...but they feel like they are. It's another side effect, called peripheral neuropathy.
Generally peripheral neuropathy is linked to diabetes, but certain chemotherapy drugs (including the class of drugs named taxenes, of which Taxol is a member) can also cause damage to the end of nerves, leaving you feeling like you've left your legs crossed for too long or like you've fallen asleep on your side and your arm and hand are now asleep. This usually occurs in the longer nerves in our bodies, which is why feet and hands are the most common areas affected.
My case, thus far, is minor. I'm having some numbness on the outside of my left foot and my heel has been numb for a couple of days, and my toes on both feet are numb and/or tingly off and on. It can progress as the drugs accumulate in your system, but I'm putting my foot down on this one, even if I can't feel it: I am not letting it get worse. The progression can include increased numbness, tingling, and even sharp, "electric" type pains. I've had a few of those to date, and they always make me jump.
Moisturizing seems to be the best way to keep it from progressing, and I've been diligent about applying a thick, natural moisturizer (Moon Valley Organics came recommended at Whole Foods; the woman there said another customer in chemotherapy said it works best, and so far I have to agree, though Eucerin Calming Creme is good too) three or four times a day. This isn't a bad habit to get into anyway, as I've been increasingly dehydrated and my skin is crazy dry.
Controlling your blood sugar has also been cited as a way to decrease the symptoms (this is for the diabetes-related neuropathy, I assume), as has the cure-all for nearly all my chemotherapy side effects, regular exercise. I try to walk regularly, mostly to counteract the aches and the heart-related side effects. Thankfully, the weather seems to be cooperating, at least for the next couple of days.
Wednesday, September 29, 2010
Thursday, September 23, 2010
Yesterday I finished the third treatment in my second round of chemotherapy. The drug I'm getting this time around is called paclitaxel (brand name Taxol). I will be getting it via injection once a week for three weeks, with a week off each cycle. It's supposed to be much better than the drugs in the first round, which one of the chemo nurses referred to as "the mack daddy of cancer treatment" (and patients can only get once in their lifetimes because it's so toxic to your heart). I'm very glad to be done with that round, though I really cannot complain about the side effects. I was tired for about three or four days after the treatment and achey (like having the flu) but that is about it. Oh, well, I'm bald too, but that didn't really hurt. But this round is either creating a cumulative effect of the drug(s) or the side effects are just more apparent.
Dry skin, dehydration and fatigue are cumulative during this round, as the treatments are more frequent, and though I'm an old pro at these I can already tell they are getting worse. The hot flashes are sticking around, unfortunately, but they are familiar and somehow that makes them tolerable. There is another side effect that the medical professionals worry about, called peripheral neuropathy, but I don't think I'm experiencing that yet. Instead I am displaying a "seldom seen" side effect called hand-foot syndrome.
This fun side effect makes the palms of my hands and the bottoms of my feet feel hot and itchy. I suppose this is tolerable, at least right now, but it's really irritating. I'm hoping (against all I've read) that this does not have a cumulative effect, but I'm afraid it will get worse.
Right now I only have an itchy feeling and at times my palms are red, but it can progress to peeling skin, tenderness, pain and even blistering. Today I've already had some discomfort walking, but no blisters or anything are evident. What's worse, they (the ubiquitous "they") really don't know what causes this reaction. It could possibly be due to the rupture of capillaries in these areas as a result of the drugs.
Moisturizing my hands and feet seems to be the most important thing, as well as elevating my feet as often as I can (at least for a week after the infusion). Thus, I spent an obscene amount on a various assortment of natural moisturizers the other day, hoping I find one that works well. So far Bert's Bee's Mama Bee cooling leg and foot creme provides some temporary relief from both the heat and the itchiness, but I'll keep you updated. I have a lot of hope for several of the other choices, as well.
Dry skin, dehydration and fatigue are cumulative during this round, as the treatments are more frequent, and though I'm an old pro at these I can already tell they are getting worse. The hot flashes are sticking around, unfortunately, but they are familiar and somehow that makes them tolerable. There is another side effect that the medical professionals worry about, called peripheral neuropathy, but I don't think I'm experiencing that yet. Instead I am displaying a "seldom seen" side effect called hand-foot syndrome.
This fun side effect makes the palms of my hands and the bottoms of my feet feel hot and itchy. I suppose this is tolerable, at least right now, but it's really irritating. I'm hoping (against all I've read) that this does not have a cumulative effect, but I'm afraid it will get worse.
Right now I only have an itchy feeling and at times my palms are red, but it can progress to peeling skin, tenderness, pain and even blistering. Today I've already had some discomfort walking, but no blisters or anything are evident. What's worse, they (the ubiquitous "they") really don't know what causes this reaction. It could possibly be due to the rupture of capillaries in these areas as a result of the drugs.
Moisturizing my hands and feet seems to be the most important thing, as well as elevating my feet as often as I can (at least for a week after the infusion). Thus, I spent an obscene amount on a various assortment of natural moisturizers the other day, hoping I find one that works well. So far Bert's Bee's Mama Bee cooling leg and foot creme provides some temporary relief from both the heat and the itchiness, but I'll keep you updated. I have a lot of hope for several of the other choices, as well.
Tuesday, September 14, 2010
Anatomy of a hot flash
I'm bald, tired, and nearly always thirsty. The chemotherapy makes me ache. It makes me tired, too, but also, just to add insult to injury, it also gives you insomnia (though that is exacerbated by the steroids they give you to make you feel better). I awake nearly every two hours throughout the night. Luckily, I can usually fall back to sleep, but there are times I do not, and those are fun. The targeted therapy I just began can cause a skin rash (similar to acne) and will cause diarrhea (they laid that out for me in no uncertain terms). But overall, the worse symptom has to be the hot flashes.
Chemotherapy messes with your hormones and suppresses ovarian function (i.e., you don't ovulate or menstruate). Thus, patients are basically thrown into a chemical-induced menopause. It's lots of fun. You are just sitting there, minding your own business, and suddenly the skin on your head, neck and chest begins to prickle. A flush climbs up your neck and reaches your cheeks, making you feel hot. But by far the best part is the sweat itself. (Personally I sweat on my back, neck and chest and head most often, but there are times when I'm lying in bed that my entire body feels sweaty. And the sweat on your bald head feels lovely, believe me.)
There is no pattern to these little flashes of hell, they come morning, noon and night. They come when I'm relaxed, when I'm running around, and when I'm sleeping. There's really no preparation.
Sometimes I have warning, heart palpitations or shortness of breath. Other times, nothing (most times, actually). Breastcancer.org defines hot flashes as follows: "the sudden, intense, hot feeling on your face and upper body, perhaps preceded or accompanied by a rapid heartbeat and sweating, nausea, dizziness, anxiety, headache, weakness, or a feeling of suffocation." It's as accurate a definition as I can find.
Why does this happen? The simple reason is the change in hormones, specifically estrogen. Low levels of estrogen affect the hypothalamus, the "termostat" of our brains, the area responsible for regulating our sleep cycles, appetite, and body temperature. The drop in estrogen levels causes the hypothalamus to misread our body's temperature and the body's response is, well, not fun, but biologically the brain signals our body (via epinephrine, serotonin and related molecules) to stop the heat, even if there wasn't any heat prior to this signal. So the heart beats faster, your blood vessels dilate (which actually helps cool the blood) and you sweat because it's the body's cooling mechanism. This is how our bodies normally regulate their temperature, but because of the screwed-up hormones it triggers these responses randomly instead of in response to overheating. (Which, incidentally, my body does not do right now, or at least it didn't this summer in the humidity and heat.)
The next time you see me sitting quietly across from you and I suddenly break out in a flush and sweat, be kind. It's terrible. And I learned this after my second hot flash: I called my mom immediately and apologized for making fun of her while she went through menopause. I really do take it all back now.
Chemotherapy messes with your hormones and suppresses ovarian function (i.e., you don't ovulate or menstruate). Thus, patients are basically thrown into a chemical-induced menopause. It's lots of fun. You are just sitting there, minding your own business, and suddenly the skin on your head, neck and chest begins to prickle. A flush climbs up your neck and reaches your cheeks, making you feel hot. But by far the best part is the sweat itself. (Personally I sweat on my back, neck and chest and head most often, but there are times when I'm lying in bed that my entire body feels sweaty. And the sweat on your bald head feels lovely, believe me.)
There is no pattern to these little flashes of hell, they come morning, noon and night. They come when I'm relaxed, when I'm running around, and when I'm sleeping. There's really no preparation.
Sometimes I have warning, heart palpitations or shortness of breath. Other times, nothing (most times, actually). Breastcancer.org defines hot flashes as follows: "the sudden, intense, hot feeling on your face and upper body, perhaps preceded or accompanied by a rapid heartbeat and sweating, nausea, dizziness, anxiety, headache, weakness, or a feeling of suffocation." It's as accurate a definition as I can find.
Why does this happen? The simple reason is the change in hormones, specifically estrogen. Low levels of estrogen affect the hypothalamus, the "termostat" of our brains, the area responsible for regulating our sleep cycles, appetite, and body temperature. The drop in estrogen levels causes the hypothalamus to misread our body's temperature and the body's response is, well, not fun, but biologically the brain signals our body (via epinephrine, serotonin and related molecules) to stop the heat, even if there wasn't any heat prior to this signal. So the heart beats faster, your blood vessels dilate (which actually helps cool the blood) and you sweat because it's the body's cooling mechanism. This is how our bodies normally regulate their temperature, but because of the screwed-up hormones it triggers these responses randomly instead of in response to overheating. (Which, incidentally, my body does not do right now, or at least it didn't this summer in the humidity and heat.)
The next time you see me sitting quietly across from you and I suddenly break out in a flush and sweat, be kind. It's terrible. And I learned this after my second hot flash: I called my mom immediately and apologized for making fun of her while she went through menopause. I really do take it all back now.
Monday, September 6, 2010
You may not know that there are different kinds of breast cancer. Researchers call these “pathways.” There’s the well-known estrogenic (estrogen positive) breast cancer, caused by an overabundance of estrogen (much of which is from the environment). There’s also progestin positive breast cancer, and the highly publicized BRCA1 and BRCA2 genetic forms of the disease. My cancer is HER2+, meaning that some of my cells make too much of the HER2 protein (this is termed “overexpression”). HER2 overexpression is the culprit in about 25% of breast cancers and has been linked to nearly 10% of ovarian cancers as well.
We breast cancer patients who overexpress HER2 proteins sometimes do not respond as well as other patients to traditional treatments such as certain chemotherapy drugs. Thankfully, the discovery of this cancer pathway allows better chemotherapy drugs to be developed and there are targeted treatments too, including Tykerb (generic name: lapatanib) and Herceptin (generic name: trastuzumab).
HER2 proteins are what is called receptor proteins, which the cells use to communicate with one another, and between the inside of the cell and the “outside.” These proteins are found on the surface of every cell and are usually exclusive; that is, if the protein doesn’t “match” the receptor it cannot bind to it. These receptors come from different “families” and work in different ways, and interact with different molecules.
This really is too intricate to get into here, so we’ll leave it at this: HER2 (also called HER2/neu) receptor molecules are signal transductors, meaning they take signals from inside the cell to the outside (or vice versa), so nearby cells can communicate with one another.
It works like this: signal—reception—transduction—response.
The reception is on the surface of the cell membrane, the transduction occurs through the cell membrane and within the cells, and the response occurs in the nucleus of the cell, in the DNA and the proteins it is told to produce. In this case, the cell is told to produce too many HER2 receptors and may not send proper signals to the cell to grow, mature and die (a process called apoptosis, which happens to of my all-time favorite words).
Finding out about these pathways is important to the increased survival in breast cancer patients, as well as to my own treatment. There are chemotherapies, called non-targeted therapy, and targeted biological therapies such as those I will be getting both in the next round of chemo and after surgery for about a year.
The latter types of therapies work in two ways. First, by binding to the HER2 receptors it “flags” them for destruction by the patient’s immune system. Next, it signals to HER2 receptors “downstream” from the one flagged that it needs to stop producing so many. Lapatanib works from inside the cell out, and herceptin from outside in, and both shrink the tumor (or so we hope!).
As I begin round two of my chemotherapy (weekly infusions of the drug Taxol) I’m also preparing to take one of the targeted therapies, lapatinib. This is part of a clinical trial, as the drug is only FDA approved for metastatic breast cancer at this point and they are researching if it works on in situ breast cancers as well. Both types of treatment provide the patient with all sorts of interesting side effects, from the really scary to the simply annoying. You’ll hear more about these soon.
We breast cancer patients who overexpress HER2 proteins sometimes do not respond as well as other patients to traditional treatments such as certain chemotherapy drugs. Thankfully, the discovery of this cancer pathway allows better chemotherapy drugs to be developed and there are targeted treatments too, including Tykerb (generic name: lapatanib) and Herceptin (generic name: trastuzumab).
HER2 proteins are what is called receptor proteins, which the cells use to communicate with one another, and between the inside of the cell and the “outside.” These proteins are found on the surface of every cell and are usually exclusive; that is, if the protein doesn’t “match” the receptor it cannot bind to it. These receptors come from different “families” and work in different ways, and interact with different molecules.
This really is too intricate to get into here, so we’ll leave it at this: HER2 (also called HER2/neu) receptor molecules are signal transductors, meaning they take signals from inside the cell to the outside (or vice versa), so nearby cells can communicate with one another.
It works like this: signal—reception—transduction—response.
The reception is on the surface of the cell membrane, the transduction occurs through the cell membrane and within the cells, and the response occurs in the nucleus of the cell, in the DNA and the proteins it is told to produce. In this case, the cell is told to produce too many HER2 receptors and may not send proper signals to the cell to grow, mature and die (a process called apoptosis, which happens to of my all-time favorite words).
Finding out about these pathways is important to the increased survival in breast cancer patients, as well as to my own treatment. There are chemotherapies, called non-targeted therapy, and targeted biological therapies such as those I will be getting both in the next round of chemo and after surgery for about a year.
The latter types of therapies work in two ways. First, by binding to the HER2 receptors it “flags” them for destruction by the patient’s immune system. Next, it signals to HER2 receptors “downstream” from the one flagged that it needs to stop producing so many. Lapatanib works from inside the cell out, and herceptin from outside in, and both shrink the tumor (or so we hope!).
As I begin round two of my chemotherapy (weekly infusions of the drug Taxol) I’m also preparing to take one of the targeted therapies, lapatinib. This is part of a clinical trial, as the drug is only FDA approved for metastatic breast cancer at this point and they are researching if it works on in situ breast cancers as well. Both types of treatment provide the patient with all sorts of interesting side effects, from the really scary to the simply annoying. You’ll hear more about these soon.
Wednesday, September 1, 2010
Old Genes
When my father was diagnosed with squamous cell carcinoma just over a year ago, I worked with a professor who said something along the lines of "if it's any consolation, remember that your father's genes are very old and they've survived for generations." It wasn't really a consolation, because at the time I had a bad feeling about my father's diagnosis, and about how far along the cancer actually was; it was aggressive and surgery revealed substantial tumor growth in his head and neck. As it turns out, my bad feelings were right, and now I am mourning his loss.
I recount this sentiment because a little over a year later I am facing a cancer diagnosis of my own. Mine isn't skin cancer, rather it's invasive ductal carcinoma, one of the most common and most treatable forms of breast cancer. I had a terrible feeling about the lump (which is why I went to the doctor) and about the biopsy. Once again, my intuition served me well, because I got the diagnosis I did not want, but was expecting. This time, those same words that professor thought may console me actually do bring me some comfort. They have me thinking about genes (cancerous ones in particular) and the fragility of life. And unlike the bad feelings I had about my father's diagnosis and my own, I do not have bad feelings about my outcome. That may be naive, but sometimes--especially in times like these--optimism is all you've got. My genes, in various forms, have been around for centuries, and even longer. Early versions existed eons and have been passed down through entire eras. Why shouldn't they serve me well?
Life is amazing when you think about it. We start out as a hollow ball of cells called a blastulae, and if somehow we make it through that simple, silly little stage without trouble and begin to differentiate, then hey, it's nothing short of a miracle. Next, as embryos, we traverse the dangerous terrain of development, where our growth and gene expression is finely tuned, thanks to millions of years of trial and error. And if we develop as planned by our DNA, our problems aren't over yet. So many things can go wrong during these stages, and if we are lucky enough to develop as specified in the DNA blueprints, we have to go out into the real world after birth, and that isn't easy either.
We get out into the world and are bombarded by chemicals and sunlight and hormones in our food. We dodge viruses and bacteria and microbes. During all of this it is business as usual at the cellular level. Signals tell the cells when to grow, how to grow and when to divide, when to die off. If you delve deeper, into the DNA, it becomes even more detailed.
The DNA double helix unwinds, the mRNA comes in to make a copy. It copies each base, or nucleotide, of the DNA one by one, and in the correct order. There are even checkpoints, like spell check or proofreading, to avoid errors. This is all built in to our bodies. The sequence of DNA nucleotides, the As, Ts, Gs and Cs, is what makes the cells what they are. The mRNA is then shuttled out of the nucleus into the cytoplasm of the cell. Once there, it is translated into the proteins which make up, well, everything in our bodies. This process is elegant, intricate, and stunning. Life goes on. But sometimes the chemicals, sunlight and viruses can cause changes in our DNA, called mutations. In the case of many cancers, it may be one slight change, as little as one nucleotide of DNA, and it is all different. A ball of cells will begin to form. They replicate themselves and grow and don't die when they should, and they stick close together like cliques in a high school cafeteria. They make a tumor. This ball of cells gone awry is what I'm planning to bring down. Beat. Survive.
Individually my cells are fragile. So very many things can go wrong and become the squeaky wheel in the well-oiled machine that is the human body. Conversely, so many things continue to go right, too, and life, in all it's fragile beauty, goes on as it should. I have faith that my body will continue on as it should, my DNA will copy and translate as it is supposed to, it will make the right protein at the right time, as these genes have been doing for eons. And I will survive.
Originally journaled 15 May 2010
I recount this sentiment because a little over a year later I am facing a cancer diagnosis of my own. Mine isn't skin cancer, rather it's invasive ductal carcinoma, one of the most common and most treatable forms of breast cancer. I had a terrible feeling about the lump (which is why I went to the doctor) and about the biopsy. Once again, my intuition served me well, because I got the diagnosis I did not want, but was expecting. This time, those same words that professor thought may console me actually do bring me some comfort. They have me thinking about genes (cancerous ones in particular) and the fragility of life. And unlike the bad feelings I had about my father's diagnosis and my own, I do not have bad feelings about my outcome. That may be naive, but sometimes--especially in times like these--optimism is all you've got. My genes, in various forms, have been around for centuries, and even longer. Early versions existed eons and have been passed down through entire eras. Why shouldn't they serve me well?
Life is amazing when you think about it. We start out as a hollow ball of cells called a blastulae, and if somehow we make it through that simple, silly little stage without trouble and begin to differentiate, then hey, it's nothing short of a miracle. Next, as embryos, we traverse the dangerous terrain of development, where our growth and gene expression is finely tuned, thanks to millions of years of trial and error. And if we develop as planned by our DNA, our problems aren't over yet. So many things can go wrong during these stages, and if we are lucky enough to develop as specified in the DNA blueprints, we have to go out into the real world after birth, and that isn't easy either.
We get out into the world and are bombarded by chemicals and sunlight and hormones in our food. We dodge viruses and bacteria and microbes. During all of this it is business as usual at the cellular level. Signals tell the cells when to grow, how to grow and when to divide, when to die off. If you delve deeper, into the DNA, it becomes even more detailed.
The DNA double helix unwinds, the mRNA comes in to make a copy. It copies each base, or nucleotide, of the DNA one by one, and in the correct order. There are even checkpoints, like spell check or proofreading, to avoid errors. This is all built in to our bodies. The sequence of DNA nucleotides, the As, Ts, Gs and Cs, is what makes the cells what they are. The mRNA is then shuttled out of the nucleus into the cytoplasm of the cell. Once there, it is translated into the proteins which make up, well, everything in our bodies. This process is elegant, intricate, and stunning. Life goes on. But sometimes the chemicals, sunlight and viruses can cause changes in our DNA, called mutations. In the case of many cancers, it may be one slight change, as little as one nucleotide of DNA, and it is all different. A ball of cells will begin to form. They replicate themselves and grow and don't die when they should, and they stick close together like cliques in a high school cafeteria. They make a tumor. This ball of cells gone awry is what I'm planning to bring down. Beat. Survive.
Individually my cells are fragile. So very many things can go wrong and become the squeaky wheel in the well-oiled machine that is the human body. Conversely, so many things continue to go right, too, and life, in all it's fragile beauty, goes on as it should. I have faith that my body will continue on as it should, my DNA will copy and translate as it is supposed to, it will make the right protein at the right time, as these genes have been doing for eons. And I will survive.
Originally journaled 15 May 2010
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