TOPIC:

Hi Sandi,

Since you asked me to write in the General Section, I want to get connected to an expert on ITP for a second opinion. Waiting for some recommendations.

Where does your mom live?

I meant to start a new post in the General Section and give your location. Usually within a few days, someone will respond with a recommendation.

You need to make a new topic so that people will see your question - go to
this same section:

Adults With ITP > General ITP Discussion

Under that you will see:
New Topic - Mark Topics Read - Subscribe

Click on "New Topic" and write your question & give it a subject line

I did respond in the other thread - asking you what Pak meant in your profile.


A lot of times there aren't "experts" in ITP where someone lives - but a really good hematologist [and they usually are oncologists too] should be fine. Some know more than others so you just have to figure that out.

Immune thrombocytopenia (ITP) represents the epitome of acquired bleeding diseases for the hematologist. Stemming from the interest for the safety of thrombopoietin-receptor agonists (TPO-ra) romiplostim and eltrombopag, recent data have investigated if thrombotic risk is also increased in this disorder. In patients not treated with TPO-ra, a slightly higher risk of venous thrombosis (VTE) is consistently found in ITP, but not to a rate demanding special attention in the generality of cases. No significant increase of arterial thrombosis (AT) is apparent. However, age, splenectomy, and personal risk factors may put some ITP patient to a particularly higher risk of venous and arterial thrombosis (three to four times higher than the average subject). Patients exposed to TPO-ra present indirect evidence of a much higher risk of both AT and VTE. Unfortunately, no matched control population is available and the prospective and registrative nature of these studies may have emphasized the incidence of thrombosis, which was recorded as adverse event. The clinician should be able to individualize the best treatment for the patient, taking also into account the thrombotic risk, limiting active treatment of ITP to those patients really at risk of bleeding. Am. J. Hematol. 91:39-45, 2016. © 2015 Wiley Periodicals, Inc.

© 2015 Wiley Periodicals, Inc.

www.ncbi.nlm.nih.gov/pubmed/26547507

www.medscape.com/viewarticle/858122

Abstract
BACKGROUND:

Because many physicians seem reluctant to recommend splenectomy for elderly patients with immune thrombocytopenia (ITP), we investigated the safety and efficacy of splenectomy and the predictive factors for response in these patients.
METHODS:

184 patients with primary ITP were retrospectively analyzed based on age at splenectomy: an elderly group (≥60 years, n = 52) and a younger group (<60 years, n = 132).
RESULTS:

There was no difference in the response rate of elderly versus younger patients (80.7 vs. 80.3%, p = 0.466). Relapse (45.2 vs. 22.6%, p = 0.006), complications, and median postoperative stay (9.5 vs. 7 days, p = 0.019) were significantly higher in the elderly group. The 5-year relapse-free survival of responders was 51.8% in the elderly group and 76.3% in the younger group (p = 0.002). Response to any treatment before splenectomy (HR 2.9, 95% CI: 1.24-6.80, p = 0.014) and platelet count on postoperative day 14 ≥200 × 109/l (HR 31.43, 95% CI: 4.15-238.28, p = 0.001) were independent factors for a favorable response.
CONCLUSIONS:

Age ≥60 years did not influence the response to splenectomy but was associated with increased relapse and postoperative complications. Splenectomy could provide a durable long-term response for elderly ITP patients.

© 2016 S. Karger AG, Basel.

www.ncbi.nlm.nih.gov/pubmed/26771656

Abstract

The etiologies of secondary idiopathic thrombocytopenic purpura (ITP) include infection, autoimmune disease, and immunodeficiency. We report the cases of three elderly patients who developed ITP after receiving influenza vaccinations. The platelet count of an 81-year-old woman fell to 27,000/μL after she received an influenza vaccination. A 75-year-old woman developed thrombocytopenia (5,000 platelets/μL) after receiving an influenza vaccination. An 87-year-old woman whose laboratory test values included a platelet count of 2,000/μL experienced genital bleeding after receiving an influenza vaccination. After Helicobacter pylori (HP) eradication or corticosteroid treatment, all of the patients' platelet counts increased. Influenza vaccination is an underlying etiology of ITP in elderly patients. HP eradication or corticosteroid treatment is effective for these patients. Clinicians should be aware of the association between ITP and influenza vaccinations.

www.ncbi.nlm.nih.gov/pubmed/26998369

LORHAM PARK, N.J.-- Protalex, Inc. (OTCQB:PRTX), a clinical-stage biopharmaceutical company, today announced that following a planned interim data review by its independent Safety Monitoring Committee (SMC), the Company is continuing enrollment and increasing the dose for subjects in its European Phase 1b study of PRTX-100 in adults with persistent/chronic Immune Thrombocytopenia (ITP) (PRTX-100-203 Study). The dose of PRTX-100 for subjects in the next treatment group (6.0 micrograms/kg) will be twice that of the initial starting dosage (3.0 micrograms/kg).

PRTX-100, Protalex’s lead drug candidate, is a highly purified form of Staphylococcal protein A (SpA) and has been the subject of ongoing clinical development in both ITP and rheumatoid arthritis (RA). PRTX-100 was recently granted Orphan Drug Designation in the U.S. and in Europe for the treatment of ITP and is currently the subject of clinical studies in both the U.S. and Europe.

The 203 Study is an open-label, dose escalating study that can enroll up to 30 patients in as many as five cohorts. Each patient will receive four weekly intravenous doses of PRTX-100 and will be monitored for up to 48 weeks thereafter. The primary study endpoint of the 203 Study is safety. Secondary endpoints include safety, platelet response, immunogenicity, and pharmacokinetics. Enrollment in the 203 Study is currently taking place at several study sites in France.

“We continue to be encouraged by the ongoing progress both in the 203 trial in Europe and in the parallel 202 trial in the U.S., which support the development of a new treatment for ITP. We are pleased to continue patient enrollment and dose escalation in the 203 Study and look forward to advancing to the next cohort of the study,” stated Richard J. Francovitch, Ph.D., Protalex’s Vice President ITP Programs.

About Immune Thrombocytopenia (ITP)

ITP is an autoimmune-mediated condition characterized by bruising and increased bleeding as a result of immune-mediated accelerated destruction of platelets and impaired production of platelets. The diagnosis of ITP is based upon a low platelet count, usually less than 100,000 per microliter of blood, in the absence of other possible causes of reduced platelet numbers such as an underlying illness or medication.

About PRTX-100

PRTX-100, a new generation immunomodulatory therapy, is a highly purified form of SpA, an immunomodulatory protein known to modify aspects of the human immune system. PRTX-100 has the ability, at very low concentrations, to bind to human B-lymphocytes and macrophages and to modulate immune processes. Pre-clinical data indicate that PRTX-100 may have the potential to treat ITP by reducing the immune-mediated destruction of the platelets. The two most recently approved drugs used to treat ITP, Nplate® (romiplostin) and Promacta®/Revolade™ (eltrombopag) both increase the production of platelets but do not appear to affect the underlying platelet destruction process.

The safety, tolerability and pharmacokinetics of PRTX-100 have been characterized in six clinical studies. In three Phase 1b clinical trials in adult patients with active RA, PRTX-100 was generally safe and well tolerated at all dose levels, and at certain higher doses, more patients showed improvement in measures of RA disease activity than did patients at the lower dose or placebo cohorts. PRTX-100 is administered as a short intravenous infusion.

Nplate® is a registered trademark of Amgen, Inc. and Promacta®/Revolade™ are registered trademarks of Novartis AG.

About Protalex, Inc.

Protalex, Inc. is a clinical-stage biopharmaceutical company focused on the development of a class of drugs for treating autoimmune and inflammatory diseases including RA and ITP. In the U.S., Protalex has open IND’s for the treatment of RA and ITP and in Europe, an open IMPD for ITP. Please visit Protalex’s website at www.protalex.com to learn more about Protalex and its lead drug candidate, PRTX-100.

Forward-Looking Statements

Statements in this press release that are not statements of historical or current fact constitute "forward-looking statements." Such forward-looking statements involve known and unknown risks, uncertainties and other unknown factors that could cause the Company's actual operating or clinical results to be materially different from any historical results or from any future results expressed or implied by such forward-looking statements. In addition to statements that explicitly describe these risks and uncertainties, readers are urged to consider statements that contain terms such as "believes," "belief," "expects," "expect," "intends," "intend," "anticipate," "anticipates," "plans," "plan," to be uncertain and forward-looking. The forward-looking statements contained herein are also subject generally to other risks and uncertainties that are described from time to time in the Company's filings with Securities and Exchange Commission.

View source version on businesswire.com: www.businesswire.com/news/home/20160502005049/en/


Released May 2, 2016


www.protalex.com/news/press-releases/detail/386/protalex-receives-positive-interim-review-from-independent

EXTEND study provides long-term safety data for Revolade that are consistent with the findings from the pivotal Phase III RAISE study[1,2]

Immune thrombocytopenia (ITP) is a rare and potentially serious blood disorder, characterized by bruising, bleeding and in some cases, serious hemorrhaging[3]

Novartis continues to build on its heritage in hematology to advance care for patients suffering from serious hematologic disorders such as ITP

Basel, June 10, 2016 - Novartis today announced data from the largest study of its kind confirming the long-term safety profile of Revolade (eltrombopag) in adults with chronic immune (idiopathic) thrombocytopenia (ITP), with data for up to 6 years in some patients (median exposure was 2.4 years).[1,2] Additional data from the study will also be presented that showed long-term oral administration of Revolade was effective in increasing and maintaining platelet counts in adult patients who had their spleens removed (splenectomized) as well as those who did not (non-splenectomized)[4]. The final results of the study and sub-analysis will be presented at the 21st Congress of the European Hematology Association (EHA) in Copenhagen, Denmark.

ITP is a rare and potentially serious blood disorder where the blood doesn`t clot as it should due to a low number of platelets. As a result, patients experience bruising, bleeding and, in some cases, serious hemorrhage that can be fatal. ITP may also affect a patient`s quality of life, as it is often associated with fatigue and depression as well as a fear of bleeding that may limit everyday activities[3].

More......

finance.yahoo.com/news/novartis-highlights-long-term-safety-063201133.html

Splenectomy remains the preferred treatment for chronic immune thrombocytopenia (ITP) after corticosteroid failure, despite the risks of despite surgical complications and infection. The aim of this study was to assess the efficacy of and tolerance to rituximab through a retrospective analysis of 35 refractory/relapsing ITP patients treated from 2004 to 2013. The median age of subjects was 46 years (14-80). Rituximab was given at a weekly dose of 375 mg/m2 for 4 weeks. Median time from diagnosis to first infusion was 17 months (1-362) and follow-up was 47 months (2-133). The overall response rates at 1 and 2 years after the first infusion were 47 and 38 %, with complete response rates of 24 and 25 %, respectively. Median duration of response was 38 months (1-123), with 37 % of patients maintaining a durable response (>1 year). Twenty-nine percent of patients had undergone splenectomy. A durable response after rituximab was more frequently observed in patients undergoing second-line therapy than those in third or later (83 versus 35 %, P = 0.01). Forty-four percent of patients experienced mild hypogammaglobulinaemia after rituximab, and no clinical infection occurred. To conclude, rituximab should be considered as an alternative treatment to splenectomy. Its efficacy and safety profile should lead us to choose this medical option therapy before surgery for ITP patients.

www.ncbi.nlm.nih.gov/pubmed/27040278

During the last two decades, new therapeutic strategies have been developed, particularly anti-CD20 agents and thrombopoietin-receptor (TPO-r) mimetics, for immune thrombocytopenia (ITP). However, although the new efficient drugs have deeply modified the therapeutic strategy and the disease prognosis, there are still unmet needs and challenges. Concerning rituximab, reassuring data concerning its safety have recently been reported. The main limitation of the treatment is its modest long-term efficacy, with frequent disease relapse. Maintenance treatment or association with other immunomodulatory drugs such as dexamethasone may achieve better long-term response. With failure of one of the available TPO-r agonists (ie, romiplostim and eltrombopag), another can be used. Switching may be beneficial, with more than 50% chance of response, and could limit the risk of platelet fluctuation occasionally observed with these treatments. According to the mechanism of action of TPO-r agonists, a rapid relapse of thrombocytopenia should be observed after they are stopped. Several recent observational studies suggested sustained responses in patients achieving complete response with TPO-r agonists and who stopped the treatments. Prospective studies to confirm these unexpected data are needed. Thrombosis in ITP is a concern, particularly with TPO-r agonists, even though the pivotal studies of eltrombopag and romiplostim did not report a higher incidence of thrombosis events with TPO-r agonists than placebo. Despite these reassuring data, the risk of thrombosis with TPO-r agonists remains unanswered, particularly with secondary ITP or in older adults.

Copyright © 2016 Elsevier Inc. All rights reserved.

www.ncbi.nlm.nih.gov/pubmed/27312163

Common variable immunodeficiency (CVID) is a heterogeneous group of diseases, characterized by primary hypogammaglobulinemia. B and T cell abnormalities have been described in CVID. Typical clinical features of CVID are recurrent airway infections; lymphoproliferative, autoinflammatory, or neoplastic disorders; and autoimmune diseases among which autoimmune thrombocytopenia (ITP) is the most common. The coexistence of immunodeficiency and autoimmunity appears paradoxical, since one represents a hypoimmune state and the other a hyperimmune state. Considering both innate and adaptive immune response abnormalities in CVID, it is easier to understand the mechanisms that lead to a breakdown of self-tolerance. CD21(low) B cells derive from mature B cells that have undergone chronic immune stimulation; they are increased in CVID patients. The expansion of CD21(low) B cells is also observed in certain autoimmune diseases. We have studied CD21(low) B cells in patients with CVID, CVID, and ITP and with ITP only. We observed a statistically significant increase in the CD21(low) population in the three pathological groups. Moreover, we found statistical differences between the two groups of CVID patients: patients with ITP had a higher percentage of CD21(low) cells. Our data suggest that CD21(low) cells are related to autoimmunity and may represent a link between infection and autoimmunity.

Copyright © 2016 Elsevier B.V. All rights reserved.


www.ncbi.nlm.nih.gov/pubmed/27392505

Allogeneic platelet transfusions are widely used for the prevention and treatment of bleeding in thrombocytopenia. Recent evidence suggests platelet transfusions have limited efficacy and are associated with uncertain immunomodulatory risks and concerns about viral or bacterial transmission. Alternatives to transfusion are a well-recognised tenet of Patient Blood Management, but there has been less focus on different strategies to reduce bleeding risk by comparison to platelet transfusion. Direct alternatives to platelet transfusion include agents to stimulate endogenous platelet production (thrombopoietin mimetics), optimising platelet adhesion to endothelium by treating anaemia or increasing von Willebrand factor levels (desmopressin), increasing formation of cross-linked fibrinogen (activated recombinant factor VII, fibrinogen concentrate or recombinant factor XIII), decreasing fibrinolysis (tranexamic acid or epsilon aminocaproic acid) or using artificial or modified platelets (cryopreserved platelets, lyophilised platelets, haemostatic particles, liposomes, engineered nanoparticles or infusible platelet membranes). The evidence base to support the use of these alternatives is variable, but an area of active research. Much of the current randomised controlled trial focus is on evaluation of the use of thrombopoietin mimetics and anti-fibrinolytics. It is also recognised that one alternative strategy to platelet transfusion is choosing not to transfuse at all.

Br J Haematol 2016(Sep); : 1-9.
Alternatives to allogeneic platelet transfusion.
Desborough MJ, Smethurst PA, Estcourt LJ , Stanworth SJ
NHS Blood and Transplant, John Radcliffe Hospital, Oxford, UK. michael.desborough@ouh.nhs.uk.

This article summarizes our approach to the management of children and adults with primary immune thrombocytopenia (ITP) who do not respond to, cannot tolerate, or are unwilling to undergo splenectomy. We begin with a critical reassessment of the diagnosis and a deliberate attempt to exclude nonautoimmune causes of thrombocytopenia and secondary ITP. For patients in whom the diagnosis is affirmed, we consider observation without treatment. Observation is appropriate for most asymptomatic patients with a platelet count of 20 to 30 × 109/L or higher. We use a tiered approach to treat patients who require therapy to increase the platelet count. Tier 1 options (rituximab, thrombopoietin receptor agonists, low-dose corticosteroids) have a relatively favorable therapeutic index. We exhaust all Tier 1 options before proceeding to Tier 2, which comprises a host of immunosuppressive agents with relatively lower response rates and/or greater toxicity. We often prescribe Tier 2 drugs not alone but in combination with a Tier 1 or a second Tier 2 drug with a different mechanism of action. We reserve Tier 3 strategies, which are of uncertain benefit and/or high toxicity with little supporting evidence, for the rare patient with serious bleeding who does not respond to Tier 1 and Tier 2 therapies.

See more at:

www.bloodjournal.org/content/128/12/1547.full

hi, my father is diagnosed with itp and in 2014 april he was diagnosed with T-cell lymphoma. he went through the entire treatment and got cured. then again to be on a safer side last may 2016 he went through stem cell transplant. it took time to recover but he recovered. now again since 1st jan 2017 he was having cold n cough and his local physician prescribed some antibiotics but not got cured. on 28 jan his condition was very critical when he was taken to the hospital. his platelets was 1k and homeoglobin was 3.3.doctors did biopsy and biopsy reports were normal so doctors concluded as itp.since then doctors tried ivig, steroids,several blood transfusions and platelets transfusions as well but nothing worked for him.He also have symptoms like bruises on his hands and blood in motion. day before yesterday doctors tried revolade but his platelets came down to 3k from 6k. from today they are starting rituximab. please tell me if it will work for him

Hi Shikha,
Unfortunately no one can say for sure if Rituxan will work for your father or not. It's a game of trial and error. Sometimes it takes time for a medication to work.

Shikha, as I understand Revolade normally takes 2 weeks to raise counts. Some 80% will respond.
As for Rituximab, that normally takes 4 to 12 weeks to raise counts and 60% will respond.

It could be a long 2 weeks. Do the doctors continue to administer platelet transfusions or IVIG to help him ?

The management of patients with immune thrombocytopenia (ITP) is rapidly evolving. Over the last 15 years, a number of novel treatments have improved practice, with many steroid-sparing agents and a reduction in the progression to splenectomy. Although this has improved clinical care, many therapeutic challenges remain. There is no diagnostic test, no biomarkers to direct treatment and few comparative studies to help management decisions. Development of up to date guidelines is difficult with little high-grade evidence. First line treatment continues to be steroids and intravenous immunoglobulins (IVIG) although both are often poorly tolerated and not curative. Common second line treatments include rituximab, immunosuppressive agents, such as azathioprine and mycophenolate mofetil, and the thrombopoietin receptor agonists romiplostim and eltrombopag. There are no comparative studies to decide between these agents and treatment is generally individualized, depending on comorbidity. Use of splenectomy has declined and is generally reserved for patients with chronic disease, although the exact position of splenectomy is subject to debate. Further understanding of the cause of disease in individual patients may help guide treatment. Randomized controlled studies of common treatments and novel treatments for refractory patients are urgently needed.

© 2017 John Wiley & Sons Ltd.

www.ncbi.nlm.nih.gov/pubmed/28295192

The author of that paper is Nichola Cooper who is said to be taking over from Drew Provan. Wish I could read the whole paper.

Anon ..I have a pdf copy but cannot load it to the site. If you message me your e mail address I can send it. Anne

Immune thrombocytopenia (ITP) is a common hematologic disorder characterized by isolated thrombocytopenia. ITP presents as a primary form characterized by isolated thrombocytopenia (platelet count < 100 × 109/L) in the absence of other causes or disorders that may be associated with thrombocytopenia, or a secondary form in which immune thrombocytopenia develops in association with another disorder that is usually immune or infectious. ITP may affect individuals of all ages, with peaks during childhood and in the elderly, in whom the age specific incidence of ITP is greatest. Bleeding is the most common clinical manifestation of ITP, with the risk of bleeding and related morbidity increased in elderly patients. The pathogenesis of ITP is complex, involving alterations in humoral and cellular immunity. Thrombocytopenia is caused by antibodies that react with glycoproteins expressed on platelets and megakaryocytes (glycoprotein IIb/IIIa, Ib/IX and others), causing shortened survival of circulating platelets and impairing platelet production. Diminished numbers and function of regulatory T cells, as well as the effects of cytotoxic T cells also contribute to the pathogenesis of ITP. Corticosteroids remain the most common first line therapy for ITP, occasionally in conjunction with intravenous immunoglobulin (IVIg) and anti-Rh(D). However, these agents do not lead to durable remissions in the majority of adults with ITP, and considerable heterogeneity exists in the use of second line approaches, which may include splenectomy, Rituximab, or thrombopoietin receptor agonists (TRAs). This review summarizes the classification and diagnosis of primary and secondary ITP, as well as the pathogenesis and options for treatment. Remarkable advances in the understanding and management of ITP have been achieved over the last decade, though many questions remain.
Much more at:
www.ncbi.nlm.nih.gov/pmc/articles/PMC3672858/

Rituximab is an effective therapy resulting in a platelet count improvement in 60% of patients with immune thrombocytopenia (ITP). Rituximab depletes B cells; thus, a reduction in platelet autoantibody levels would be anticipated in patients who achieve a clinical response to this treatment. The objectives of this study were to determine whether rituximab was associated with a reduction in platelet autoantibody levels, and to correlate the loss of autoantibodies with the achievement of a treatment response. We performed a case-control study nested within a previous randomized controlled trial of standard therapy plus adjuvant rituximab or placebo. We measured platelet-bound anti-glycoprotein (GP) IIbIIIa and anti-GPIbIX using the antigen capture test. Of 55 evaluable patients, 25 (45%) had a detectable platelet autoantibody at baseline. Rituximab was associated with a significant reduction in anti-GPIIbIIIa levels (P = 0·02) but not anti-GPIbIX levels (P = 0·51) compared with placebo. Neither the presence of an autoantibody at baseline nor the loss of the autoantibody after treatment was associated with a response to rituximab. The subset of patients with persistent autoantibodies after treatment failed to achieve a platelet count response, suggesting that persistence of platelet autoantibodies can be a marker of disease severity.

© 2017 John Wiley & Sons Ltd.

www.ncbi.nlm.nih.gov/pubmed/28444742

Over the past decades, a wealth of information has been reported about the pathogenic features of immune thrombocytopenia (ITP). To this day, however, it is unclear whether the immune abnormalities associated with ITP play causative roles in the disease or are secondary epiphenomena brought on by the inflammatory processes that are associated with the disorder. Like the majority of all autoimmune diseases, ITP is an organ‐specific disease and abnormalities in immune cell types, such as antigen‐presenting cells (APC), T cells and B cells have been shown to play some sort of role in the initiation and/or perpetuation of the disease. This review will discuss recent advances in understanding three immune cells important in ITP pathophysiology: APC, T cells and B cells, and will review how they interact with each other to initiate and perpetuate ITP, particularly the chronic form of the disorder. It will also focus on new data related to the genetics of the disorder and discuss relevant animal models of ITP.
See more.......

onlinelibrary.wiley.com/doi/full/10.1111/bjh.12480

83 yr old post splenectomy as a child - count usually around 98,000, but when I had the Type A Flu in January 2020 (now wonder if it was COVID) and count went down to 30,000. After 2 days in hospital pumped full of TamiFlu, Azityromycin, IV fluids and 1 IV dose of Prednisone, at 10 day follow-up with my Internist, platelet count 450,000! It has never in my lifetime been that high. Weird! Anyone else had a similar experience?

Reading your bio encouraged me that one can have a long life with itp )
Salute!

rwrourk@gmail.com wrote:

83 yr old post splenectomy as a child - count usually around 98,000, but when I had the Type A Flu in January 2020 (now wonder if it was COVID) and count went down to 30,000. After 2 days in hospital pumped full of TamiFlu, Azityromycin, IV fluids and 1 IV dose of Prednisone, at 10 day follow-up with my Internist, platelet count 450,000! It has never in my lifetime been that high. Weird! Anyone else had a similar experience?

If you do a search on PDSA website of the word 'TamiFlu' you'll find ITP'ers who have reported count rises with it.
pdsa.org/discussion-group/search.html?query=TamiFlu&searchdate=all&order=inc&childforums=1&limit=30&start=0
Specifically users: 'Tara0815' and 'semd'.

Thread on the subject of TamiFlu:
pdsa.org/discussion-group/7-treatment-general/28670-tamiflu-and-increased-platelet-count-in-husband.html#48148

Best I can gather,
1) those that respond to TamiFlu are either row 2 or row 2/1 in my treatments table. Other ITP'ers don't get a count rise with the drug.
bottools.com/Hal/ItpTypes.html

2) Flu Type A(H3) seems to cause the most trouble. Newly triggered ITP or relapse either one.
pdsa.org/discussion-group/7-treatment-general/30169-no-response-to-ivig-ack.html#65712

If you go to CDC data on the Flu, and click on 'group by virus', it looks like A(H3), A(H1N1), and B(Victoria) are the Flu strains active right now.
gis.cdc.gov/grasp/fluview/flu_by_age_virus.html

If you want to get a better understanding of what is theorized to be going on, on that first link above, look for 'desialylation' (or desilylated) and what that is and does to platelets. It's all about the liver.