Decreased mortality rates associated with SLE can be attributed to earlier diagnosis (including milder cases), improvement in disease-specific treatments, and advances in general medical care. According to the CDC, one third of SLE-related deaths in the United States occur in patients younger than 45 years, making this a serious issue despite declining overall mortality rates.

Infectious complications related to active SLE and immunosuppressive treatment are now the most common cause of death in early active SLE, and accelerated arteriosclerosis is a key cause of late mortality.  The Framingham Offspring Study demonstrated that women aged 35-44 years with SLE were 50 times more likely to develop myocardial aschemia than healthy women.  Causes of accelerated coronary artery disease (CAD) in persons with SLE are likely multifactorial, including endothelial dysfunction, inflammatory mediators, corticosteroid-induced atherogenesis, and dyslipidemia associated with renal disease.

This study is very disturbing!   I know medicine has made lots of advances in the past 50 years which has significantly decreased mortality rates in lupus but still NO new drug has come out in over 50 years!  Benlysta and others are on their way and will hopefully all be FDA fast tracked and this time next year our conversations on drug choices should be very different then they are today and not include drugs used now as much like MTX, methotexrate, and I know there are a lot more total immunosuppresants that others could list so feel free to comment and add on to this list.  Steroids & prednisone might always be needed with lupus but hopefully with much less frequency and length of time as they are prescribed now.  We need more drug companies focusing on lupus to get more drugs options available for us and as a result, increase the successful treatment of a higher % of lupus patients.

This new study says 1/3 of lupus deaths are in patients younger than 45 years old and it looks like they attribute it mainly to infections from active SLE and/or immunosuppresants .  For older cases of death, it was primarily from heart issues.  I am supposed to go on an immunosuppressant next, I am 38 and I have never had my heart checked other than blood work at initial diagnosis and the stethoscope.  My heart risks besides having LUPUS:  1) I have the MTHFR gene - only one if I remember right 2) I have high homocysteine levels (low in the high range but still high enough that I am on folbee every day for the rest of my life).  3) I have very low HDL levels (lowest around 6, highest 18 although with lupus fog I can ALWAYS be a little off especially when I am trying to pull something out from my brain).  All alone might mean nothing but the three combined with this lupus study data?  I think it is time to look at my heart some more for inflammation or other issues.  And probably the same for many of you!

They are saying we are 50 times more likely than other women to have myocardial aschemia!  I have no idea what it is but I will research it and post some more info. soon. Any suggestions on what heart testing I should request from my gp doctor? 

This disease is never ending and the doctor appointments alone are so exhausting but I owe it to my kids to try to stay as healthy as possible and educated about my risks.  Then with the help of my doctors and any advice anyone reading my blog wants to share to determine which I think are my most dangerous risks and test / treat anything needed.  I will live with this pain for a lifetime, I just want to be given the opportunity to continue to live long enough to raise my babies and see them settled and finally give me some daughters to spoil until they give me some grandchildren and then I will be moving next door to one for 6 months and the other for 6 months.  Better yet, my husband and I will rent a huge RV and drive it 6 months to one son & 6 months to the other   Can you imagine my poor daughter in laws?  haha...all out of love.

XOXO

Lupus Celebrity

Mortality/Morbidity

The natural history of SLE varies from relatively benign disease to rapidly progressive and even fatal disease. SLE often waxes and wanes in affected individuals throughout life, and features of the disease vary greatly between individuals. The disease course is milder and survival rate higher among persons with isolated skin and musculoskeletal involvement than in those with renal and CNS disease.

SLE carries an average 10-year survival rate that now exceeds 90%.  Prior to 1955, the 5-year survival rate was less than 50%. Decreased mortality rates associated with SLE can be attributed to earlier diagnosis (including milder cases), improvement in disease-specific treatments, and advances in general medical care. According to the CDC, one third of SLE-related deaths in the United States occur in patients younger than 45 years, making this a serious issue despite declining overall mortality rates. In 1976, Urowitz first reported bimodal mortality in early versus late SLE, noting that SLE-related deaths usually occur within the first 5-10 years of symptom onset.

Infectious complications related to active SLE and immunosuppressive treatment are now the most common cause of death in early active SLE, and accelerated arteriosclerosis is a key cause of late mortality.  The Framingham Offspring Study demonstrated that women aged 35-44 years with SLE were 50 times more likely to develop myocardial aschemia than healthy women.  Causes of accelerated coronary artery disease (CAD) in persons with SLE are likely multifactorial, including endothelial dysfunction, inflammatory mediators, corticosteroid-induced atherogenesis, and dyslipidemia associated with renal disease.