Aa
hgb dropped after stopping incevik
Hi all. Quick tx history. Started peg, riba, incevik 13 weeks ago. I got anemic immediately...was @ 8.2 after 2 wks. I got transfused and drop riba to 600mg but after 2 wks was back down to 7.9. Another transfusion and started procrit shots (and stopped working). Bottom line is the procrit held me steady at 7.2 for 8 weeks, without working it was tolerable. Stopped the incevik at 12 weeks, felt much better and thought for sure my hgb had gone up only to get my cbc's and found hgb had dropped to 6.6?? I was hoping to be out of the woods at 12 weeks!!! BTW, NDT at 4, 8 and 12 weeks. Hemo dr was pushing for transfuse but I declined based on how I'm feeling and the fact I'm taking 1 less drug. Just wondering if anyone else had hgb drop after stopping incevik, how much drop and how long before it came up?
I suspect after some reading I may have caused the drop due to feeling better I started being a little more active...short walks, running errands etc.
The thing is I'm not feeling that bad...I felt much worse in the 8's and working than in the 6's taking it easy. After declining the transfusion the nurse took blood pressure while sitting, standing and walking and stayed steady 140/80 during all. Just a little scared of the 6.6 even though feeling ok. I really want to avoid another transfusion if possible, especially since they only last for a week or so. Hoping for some encouraging feedback on incevik hgb drop.
Thanks
I suspect after some reading I may have caused the drop due to feeling better I started being a little more active...short walks, running errands etc.
The thing is I'm not feeling that bad...I felt much worse in the 8's and working than in the 6's taking it easy. After declining the transfusion the nurse took blood pressure while sitting, standing and walking and stayed steady 140/80 during all. Just a little scared of the 6.6 even though feeling ok. I really want to avoid another transfusion if possible, especially since they only last for a week or so. Hoping for some encouraging feedback on incevik hgb drop.
Thanks
good luck dan....my tx was nasty...i had to be driven around...my gf was a great help...i took zoloft..started 2 months before tx...now cutting way back..soon i'll be off of it..i feel really good off tx even though i had an awful time on tx...try not to do much of anything...low 8 are tough for some...i'll bet you'll feel a little better soon...just the anticipation of getting off the incivek followed by the let down of not feeling good is a drag..together with very low hgb...a double let down.....the riba also can be really tough...you gotta hang in there....soon your tx will be history....billy
10 days off incevik and still terrible withdraw sx. Hands so shaky, pupils the size of quarters, skin, muscles, nerves tense. Slept last night for first in 4 days. Tried sleep aids but that just makes me sleepy and unable to sleep. Gastro doc gave a mild anxiety med..didn't seem to help. Almost went to ER yesterday but decided instead to go to hematologist sense I had an appointment. I was so bad my wife had to drive me. cbc were relatively good, hgb up to 8.2. The Doc felt the anxiety was most likely from the incevik. He felt My Gastro doc gave me an anxiety med that takes 2-3 weeks to work. He recommended I call my family dr and get atiban which works faster. My wife had some in the house so tried the atiban....as I said it was the first night of sleep in a while...really hope this clears soon. Thanks for all the good reply's.
Dan
Dan
My husband had some interesting creepy/crawly skin, tingling, twitching (kind of like neuropathy) symptoms right around or shortly after finishing Incivek. I think it went away within a week or two after finishing Incivek. He's in week 20 right now, and the side effects are mild (metallic taste in mouth, mild fatigue), but much better than while on Incivek. It will get better! Have you tried Ambien (Zolpidem) for sleep?
Advocate1955
Advocate1955
Well got some good news in the middle of this storm. Got mid week cbc and hgb is back up to 7.6 (and hopefully rising). Bad news is I haven't slept in 3 days. It's my opinion I am experiencing incevik withdraw. I'm shaking, skin is crawling, muscles tense,...on top of be anemic it's freakin hell. Felt good first 3 days off incevik then down hill. Been off inc 8 days now, hopefull things will start getting better. Doc called me in an anxiety med, not sure what till I pick it up....hope that helps me get some sleep!!
Good luck to everyone and thanks for the reply's.
Dan
Good luck to everyone and thanks for the reply's.
Dan
my hgb was low throughout tx...i thought after incivek my hgb would go up....it never did...i felt real good for the first 3 to 4 days after stopping incivek...that was it...then more low hgb...the riba was pretty nasty too..but it was the interferon that stopped me at 19+ weeks...eye problems...you just got to hang in there ...i wouldn't expect it to get better physically but mentally i felt much better off incivek which made it easier to tolerate low hgb...good luck....billy
Dan, I also dropped HGB after finishing TX. I went to 7.4 stopped riba and was already on procrit. I couldn't even lift my head off the pillow at 7.4 - I would suggest speaking to your Dr - anemia is nothing to mess with - Good luck - Fred
Sorry, you asked about side effects. Really only side effect is shortness of breath after walking. Feeling better than I have in months, which is why I was flabbergasted when the told me hgb was 6.6.
Thanks frijole. Reduced riba from 1200 to 600 @ week 4 I think. I think yesterday was my 7th procrit shot, first 5 were @ 40000 and last 2 @ 60000. Where I'd rather be on 1200 riba, studys seem to support that riba reduction when early NDT is achieved has little if any effect on SRV. However, 2 days before I had my last CBC (yesterday) and 2 days after stopping incevik my Dr had me increase back to 1200 on riba. I stated my objection (even though feeling better)I would rather wait for cbc till increasing but against my judgement I did as he said...dont know if only 2 days of 1200 riba would cause the drop or it was stopping the incevik that caused the drop. Since cbc yesterday I took it upon myself to go back to 600.
I only declined the transfusion, 1 because I dont feel like 6.6 (feeling fairly good) and 2 because I feel I'm so close to it going up....just hoping for some feedback to support that feeling. Hopefully with another procrit shot and returning to 600 riba will help.
Thanks,
Dan
I only declined the transfusion, 1 because I dont feel like 6.6 (feeling fairly good) and 2 because I feel I'm so close to it going up....just hoping for some feedback to support that feeling. Hopefully with another procrit shot and returning to 600 riba will help.
Thanks,
Dan
welcome to the forum. As much as I would not like to transfuse, I cannot believe you are not transfusing at 6.6. If the procrit is not bringing your hgb up, I think you need to. How much procrit do you take each week? How much riba are you taking? Have they reduced riba dose? I am taking Victrelis so I don't know what it is like to come off the Incevik, but I was anemic on SOC without any PI so I can relate to that. I sounds like you have great sensitivity to the ribavirin. The good news is that patients who go anemic have a higher rate of SVR
But anemia is bad stuff - don't forget that. What are your anemic side effects -- pale skin? swelling in your ankles? Here is a pretty good paper on anemia and what it can do.
http://web2.iadfw.net/uthman/unanemia/unanemia_ch1.html
Increased cardiac output. The volume of blood the heart pumps through itself per unit time is called the cardiac output. In the normal resting state, the heart pumps about 5 liters of blood every minute, abbreviated 5 L/min. This means that the heart is easily capable of pumping the body's total blood volume through its chambers in one minute. Actually it is capable of much more than that. When there is a greater demand for oxygen, as during vigorous exercise, the heart can increase its output manyfold, to as much as 30 L/min. It does this by increasing not only the number of beats per minute (the heart rate) but also the volume of blood pumped with each stroke (the stroke volume). Mathematically, the cardiac output can be calculated by multiplying the heart rate times the stroke volume. In anemia, the cardiac output increases, and that allows more hemoglobin to be exposed to the peripheral tissues, making up for the decreased hemoglobin concentration. Accordingly, the heart rate increases, which gives us one of the cardinal clinical manifestations of anemia, tachycardia, or fast heart rate.
The heart does not act alone to increase the cardiac output. It has to have cooperation from the peripheral tissues and the blood itself. If nothing changes in the body but the heart rate and stroke volume, the heart will be trying to pump blood faster into a fixed, unchanging bed of blood vessels. This is like trying to squeeze thick dishwasher detergent gel out of its container by pushing harder. The only way to make the gel dribble out faster is to increase the pressure. Analogously, in the body, to push more blood through an ungiving vascular bed would require a higher blood pressure. Higher blood pressure would cause the heart to work harder, because it would have to pump against a high pressure head, just like a muscle has to work harder to lift a heavier weight. Clearly this is not in the best interest of the body. Fortunately, the blood pressure is kept from going up by two factors. The first is the viscosity of anemic blood. Viscosity is the quality of a fluid which tends to cause it to resist being propelled through a tube or opening. Thin, anemic blood is less viscous than normal blood and can be pushed through the vascular bed with less pressure. The second factor is the blood vessels themselves. The wall of each small artery or vein contains one or more layers of muscle capable of responding to nerve signals by contracting. This causes the vessel to close down to a smaller caliber and be more resistant to the flow of blood. Other nerve impulses cause the muscles to relax, letting the vessels expand to a wider caliber and allowing more blood to flow with less resistance. In the anemic patient, the brain sends signals to the muscles around the small vessels telling them to relax and open up. The result is less impediment to the flow of blood. Therefore, because of less peripheral vessel resistance and thinnet, less viscous blood, the cardiac output can rise without causing the blood pressure to go up.
Redistribution of blood flow. The various organs of the body are quite capable of cutting deals among themselves when times are bad. In the case of anemia, all the organs conjoin to protect the two most oxygen-demanding organs in the body, the brain and the heart. If these organs don't get enough oxygen, the rest of the body is in real trouble. Fortunately, two other organs can get by without nearly as much blood as they normally enjoy in good times. The first of these is the skin. As a response to anemia, small blood vessels in the skin contract, causing a greater resistance to the flow of blood than is present in more vital organs. Since the blood being pumped out of the heart will preferentially follow the path of least resistance, it will go through the more vital organs faster than it will through skin with contracted vessels. The result is a partial diversion of blood from the skin to other organs. The second organ which sacrifices its right to blood supply is the kidney. Now the kidney is a very vital organ, to be sure, but it is normally endowed with much more blood flow than it needs to stay alive and function properly. Both kidneys, taken together, weight about 350 grams (or about 1/2 of 1 percent of the total body weight), but they receive 20 percent of the cardiac output, or about 1 liter per minute. Gram for gram, then, the kidneys receive 50 times the cardiac output of the body as a whole. Clearly they could give up some of that for the benefit of their fellow organs, and as part of the adaptation to anemia, they do so.
The diversion of blood flow from the skin causes one of the cardinal clinical features of anemia--pallor. Pallor is the pale color observed in the skin of a light-skinned anemic individual, and in the mucous membranes and nailbeds of all anemic individuals, light-skinned or otherwise. It should be noted that anemic patients are pale not because their blood is thin (anemic blood is just as opaque and highly colored as normal blood), but because the diversion of blood means that there is less of it in the skin, and more of the pale color of bloodless human tissue shows through.
Decrease of hemoglobin-oxygen affinity. Earlier we discussed how the affinity (or the "willingness" to bind) between oxygen and hemoglobin changed with the number of oxygen molecules gained or lost by hemoglobin. It turns out that hemoglobin-oxygen affinity can be accomplished by other chemical means as well. There is a simple organic acid, called 2,3-diphosphoglycerate (2,3-DPG) that is elaborated within the red cell under anemic conditions. This 2,3-DPG causes hemoglobin to bind oxygen less avidly and to give up as much to the starved tissues as possible. Of course, the other side of the coin is that oxygen is more difficult to pick up in the lungs, but, since the respiratory system is not the main concern in an anemic patient, something has to give, and the healthy system ends up taking up the slack for the sick one.
But anemia is bad stuff - don't forget that. What are your anemic side effects -- pale skin? swelling in your ankles? Here is a pretty good paper on anemia and what it can do.
http://web2.iadfw.net/uthman/unanemia/unanemia_ch1.html
Increased cardiac output. The volume of blood the heart pumps through itself per unit time is called the cardiac output. In the normal resting state, the heart pumps about 5 liters of blood every minute, abbreviated 5 L/min. This means that the heart is easily capable of pumping the body's total blood volume through its chambers in one minute. Actually it is capable of much more than that. When there is a greater demand for oxygen, as during vigorous exercise, the heart can increase its output manyfold, to as much as 30 L/min. It does this by increasing not only the number of beats per minute (the heart rate) but also the volume of blood pumped with each stroke (the stroke volume). Mathematically, the cardiac output can be calculated by multiplying the heart rate times the stroke volume. In anemia, the cardiac output increases, and that allows more hemoglobin to be exposed to the peripheral tissues, making up for the decreased hemoglobin concentration. Accordingly, the heart rate increases, which gives us one of the cardinal clinical manifestations of anemia, tachycardia, or fast heart rate.
The heart does not act alone to increase the cardiac output. It has to have cooperation from the peripheral tissues and the blood itself. If nothing changes in the body but the heart rate and stroke volume, the heart will be trying to pump blood faster into a fixed, unchanging bed of blood vessels. This is like trying to squeeze thick dishwasher detergent gel out of its container by pushing harder. The only way to make the gel dribble out faster is to increase the pressure. Analogously, in the body, to push more blood through an ungiving vascular bed would require a higher blood pressure. Higher blood pressure would cause the heart to work harder, because it would have to pump against a high pressure head, just like a muscle has to work harder to lift a heavier weight. Clearly this is not in the best interest of the body. Fortunately, the blood pressure is kept from going up by two factors. The first is the viscosity of anemic blood. Viscosity is the quality of a fluid which tends to cause it to resist being propelled through a tube or opening. Thin, anemic blood is less viscous than normal blood and can be pushed through the vascular bed with less pressure. The second factor is the blood vessels themselves. The wall of each small artery or vein contains one or more layers of muscle capable of responding to nerve signals by contracting. This causes the vessel to close down to a smaller caliber and be more resistant to the flow of blood. Other nerve impulses cause the muscles to relax, letting the vessels expand to a wider caliber and allowing more blood to flow with less resistance. In the anemic patient, the brain sends signals to the muscles around the small vessels telling them to relax and open up. The result is less impediment to the flow of blood. Therefore, because of less peripheral vessel resistance and thinnet, less viscous blood, the cardiac output can rise without causing the blood pressure to go up.
Redistribution of blood flow. The various organs of the body are quite capable of cutting deals among themselves when times are bad. In the case of anemia, all the organs conjoin to protect the two most oxygen-demanding organs in the body, the brain and the heart. If these organs don't get enough oxygen, the rest of the body is in real trouble. Fortunately, two other organs can get by without nearly as much blood as they normally enjoy in good times. The first of these is the skin. As a response to anemia, small blood vessels in the skin contract, causing a greater resistance to the flow of blood than is present in more vital organs. Since the blood being pumped out of the heart will preferentially follow the path of least resistance, it will go through the more vital organs faster than it will through skin with contracted vessels. The result is a partial diversion of blood from the skin to other organs. The second organ which sacrifices its right to blood supply is the kidney. Now the kidney is a very vital organ, to be sure, but it is normally endowed with much more blood flow than it needs to stay alive and function properly. Both kidneys, taken together, weight about 350 grams (or about 1/2 of 1 percent of the total body weight), but they receive 20 percent of the cardiac output, or about 1 liter per minute. Gram for gram, then, the kidneys receive 50 times the cardiac output of the body as a whole. Clearly they could give up some of that for the benefit of their fellow organs, and as part of the adaptation to anemia, they do so.
The diversion of blood flow from the skin causes one of the cardinal clinical features of anemia--pallor. Pallor is the pale color observed in the skin of a light-skinned anemic individual, and in the mucous membranes and nailbeds of all anemic individuals, light-skinned or otherwise. It should be noted that anemic patients are pale not because their blood is thin (anemic blood is just as opaque and highly colored as normal blood), but because the diversion of blood means that there is less of it in the skin, and more of the pale color of bloodless human tissue shows through.
Decrease of hemoglobin-oxygen affinity. Earlier we discussed how the affinity (or the "willingness" to bind) between oxygen and hemoglobin changed with the number of oxygen molecules gained or lost by hemoglobin. It turns out that hemoglobin-oxygen affinity can be accomplished by other chemical means as well. There is a simple organic acid, called 2,3-diphosphoglycerate (2,3-DPG) that is elaborated within the red cell under anemic conditions. This 2,3-DPG causes hemoglobin to bind oxygen less avidly and to give up as much to the starved tissues as possible. Of course, the other side of the coin is that oxygen is more difficult to pick up in the lungs, but, since the respiratory system is not the main concern in an anemic patient, something has to give, and the healthy system ends up taking up the slack for the sick one.
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