Antiphospholipid syndrome

[Guest guest]

nne,

I also have the antiphospholipid syndrome. It was discovered in July when I went to the first appt with my new rheumy. I was diagnosed with lupus back in 96 and under the care of my old rheumy for 6 years but he never bothered to test me for the antiphospholipid syndrome despite the fact that they found out in 2000 that I have a 60% blockage in my right renal artery. Anyway, I am on coumadin for the antiphospholipid syndrome but I would assume that since your clotting times are not good, coumadin would not be necessary for you at this time. I was on 4 mg of coumadin a day prior to finding out I have AIH and going on prednisone in January. They keep having to up my coumadin. I was on 6 mg coumadin daily and my last protime was 12.3 and my INR was 1.1. The doctors want my INR to be in the range of 1.5-2.0, so they just upped my coumadin to 7 mg daily and I'll have my protime checked next week. I think that since it is taking higher doses of coumadin to keep my protime/INR up that maybe that means the prednisone is doing it's job and helping my liver work better.

I'm not trying to scare you but having the antiphospholipid syndrome also puts you at an increased risk for strokes and heart disease (or blockage in any arteries). I consider myself one of the lucky ones. Most of the time the antiphospholipid syndrome is not discovered until after you've had a blood clot, stroke, or heart attack! Taking coumadin for life sounds a lot better than the alternative! My grandmother spent the last 3-4 years of her life in a nursing home after her first stroke. She was totally bedridden and we're not sure she even knew anyone. She had multiple strokes during her last years and was eventually killed by a stroke. The thought of a stroke is terrifying to me so I'll take the coumadin, even though at this point it seems it's going to take a dose high enough to kill a horse to keep my INR where they want it. They've told me if I ever do have a blood clot, stroke, or signs of heart disease, they'll have to keep my INR from 2.0 to 2.5. If that happens, I guess I'd better just take out stock in coumadin!

My daughter is 21 and I worry about her having the antiphospholipid syndrome. She was diagnosed with JRA at 15 and our current rheumy is watching her to make sure she doesn't also have lupus. The one time the old rheumy checked her ANA it was a low positive (1:80), but he didn't bother to tell us. When the new rheumy checked her ANA it was also 1:80. I have told my daughter that before she starts trying to get pregant (in about 4 years) she definitely needs to be tested to make sure she does not have the antiphospholipid syndrome.

My older sister has an appointment with my rheumy the end of May. We are pretty sure she has lupus because she tested positive to the Anti-smith antibody and the anti-rnp antibody. The anti-smith is pretty specific for lupus according to my rheumy and what I've read on the internet. I also have 3 male cousins with RA and had an uncle with RA, but he's now deceased.

For me, AIH was autoimmune disease number 3, unless they end up deciding that interstitial cystitis and is an autoimmune disease. I am hoping my daughter doesn't end up as lucky as me, but the autoimmune problems began at a much younger age for her than they did for me, so it's kind of scary thinking about what the future may hold for her. I mostly try not to think about it and do a lot of praying!

Yesterday was a beautiful day here. I woke up not feeling well, but after two phenergan, I felt pretty good. We went to my sister's house and hung out with family. The day was the perfect temperature to be outside. Today I get to go for a mammogram. I am so excited! NOT! However, it looks like today is just as nice as yesterday outside.

Hope everyone has a great day today.

W

[Guest guest]

,

THanks for the info. I guess the one good thing was I learned

finally why I had so many problem pregnancies. Now I worry what that

could mean for from my daughter. Of course the news about the blood

clot protential was not really what I wanted to hear.

nne

> nne,

> I also have the antiphospholipid syndrome. It was discovered in

July when I went to the first appt with my new rheumy. I was

diagnosed with lupus back in 96 and under the care of my old rheumy

for 6 years but he never bothered to test me for the antiphospholipid

syndrome despite the fact that they found out in 2000 that I have a

60% blockage in my right renal artery. Anyway, I am on coumadin for

the antiphospholipid syndrome but I would assume that since your

clotting times are not good, coumadin would not be necessary for you

at this time. I was on 4 mg of coumadin a day prior to finding out I

have AIH and going on prednisone in January. They keep having to up

my coumadin. I was on 6 mg coumadin daily and my last protime was

12.3 and my INR was 1.1. The doctors want my INR to be in the range

of 1.5-2.0, so they just upped my coumadin to 7 mg daily and I'll

have my protime checked next week. I think that since it is taking

higher doses of coumadin to keep my protime/INR up that maybe that

means the prednisone is doing it's job and helping my liver work

better.

>

> I'm not trying to scare you but having the antiphospholipid

syndrome also puts you at an increased risk for strokes and heart

disease (or blockage in any arteries). I consider myself one of the

lucky ones. Most of the time the antiphospholipid syndrome is not

discovered until after you've had a blood clot, stroke, or heart

attack! Taking coumadin for life sounds a lot better than the

alternative! My grandmother spent the last 3-4 years of her life in

a nursing home after her first stroke. She was totally bedridden and

we're not sure she even knew anyone. She had multiple strokes during

her last years and was eventually killed by a stroke. The thought of

a stroke is terrifying to me so I'll take the coumadin, even though

at this point it seems it's going to take a dose high enough to kill

a horse to keep my INR where they want it. They've told me if I ever

do have a blood clot, stroke, or signs of heart disease, they'll have

to keep my INR from 2.0 to 2.5. If that happens, I guess I'd better

just take out stock in coumadin!

>

> My daughter is 21 and I worry about her having the antiphospholipid

syndrome. She was diagnosed with JRA at 15 and our current rheumy is

watching her to make sure she doesn't also have lupus. The one time

the old rheumy checked her ANA it was a low positive (1:80), but he

didn't bother to tell us. When the new rheumy checked her ANA it was

also 1:80. I have told my daughter that before she starts trying to

get pregant (in about 4 years) she definitely needs to be tested to

make sure she does not have the antiphospholipid syndrome.

>

> My older sister has an appointment with my rheumy the end of May.

We are pretty sure she has lupus because she tested positive to the

Anti-smith antibody and the anti-rnp antibody. The anti-smith is

pretty specific for lupus according to my rheumy and what I've read

on the internet. I also have 3 male cousins with RA and had an uncle

with RA, but he's now deceased.

>

> For me, AIH was autoimmune disease number 3, unless they end up

deciding that interstitial cystitis and is an autoimmune disease. I

am hoping my daughter doesn't end up as lucky as me, but the

autoimmune problems began at a much younger age for her than they did

for me, so it's kind of scary thinking about what the future may hold

for her. I mostly try not to think about it and do a lot of praying!

>

> Yesterday was a beautiful day here. I woke up not feeling well,

but after two phenergan, I felt pretty good. We went to my sister's

house and hung out with family. The day was the perfect temperature

to be outside. Today I get to go for a mammogram. I am so excited!

NOT! However, it looks like today is just as nice as yesterday

outside.

>

> Hope everyone has a great day today.

>

> W

[Guest guest]

, That seems like a legitimate whine, sorry to hear about Nikki's health stuff. You can even have a pity party if you want... although then you have to invite the rest of us.

Patty

-----Original Message-----From: Weston [mailto:karenw@...] Sent: Friday, August 01, 2003 12:27 AMLupies group; Subject: [ ] antiphospholipid syndrome

As I write this I feel a little guilty that this news has me bummed out (and scared), but I needed to get it off my chest so I can put things in perspective and go on.

My daughter, Nikki, got a phone call from our rheumy today telling her that she does have the autoimmune clotting disorder that I have. (antiphospholipid syndrome) She is to begin taking an asprin daily and will take it and/or stronger blood thinners for the rest of her life. It is truly a blessing that this was discovered now and not AFTER Nikki had already had a blood clot, stroke, or miscarriage. Chances are these things can now be prevented. However, just knowing that Nikki now has a second autoimmune disease is so frightening for me. She was diagnosed with rheumatoid arthritis at 15 and she is now 21. So far, her RA has remained relatively mild but she does have a good deal of joint pain, swelling, and fatigue. I know that things could be soooo much worse and I truly am thankful that they are not. However, even at 21, she is my baby girl and I hate knowing that she already has so many health issues to deal with.

At least now we know about the clotting disorder and Nikki will be followed closely, especially when she does decide to begin having children. Chances are that all the things that could be caused by the clotting disorder can now be prevented.

Thanks for listening and letting me whine.

W

[Guest guest]

,

It is a good thing to know ahead of time, but still when it is your

baby girl (no matter how old she gets, she still will be your baby)

it just makes you nuts that you can't protect her from things like

this.

Take care, ...will keep you and your daughter in my prayers.

nne

> As I write this I feel a little guilty that this news has me

bummed out (and scared), but I needed to get it off my chest so I

can put things in perspective and go on.

>

> My daughter, Nikki, got a phone call from our rheumy today telling

her that she does have the autoimmune clotting disorder that I have.

(antiphospholipid syndrome) She is to begin taking an asprin daily

and will take it and/or stronger blood thinners for the rest of her

life. It is truly a blessing that this was discovered now and not

AFTER Nikki had already had a blood clot, stroke, or miscarriage.

Chances are these things can now be prevented. However, just

knowing that Nikki now has a second autoimmune disease is so

frightening for me. She was diagnosed with rheumatoid arthritis at

15 and she is now 21. So far, her RA has remained relatively mild

but she does have a good deal of joint pain, swelling, and fatigue.

I know that things could be soooo much worse and I truly am thankful

that they are not. However, even at 21, she is my baby girl and I

hate knowing that she already has so many health issues to deal with.

>

> At least now we know about the clotting disorder and Nikki will be

followed closely, especially when she does decide to begin having

children. Chances are that all the things that could be caused by

the clotting disorder can now be prevented.

>

> Thanks for listening and letting me whine.

>

> W

[Guest guest]

Alice here, could you give a definition please? Thanks

On Friday, August 19, 2005, at 07:10 PM, ci_sme wrote:

> Does anyone here suffer from antiphospholipid syndrome, a sister

> disease to Lupus?

>

>

>

[Guest guest]

Background: Antiphospholipid syndrome (APS) is a disorder characterized by

recurrent venous or arterial thrombosis and/or fetal losses associated with

typical laboratory abnormalities. These include persistently elevated levels of

antibodies directed against membrane anionic phospholipids (ie, anticardiolipin

[aCL] antibody, antiphosphatidylserine) or their associated plasma proteins,

predominantly beta-2 glycoprotein I (apolipoprotein H), or evidence of a

circulating anticoagulant.

Multiple terms exist for APS. Unfortunately, some synonyms can be confusing.

Lupus anticoagulant (LA) syndrome, for example, is misleading because

patients may not necessarily have systemic lupus erythematosus (SLE) and LA is

associated with thrombotic rather than hemorrhagic complications. In an attempt

to

avoid further confusion, APS is the currently preferred term for the clinical

syndrome (as described below).

APS can occur in patients without evidence of any definable associated

disease (primary APS). It may also occur in association with SLE or another

rheumatic or autoimmune disorder (secondary APS). Although antiphospholipid

(aPL)

antibodies are clinically linked to APS, whether they are involved in the

pathogenesis or are an epiphenomenon is unclear. (aPL antibodies are known to

occur

in up to 5% of healthy individuals.)

Pathophysiology: An alteration of the homeostatic regulation of blood

coagulation occurs; however, the mechanisms of thrombosis are not yet defined.

One

hypothesis postulates a defect in cellular apoptosis, which exposes membrane

phospholipids to the binding of various coagulation proteins. Once bound, a

phospholipid-protein complex is formed and a neoepitope is uncovered, which

subsequently becomes the target of autoantibodies.

Other proposed mechanisms for the hypercoagulable effect of aPL antibodies,

which may or may not be dependent on beta-2 glycoprotein I, include the

following:

• Activation of platelets to enhance endothelial adherence

• Activation of vascular endothelium, which, in turn, facilitates the binding

of platelets and monocytes

• Production of antibodies against coagulation factors, including

prothrombin, protein C, and protein S

• Reaction of antibodies to oxidized low-density lipoprotein, thus

predisposing those individuals to atherosclerosis and myocardial infarction

• Activation of complement (contributes to pregnancy loss)

The series of events that leads to hypercoagulability and recurrent

thrombosis can affect the extremities and virtually any organ system, including

the

following:

• Peripheral venous system (deep venous thrombosis [DVT])

• Central nervous system (cerebrovascular accident [CVA], sinus thrombosis)

• Hematologic (thrombocytopenia, hemolytic anemia)

• Obstetric (pregnancy loss, eclampsia)

• Pulmonary (pulmonary embolism, pulmonary hypertension)

• Dermatologic (livedo reticularis, purpura, infarcts/ulceration)

• Cardiac (Libman-Sacks valvulopathy, myocardial infarction)

• Ocular (amaurosis, retinal thrombosis)

• Adrenal (infarction/hemorrhage)

• Musculoskeletal (avascular necrosis of bone)

Medical Care: Patients with APS may be evaluated in an outpatient setting.

Inpatient evaluation is required if the patient presents with a significant

clinical event. Patients with CAPS require intense observation and treatment,

often in an intensive care unit setting.

In general, treatment regimens for APS must be individualized according to

the patient's current clinical status and history of prior thrombotic events.

Prophylactic therapy

Eliminate other risk factors, such as oral contraceptives, smoking,

hypertension, or hyperlipidemia.

Low-dose aspirin is used widely in this setting; however, the effectiveness

of low-dose aspirin as primary prevention for APS remains unproven. Clopidogrel

has anecdotally been reported to be helpful in persons with APS and may be

useful in patients allergic to aspirin.

Consider the use hydroxychloroquine in patients with SLE (may have intrinsic

antithrombotic properties).

Thrombosis

Perform full anticoagulation with intravenous or subcutaneous heparin

followed by warfarin therapy.

Based on the most recent evidence, a reasonable target for the international

normalized ratio (INR) is 2.6-3 for a minimum of 6 months for a first

thrombosis. Patients with recurrent thrombotic events while well maintained on

the

above regimen may require an INR of 3-4 and generally receive anticoagulation

therapy for life. For severe or refractory cases, a combination of warfarin and

aspirin may be used.

Obstetric considerations

Subcutaneous heparin (unfractionated or low–molecular-weight heparin [LMWH])

and low-dose aspirin are used. Therapy is held at the time of delivery; it is

restarted after delivery and should be continued for as long as 6 weeks

postpartum. Most authors avoid warfarin (Coumadin) because it is category X in

pregnancy.

If the patient also has a history of thrombosis, then long-term

anticoagulation is needed.

Corticosteroids have not been proven effective for persons with primary APS,

and they have been shown to increase maternal morbidity and fetal prematurity.

Heparin and warfarin may be used while breastfeeding.

Catastrophic APS

These patients generally are very ill, often with active SLE.

Treatment with intensive anticoagulation and plasmapheresis appears

beneficial, but no controlled trials have been performed.

Additionally, corticosteroids, cyclophosphamide, and intravenous

immunoglobulin may be used.

Surgical Care: Recurrent DVT may necessitate placement of an inferior vena

cava filter.

Consultations:

• Rheumatologist

• Hematologist

• Neurologist, cardiologist, pulmonologist, hepatologist,

ophthalmologist (depending on clinical presentation)

• Obstetrician with experience in high-risk pregnancies

Diet:

• If warfarin therapy is instituted, instruct the patient to avoid

excessive consumption of foods containing vitamin K.

Activity:

• No specific limitations on activity are necessary.

• Individualize the activity according to the clinical setting.

• Instruct the patient to avoid sports with excessive contact if taking

warfarin.

• Limit activity in patients with acute DVT.

• Instruct the patient to avoid prolonged immobilization

Hope this helps

Babs