis is difficult to estimate, it is higher than that of PV. Secondary erythrocytosis affects 6%8% of patients with chronic obstructive pulmonary disease4 and 2%8% of patients with obstructive sleep apnea.5,6

In this review, we summarize a contemporary approach to differentiating PV from other causes of erythrocytosis, and review the natural history, diagnosis and management of PV (Box 1).

We reviewed current guidelines on the management of polycythemia vera. For questions regarding the diagnostic investigation of erythrocytosis and the utility of specific laboratory tests such as the erythropoietin level, we searched MEDLINE to January 2020 for terms such as polycythemia vera, erythrocytosis or secondary erythrocytosis AND diagnosis, erythropoietin level, bone marrow biopsy and JAK2. We considered original research and review articles published between 2010 and January 2020, and searched reference lists of selected articles to identify additional studies of interest. We specifically reviewed landmark randomized trials in polycythemia vera such as the Cytoreductive Therapy in Polycythemia Vera (CYTO-PV) study,7 the European Collaboration on Low-Dose Aspirin in Polycythemia Vera (ECLAP) study,8 the Randomized Study of Efficacy and Safety in Polycythemia Vera with JAK Inhibitor INCB018424 versus Best Supportive Care (RESPONSE),9 the RESPONSE-210 and older studies conducted by the Polycythemia Vera Study Group.

Relative erythrocytosis results from any condition that reduces plasma volume, such as gastrointestinal fluid losses or diuretic use. Absolute erythrocytosis can be driven by a clonal bone marrow disease (PV) or be secondary to another disease, including a physiologic response to increased erythropoietin secondary to hypoxia, drugs11 or erythropoietin-producing solid tumours12,13 (Box 2). Congenital causes of erythrocytosis include high-oxygenaffinity hemoglobins, erythropoietin receptor mutations and alterations in oxygen-sensing molecular pathways.

Hypoxia-driven

Generalized tissue hypoxia

Smoking

Carbon monoxide poisoning

Hypoxic lung disease

Obstructive sleep apnea

Right to left cardiopulmonary shunt (e.g., cyanotic congenital heart disease)

High altitude

Local renal hypoxia

Drug-associated

Testosterone

Erythropoietin

Pathologic erythropoietin production

Miscellaneous

Erythrocytosis after renal transplantation

Idiopathic erythrocytosis*

Polycythemia vera is a myeloproliferative neoplasm characterized by increased erythrocyte mass, thrombosis and vasomotor symptoms. A gain-of-function mutation in Janus kinase 2 (JAK2) underlies 98% of PV cases.15

The history-taking and physical examination should be directed toward ruling out relative erythrocytosis and then distinguishing between primary and secondary erythrocytosis. For secondary erythrocytosis, this includes a review of cardiac, respiratory and abdominal signs and symptoms. Patients should be asked about tobacco smoking, medications (especially androgenic steroids, including testosterone11), exposure to carbon monoxide and symptoms of obstructive sleep apnea. A full cardiopulmonary examination should be completed, and the abdomen should be examined for organomegaly or erythropoietin-producing intraabdominal tumours (e.g., hepatocellular or renal cell carcinoma).

Oxygen saturation less than 92% on room air by pulse oximetry suggests that erythrocytosis is secondary to hypoxic cardiopulmonary disease.14 Some causes of hypoxia may present with a normal or falsely elevated oxygen saturation value (e.g., obstructive sleep apnea, high-oxygen-affinity hemoglobins, or carboxyhemoglobinemia from tobacco smoking or carbon monoxide poisoning).

The World Health Organization diagnostic criteria for PV were updated in 2016 (Box 3).16 Patients with PV may have symptoms of splenomegaly, constitutional symptoms or vasomotor symptoms such as headache, visual disturbances or light-headedness. Two specific symptoms for myeloproliferative neoplasms are pruritus and erythromelalgia.15 Pruritus is often aquagenic and may be debilitating. Erythromelalgia is a recurrent burning sensation accompanied by erythema and warmth, most commonly affecting the hands.

Diagnosis of polycythemia vera requires all 3 major criteria OR the first 2 major criteria and the minor criterion

Major criteria

Hemoglobin level > 165 g/L in men, > 160 g/L in women OR hematocrit > 0.49 in men, > 0.48 in women OR increased erythrocyte mass

Bone marrow biopsy showing hypercellularity for age with trilineage growth (panmyelosis) including prominent erythroid, granulocytic and megakaryocytic proliferation with pleomorphic, mature megakaryocytes*

Presence of JAK2 V617F or JAK2 exon 12 mutation

Minor criterion

* Bone marrow biopsy is not required for patients with sustained absolute erythrocytosis, defined as a hemoglobin level greater than 185 g/L in men (hematocrit 0.55) or greater than 165 g/L in women (hematocrit 0.50) if the third major criterion and the minor criterion are met.

Initial tests to differentiate primary from secondary erythrocytosis include a complete blood count, peripheral blood film, renal and liver function tests, and determination of the ferritin level.14 Erythrocyte mass can be measured directly to confirm absolute erythrocytosis by nuclear isotope dilution, but this test is not widely available in Canada.1 As PV is associated with panmyelosis (expansion of all myeloid elements of the bone marrow), patients often have mild to moderate leukocytosis and thrombocytosis rather than isolated erythrocytosis.15 Many patients with PV are iron deficient at diagnosis owing to erythroid expansion and altered iron metabolism. 17 A low mean erythrocyte volume and low ferritin level (< 3545 ng/mL) support a diagnosis of iron deficiency.18 Baseline abdominalpelvic imaging is indicated when the clinical examination for splenomegaly gives equivocal findings or when endogenous erythropoietin production is suspected.19

The serum erythropoietin level can differentiate between primary and secondary erythrocytosis. In a cohort study of 125 patients, a low erythropoietin level (< 2.9 mU/mL) was specific (92%) and moderately sensitive (64%) for the diagnosis of PV.20 A high erythropoietin level (> 15.1 mU/mL) was specific (98%) but had poor sensitivity (47%) for the diagnosis of secondary erythrocytosis.20

Ninety-five percent of patients with PV have a V617F point mutation in exon 14 of JAK2.21 JAK2 V617F-negative PV is rare, and mutations in exon 12 of JAK2 account for most of these cases.22 The JAK2 V617F mutation is not specific to PV; it can also be seen in other myeloproliferative neoplasms including essential thrombocythemia and primary myelofibrosis.21 Some cases of PV with iron deficiency may resemble essential thrombocythemia. 17 In these cases, erythrocytes are microcytic, the hemoglobin level is low or within normal limits, and there is marked thrombocytosis.

Our approach to sequencing investigations is adapted from Canadian consensus recommendations1 and a British guideline for the diagnosis and management of PV14 (Figure 1). Front-line tests are selected based on the pretest probability of PV and the availability of JAK2 mutation testing.

Practical diagnostic approach to erythrocytosis. *Some clinicians order determination of the erythropoietin level and JAK2 V617F mutation testing concurrently in settings when there is a high probability of diagnosing polycythemia vera. Bone marrow biopsy is required to meet the World Health Organization 2016 diagnostic criteria16 if the hemoglobin level is less than 185 g/L (hematocrit 0.55) in men or less than 165 g/L (hematocrit 0.50) in women.

In the primary care setting, where the probability of PV is low, clinical evaluation for secondary causes of erythrocytosis paired with a high erythropoietin level can rule out PV in most patients. In hematology clinics, where the probability of PV is higher, erythropoietin level and JAK2 V617F mutation testing are done concurrently. Patients with a low or normal erythropoietin level and no JAK2 V617F mutation are further evaluated with JAK2 exon 12 mutation testing (on peripheral blood or marrow aspirate, based on local practice) and a bone marrow biopsy.14 Findings on bone marrow biopsy in a patient with PV are shown in Figure 2.

Bone marrow biopsy specimen of a patient with polycythemia vera. (A) Hypercellularity for age and panmyelosis (expansion of all myeloid elements of the bone marrow) (hematoxylineosin, 40 magnification). (B) Panmyelosis and pleomorphic megakaryocytes (hematoxylineosin, 200 magnification). Images courtesy of Dr. Catherine Ross, Pathology and Molecular Medicine, Juravinski Hospital, Hamilton, Ontario.

When no diagnosis is made, selected patients with onset of erythrocytosis at a young age or compatible family history should undergo testing for high-oxygen-affinity hemoglobins, and gene sequencing for mutations involving the erythropoietin receptor or oxygen-sensing pathways.14,23 Idiopathic erythrocytosis is a diagnosis of exclusion.

Investigations for secondary erythrocytosis should be symptom-directed and may include chest radiography, overnight oximetry for suspected sleep apnea, pulmonary function tests for hypoxic lung disease, venous blood gas sampling (carboxyhemoglobin level) and echocardiography to rule out right to left cardiac shunting. Abdominalpelvic imaging can help exclude an erythropoietin-producing tumour or conditions associated with local renal hypoxia (Box 2). Neuroimaging to rule out meningioma or cerebellar hemangioblastoma should be ordered for patients with unexplained neurologic symptoms as these tumours have been associated with autonomous erythropoietin production.14

There are no established criteria for referral to a hematologist. Patients with a low or normal erythropoietin level and negative findings on investigation for secondary erythrocytosis are typically referred to a general internist or hematologist to arrange additional investigations starting with JAK2 V617F testing (Figure 1). Internists or hematologists often manage patients who require phlebotomy. Referral to a hematologist is warranted for women with PV who desire pregnancy, patients who are refractory or intolerant to treatment with hydroxyurea, and patients with no diagnosis despite extensive appropriate investigations.

The goals of treatment of PV are to reduce the risk of arterial and venous thromboembolism, and minimize symptoms.14 Unfortunately, existing treatments do not successfully reduce the risk of transformation to myelofibrosis or acute leukemia.

Thrombosis in PV is common and highly morbid. Up to 15% of patients with newly diagnosed PV have a history of arterial or venous thromboembolism.15,24 Patients with PV have venous thrombosis at unusual sites, such as the splanchnic or cerebral veins.25 A meta-analysis of observational studies showed that more than 15% of patients with splanchnic vein thrombosis or BuddChiari syndrome are later diagnosed with a myeloproliferative neoplasm.26

In a cohort of 1638 patients with PV, cardiovascular mortality accounted for 45% of all deaths over more than 4000 person-years of follow-up.27 The 2 most important predictors of cardiovascular events were age greater than 65 years and prior thromboembolism. Patients with neither, 1 or both risk factors experienced 2.5, 5.0 and 10.9 cardiovascular events per 100 person-years, respectively. Treatment guidelines classify patients as being at high risk for thromboembolism if they are more than 60 or 65 years old or have a history of thrombosis, or both.14,28 Patients who meet neither of these criteria are considered to be at low risk.

Patients with PV are treated with daily low-dose acetylsalicylic acid (ASA) and phlebotomy to achieve a target hematocrit value of less than 0.45 based on the results of 2 randomized trials.14,28 Patients are monitored regularly (every 36 mo) for symptoms, treatment complications, cardiovascular events and disease progression.

In the European Collaboration on Low-Dose Aspirin in Polycythemia Vera (ECLAP) study,8 518 patients with PV were randomly allocated to receive low-dose ASA (100 mg/d) or placebo. Acetylsalicylic acid reduced the composite outcome of nonfatal myocardial infarction, nonfatal stroke, venous thrombosis or death from cardiovascular causes by 60% (relative risk [RR] 0.40, 95% confidence interval [CI] 0.180.91), with no statistically significant increase in major bleeding.

In the Cytoreductive Therapy in Polycythemia Vera (CYTO-PV) study, 365 adults with PV were randomly allocated to a low hematocrit target (< 0.45) or a less-intensive hematocrit target (0.450.50).7 The primary outcome of death from cardiovascular causes or major thrombotic events was observed in 5 of 182 patients (2.7%) in the low-hematocrit group compared to 18 of 183 patients (9.8%) in the higher-hematocrit group (RR 3.91, 95% CI 1.196.12), with no significant difference in adverse events between the groups.

Most patients with an indication for anticoagulation therapy should receive an anticoagulant in place of ASA. A multicentre observational study of 2510 patients with PV showed that patients who received both an anticoagulant and ASA had a fourfold increased risk of bleeding (95% CI 2.576.94) compared to those who received either treatment alone or no treatment.29 We could not identify any high-quality data comparing warfarin to direct anticoagulants for oral use in PV.30 The British guideline recommends that cardiovascular risk factors, including blood pressure, lipid control, and counselling around smoking cessation and weight loss, be addressed in all patients.14

Observational studies suggest that patients with high-risk PV benefit from cytoreductive therapy in addition to low-dose ASA therapy and phlebotomy.14,28 In North America, hydroxyurea (hydroxycarbamide), an orally administered antimetabolite chemotherapy drug that causes myelosuppression, is used owing to its known efficacy, low cost, oral formulation and acceptable toxicity profile (discussed below). A study showed that 51 patients with PV treated with hydroxyurea had a lower incidence of thrombosis at 2 years than historical controls treated with phlebotomy alone (7% v. 14%).31 Some clinicians titrate the dosage of hydroxyurea to achieve peripheral blood count remission (hematocrit < 45% without phlebotomy, platelet count 400 109/L and leukocyte count < 10 109/L).32 Response definitions for PV have been created for use in clinical trials, but their routine application to clinical practice is not evidence-based.32 Other clinicians titrate the dosage of hydroxyurea to minimize the need for phlebotomy. An observational study showed that patients receiving hydroxyurea who needed 3 or more phlebotomy procedures per year had a significantly higher rate of thrombosis than those who required fewer phlebotomy procedures (21% v. 5% at 3 yr, p < 0.001).33

Alternatives to hydroxyurea include pegylated interferon or busulfan. The former can be used safely during pregnancy and induces molecular remission in some patients; for these reasons, it is often used as front-line therapy for young patients or women desiring pregnancy.34

Ruxolitinib, an orally administered JAK1 and JAK2 inhibitor, is a second-line agent for patients who are refractory or intolerant to hydroxyurea.9,10 The Randomized Study of Efficacy and Safety in Polycythemia Vera with JAK Inhibitor INCB018424 versus Best Supportive Care (RESPONSE) investigators randomly allocated 222 such patients with splenomegaly to ruxolitinib versus best available therapy.9 The composite primary outcome of hematocrit control and at least a 35% reduction in spleen volume was achieved in 20.9% of the patients in the ruxolitinib arm, compared to 0.9% of those in the best-available-therapy arm (p < 0.001). The RESPONSE-2 investigators enrolled similar patients without splenomegaly and found that a higher proportion of ruxolitinib-treated patients than patients who received best available therapy achieved hematocrit control (62% v. 19%, p < 0.001).10

Hydroxyurea is well tolerated, but common adverse effects include complications from cytopenia, oral and leg ulcers, gastrointestinal upset, drug fever, and skin and nail changes. An international retrospective cohort study of 1545 patients with PV showed that hydroxyurea does not increase the incidence of leukemia.15

Ruxolitinib is the most effective treatment for pruritus in PV. A phase III randomized trial showed that patients treated with ruxolitinib were more likely to experience alleviation of pruritus than those who received hydroxyurea (54% v. 32%, p = 0.03).35 Other treatments for pruritus are supported by lower-quality evidence, mostly from case series. These include selective serotonin reuptake inhibitors, interferon , psoralen and ultraviolet A, and antihistamines.36

The prevalence of PV among females of reproductive age is less than 0.3 per 100 000,37 so management recommendations are based on case series or extrapolated from essential thrombocythemia. 5,34 The hematocrit is maintained in the normal range for gestation.5 Women without a contraindication receive low-dose ASA throughout pregnancy, and interferon is used for women who require cytoreductive therapy. Thromboprophylaxis with low-molecular-weight heparin, in addition to ASA, may be beneficial for selected patients at high risk.5,28

Treatment should be directed at the underlying cause. There is no definitive evidence that the risk of thromboembolism is increased in patients with secondary erythrocytosis, and, therefore, phlebotomy is not recommended routinely.38 We direct the reader to a recently published guideline on the management of secondary erythrocytosis,5 which recommends the following approach:

Long-term oxygen therapy should be considered in patients with hypoxic lung disease.

Testosterone should be discontinued in patients with moderate to severe testosterone-induced erythrocytosis and can be resumed at lower dosages once the hematocrit normalizes11,39

Erythrocytosis after renal transplantation should be treated with an angiotensin-converting-enzyme inhibitor or angiotensin receptor blocker.

Patients with cyanotic congenital heart disease or high-oxygen-affinity hemoglobins have physiologic erythrocytosis and should be under specialist care. These patients are at risk for thrombosis, although optimal target hematocrit values are unknown.

Idiopathic erythrocytosis is a diagnosis of exclusion that carries a low risk of thrombosis and bleeding.40 However, some experts recommend an arbitrary target hematocrit value of 0.450.55 for patients with symptomatic hyperviscosity or a history of thrombosis.5

Secondary erythrocytosis can be distinguished from PV in most patients with a focused clinical evaluation and, where available, determination of the erythropoietin level and JAK2 V617F mutation testing. Goals of treatment in PV are to alleviate symptoms, reduce the risk of thromboembolism, and monitor patients for transformation to myelofibrosis or acute leukemia. The majority of patients with PV should be treated with low-dose ASA and phlebotomy to achieve a target hematocrit value of less than 0.45. Cytoreduction, most commonly with hydroxyurea, should be considered in patients at high risk for thrombosis. Treatment of secondary erythrocytosis should be directed at the underlying cause.

Competing interests: Christopher Hillis received grant funding from Novartis Oncology and personal fees from Novartis Oncology, Bristol Myers Squibb and Celgene outside the submitted work. Mark Crowther serves on the advisory boards of Servier Canada, Asahi Kasei Corporation and Precision BioLogic, and the data safety and monitoring board of Bayer. He has received speaking fees from Pfizer, CSL Behring and Diagnostica Stago. He has equity ownership in Alnylam Pharmaceuticals. He is also the Leo Pharma Chair in Thromboembolism Research at McMaster University. No other competing interests were declared.

This article has been peer reviewed.

Contributors: Siraj Mithoowani conceived of the work. Siraj Mithoowani and Marissa Laureano drafted the manuscript, and Mark Crowther and Christopher Hillis revised it critically for important intellectual content. All of the authors made substantial contributions to the design of the work, approved the final version to be published and agreed to be accountable for all aspects of the work.

Funding: Siraj Mithoowani is supported by a CanVECTOR fellowship. The CanVECTOR Network receives grant funding from the Canadian Institutes of Health Research (funding reference CDT-142654).

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Investigation and management of erythrocytosis - CMAJ

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Aug 11th, 2020 | Filed under Testosterone

There are probably many reasons why you wanted to leave your teen years behind, and saying goodbye to your acne was surely one of them. But dont freak out if those pesky pimples stuck around. Adult acne in women is super common, says Nazanin Saedi, M.D., director of the Jefferson Laser Surgery and Cosmetic Dermatology Center in Philadelphia. The main cause: hormonal imbalance. Thats why dermatologists often recommend medications like birth control, which can help keep hormones like estrogen and testosterone in check.

However, what you put on your face also matters. The first step in your anti-acne regimen? A face wash that you can lather up with morning and night. Nighttime cleansing washes off dirt and excess oil thats sitting on skin, while morning cleansing will clear off anything that accumulated overnight, says Dr. Saedi.

Look for actives: A few ingredients to look for in your face wash include benzoyl peroxide (to clean out the P. acnes bacteria that contributes to acne), salicylic acid (to exfoliate and remove pore-clogging debris and break up blackheads and whiteheads), sulfur (to lessen inflammation), or glycolic acid (an alpha hydroxy acid that clears away dead skin cells).

But go mild if need be: One downside is that face washes with anti-acne ingredients can be drying. You may also be tempted to overdo it on cleansingand see skin irritation as a result. Pro tip: If you do get a bit dry or flaky, scale back to every other day and follow with a noncomedogenic moisturizer designed for oily or acne-prone skin.

Or, if youre using a super-drying medication, stick with a mild nothing cleanser to minimize your irritation. These face washes are formulated for sensitive skin and really just prep your base (cleaning out makeup, oil, and dirt) so your acne medication (say, a prescription retinoid) or spot treatment can do the heavy lifting.

Listen to your skin: Finding the right cleanser for your acne-fighting routine can be tricky, and youll like have to try both cleansers for sensitive skin and those formulated with active ingredients to figure out which you prefer. If your skin gets red, itchy, flaky, or irritated in general, talk to your doctor about switching to a milder formula instead.

When it comes to cleanser, you dont have to pick an expensive onedrugstore buys will get the job done, says Dr. Saedi. But there are options in every price category: Here, dermatologists share the best face washes for acne-prone skin, from those with ultra-mild properties to top-notch pimple-fighting power.

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Dermatologists Say These Are the *Best* Face Washes for Acne-Prone Skin - MSN Money

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Aug 11th, 2020 | Filed under Testosterone

Every day on social media we see soaring stories of people standing tall. But what about the moments we live small?

Lately I've been loitering inside my memory bank with an experience that no matter how I twist and contort to escape, it has no alternate ending.

I lived small.

I was a junior in high school when I landed a beefy role in a play. I'd been acting for a few years and was thrilled my dynamite drama teacher and director had trusted me with the part.

We had little time to prepare and I'll never forget reading the script for the first time. The dialogue fizzed and popped like an afterschool Pepsi.

And then it all went flat.

My character had one particularly profane line that I shouldn't, wouldn't, couldn't say. I'd never said those words. I still don't.

At our first rehearsal I mumble-whispered the line and hoped with so many distractions on stage the director wouldn't notice.

She didn't.

Over three wild weeks of rehearsals, I convinced myself I could keep faking it. Then, when the curtain finally rose with an audience, maybe I'd feel fine about saying it just once at full volume.

On the night of the open dress rehearsal, I was nervous to see an older couple from church - the Ehlers - seated in the auditorium. They were forever friends of our family and I had no idea they'd be there.

When the big moment arrived - with adrenaline, testosterone, and gummy bears racing through my system - I went for it.

$#*%!

I remember the moment. Where I stood. How it sounded. How I felt.

After the show, the Ehlers met me in the school lobby with cheers, a hug, and some snappy dialogue of their own.

Certainly after all these years this cannot be considered verbatim. Still, sadly, I know it's close. Regrets have a way of adding color to otherwise gray memories.

Mrs. Ehlers looked at me. "Jason, that was quite some language. You surprised us."

"I know. I didn't want to say it."

"Why didn't you tell the director you didn't want to say the line? I bet you could have changed it."

I studied my black and white checkered sneakers. "She wouldn't have let me," I said.

"Maybe," Mrs. Ehlers said with a soft smile. "Or maybe not. But we have to stand up sometimes, don't we? Either way, we're proud of you."

I said goodbye and lingered around the drama room until our director appeared and the other cast members vanished.

With my heart thumping and my palms sweating, I stood near her desk and casually asked if I might maybe, sort of, I don't know, possibly perhaps like change the profane line in the play to something more PG.

"Of course! You're right. We really should. I wish you'd said something earlier."

Ouch.

Soon I walked away juggling gratitude, humility, respect, and shame.

Later when I relayed the story to the Ehlers, they gave me more cheers, hugs and unconditional love.

So, how about that alternate ending?

Why didn't I immediately make a stand? Why hadn't I clung to my standards? Refused to bend? I could have made my case without ego, pride, or self-righteous judgement.

What a story it could've been!

"Hey kids. Have I ever told you about the time I made a tough call and refused to give in?"

Instead, my spine shrank. It was a golden moment to be brave, to speak up, to stand tall.

Instead I was weak, went silent, lived small.

Years later I can remember other times I handled those character moments much better. How thankful I am for those second chances.

Yet here I am, sharing a what-if regret in the spirit of transparency.

If we can't share the good times with the bad and the falls and failures with the big wins, what's the point of sharing at all?

Life and her hard lessons aren't meant to be lived and learned through a fancy filter.

Because heaven knows the moments we live small are just as important in our book of life as the days we stand tall.

Jason F. Wright is a New York Times bestselling author, columnist, and speaker. His newest book, "Seen, Loved, Lifted: How Seeing, Loving and Lifting Others Can Change Your Life" is available at Amazon. Join Jason on Facebook, Instagram and Twitter.

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Jason F. Wright: The day I went silent, lived small - Northern Virginia Daily

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Jul 18th, 2020 | Filed under Testosterone

(UroToday.com)In this debate, a clinical case of a 65-year-old gentleman who was diagnosed with prostate cancer Gleason grade group 2 on biopsy was presented byGiorgio Gandaglia, MD. The patient underwent robotic-assisted radical prostatectomy, demonstrating pT3a, Gleason grade group 4 with negative margins on final pathology, with no lymph node dissection performed. The first postoperative prostate-specific antigen (PSA) was undetectable, but later, PSA started to rise from 0.25 to 0.65 with a PSA doubling time of 1.4 months. The patient received salvage radiotherapy to the prostatic fossa and pelvic lymph nodes + concomitant androgen deprivation therapy (ADT) for 36 months.

Following salvage treatment, the PSA started to rise again from a nadir of 0.1 to 0.3, 1.2, and finally, 1.5 ng/ml with castrated testosterone. The patient was defined as having castrate-resistant prostate cancer. The patient had a negative multiparametric magnetic resonance imaging (MRI) and a negative bone scan, an abdominal pelvic CT scan. Later, PET prostate-specific membrane antigen (PSMA) was performed and showed two positive spots in the common iliac and presacral lymph nodes (Figure 1). The question that was presented by Dr. Gandaglia was whether this patient should be considered for androgen receptor-targeted treatment (ARTA).

Figure 1 Positive PET PSMA in the presented patient:

First, Alicia Morgans, MD, MPH, discussed why she believes ARTA should be given to this patient.According to Dr. Morgans, regardless of molecular imaging results, patients with rising PSA on ADT with conventional negative imaging meet the trial definition of M0 CRPC.The important question is whether this patient has M0 CRPC or oligo-progressive mCRPC and whether he could have both, and if so, does it really matter?

M0 CRPC occurs in patients with:

Oligo-progressive oligo-metastatic CRPC occurs in patients with:

In the next part of the discussion, Dr. Morgans discussed the various available treatment options for these patients. She began with metastasis directed therapy (MDT) in M0 CRPC. In a retrospective analysis, targeted ablation of three or fewer sites identified by molecular or standard imaging was performed. PSA doubling time and freedom from progression were calculated. In this retrospective analysis, 73% had a PSA response with a mean of 86% reduction of PSA and a clear advantage in patients treated with ARAT (Figure 2).

Figure 2 Metastasis directed therapy in patients with oligometastatic prostate cancer1

In another retrospective analysis2, MDT was associated with an improved median time to PSA failure, time to next intervention, and distant metastases free-survival. The challenges with studies of MDT in M0 CRPC include the fact that these are mostly retrospective analysis with variability in the treatments and imaging used. Most studies are small and nonrandomized. The studies do not regularly include currently available next-generation AR antagonist treatment, and the outcomes may not be meaningful or rigorously documented.

To date, the only level one evidence of benefit has been shown by providing intensified systemic therapy, in the form of either apalutamide, darolutamide, or enzalutamide to patients with MO CRPC and a high risk of developing Metastasis (PSA doubling time of fewer than ten months). This level one evidence comes from the three recently landmark published trials, SPARTAN3, PROSPER4, and ARAMIS5 (Figure 3). All three trials demonstrated significant improvement in metastases free survival (Figure 4) and overall survival in the updated results (Figure 5). Importantly, Enzalutamide and apalutamide were associated with stable to improved quality of life.

Figure 3 ARAMIS, PROSPER, and SPARTAN trials:

Figure 4 - Metastasis free survival in ARAMIS, PROSPER, and SPARTAN:

Figure 5 - Overall survival in ARAMIS, PROSPER, and SPARTAN trials:

Therefore, regardless of molecular imaging results, level one evidence suggests improved metastasis-free survival, overall survival, and quality of life associated with ARAT in M0 CRPC patients.

Concluding her excellent talk, Dr. Morgans stated that Imaging advances blur the distinction between patient types, and applying the criteria for M0 CRPC from clinical trials still remains valid. Additionally, MDT for oligo progressive CPRC appears promising, but to date, there is insufficient evidence available to apply this outside of a clinical trial. Lastly, there is level 1 evidence, and the EAU guidelines themselves support the use of apalutamide, darolutamide, or enzalutamide for M0 CRPC with improvement in metastasis-free survival, overall survival, and quality of life.

In the last part of this debate, Jens Bedke, MD, gave a talk explaining why he thinks there is no role for ARAT in M0 CRPC.

According to Dr. Bedke, the presented patient is not a true M0 CRPC patient, as his PET PSMA was positive for two distinct lymph nodes.

The patients included in SPARTAN3 study were required to have no local or regional nodal disease (N0) or to have malignant pelvic lymph nodes that measured less than two centimeters in the short axis (N1) that were located below the aortic bifurcation. According to Dr. Bedke, the predominant effect of apalutamide was in patients with cM1a (HR 0.15), with the outcome of cM0 patients remaining to be unknown.

The time to metastases without treatment was 14-18 months in PROSPER, SPARTAN, and ARAMIS trials (Figure 6). This time to metastases in patients who did not receive any treatment is quite important as patients on these therapies had significant adverse events (Figure 7).

Figure 6 Time to metastases without treatment in PROSPER, SPARTAN, and ARAMIS:

Figure 7 Adverse events in PROSPER, SPARTAN, and ARAMIS:

The other problem in these three landmark large trials are the fact that there was a high crossover rate, with 56-65% of patients in the placebo arm receiving subsequent therapies with no clean comparison, as these trials were basically a comparison of early treatment vs. late treatment.

Additionally, phase 3 non-metastatic CRPC trials have shown a 14-18 months time to metastases without treatment. Based on this data, there is a high probability of undetected cM1 disease. In PROSPER, SPARTAN, and ARAMIS, the PSA doubling time was in the range of 3 to 8.9 months.

According to Dr. Bedke, there is a data gap in the true treatment of cM0 CRPC.

Dr. Bedke concluded his talk emphasizing that the large three trials assessing non-metastatic CRPC patients included M1a patients as well. M1 status is defined by the modality of imaging, and only PET PSMA CT can define MO CRPC and not conventional imaging. Dr. Bedke believes that not every patient with M0 CRPC needs ARTA. The PSA doubling time determines the risk of metastases and death in patients with M0 CRPC. ARTA should be given to M0 CRPC patients with PSA doubling time of fewer than three months. Lastly, it is important to remember that ARTA has significant adverse effects that need to be considered, as well.

Presented by:

Written By: Hanan Goldberg, MD, MSc., Urology Department, SUNY Upstate Medical University, Syracuse, NY, USA, Twitter: @GoldbergHananat the Virtual 2020EAUAnnual Meeting #EAU20, July 17-19, 2020.

References:

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EAU 2020: M0 CRPC: Androgen Receptor Targeted Treatment (ARTA) - UroToday

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Jul 17th, 2020 | Filed under Testosterone

JACKSONVILLE, Ore. Its a name you see all over Jacksonville, but who was Beekman?

First things first, his name was Cornelius Beekman, and he opened the very first bank in the Pacific Northwest in the 1860s. Its still standing in downtown Jacksonville, but unfortunately, a lot of people seem to walk by without paying it much attention.

Local historian Ben Truwe spends a lot of time behind the counter of the Beekman Bank, full of information on why the building should pique your interest. Even if you were to enter the bank without a guide, youd find plenty relics keep you occupied.

He ran his bank here for 50 years and when he died everything was left in place, Truwe said. This is a national treasure. The board youre standing on is 150 years old.

Much of what youll find in the bank is authentic. Some of the items are so outdated, visitors play a guessing game with Truwe trying to figure out what the devices were used for. Everything from check presses and cutters, to envelope seals and vaults. Antique, dust-covered books line the floor-to-wall bookshelf, and Truwe says many of them are original to the bank. Though, he admits others are imposters.Actually, Truwe is brutally honest about any modification made to the bank to lure in tourists, including the phony back room.

Truwe said its one of Beekmans original items that draws the most attention; a giant vault that you can walk inside. Inside the safe you can see what Truwe says is 50 years of soot and cigar smoke on the walls, as well as a tin of marshmallows.

Yeah, Beekman liked marshmallows, Truwe said with a laugh.

While the vault appears quite impressive to anyone who sees it, Truwe said it would not have been hard to rob the Beekman Bank back in the 1860s.

It was a lot of smoke and mirrors, Truwe said. He went on to explain that the walls of the big safe were thick and sturdy, but a quick tap on the roof and door is proof that the safe was wellnot so safe.

Pretty much put together with a bunch of junk, Truwe said.It was to impress the miners that this was the place to do business.

So, Beekmans safe may not have been the safest place to store gold or cash, but thats not exactly how he operated.

When you sold your gold either that would give you an account on Beekmans bank that you could draw on, or he would give you a Wells Fargo check, Truwe explained. A Wells Fargo check you could cash anywhere in the world. So it was better than money.

Back to where we started, who exactly is Beekman? Like many men in the 1850s, Beekman came out west with the Gold Rush, arriving in Jacksonville in 1853.

5,000 young, single testosterone-fueled men digging in the dirt trying to make their fortune, Truwe said. He went on to explain that Beekman would travel back and forth to Yreka (about a 20 hour round trip at the time) several times a week.

Well, he was in his 20s he was superman he could tolerate that, Truwe added.

When the company Beekman rode for went bankrupt, he decided to buy it. Then, Beekmans Express became a Wells Fargo agency and, in 1862, it became a bank.

[Beekman Bank] was actually the first bank in Oregon territory. There were no banks north of California when this bank began, Truwe said.

Its a place where southern Oregons history is still intact, and yet, Truwe says too many people just walk on buy without taking so much as a glance.

People will come in and look at the brochures Stick their head in and then theyll leave, Truwe said. Who knows they could come in and I could sell them a timeshare. It could be that bad!

Its far from a timeshare, but if you visit the Beekman Bank, you will take a trip through time.

Theres a national treasure here that you really shouldnt miss.

NBC5 News anchor and reporter Kristina Zagame is from Boston, Massachusetts. She comes to us from KQTV in St. Joseph, Missouri where she was the evening anchor and executive producer.

Kristina received her degree in Broadcast Journalism from the University of South Carolina. She spent a summer interning for an international online magazine in Santiago, Chile. She also covered Hurricane Maria relief efforts in the Virgin Islands.

When shes not in the newsroom, Kristina loves exploring, dancing and live music.

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Unknown Stories Pt. 5: The first bank in the Pacific Northwest - KOBI-TV NBC5 / KOTI-TV NBC2

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Jul 17th, 2020 | Filed under Testosterone

Testosterone Replacement Therapy Market Research 2020

The most recent research report published by Regal Intelligence presents a scientific analysis titled as worldwide Testosterone Replacement Therapy Market 2020. The report contemplates in a brief manner the presentation of both historical records alongside the ongoing patterns. It incorporates a complete analysis of various traits, for example, manufacturing base, type, and size. This report assesses the market division alongside the competitive landscape at worldwide as well as local level.

This study considers the Testosterone Replacement Therapy-value generated from the sales of the following segments:

The key manufacturers covered in this report: AbbVie, Pfizer, Eli Lilly, Teva Pharmaceuticals, Mylan, Bayer HealthCare Pharmaceuticals, Antares Pharma, Ferring Pharmaceuticals, Allergan, Antares Pharma, Sandoz, Clarus Therapeutics, Juniper Pharmaceuticals, Endo International, Acerus Pharmaceuticals, Forendo Pharma, MetP Pharma, Repros Therapeutics,

Segmentation by product type: Gels, Injectables, Patches, Other,

Segmentation by application: Hospitals, Clinics, Other

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Market Segment by Regions, regional analysis covers:

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Global Testosterone Replacement Therapy Market by Manufacturers, Regions, Type and Application, Forecast to 20261 Report Overview1.1 Definition and Specification1.2 Report Overview1.2.1 Manufacturers Overview1.2.2 Regions Overview1.2.3 Type Overview1.2.4 Application Overview1.3 Industrial Chain1.3.1 Testosterone Replacement Therapy Overall Industrial Chain1.3.2 Upstream1.3.3 Downstream1.4 Industry Situation1.4.1 Industrial Policy1.4.2 Product Preference1.4.3 Economic/Political Environment1.5 SWOT Analysis2 Market Assessment by Type2.1 Gels Sales (K Units), Revenue (M USD) and Growth Rate 2014-20202.2 Injectables Sales (K Units), Revenue (M USD) and Growth Rate 2014-20202.3 Patches Sales (K Units), Revenue (M USD) and Growth Rate 2014-20202.4 Other Sales (K Units), Revenue (M USD) and Growth Rate 2014-20203 Asia Pacific Testosterone Replacement Therapy Market Assessment by Type3.1 Asia Pacific Market Performance (Sales, Revenue)3.2 Key Players in Asia Pacific4 North America Testosterone Replacement Therapy Market Assessment by Type4.1 North America Market Performance (Sales, Revenue)4.2 Key Players in North America5 Europe Testosterone Replacement Therapy Market Assessment by Type4.1 Europe Market Performance (Sales, Revenue)4.2 Key Players in Europe6 South America Testosterone Replacement Therapy Market Assessment by Type4.1 South America Market Performance (Sales, Revenue)4.2 Key Players in South America7 Middle Easr and Africa Testosterone Replacement Therapy Market Assessment by Type4.1 Middle Easr and Africa Market Performance (Sales, Revenue)4.2 Key Players in Middle Easr and Africa

Read Complete Report with TOC: https://www.regalintelligence.com/request-toc/95904

To conclude the report sums up present analysis dependent on factors which are relied upon to show positive development of the market. The report studies market estimation for 2020 to 2026. Pertinently, the report and company profiles determine the key drivers that are affecting the interest in worldwide Testosterone Replacement Therapy markets.

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Testosterone Replacement Therapy Market Research Report: Latest Industry Status and Future Growth Outlook - Cole of Duty

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Jul 16th, 2020 | Filed under Testosterone

Transparency Market Research (TMR) has published a new report titled, Testosterone Replacement Therapy Market Global Industry Analysis, Size, Share, Growth, Trends, and Forecast, 20192027. According to the report, the globalTestosterone Replacement Therapy marketwas valued at US$ 1,613.7 Mn in 2018 and is projected to expand at a CAGR of 4.4% from 2019 to 2027.

Overview

Growing Awareness about Testosterone Replacement Therapy to Drive Market

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Competitive Landscape

The global Testosterone Replacement Therapy market has been segmented as follows:

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Impact of the Coronavirus on Testosterone Replacement Therapy Market - Jewish Life News

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Jul 16th, 2020 | Filed under Testosterone

COLLIER COUNTY

Collier County Sheriffs Office arrested a 37-year-old man on drug trafficking charges Wednesday after they found heroin, fentanyl and other drugs in his North Naples hotel room.

Joshua James Pyles of East Naples is charged with fentanyl trafficking, heroin trafficking, cocaine trafficking, amphetamine trafficking, and possession of a controlled substance.

CCSO says deputies pulled over Pyles outside the hotel he was staying at in the 4000 block of U.S. 41 North. During the stop, deputies determined that Pyles Florida drivers license was not valid.

Deputies also found methamphetamine in his possession.

Hotel management requested deputies assistance in evicting Pyles from the room he was renting. Deputies escorted Pyles to his room to retrieve his belongings. Pyles opened a dresser drawer where deputies saw small plastic bags containing what they suspected to be marijuana and methamphetamine.

CCSO says deputies conducted a field test on the methamphetamine which came back a positive reaction for amphetamines. Deputies halted the eviction process and began the process for a search warrant.

Around 4:30 p.m. detectives with the Vice and Narcotics Bureau, along with Special Enforcement Team deputies, executed a search warrant at the room where Pyles had been staying.

A search of the room turned up the following items: 166.1 grams of heroin 60 grams of fentanyl 414 grams of methamphetamine 139 grams of cocaine 24 grams of Adderall 52.2 grams of testosterone .6 grams of LSD

Deputies placed Pyles under arrest and transported him to the Collier County jail.

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East Naples man arrested with heroin, fentanyl, meth, cocaine and other drugs in a hotel room - Wink News

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Jul 16th, 2020 | Filed under Testosterone

Coherent Market Insights has recently published the Global research Report Titled Testosterone Replacement Therapy Market. The study provides an overview of current statistics and future predictions of the Testosterone Replacement Therapy Market. The study highlights a detailed assessment of the Market and displays market sizing trends by revenue & volume (if applicable), current growth factors, expert opinions, facts, and industry validated market development data.

The Global Testosterone Replacement Therapy Market research report assembles data collected from different regulatory organizations to assess the growth of the segments. In addition, the study also appraises the global market on the basis of topography. It reviews the macro- and microeconomic features influencing the growth of the in each region. Various methodological tools are used to analyze the growth of the worldwide Testosterone Replacement Therapy Market.

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AbbVie, Inc., Bayer AG, Endo Pharmaceuticals, Inc., Eli Lilly and Company, Kyowa Kirin International plc, Pfizer, Inc., Acerus Pharmaceuticals Corporation, and Perrigo Company plc.

Detailed Segmentation:

By Active Ingredient TypeTestosteroneMethyl TestosteroneTestosterone UndecanoateTestosterone EnanthateTestosterone CypionateBy Route of AdministrationInjectablesParenteral

Major Regions as Follows:

North America (USA, Canada and Mexico)

Europe (Germany, France, the United Kingdom, Netherlands, Russia , Italy and Rest of Europe)

Asia-Pacific (China, Japan, Australia, New Zealand, South Korea, India and Southeast Asia)

South America (Brazil, Argentina, Colombia, rest of countries etc.)

Middle East and Africa (Saudi Arabia, United Arab Emirates, Israel, Egypt, Nigeria and South Africa)

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Part 01: Executive Summary

Part 02: Scope of the Report

Part 03: Research Methodology

Part 04: Market Landscape

Part 05: Pipeline Analysis

Part 06: Market Sizing

Part 07: Five Forces Analysis

Part 08: Market Segmentation

Part 10: Regional Landscape

Part 11: Decision Framework

Part 12: Drivers and Challenges

Part 13: Market Trends

Part 14: Vendor Landscape

Part 15: Vendor Analysis

Part 16: Appendix

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Impact of COVID-19 on Testosterone Replacement Therapy Market How will Growth Develop And Forecast to 2027 | Endo Pharmaceuticals, Inc., Eli Lilly and...

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Jul 16th, 2020 | Filed under Testosterone

by: Erin Coulehan and Nexstar Media Wire

EL PASO, Texas (KTSM) Scientists and medical experts are grappling to learn as much as possible about the biological impact of COVID-19 on the body.

New research examining COVID-19 and human sperm suggests potential risks for male infertility as well as sexual transmission.

A study published last month in JAMA analyzed semen samples of 38 COVID-19 patients and found the presence of the virus in 15% of them.

According to researcher Dr. John Aitken, COVID-19s pathological impact on those tested is underscored by data that shows active cases dramatically reduce testosterone to luteinizing hormones. Reduction in testosterone has a significant impact on the bodys responsiveness to Leydig cells, which stimulate the secretion of sex steroids.

Aitken said the finding is to be expected because the blood-testis barriers offer little defense against viral invasion. Pathogenic viruses such as HIV, hepatitis, mumps and HPV have been linked to testes damage that causes host infertility. The presence of the virus in the testes also leaves the host susceptible to transmitting the disease to sexual partners.

It should be emphasized spermatozoa have a demonstrable capacity to carry viral infections from the male to the female reproductive tract, said Aitken. As happens during the sexual transmission of Zika, for example. Zika virusis a mostly mosquito-borne virus that can also be sexually transmitted.

With the coronavirus, the corona-shaped spike that gives the virus its name targets ACE2 enzymes that are found in many testes cell types. Additionally, the COVID-19 virus may also gain access to male sperm cells once they leave the testes, which could be very dangerous in terms of transmission.

Mature sperm have all the equipment needed to bind and fuse with COVID-19, and then reverse transcription of viral RNA into proviral DNA. The reverse transcription produces double-stranded DNA that is integrated into the genetic material of the person. This means that human sperm can act as a vehicle for sexually-transmitted COVID-19 transmission.

A COVID-19 attack on human sperm leads to a build-up of angiotensin II, which is a hormone that regulates kidney function and blood pressure. Increased levels of this hormone cause an immune response against the invading COVID-19 virus particles that increases the availability of reactive oxygen species that causes cell death.

Prolonged exposure to elevated angiotenstin II levels can lead to cell death in sperm.

The available research suggests that when the ACE2 enzyme cleaves at specific amino acids, the exposure causes decreased sperm viability and function and can ultimately result in a loss of male fertility.

Originally posted here:
Coronavirus can cause male infertility and be transmitted sexually according to new research - WJW FOX 8 News Cleveland

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Jul 16th, 2020 | Filed under Testosterone
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