I have now been diagnosed with steroid induced diabetes and steroid induced liver disease. The hardest part of that is that when I am in a flair typically the only thing that words is steroids. So, I still need to take them, but yet I shouldn’t because of the other two diseases they have caused in my body. My doc is amazing, and has started having me take the steroids in a longer period of time so less goes in my body at one time. But still it is one of those catch 22 things of lupus.
I was diagnosed 13 years ago, however the doctors think I have been dealing with it since I was about 15 years old. I am a mom of 3 amazing kids and one seriously awesome grandson. I am also a writer. Lupus has definaately affected my life, but trying to have as positive an attitude as you can helps on those days when it seems like life will never be normal or pain free again.
When ingested, PCP is rapidly transported from the blood into brain and adipose tissue with a distribution half-life of 1 to 4 h and a plasma clearance of - L/kg/h. The plasma elimination half-life varies depending on dosage. In overdose patients the elimination half-life ranges from 11 to 89 h, while in volunteers given low doses of the drug, half-life is in the range of 7 to 50 h (mean h). Frequent users exhibit a 2-compartment elimination mechanism where PCP is slowly released from tissue compartments over a long period of time. The existence of a large tissue store of the drug is supported by a large apparent volume of distribution (- L/kg/hr). In rats, the brain/plasma PCP ratio is about 7:1 after a single dose, and the fat/plasma ratio can be as high as 100:1.
PCP has also been shown to cause schizophrenia-like changes in N -acetylaspartate and N -acetylaspartylglutamate levels in the rat brain, which are detectable both in living rats and upon necropsy examination of brain tissue.  It also induces symptoms in humans that mimic schizophrenia.  PCP not only produced symptoms similar to schizophrenia, it also yielded electroencephalogram changes in the thalamocortical pathway (increased delta decreased alpha) and in the hippocampus (increase theta bursts) that were similar to those in schizophrenia.  PCP induced augmentation of dopamine release may link the NMDA and DA hypothesis of schizophrenia.