Has anyone found anything you can do about the side effects of Zometa? Is there anything that can help the terrible calf pain, other than pain meds? What about the fever? And the headache, and general fatigue?
For those who get these reactions, what kind of things work for you to get though this?
Forums
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heddleandhook - Name: heddleandhook
- Who do you know with myeloma?: self
- When were you/they diagnosed?: Jan 2015
- Age at diagnosis: 68
Re: Zometa side effects - what can be done about them?
I don't know about anyone else, but when I get my 3 month Zometa infusion (usually on a Friday) I usually just mark off the weekend.
I feel like I have the Flu for 3-4 days. I treat it like the flu. Supportive meds, fluids, sleep, etc.
I have not found anything that will stop it. Yeah, stuff that will lessen it's effects---but it's a 3-4 day flu, no matter what.
Lately, I have been drinking a fair amount of Tonic water--and it helps me greatly. I'm a cynical bastard when it comes to things like "Tonic Water"---but it relieves my muscular cramps, moreso than narcotics or Muscle relaxers. My GI tract also settles down, a bit.
Good luck.
I feel like I have the Flu for 3-4 days. I treat it like the flu. Supportive meds, fluids, sleep, etc.
I have not found anything that will stop it. Yeah, stuff that will lessen it's effects---but it's a 3-4 day flu, no matter what.
Lately, I have been drinking a fair amount of Tonic water--and it helps me greatly. I'm a cynical bastard when it comes to things like "Tonic Water"---but it relieves my muscular cramps, moreso than narcotics or Muscle relaxers. My GI tract also settles down, a bit.
Good luck.
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Rneb
Re: Zometa side effects - what can be done about them?
To both of you: I am not sure that this will be helpful, but here goes. The first time I received a Zometa infusion, I developed the flu symptoms as described. After that, the nurse increased the timing of the infusion from 30 minutes to 45 minutes. The flu symptoms and Zometa side effects did not recur.
I have been told that sometimes patients experience the side effects only initially and are okay after subsequent infusions. I have also been told that some patients always experience side effects from the Zometa. In any event, if you have not tried increasing the delivery time, why not give it a try and see what happens.
I have been told that sometimes patients experience the side effects only initially and are okay after subsequent infusions. I have also been told that some patients always experience side effects from the Zometa. In any event, if you have not tried increasing the delivery time, why not give it a try and see what happens.
Re: Zometa side effects - what can be done about them?
Also tried "Chilled" Zometa.... drinking lots of ice-water at infusion, a couple pieces of toast, and in addition to slower infusions, as you suggest.
I even tried flirting with Nurses...
No help.
I even tried flirting with Nurses...
No help.
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Rneb
Re: Zometa side effects - what can be done about them?
This was my third infusion, I don't remember any bad effect after the first, except for some cold drenching sweats at night, which could have been from the Velcade and dex given at the same time.
But the second Zometa gave me a fever of 100.6 F (38.1 C), and general achiness. Doc wanted to put me on antibiotics thinking it was a virus, but I resisted, and it only lasted about 24 hours.
This third time, again the temp went up to 100.6 F ( maybe even more, but I took Tylenol every 4 hours this time for the pain) as I got much worse achiness and fatigue, along with so much pain and stiffness in my legs – calves mostly – that I could hardly walk this morning. That's what got me scared, wondered if I was getting a blood clot.
I had talked to the doc and nurses about the slower infusion and they said no. They have to bill by the time it takes and blah blah blah.
So it seems it is getting worse with each infusion for me. At least I don't have any side effects to speak of with my RVD (Revlimid, Velcade, and dex).
Wondering about a heating pad for my legs, and investigating the magnesium or tonic for next time.
I also would like to know what the mechanism is that is causing the leg pains. Knowing WHY things happen can help understanding and helps make it more bearable.
But the second Zometa gave me a fever of 100.6 F (38.1 C), and general achiness. Doc wanted to put me on antibiotics thinking it was a virus, but I resisted, and it only lasted about 24 hours.
This third time, again the temp went up to 100.6 F ( maybe even more, but I took Tylenol every 4 hours this time for the pain) as I got much worse achiness and fatigue, along with so much pain and stiffness in my legs – calves mostly – that I could hardly walk this morning. That's what got me scared, wondered if I was getting a blood clot.
I had talked to the doc and nurses about the slower infusion and they said no. They have to bill by the time it takes and blah blah blah.
So it seems it is getting worse with each infusion for me. At least I don't have any side effects to speak of with my RVD (Revlimid, Velcade, and dex).
Wondering about a heating pad for my legs, and investigating the magnesium or tonic for next time.
I also would like to know what the mechanism is that is causing the leg pains. Knowing WHY things happen can help understanding and helps make it more bearable.
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heddleandhook - Name: heddleandhook
- Who do you know with myeloma?: self
- When were you/they diagnosed?: Jan 2015
- Age at diagnosis: 68
Re: Zometa side effects - what can be done about them?
Hah! I had terrible calf pain last Zometa that kept me in bed on Vicodin (hydrocodone and acetaminophen / paracetamol) for 2 days! I hadn't heard of other people getting that in particular before now! My first treatment I also got a fever, and get the flu-like thing every cycle.
I asked my doc at Dana Farber, and next time I'm going to switch to pamidronate (Aredia) and see if that helps. If it doesn't help, I'm going back to Zometa and we'll slow down the infusion a lot. I'll let you know.
I asked my doc at Dana Farber, and next time I'm going to switch to pamidronate (Aredia) and see if that helps. If it doesn't help, I'm going back to Zometa and we'll slow down the infusion a lot. I'll let you know.
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Tracy J - Name: Tracy Jalbuena
- Who do you know with myeloma?: Me
- When were you/they diagnosed?: 2014
- Age at diagnosis: 42
Re: Zometa side effects - what can be done about them?
As I recall, the first bunch of Zometa infusions I underwent, I also had Velcade/Dex on Board. Zometa didn't bother me so much--as the Velcade/ Dex was pretty harsh on my system--like a Yo-yo.
I hate Velcade/ Dex.
Later, after Induction was finished, I noticed the Flu-like symptoms, as the Velcade/ Dex were gone. Zometa infusions have gotten no worse, since then. Just an acceptance that I'm gonna feel "yucky" for a few days--so I take a few ibuprofen or an Advil, before I go in to be infused. I keep fluids up. I sleep if I feel tired. I get a minor fever, as you describe. I get cranky joints and a few cramps. Headaches. Neck aches. Eyes hurt--just regular old Flu-like stuff.
I keep unsalted tops crackers, 7-up, and Tonic, and ice water handy ( basically a poor man's "Banana Bag"--D5 lactated ringers) --and try to get comfortable and sleep off an uncomfortable 48-72 Hrs. Reading and computer work is fair--I watch TV, lounge in bed, and make to-do lists. Rarely do I have to take anything stronger than Pepto, for my tummy ache. Stool softener helps avoid constipation. Miralax doesn't taste too good, during these weekends--but all of the above comes with myeloma. It's not a major sacrifice, as the myeloma itself makes me tired--and I catch up on sleep over the weekends, anyway. ( Where possible).
It gets no worse, with subsequent infusions, has been my experience. I have never even considered switching to Aredia, as the Zometa is supposed to be superior.
Just one of those things "that you make peace with", as part of the Myeloma experience.
The mechanism of action is the Zometa helps activate and balance the Osteoclast / Osteoblast bone process(es) in your body. Those aches are the healing / re-contouring of your bones. Myeloma upsets the delicate balance of Osteoclasts/Osteoblasts--such that the Osteoblasts hungrily over eat bone and basically "poop" calcium. Osteoclasts don't / can't keep up--and your bones fall apart--literally. Excess Calcium floods into your Blood stream, Kidneys, Organs, etc.
That is one reason why your Proteins and calcium get out of whack, with Myeloma.
Good luck.
I hate Velcade/ Dex.
Later, after Induction was finished, I noticed the Flu-like symptoms, as the Velcade/ Dex were gone. Zometa infusions have gotten no worse, since then. Just an acceptance that I'm gonna feel "yucky" for a few days--so I take a few ibuprofen or an Advil, before I go in to be infused. I keep fluids up. I sleep if I feel tired. I get a minor fever, as you describe. I get cranky joints and a few cramps. Headaches. Neck aches. Eyes hurt--just regular old Flu-like stuff.
I keep unsalted tops crackers, 7-up, and Tonic, and ice water handy ( basically a poor man's "Banana Bag"--D5 lactated ringers) --and try to get comfortable and sleep off an uncomfortable 48-72 Hrs. Reading and computer work is fair--I watch TV, lounge in bed, and make to-do lists. Rarely do I have to take anything stronger than Pepto, for my tummy ache. Stool softener helps avoid constipation. Miralax doesn't taste too good, during these weekends--but all of the above comes with myeloma. It's not a major sacrifice, as the myeloma itself makes me tired--and I catch up on sleep over the weekends, anyway. ( Where possible).
It gets no worse, with subsequent infusions, has been my experience. I have never even considered switching to Aredia, as the Zometa is supposed to be superior.
Just one of those things "that you make peace with", as part of the Myeloma experience.
The mechanism of action is the Zometa helps activate and balance the Osteoclast / Osteoblast bone process(es) in your body. Those aches are the healing / re-contouring of your bones. Myeloma upsets the delicate balance of Osteoclasts/Osteoblasts--such that the Osteoblasts hungrily over eat bone and basically "poop" calcium. Osteoclasts don't / can't keep up--and your bones fall apart--literally. Excess Calcium floods into your Blood stream, Kidneys, Organs, etc.
That is one reason why your Proteins and calcium get out of whack, with Myeloma.
Good luck.
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Rneb
Re: Zometa side effects - what can be done about them?
Used to wake up after infusions with terrible calf cramps, actually called my doctor at 3:00 a.m. He seemed to think that it was hydration problem and recommended pidiacare.
Since then, I make sure I am well hydrated and usually drink Gatorade or some other liquids during the infusions. Seems to help. Have not had any problems for the last 3 infusions. My doctor did explain the Zometa hydration relationship and it has ameliorated the cramping.
Hope this helps. Life with multiple myeloma is tough enough.
John Wing
12 year survivor
Since then, I make sure I am well hydrated and usually drink Gatorade or some other liquids during the infusions. Seems to help. Have not had any problems for the last 3 infusions. My doctor did explain the Zometa hydration relationship and it has ameliorated the cramping.
Hope this helps. Life with multiple myeloma is tough enough.
John Wing
12 year survivor
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johnwing13
Re: Zometa side effects - what can be done about them?
Zometa and Aredia side effects are awful, but my bones (skull, hips, spine) were riddled with lesions! Fortunately, my oncologist / hematologist was not convinced of their efficacy. He stated that he had never read anything that he found really persuasive.
After 2 treatments with Zometa and 1 treatment with Aredia, and horrid side effects, I chose to discontinue both. I have never regretted that decision. As others have stated, RVD side effects are way more than bad enough!
Oh, and by the way, I just celebrated my 2 year post ASCT with no bone or lesion problems of any kind....
Rneb, you make the following statement:
I'm confused. Don't osteoblasts rebuild the bone, while osteoclasts break down bone structure? So wouldn't it be the osteoclasts, and not the osteoblasts, that would be hungrily over-eating the bone?
Aloha
Daniel
After 2 treatments with Zometa and 1 treatment with Aredia, and horrid side effects, I chose to discontinue both. I have never regretted that decision. As others have stated, RVD side effects are way more than bad enough!
Oh, and by the way, I just celebrated my 2 year post ASCT with no bone or lesion problems of any kind....
Rneb, you make the following statement:
Myeloma upsets the delicate balance of Osteoclasts/Osteoblasts--such that the Osteoblasts hungrily over eat bone and basically "poop" calcium. Osteoclasts don't / can't keep up--and your bones fall apart--literally."
I'm confused. Don't osteoblasts rebuild the bone, while osteoclasts break down bone structure? So wouldn't it be the osteoclasts, and not the osteoblasts, that would be hungrily over-eating the bone?
Aloha
Daniel
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DanielR - Name: Daniel Riebow
- Who do you know with myeloma?: Self
- When were you/they diagnosed?: 12/2012
- Age at diagnosis: 59
Re: Zometa side effects - what can be done about them?
Daniel:
Perhaps I oversimplified on the cell Biology. Here is a more definitive statement for you, and part of a cell biology article, explaining the relationship.
"Osteoclasts and Osteoblasts are felt to overlap, and their functions are often dependent upon phase, factor, protease presence, RANKL,TRANCE,OPGL,ODF, etc." (ie. promyeloid precursor)
Glad things are going well for you.
* * * *
H. Kalervo Väänänen*, Haibo Zhao, Mika Mulari and Jussi M. Halleen, "The cell biology of osteoclast function", Skeletal Research Program, Department of Anatomy, Institute of Biomedicine, University of Turku, 20520 Turku, Finland (full text of article [PDF])
SUMMARY
Osteoclasts are multinucleated cells responsible for bone resorption. They have developed an efficient machinery for dissolving crystalline hydroxyapatite and degrading organic bone matrix rich in collagen fibers. When initiating bone resorption, osteoclasts become polarized, and three distinct membrane domains appear: a ruffled border, a sealing zone and a functional secretory domain. Simultaneously, the cytoskeleton undergoes extensive re-organisation. During this process, the actin cytoskeleton forms an attachment ring at the sealing zone, the membrane domain that anchors the resorbing cell to bone matrix. The ruffled border appears inside the sealing zone, and has several characteristics of late endosomal membrane. Extensive vesicle transport to the ruffled border delivers hydrochloric acid and proteases to an area between the ruffled border and the bone surface called the resorption lacuna. In this extracellular compartment, crystalline hydroxyapatite is dissolved by acid, and a mixture of proteases degrades the organic matrix. The degradation products of collagen and other matrix components are endocytosed, transported through the cell and exocytosed through a functional secretory domain. This transcytotic route allows osteoclasts to remove large amounts of matrix-degradation products without losing their tight attachment to underlying bone. It also facilitates further processing of the degradation products intracellularly during the passage through the cell.
Key words: Bone, Osteoclast, Cell biology
INTRODUCTION
Bone resorption is necessary for many skeletal processes. It is an obligatory event during bone growth, tooth eruption and fracture healing, and is also necessary for the maintenance of an appropriate level of blood calcium. In the adult human skeleton, continuous physiological remodelling of bone is exclusively dependent on bone resorption. In several human diseases (e.g. malignant hypercalcemia and postmenopausal osteoporosis) enhanced bone resorption is the key pathophysiological event, and therapies for these diseases are currently based on its inhibition. In contrast, some rare genetic disorders are manifested as decreased resorption and lead to osteopetrosis.
*** Osteoclasts are multinuclear cells derived from hematopoietic stem cells (Suda et al., 1992). Their differentiation pathway is common to that of macrophages and dendritic cells. Thus a promyeloid precursor can differentiate into either an osteoclast, a macrophage or a dendritic cell, depending on whether it is exposed to receptor activator of NF-κ B ligand (RANKL; also called tumor necrosis factor-related activation-induced cytokine (TRANCE), osteoprotegerin ligand (OPGL) or osteoclast differentiation factor (ODF)) macrophage colony-stimulating factor (M-CSF) or granulocyte-macrophage colony-stimulating factor (GM-CSF), respectively (Kong et al., 1999; Nutt et al., 1999; Rolink et al., 1999; Suda et al., 1999). Simonet et al. (1997) found that several cells and tissues produce a soluble factor, osteoprotegerin (OPG), that strongly inhibits osteoclast formation in vitro and in vivo.
^^^^^ More recently, several groups demonstrated that bone marrow stromal cells and osteoblasts produce membrane bound and soluble RANKL/TRANCE/OPGL/ODF, an important positive regulator of osteoclast formation (Lacey et al., 1998). The inhibitory effect of OPG on the osteoclast differentiation is due to the fact that it can prevent the binding of RANKL to its receptor, RANK (Hsu et al., 1999). Major breakthroughs in osteoclast differentiation have thus been made, and some excellent reviews on this topic has been written recently (Suda et al., 1999; Roodman, 1999).
^^^^^^ Here, we do not discuss any further details of the osteoclast differentiation and its regulation but encourage readers to familiarise themselves with the above-mentioned articles.
*** Osteoclasts have developed efficient and unique machinery for dissolving mineral and degrading organic bone matrix. Our understanding of the cellular and molecular processes that are utilized by these professional hard-tissue destroyers has also significantly increased during the past decade. Here, we discuss the recent progress in the understanding of the cell biology of osteoclasts function and activation. Furthermore, we suggest that these cells represent good model systems for addressing some general questions in cell biology.
Perhaps I oversimplified on the cell Biology. Here is a more definitive statement for you, and part of a cell biology article, explaining the relationship.
"Osteoclasts and Osteoblasts are felt to overlap, and their functions are often dependent upon phase, factor, protease presence, RANKL,TRANCE,OPGL,ODF, etc." (ie. promyeloid precursor)
Glad things are going well for you.
* * * *
H. Kalervo Väänänen*, Haibo Zhao, Mika Mulari and Jussi M. Halleen, "The cell biology of osteoclast function", Skeletal Research Program, Department of Anatomy, Institute of Biomedicine, University of Turku, 20520 Turku, Finland (full text of article [PDF])
SUMMARY
Osteoclasts are multinucleated cells responsible for bone resorption. They have developed an efficient machinery for dissolving crystalline hydroxyapatite and degrading organic bone matrix rich in collagen fibers. When initiating bone resorption, osteoclasts become polarized, and three distinct membrane domains appear: a ruffled border, a sealing zone and a functional secretory domain. Simultaneously, the cytoskeleton undergoes extensive re-organisation. During this process, the actin cytoskeleton forms an attachment ring at the sealing zone, the membrane domain that anchors the resorbing cell to bone matrix. The ruffled border appears inside the sealing zone, and has several characteristics of late endosomal membrane. Extensive vesicle transport to the ruffled border delivers hydrochloric acid and proteases to an area between the ruffled border and the bone surface called the resorption lacuna. In this extracellular compartment, crystalline hydroxyapatite is dissolved by acid, and a mixture of proteases degrades the organic matrix. The degradation products of collagen and other matrix components are endocytosed, transported through the cell and exocytosed through a functional secretory domain. This transcytotic route allows osteoclasts to remove large amounts of matrix-degradation products without losing their tight attachment to underlying bone. It also facilitates further processing of the degradation products intracellularly during the passage through the cell.
Key words: Bone, Osteoclast, Cell biology
INTRODUCTION
Bone resorption is necessary for many skeletal processes. It is an obligatory event during bone growth, tooth eruption and fracture healing, and is also necessary for the maintenance of an appropriate level of blood calcium. In the adult human skeleton, continuous physiological remodelling of bone is exclusively dependent on bone resorption. In several human diseases (e.g. malignant hypercalcemia and postmenopausal osteoporosis) enhanced bone resorption is the key pathophysiological event, and therapies for these diseases are currently based on its inhibition. In contrast, some rare genetic disorders are manifested as decreased resorption and lead to osteopetrosis.
*** Osteoclasts are multinuclear cells derived from hematopoietic stem cells (Suda et al., 1992). Their differentiation pathway is common to that of macrophages and dendritic cells. Thus a promyeloid precursor can differentiate into either an osteoclast, a macrophage or a dendritic cell, depending on whether it is exposed to receptor activator of NF-κ B ligand (RANKL; also called tumor necrosis factor-related activation-induced cytokine (TRANCE), osteoprotegerin ligand (OPGL) or osteoclast differentiation factor (ODF)) macrophage colony-stimulating factor (M-CSF) or granulocyte-macrophage colony-stimulating factor (GM-CSF), respectively (Kong et al., 1999; Nutt et al., 1999; Rolink et al., 1999; Suda et al., 1999). Simonet et al. (1997) found that several cells and tissues produce a soluble factor, osteoprotegerin (OPG), that strongly inhibits osteoclast formation in vitro and in vivo.
^^^^^ More recently, several groups demonstrated that bone marrow stromal cells and osteoblasts produce membrane bound and soluble RANKL/TRANCE/OPGL/ODF, an important positive regulator of osteoclast formation (Lacey et al., 1998). The inhibitory effect of OPG on the osteoclast differentiation is due to the fact that it can prevent the binding of RANKL to its receptor, RANK (Hsu et al., 1999). Major breakthroughs in osteoclast differentiation have thus been made, and some excellent reviews on this topic has been written recently (Suda et al., 1999; Roodman, 1999).
^^^^^^ Here, we do not discuss any further details of the osteoclast differentiation and its regulation but encourage readers to familiarise themselves with the above-mentioned articles.
*** Osteoclasts have developed efficient and unique machinery for dissolving mineral and degrading organic bone matrix. Our understanding of the cellular and molecular processes that are utilized by these professional hard-tissue destroyers has also significantly increased during the past decade. Here, we discuss the recent progress in the understanding of the cell biology of osteoclasts function and activation. Furthermore, we suggest that these cells represent good model systems for addressing some general questions in cell biology.
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Rneb
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