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Polycythemia
Vera--Treatment
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Please
email us your suggestions and experiences.
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Outline
the treatments that have been used historically and then why most of
them are counterindicated at this time. Site recent research on phlebotomy,
interferon, hydroxia etc.
Personal experiences from people who are using different treatments. Treatments of symptoms. |
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Phlebotomies decrease blood-iron levels, which controls the amount of HG produced, which in turn lowers the HCT. Recent studies have shown that decreased iron levels decrease the incidence of heart disease. Also, according to well known PV specialist at Johns Hopkins, Dr. Spivak: "Iron deficiency-related hyperviscosity is a test tube artifact tha also has no physiologic basis. A state of chronic iron deficiency that limits erythropoiesis is actually the ultimate goal of phlebotomy therapy in polycythemia vera, a goal this is unfortunately frequently not achieved judging from published results."
Reference to Iron intake from Dr. Spivak in an article he wrote in December 2002 for the American Society of Hematology: " Chronic iron deficiency that limits erythropoiesis is actually the ultimate goal of phlebotomy therapy in polycythemia vera, a goal that is unfortunately frequently not achieved judging from published results. . . Venesection is a safe and immediately effective therapy and its desired side effect, iron deficiency, is not a liability, claims that cannot be made for any of the surrogate therapies for polycythemia vera that have been proposed to date. Reduction of the red cell mass and maintaining it at a physiologic level removes a major source of complications and may also alleviate systemic hypertension and pruritus and reduce splenomegaly . . . Occasionally, with blood loss or overzealous phlebotomy, symptomatic anemia can ensue. Judicious iron replacement can accelerate the recovery process but too much iron will result in an explosive increase in red cell mass."
MPD VOICEETM, Newsletter volume 4 No. 1, February 1999: What About Iron in Patients Treated With Phlebotomy? "Of necessity, if it (iron) is not replaced it will decrease. In fact, the long term objective of phlebotomy is to inhibit red blood cell production by creating a state of iron deficiency. Red blood cell production requires iron store in the bone marrow. The iron is incorporated into hemoglobin (Hg). When iron is absent, the red blood cell parent cells (precursors) will turn out RBC that contain less Hg. That is why they are smaller in size and the mean corpuscular volume (MCV) is low. It is not appropriate to replenish the iron stores if the PV is still active because this will stimulate production of red blood cells and raise the HCT and blood viscosity and you will be back where you started-needing more frequent phlebotomies. What Is The Effect of Iron Deficiency on Your Body At a normal HCT, there should be non. In the immediate post-phlebotomy period the symptoms of weakness, headache, etc. are due to the acute change in blood volume. The state of iron deficiency in patients without PV leads to iron deficiency anemia and when the HCT gets low enough they will feel weak and tired and have headaches and other symptoms. That is due to a low HCT with compromise of oxygen delivery. This is not the case in an iron deficient PV patient who has a normal HCT. Ir5on is needed for many metabolic tasks in the body, but these take priority over hemoglobin synthesis, so that the iron left in your body is usually sufficient for these needs. If your body does not need the excess red blood cells that your are making, then you are better off without them and there should be a net gain in your health status and a net decrease in your risk of thrombosis or bleeding. You should be cheered by the recent report that iron contributes to cardiovascular and coronary heart disease and that iron deficiency may protect against heart attacks. Wouldn't it be a laugh if your phlebotomies were doing more that just correcting your blood viscosity and were actually contributing to your increased survival? As we will discuss in the future, I have often wondered why patients with PV and all the risks that the disease poses have a normal life expectancy. It certainly suggests that there are factors at play that prolong life. I'll talk about cholesterol metabolism in PV and other MPDs in a future edition of the MPD Voice." I think that the above article fails to mention that the body naturally rejects the red blood cells that are misshapen due to lack of iron. In other words, the body with PV continues to make too many RBCs, but they are mutated because of the lack of iron and so are rejected by the body. And so the body needs less phlebotomies after iron stores are reduced. I'll try to find the reference for this too if anyone is interested.
Hydroxia User Personal Testimonials:
From: "Nelson Kennedy" Date: Tue Dec 28, 2004 12:00 pm Subject:
Why take HU?
I've been taking HU for three years now. I started at around 10 caps per week
and I'm now on 14 (1 gram per day) and I am hopeful of having the dosage reduced
a little when I go back to my haematologist in January as a recent CBC shows
my HCT at around 42 and it can stand being a little bit higher than that.
The reason I take HU is because I have an adverse reaction to venisection
(phlebs). My platelets shoot up when I have blood taken off because my system
says 'oops, major bleeding, need more platelets' - quite the opposite effect
to that which we wanted. At diagnosis my HCT was around .64 and platelets
around 900. HU has maintained my HCT at <.45 and platelets at <500, sometimes
as low as 375. I'm coming up to my 63rd birthday, so some of what I am about
to say may be related to that rather than exclusively to HU, but I have the
impression that I am aging more quickly since taking HU. This shows in these
ways: Aging of the skin - my hands are becoming the hands of an old man, thin
skin, easily broken when knocked, bleeding easily but also quickly stopped
with a band aid. My skin in general has become very soft, particularly upper
legs and I have lost hair from my legs. I was balding severely before PV -
as is the norm for males in my family - and that does not seem to have become
any worse, but my remaining 'friars fringe' is incredibly soft to touch. My
beard does not grow as strongly as before and it too is quite soft - I had
occasion to grow it for a minor theatrical piece a couple of months ago when
I played (the late) Maurice Gibb. I took the lead in 'Words' and chorus in
'Gotta Get a Message to You'. I am prone to some infection. I did not have
a head cold for more than ten years, but since taking HU I have had one or
two each year. No big deal. It's just something I used to be able to fend
off but now don't. I have a tendency towards cellulitis which flares up in
my legs without much provocation. We're working on this with some lab work
at present. It may be quite unrelated to the HU. On balance I think HU has
been good for me. With my numbers being kept close to normal I have no issues
with itching. Life for me is about as normal as it gets. I have made the concession
of getting out of a high pressure occupation (I was CEO of a major charity)
by retiring a few years ahead of time and now work on a contract basis at
my own pace. Whether or not to take HU requires, in my opinion, sufficient
information to make an informed decision. I was blessed by a haematologist
who was very open and worked through the alternatives with me. For me, I felt
HU was a better option than Interferon. We talked openly about the risks.
She was able to tell me that in about twenty years of practice she has never
yet lost a PV patient on HU to progression to leukemia. I'm not planning on
being the one to break that pattern! Nelson Kennedy Christchurch, New Zealand
More From Nelson December 17 2005:
We walk a fine line sometimes. The way the HU (Hydroxyurea)
works is to cull out stem cells in the bone marrow before they
form into either red, while or platelet cells. So it does not discriminate
and ought to result in a lowering of all three cells types. We can get by
with relatively low platelets – 375 to 750 I think is regarded as the norm
– quite a range. And of course, reducing the reds is largely what it is about
for us. But reducing the whites does have its downsides. They are an important
part of our immune system and I won’t claim to be free of unwanted side effects.
I am now prone to cellulitis in one leg (why not the other I don’t know!)
and I have learned to humour it and keep it under control although I did get
caught earlier this year when I seemed to be attacked on several fronts at
once with flu like symptoms and my leg got away on me and required antibiotics
to get it back under control. I went for years without even getting a head
or chest cold – at least ten years, maybe 15. But the last few years I have
succumbed to a head cold a couple of times a year and I can get a bit bronchial
if I don’t keep warm in winter. Maybe HU has just made me ‘normal’! I acknowledge
the risk of progression to leukemia but I play it down because the stats are
not alarming, in my opinion. About a 5% chance of that happening compared
with a general populace risk of 2 to 3%. The reality for me is that HU keeps
me alive! And I’m grateful for that. If the stats are right – and I have no
reason to disbelieve them, then on mean survival rates I should have started
pushing up daisies about 3½ years ago had I not been diagnosed and treated.
Alleluia!
Hi there, I have been reading everyone's comments with great interest. You all have a different story to tell and the support for others is tremendous. Just wanted to give some encouragement to those that are concerned about getting the disorder earlier in life and having to take hydroxyurea. I was 37 when first diagnosed (taken from work to hospital with a thrombosis) and was informed, after the bone marrow test, that I'd had polycythemia for at least 12 months. I'm now 51 years of age and have been taking hydroxyurea for 14 years. (Reduced the dose recently and all's well). I feel sure that I've still got a lot of years left, and a holistic approach to this disorder along with a healthy respect for my specialist are all important factors in getting along with my everyday life. A good attitude takes you far. Came across the site by accident, and am very grateful for the discovery! Best wishes to you all and, please, don't worry.... Best Wishes Jeanette - Perth, Western Australia May 16, 2006 jeanette.han@...>
New Side Effects Reported:
Hi everyone, My name is Joanne and for those of you who don't know me I am
a nurse but also a person with PV. Today when I opened my critical care newsletter
there was an article on Hydrea and new side effects reported from patients
who are taking it. According to the report vasculitic ulcerations and gangrene
are to be added to the side effect list. I felt as though I should let all
of you know . For those of you on hydrea if you are showing any ulcerations
make sure you let your doctor know. I'm not sure if this number is for health
care professionals only but you can call if you have questions. 1-800-321-
1335. You can speak with a representative directly. Also ask for adverse Event
Report document form code #2000. I was told when I called that side effects
are noted more on patients who are also on interferon. If I receive any info
(good or bad) I will keep all of you informed. Sincerely, Joanne oven3broke"
DATE: 29 Jan 1997 TO: MPD-SUPPORT-L FROM: R. Freeburg SUBJECT: review of Silver's new article INTERFERON ALFA: EFFECTS OF LONG-TERM TREATMENT FOR POLYCYTHEMIA VERA by Richard Silver, published in Seminars in Hematology, Vol.34, No. 1, 1997. NEED: Silver begins with the problems of the "standard," existing treatments for PV - phlebotomy-only and hydroxyurea (HU). Here, and again later in the article, he emphasizes that PV, treated only by phlebotomy, progresses sooner to myelofibrosis. He uses the Najean data (which we have listed before) and states that "some form of myelosuppression, especially for younger patients, is mandatory." (This is consistent with the other current literature by Najean, Rain, Boivin, and - with respect to platelets- Messinezy.) The problems with HU (also introduced here and mentioned through out the article) include the potential for leukemia - chromosome abnormalities have been found in HU cell cultures and in 36% of patients treated with HU (one study). Other problems - failure to control the disease (platelets, hematocrit, splenomegaly), constitutional problems (pruritus, night sweats), and toxicity (thrombocytopenia/leukopenia, gastric symptoms, rash). Macrocytosis is also caused by HU (the BIG red blood cells). Silver notes later that previous PVSG "control of the disease" allowed for a hematocrit of up to 50% and permitted more than 6 phlebotomies per year. He states that this is no longer considered satisfactory (controlled). DATA: The article includes the data on 28 patients treated with interferon (IFN) making it the largest and longest follow-up of PV patients treated with IFN. Sixteen of the patients have been followed for more than 6 years (as of the cut-off date of December, 1995). Prior treatment was phlebotomy-only (18 patients) or hydroxyurea (10 patients). It is noted with interest that 23% were under 40 years old. (I can't read all the graphs clearly on my faxed copy, but I guess that must mean 9 patients.) IFN dose was targeted to reach 3 mu/3 x's per wk (or sometimes 5 mu) and adjusted accordingly to keep hematocrit below 45% - an increase or decrease of 25% every 2 months. Although originally, 3 mu was the starting dose, later (to minimize side-effects), all patients were started with 1 mu/3 x's per wk and increased every 2 to 4 weeks by .5 mu until the target dose was reached. Median dose at the end of one year was 10.5 mu/week and at the end of the 2nd year was 7.5 mu/week. So by the end of the second year, most patients were taking LESS than 3 mu/3 x's per week. CLINICAL RESULTS: Phlebotomy requirement before IFN was a median of 10/yr in the phleb-only group and 7/yr in the HU group. Although phlebotomies were still required in 16 patients during the first year (to keep hematocrit below 45%), only 2 patients required phlebotomies the second year. (!!!!) Platelet counts are also charted and again showed a significant response. Only one patient from phleb-only had a platelet count of 625,000 after two years, and the HU group also significantly decreased. Spleen size had also diminished by the end of the second year in all 13 patients who started with splenomegaly. (Even those patients with HUGE spleens - three had over 15 cm below left costal margin when starting.) Iron stores were replenished; hypochromic/microcytic anemia (that's the little red blood cells with little hemoglobin - meaning poor oxygen-carrying capacity - caused by phlebotomies) was corrected. Macrocytosis from HU also corrected. There were no thrombotic events. SIDE EFFECTS: These were generally dose-related and, mainly, of the influenza variety. Thirteen patients reported nothing significant after six months; 15 continued to have some for another six months. Only two patients discontinued the IFN. One lady on IFN for six years was apparently persuaded by another hematologist to switch to HU (this is my drift, not the way Silver stated it) and another went off after developing a bilateral lower extremity neuritis. This did clear up and the 62 yr old woman went on HU plus phlebotomy. One thyroid problem was cleared up; any liver problems returned to normal with temporary cessation of the IFN. (.....Silver does not mention any problems with drug-induced autoimmune disease - unless the thyroid problem could be considered here. IFN-induced autoimmune disease is found in the literature and mentioned to us by Dr. Krieg - a lupus specialist - but, it is seldom severe and, apparently, reversible when it does occur. And, although called "maintenance dose" levels in at least one of the reports on CML, I'm not sure what that dose was.........) Silver notes, interestingly, that tolerance/toxicity are somewhat variable terms that can depend on the physician and patient's conviction about the merits of a treatment. BONE MARROW: Although consistent chromosome abnormalities have not been noted in PV, IFN has given improvement in some instances. However, Silver's patients (other than 2 who remained in clinical remission after a year) needed continued IFN treatment, while bone marrow hypercellularity and reticulum (fiber) remained. Silver emphasizes that IFN in PV is "suppressive," not "curative." UNIQUENESS OF IFN: Megakaryocytes (platelets) are believed to play a special role in the development of myelofibrosis in MPD. (......Remember the strong statements about this in the Messinezy article. We've also noted an interesting article about MPD developing in frequent blood donors and, in another article, it is noted that frequent blood donors have higher concentrations of megakaryocyte colony-forming progenitors. These are strictly my comments, not Silver's!!!.....) Silver notes that platelet-derived growth factor (PDGF) is involved in this fibrosis, along with other growth factors ((including transforming growth factor beta (TGF-beta)). - IFN is known to antagonize (suppress) PDGF. - IFN causes TGF-beta to return to normal levels. - IFN is ANTIangiogenic. (Angiogenesis is the first step in the formation of new blood vessels. This is very important in the growth of malignancies. ) In addition, TGF-beta is a strong promoter of angiogenesis. -IFN inhibits erythroid progenitors in vitro (test tube) and affects platelet maturation, etc. In some reports IFN had corrected biochemical abnormalities of platelets. So IFN is the first drug offered as treatment for PV that actually may be able to alter the course of the disease. Silver calls it the "therapeutic evolution of the PVSG" in its search for PV treatment. (Since phlebotomy-only and hydroxyurea as PV treatments came FROM the PVSG in 1986 -this is VERY interesting as coming in the "last official publication of the PVSG.") Silver summarizes the reasons for using IFN in PV including abatement of constitutional symptoms (like pruritus), maintenance of hematocrit & platelets, avoidence of iron-deficient anemia (from phlebotomies) and macrocytosis (from HU). He also states the LACK OF MUTAGENICITY and PREVENTION OR DELAY OF POST-POLYCYTHEMIA MF if used EARLY in PV (emphasis is mine). RECOMMENDATIONS: Silver concludes with his recommendations for the treatment of PV. It includes phlebotomy to keep hematocrit between 40 and 45% with strict attention to platelets. Interferon (IFN) gradually increasing from 1 mu/3 x's per wk to a target dose of 3 or 5 mu/3 x's per week which then may be modified to keep hematocrit below 45%. He says only occasional phlebotomies should be required after the second year on IFN. He does include aspirin - enteric-coated, 80 mg daily. For YOUNG patients who can not accept IFN, he considers anagrelide (for platelet control) with phlebotomies. For ELDERLY (over 70 years), he considers radioactive phosphorus (P32) or HU.
Interferon Users Personal Testimonials:
Joanne, When my husband was diagnosed, he was 42 and his platelet count was 4 million. He has never had phlebotomies, his doctor told him that they don't work when counts are that high. They immediately put him on hydroxurea, which started his count down. It is three years later, his platelet count is 450,000. He gives himself a shot of interferon once a week and takes hydrea and a baby aspirin daily. Although this has not been fun, he is doing fine. He has his blood drawn about every other week now just to check his counts and he sees a specialist 3 times a year. Over the last 6 months or so, he has been able to reduce the amount of interferon he gets from the shot. A specialist from the Mayo Clinic in Rochester, MN put him on the interferon. The hydrea was making his counts roller coaster and the interferon stabilized them. If your pcp is alarmed, I think its time to find a specialist. My husband went through several different doctors, before he even go a diagnosis. I don't think that this is something a pcp can handle. Kim
I am surprized that your doctor has you on hydroxyurea. Are
you having problems with phlebotomies? The second line of defense for younger
patients is usually Interferon-Alpha. Only if you show an intollerance to
phlebotomies, and then Interferon do informed doctors put their patients on
hydroxyurea. There is a new Interferon treatment that is reportedly easier
to adjust to, and can be taken orally. Also, there is no evidence that shows
any warranted treatment for platelets as low as yours. The best researchers
don't put a patient on medication until their platelets go over 1,500,000.
Treating your for platelets of only 600,000 makes me wonder if your doctor
is keeping up on current findings. There seem to be very few doctors who stay
current with PV treatment because it is such a rare disorder. Dan
Here's some great news! This is a quote from a recent article that my wife found: A new study is first to show that dark chocolate inhibits platelet clumping (aggregation), a major cause of blood clots (thrombi) that trigger heart attacks and stroke. The study, from Ninewells Hospital, Scotland, was reported recently at the XIX Congress of the International Society on Thrombosis and Haemostasis, held in the UK in July 2003. Thirty subjects were randomized to receive 100 grams of white chocolate, milk chocolate, or dark chocolate. Four hours later, blood samples of each group were tested in vitro to see if chocolate intake modified platelet aggregation. While white chocolate had no effect and milk chocolate showed a trend towards reducing clumping, dark chocolate inhibited platelet aggregation by 92%. Of the trhee types of chocolate, dark chocolate has the highest content of flavonoids, known to inhibit cyclooxygenase (COX1) that helps block platelet aggregation. The researchers suggest that dark chocolate has potential to reduce thromboembolism and cardiovascular diseases. By Carmia Borek, Ph.D.
Green Tea: Many people are reporting decrease in symptoms and longer intervals between phlebotomies. http://www.polycythemia.org/GreenTea.htm
Vitamin E benefits: Natural anti-thrombin - circulates in the blood and prevents platelet aggregation or clots occurring inside the vessel, but does not interfere with the normal clotting process in wounds or with normal healing. In fact, it actually accelerates healing of burns and wounds. This is important not only in the treatment of heart disease, but in treating phlebitis and varicose veins caused by blood clots and venous obstructions. Tocotrienols also inhibit platelets by blocking thromboxane A2, which is exactly how aspirin works to cut the risk of heart attacks. Of course, Vitamin E does not have the possible side effects of aspirin. Sesame oil further reduces the risk of thrombi. http://www.vitasentials.com/e400toco.htm
Kiwi I have been told kiwi fruit is
"absolutely" great for platelet reduction. They supposedly don't know why
it works the way it does though. Having said that, I am also told that Vitamin
C is not good as it holds Iron in the body, and kiwi fruit is full of vitamin
C, gets confusing. Cacium (milk) breaks down vitamin C. Thanks for replies
re alternatives to Asprin. Will need to check if they are available in Australia.
Malcolm Fallon
Grape Juice Grape juice (purple) is
also good for those thick overpopulated platelets we have.....somehow it
"unsticks" them, which in turn, greatly reduces the risks of blood clots.
Thanks for the tip on Kiwi...which I just happen to really like.
Also, on the aspirin problems you have......I
work for a group of Cardiologists and we use Ticlid
on patients who are allergic to, intolerant to, or have failed aspirin therapy.
It's much cheaper then Plavix. You may want to look into this if you From:
Susan
Asperin Substitutes: Besides Kiwi,
purple (not white) grape juice, also works well with keeping the blood thin.
For those allergic to or cannot tolerate aspirin, Ticlid can be used in
its place. Best wishes to all, Susan freetobefifty
There is also a new drug called Paroxitine used to treat depression that some of the latest reports suggest could be effective in controlling platelets in people getting phlebotomies as a treatment for PV. In an article by Ayalew Tefferi, MD at Mayo Clinic she says: "Interestingly, a recent study showed a response rate higher than 80% in PV associated pruritus treated with paroxetine, a selective serotonin ruptake inhibitor. (I'll stick to dark chocolate for as long as I can, this stuff is too new and I don't have more info yet).
A safe treatment for PV may be coming very soon!!! http://mpdfoundation.org/webarticle.htm
Gout is a metabolic disorder that may be inherited. It is characterised by recurrent acute joint inflammation (gouty arthritis) in the extremities, caused by crystals that are deposited in and around the joints. These crystals come from body fluids that contain markedly high concentrations of uric acid (urate), a waste product of digestion that is normally excreted in urine. Symptoms include heat, red shiny skin and extreme tenderness and pain in the affected joints. It tends to affect the peripheral joints, most often those in the big toe, but can also affect the knees, elbows, thumbs or fingers. The arthritis may become chronic and cause joint deformity. Tophi - small, hard lumps of urate deposits - may also form around the ankles, hands, tips of the elbows and earlobes. The tophi may erupt, causing a discharge. Collection of urate crystals in the kidneys can lead to kidney stones. Not all persons with high urate levels in their blood (hyperuricaemia) develop gout, but the greater the degree and duration of hyperuricaemia, the greater the risk of crystal deposition and acute gout attacks. Gout is a common disease and one of the oldest in medical literature. One of the oldest drugs in therapeutics, colchicine, is used for the symptoms of gout. Prevention · Avoid certain protein-rich foods that can lead to decreased urate excretion: organ meats (liver, brains and kidneys), shellfish, fatty fish, asparagus, spinach and most dried beans. Some people find particular foods which affect them as individuals. These should be avoided in that instance. · Increase your fluid intake - this is very important to decrease the possibility of urate crystal formation in the kidney tracts. · Avoid alcohol, as it retards elimination of urate. · If you are obese, control your body weight. If you are a man and gouty arthritis runs in your family, these preventative measures are particularly important. Blood and urine tests during routine check-ups will alert your doctor to a potential for gout attacks. He or she may prescribe drugs to reduce the body's production of urate and to encourage the excretion of excess urate. It is a treatable disease. Reviewed by Dr David Gotlieb, rheumatologist, MBChB FCP(SA). 10/9/2004
Gout Subject: Re: [PVSupport] Bleeding
ulcer and nose bleed drpeterlok Offline Send Email Invite to Yahoo! 360º
Thanks for your input on the nose bleeding. Here is an info on gout from
the internet: " If you suffer from an acute attack of gout, you will probably
want to take pain relievers. Be sure to use the right one. Aspirin can actually
worsen your symptoms by inhibiting the excretion of uric acid. The best
over-the-counter pain reliever for gout is ibuprofen, available by various
names including Nuprin and Advil. Ibuprofen reduces inflammation and is
more effective than other pain relievers including acetaminophen. If your
symptoms persist, consult your doctor." http://alternative-medicine-and-health.com/conditions/gout.htm
Peter Lok
Anyone who suffers during a phleb, please recommend that they numb you first. I had that done last time and it was so much less painful. There is a cream that you can put on to numb your arm instead of a needle also. I cannot figure out why nobody told me about this numbing before. I was in quite a bit of pain getting phelbs before this time. At the hospital I went to,it is standard procedure. I totally recommend for people with small or hard to get to veins. Jeffry Markland Yahoo PV Forum Date: Sat May 7, 2005
One person's cure for itchiness. I
find the itchiness is more prelevant at bedtime; I shower before bed, take
an antihistamine and keep away from caffine at night and normally have no
problems sleeping any more. Before taking the antihistamine, I was not able
to sleep well because of the itchiness. The itch is from a release of histamines.
To stem the reaction of the body to the histamines one needs to take an
anti-histamine like Benedryl. Only thing is, I think we become immune to
such products over time. The trick, for me, is to take the anti-histamine
once every 5 days or so and it seems to work well for that period of time.
I was taking one every night anticipating the "itch". Now, however, taking
a couple at night every 4 or 5 days seems to control it. And, I haven't
had a "bath" in years - showers only - so I'm able to keep the temperature
lukewarm as opposed to hot. I also swim every day from June through Sept.
and so far, the chlorine and other chemicals haven't affected my skin or
the itch. It is definitely not something that is affected by external applications,
at least not in my case. Bev (pond2view@yahoo.com age 67 PV 3/04/moderate
HBP phlebs & aspirin
I also find swimming and getting a little
sun is a huge help. During the months I can't swim or get sun I itch much
more. Your Mom might want to check with a dermatologist about sun beds.
Sue PV (Hydrea, phlebs, iron, aspirin and a plethora more lol)
Alcohol is what i use for a blood thinner.
Not enough to get drunk. I sip on 2 or 3 cans of tilt about 4 days a week
and my blood hasnt been thick in 6 month and i havnt had a pholb. since
October. No meds what so ever. So sto freaking out and sit down and have
a beer. ----- Original Message ----- From: April Hentz cybrarian2004@yahoo.com
To: polycythemia_vera@yahoogroups.com Sent: Wednesday, January 24, 2007
5:47 PM
(Caution: alcohol can dehydrate you, which can raise blood levels)
Swollen Painful Fingers: I had the yearly consult with Spivak yesterday. As always, he reiterated the critical importance of low hematocrit: <42 for women. He was still okay with my >1,000,000 platelets. However, since I've recently developed occasional swelling/pain in some fingertips, he recommended baby aspirin every day instead of every other day. (Because high platelets in PV can result in either hemmoraging or thrombosis, he has been conservative in using aspirin.) Significantly I thought, because of his hesitation to recommend meds for me, he will prescribe low-dose anagrelide to keep the platelets in order if the aspirin doesn't work. He said emphatically that high platelet counts are common to PV and shouldn't be looked at separately as ET (essential thrombocythemia), although I'm not sure how significant the distinction is in regard to treatment. Emily Aug 9, 2007