My friend bought me a beer on May 7, 2016 before a road rally. That was the last time I had a drink until this past Saturday, memorial weekend, when I bought a 6 pack of budlight lime, and drank them all at a friend's party. Sunday morning, I woke up with extreme pain in my left shoulder/ shoulder blade, and it hurts to take a deep breath. My neighbor had a party Sunday, and I did not drink anything other than water and coffee, and today, Memorial Day, I am still in pain. I can not move my head to the left, and it hurts to take a deep breath and move my left arm. So, my note to self is to never drink alcohol again. Period. Having a few drinks with my friends is not worth the pain that those few drinks cause. I can not drink alcohol anymore!
It's was a painful week that led to a shoulder blade attack at 3am Friday morning. At 6am I gave myself my humira shot. I should have injected a couple days early this week to maybe have avoided the pain in my shoulder blade, and I will try and remember that next time. Both shoulder blades had hurt all week, but whatever happened at 3am, I never want to experience again. I woke up to, what felt like to me, was someone stabbing me over and over again in my right shoulder. I got up and took a norco and 2 neurontin, and proceeded to fight through the constant intense pain. I went outside to avoid waking anyone up, sat on my stool, and smoked a cigarette to try and calm myself down, and wait for my medicine to start working. It was an exhausting and overwhelming experience. I went back to bed an hour later and slept for another hour and a half. After waking my son up for school, I took my humira shot. My right arm and hand felt sore and numb, like someone had punched me in that area. I felt this way pretty much all day, and very tired. Probably because a couple extra neurontin, but I would rather try and stay ahead of the pain. Humira felt like it started working within an hour too. I believe I would die without this medicine. And that is another story. I have not accomplished too much all week, but I feel grateful for the moments I have experienced, and am ready for a new week.
My Frustrating experience this month: I went to see my rheumatologist on April 4. I asked her if she could start filling my norco prescription. She said yes, but I would have to get out of my 'pain contract' with my neurologist. On April 26, I had a followup visit with Dr. Turk, my neurologist, from my transferaminals that I had on March 21, and April 11. April 26th was his last day...he has only been here a year and a half. My appointment was at 9:45. I arrived at 9:30, and the nurse called me back at 9:35. She told me today was the Dr.'s last day, and that this appointment should be pretty quick. HA! The Dr. came in to see me at 10:40. He released me from my pain contract. The appointment with him was so frustrating, I am happy he is leaving. Maybe now I can be seen by a Doctor who actually speaks English, and knows what I am asking. The Dr. had an assistant with him this time. I asked the Dr. if I could have a 3rd transferaminal this time to hopefully get me through this year. The injections I had last year worked for 7 months...they wore off right before Thanksgiving last year, which meant I had to have cortisone injections in November, December, and January. Anyway, the Dr. could not understand my request. The assistant had to ask him the same exact thing I did, and his answer was no. He scheduled another appointment for me in 2 months. While waiting at the front desk to be rescheduled, I asked the receptionist if I could get a copy of my 'release of pain contract'. She said yes, but she would have to go to the back to get it. I asked her what time it was, and she said 10:50. I was late for my next Dr. appointment which was at 10:45, so I said never mind, and left quickly to speed to my late appointment! When I got home later that day, I called my rheumatologist and left a message letting her know I had been released from my pain contract. The rheumatologist's office called me back the next day, April 27th, saying the Dr. had called in my new prescription for norco to my pharmacy. My other 3 prescriptions for Humira, Neurontin, and Arava could be refilled on the 28th, so I called them in, and on Friday afternoon I go to the pharmacy to pick them up. My Humira was all screwed up. The pharmacy received the syringe, not the pen, so they have to call the Dr. to get approval for the pen. I received the other 3, but when I get out to the car, I check the prescriptions and my Norco was horribly wrong. My neurologist had been prescribing 75 pills, 1 pill 3x a day, and they were 325/10. The prescription I received was 60 pills, 325/5mg. When I got home, I call the rheumatologist. I explained to her what had happened. She said that since I picked up the prescription, there was nothing she could do. I said that wouldn't do. I will have to take 6 pills a day to get the same relief as I was from the 3. The nurse says "well, you're going to run out then." I told her to speak with Dr. VanDellen and get back to me to see how we can make this right. All this happened on FRIDAY! Monday morning, Tammy from Dr. VanDellen's office called. She said she had left a message at Dr. Turk's on Friday and today, and no one had sent her the fax she needs proving that I was released from my pain contract. She said that once she receives that, Dr. VanDellen could refill my prescription in 2 weeks at the correct dose. I called Dr. Turk's office and left an angry message. Tammy called me back later that morning and said she had heard from Dr. Turk's office saying they would send her a fax, but she had not received anything yet. I waited until Tuesday to call Tammy to see if she had received the fax, and she said yes. So, hopefully my medication will finally be right. I guess I will just have to wait to find out.
I had saved this information on my computer in 2014, just found it, and wanted to share it.
The genetic marker: HLA-B27 is a MHC (Major histocompatibility complex) class I molecule consisting of an alpha chain encoded in the MHC region on chromosome 6 and a non-MHC encoded beta chain I32 microglobulin, and is highly recognized as being associated with certain Rheumatic and Inflammatory Autoimmune Conditions. Similar information, statistics, geographical similarities and other associations between Rh- individuals and many of the various Autoimmune Conditions. According to Randall Johnson at the Baylor College of Medicine in Houston, “Only 7% of the US population tests positive for the HLA-B27 gene; this gene, found only in persons with Rh- blood, can trigger the immune system to operate overtime at WARP SPEED in times of medical emergency.” Can the HLA-B27 genetic marker be found in Rh+ individuals? Autoimmune diseases are disorders where the primary cause is an inflammatory reaction caused by the body’s own immune system attacking the body’s own tissues. It has been established that the Rh- factor can be recessive, but it does not disappear. Where do the Rh- cells, that one without the Rh protein go to hide within the body? Could this incompatibility be the result in Autoimmune diseases? Recessive Rh- blood cells do not just morph into Rh+ blood cells because if they did, a parent could not pass it down from their recessive gene pool. What is the relationship of Rh- and HLA-B27 Positive? The HLA profile defines the cells from an individual or “self”, distinguishing them from those from other individuals showing a different HLA profile “non-self”. Autoimmunity is the failure of an organism to recognize its own constituent parts as “self”, which allows an immune response against its own cells and tissues. Knowing our true blood type and factors makes a big difference to our health.
This information led me to 23andme.com, looking for the HLA-B27 genetic marker. My search brought up no results, so I typed in A- Blood. This search led me to the following information:
Non-ABO Blood Groups Most people think of their blood type as A+ or O- (or some other combination of A, B, O, +, and -) but there actually are more than 25 different blood groups that go into your particular "type." All of these blood groups can be important in the event that you need a blood transfusion. Blood type is also important during pregnancy—some types of mismatch between mother and fetus are potentially dangerous to the developing baby. In both cases, reactions to mismatched blood happen because the immune system can't tell the difference between foreign red blood cells and dangerous foreign cells like bacteria. The following results are based on Established Research for 4 reported markers.
My Genotype Genetic Marker rs2285644 is GG di(a-b+) on the SLC 4A1 Gene. The SLC 4A1 determines the "Diego" blood group.
Blood type is high heritable. Each of the different blood types are determined by genotype at just one or two SNP's. The Diego, Kidd, and Kell blood types are inherited in a codominant manner. This means the red blood cells of heterozygotes actually present two different versions of a protein on their surface. (For example, Diego heterozygotes have the Di)a+b+) blood type - their blood cells have both Di(a) and Di(b) proteins.
The SLC4A1 gene determines the "Diego" blood group. It makes a protein that transports ions in and out of red blood cells and plays an essential role in enabling the red blood cells to transport the waste product carbon dioxide to the lungs, where it can be removed from the body. The different versions of the SLC4A1 protein are call Di(a) and Di(b). A single SNP that changes the protein sequence determines which one of these blood group antigens will be made. Immune responses to blood mismatched for the Diego blood group can cause moderate to severe transfusion reactions and mild to severe hemolytic disease of a newborn. The Diego blood group is interesting to anthropologists because the distribution of the various blood types is different in diverse populations from around the world. The Di(a) version of this blood group is mainly found in populations of Mongolian descent. It is found in 36% of South American Indians, 12% of Japanese, and 12% of Chinese, but is rare in Caucasians and Blacks (0.01%). Interestingly, the Di(a) antigen is less rare in the Polish population (0.47%) compared to most Caucasian populations (0.01%). This may reflect the invasion of Poland by Tatars (who have Mongolian heritage) many centuries ago. The Di(b) blood group antigen is found in almost every population. Frequencies of the Diego blood types: Di(a-b+) is found in more than 99.9% of Europeans and Africans and >90%of Asians. Di(a+b+) is found is less than 0.1% of Europeans and Africans and in 10% of Asians. Di(a+b-) is found in less than 0.01% of Europeans, Africans and Asians.
Di(a-b+) is found in more than 99.9% of Europeans and Africans and >90% of Asians. Di(a+b+) found in less than 0.1% of Europeans and Africans and in 10% of Asians. Di(a+b-) found in less than 0.01% of Europeans, Africans, and Asians.
My Genotype Genetic Marker rs8176058 is GG K-k+ for the KEL Gene.
The KEL gene determines the Kell blood group. It encodes a protein that cuts another protein called endothelin-3, producing a short form of endothelin-3 that causes blood vessels to constrict. Several different antigens are determined by the KEL gene. (23andMe reports data on 2 of these.) SNP rs8176058 determines the K/k antigen. SNP rs817059 determines the Kpa/Kpb antigen. In both cases the SNPs are affecting the sequence of the protein made by the KEL gene. Immune responses to blood mismatched for the Kell blood group can cause severe transfusion reactions and severe hemolytic disease of the newborn (reactions against K are stronger than against k, Kpa, or Kpb). In the case of hemolytic disease of the newborn, the mother's antibodies prevent red blood cells from being made in the fetus. The k version of this blood group antigen is much more common than the K version in most populations. The K-k+ blood type is found in 98% of Africans and 91% of people of European ancestry. 25% of people with Arabic ancestry have the K version on their red blood cells. The Kp(a-b+) blood type is found in 97.7% of Europeans and 100% of Africans.
My Genotype Genetic Marker rs1058396 is GG k(a+b+) on SLC14A1 Gene. The SLC14A1 Gene determines the Kidd blood group. This gene encodes a protein that transports a chemical called urea in and out of red blood cells, keeping the ion concentration of the cells balanced, and maintaining the shape of the red blood cells. The different versions of the SLC14A1 protein are called Jka and Jkb. A single SNP that affects the protein sequence determines which one of these blood group antigens will be made. Immune responses to mismatched blood for the "Kidd" blood group can cause moderate transfusion reactions and mild hemolytic disease of the newborn. In fact, the reactions are so mild that antibodies against Kidd blood group antigens can be difficult to detect when a doctor does a cross-matching test, so transfusion reactions due to Kidd group mismatches end up happening more often that with other blood groups.
23andme use a set of 11 SNPs in the ABO gene to determine our ABO blood type: rs8176719, rs1053878, rs785389, rs8176740, rs8176743, rs8176746, rs41302905, rs41302905, rs8176747, i4000504, rs8176749, i4000505. However, there are many other mutations and deletions in the ABO gene that can affect blood type. If you have one of these more rare mutations, your actual blood type could be different than that predicted by these SNPs. It often takes more than a single mutation to differentiate between the A, B, and O versions of the ABO gene. This complicates the analysis of probable blood type. Take for example, a SNP that distinguishes between the A and B versions of the gene. If you have a copy of the "A" version from parent and a copy of the "B" version from the other parent, it would seem obvious that you have type AB blood. But if you also have a variant that indicates an O version of the gene (O SNPs make the protein encoded by the ABO gene non-functional, effectively cancelling out A and B versions), things get complicated. That "O" SNP could be in the A copy of the gene, or the B copy of the gene. In the first case, you would be "B/O", or type B. In the latter case, you would be "A/O", or type A. Knowing for sure which versions of different SNPs are in the same copy of a gene thakes complicated calculations that 23andMe does not currently perform. To make this experimental feature work, 23andMe has implemented a simplified version of the procedure, which is known as phasing. However, this method may introduce errors into your predicted blood type. There are multiple subtypes of the A,B, and O families. My data indicates that I probably have either the subtyp
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