You've had some recent stress to your liver which caused the elevated enzyme level. I've had the same with a bout of food poisoning, solved it with short term glutathione injections and daily NAC... Levels are back in the 30s.
A 25 year old male claims he is on PCT,but i hardly believe him.On the contrary,i am possitive he is abusing AAS at the moment.
1) Primary hypogonadism and almost inactive hypophysis (LH/FSH< 0.5)
2) High beta estradiol,as a result of estrogenic AAS (methandienone),or use of Testosterone without aromatase inhibitors.
3) Prolactinemia,as a result of possible nandrolone use
4) High TT/FT due to AAS abuse
5) Perhaps the use of mesterolone (synthetic DHT) that binds tightly to SHBG,leaves enough FT to circulate in plasma and libido is high,as SHBG is low.
There are three ways to test testosterone levels: saliva sample, urine sample, and blood sample. Each method has its pros and cons. I am going to have my blood serum test this week.
There are three ways to test testosterone levels: saliva sample, urine sample, and blood sample. Each method has its pros and cons. I am going to have my blood serum test this week.
CVD panel also includes: Homocysteine and Lipoprotein A In CBC when MCV is lower than 70, we have thalasemia.This is a non treated anemia,where RBCs appear to be smaller in size. H/H in these patients never gets above 45%/15 and is usually its close to 40%/13.5 ALP & GGT are cholestatic enzymes,that raise with bilurubin during jaundice.Alcoholism,EBV, HBV,HCV infection, prolonged 17 alkylated AAS abuse.In urine urobilinogen is found.
However ALP deals also with bones and osteopenia.In puberty ALP goes up as teens catch up in height.
In CBC,eosinophils are a type of WBCs that elevate under allergic reactions
(e.g. yeast).
Potassium is the main intracellular element.
Must be strictly under higher range,cause it leads to heart arrythmias.
AST & ALT elevate both in AMI (heart attack), pharmaceutical hepatitis and in rhabdomiolysis. However during AMI,CKMB raises,unlike CPK in later.Moreover,heart attack is clarified by troponin protein and C Reactive Protein.
LDH is an enzyme that elevated under circumstances of cellular death.
For instance in AMI,where myocardium turns into necrotic scar tissue.
Also in rhabdomiolysis,when skeletal muscle is ruptured.
And under hemolysed RBCs,either in thalasemia,or during a poor technique of blood suction.
ESR is another inflammatory marker,less accurate than CRP.
But its affected under anemia and RBCs size.
In CBC we evaluate RBCs,WBCs,PLT.
This was a case of a patient who had iron deficiency anemia.MCV was considerable high,but H/H were frustrating low,so were iron & ferritin.Thalasemia patients have considerable low MCV and they are obligated to take folic acid for life.The cell membrane of their RBCs is more fragile and ruptures.Because folate takes part in DNA synthesis,folate prolonges their short life span.Otherwise death occurs and billuruin is flushed in bloodstrea,This is why thalasemia patients are yellowish in skin colour,if they fail to treat with folic acid.
fter four bottles (16ml/16gr) of Nebido/Aveed (Testosterone Undecaonate) 25mg TU every day 25mg DHEA every day 25mg DHT every day
100iu HCG every day
1mg Anastrozol per week
July 2017/November 2017
45yo male with primary hypogonadism,undergoes a PCT with HCG & SERMs use. Libido was improved with overall mental/physical state. DHEA supplementation seems obligatory. A typical laboratory finding of andropause
Transaminemia (AST/ALT) and dislipidemia (HDL/LDL/TC),as a result of AAS abuse. Slight rhabdomyolysis effect as well. All labs were back to normal,six weeks after. NAC,LIV52,Milk thisle,Lecithin,Οmega 369, Phytosterols,Niacin and Krill oil use used on a daily basis plan.
A 50yo male visited me,in order to evaluate his HPTA. His major concern was if there is any case of andropause. However,during the medical history,there were no clinical symptoms of hypogonadism.As we are aware of,symptoms have to be followed by labs in order to diagnose andropause. It is obvious in this blood work,that there is no sign of primary,or secondary hypogonadism.We have to realise that TRT/HRT is not something trendy that every active man should follow.
It's a replacment therapy instead,for those who undergo clinically and laboratory the signs of andropause.
For the history,my suggestion to the client was the use of synthetic DHT (mesterolone),in order to lower his SHBG and let more Free Testosterone to circulate.Therefore,he will improve his self esteem,sexual drive,cognitive function,etc.This FT would eventualy aromatise,but his E2 is relatively low,so there is no major concern of a slight aromatisation.
I also advised him to use DHEA,in order to boost his SDHEA higher than the mid range value.
Rhabdomyolysis,as a result of hypertraining and cocaine use.Transaminemia,as skeletal muscles have common receptors with liver and myocardium.Slight hyperkalemia as a result of striated muscle breakdown (Potassium is the main inrracellular element).Creatinine at higher optimal range,due to toxic myoglobin release from contractile muscles damage.Urea just above highest optimal range,possibly because overtraining is frequently accompanied with dehydration.
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