LFT Basics

Apex Peptides

New member

 

 How familiar are you guys with your liver…or livers in general? Everyone thinks of their liver as a blood “filter”. While this is true in some ways, it does waaaay more than most people give it credit for. The liver manufactures bile to facilitate fat absorption, converts proteins, carbs and fat into other essential elements. It also caches fat-soluble vitamins, B12 and carbs as glycogen. It processes drugs, creates blood-clotting factors, maintains BGL by means of glycogen breakdown and discharges it into blood as glucose. There’s probably about 300 more things it does, but who’s counting.

 I’ve been a BSN-RNFA, CNOR for about 11 years and have spent most of that time in solid organ transplant…..and weight lifting. I know that doesn't make me an expert, but during this time, I’ve seen a lot of jacked up livers. While I do use AAS recreationally, I certainly try to use them responsibly. Hopefully, all of you do too. If you use steroids, you likely know that oral steroids can mess up your liver, right?  In turn, anyone who knows anything about steroids has heard of “c-17-alpha alkylated”. The description “c-17-alpha alkylated” refers to a change made on position 17 of the basic steroid structure. This concept isn’t too daunting. Anyone who has taken a chemistry course will likely understand. In very oversimplified terms; the c-17aa modification aids the drug to endure first pass metabolism. First pass metabolism occurs when a drug is absorbed from the GI tract and passes via the portal vein into the liver where the drug is metabolized. Sometimes, the result of first pass metabolism means that only a proportion of the drug reaches systemic circulation.  

Moreover, this c-17aa modification allows a very large portion of the drug to enter the blood stream and not be simply deactivated during portal circulation. This whole process sounds great, but… C-17 alkylated androgenic steroids have all been implicated in cases of liver injury, including prolonged cholestasis, peliosis hepatis, nodular regeneration, hepatic adenomas and hepatocellular carcinoma. In addition, they can also hammer your HDL level which is a beneficial cholesterol carrier in the blood. A lowered HDL level is considered a risk factor for cardiovascular disease.  This is why ALL oral cycles should be limited in length and LTFs should be acquired to ensure enzyme levels are not greatly elevated.

LFT (liver function test)

 Certain labs may include different panels in their own specific LFT. Sometimes, their values may vary. However, this should give you a roundabout idea of what to look for. I feel that whenever you’re going to run a cycle of any type, it’s a great idea to obtain blood work BEFORE you begin. This will give you some baseline data to compare any aberrant findings. A typical LFT will consist of AST, ALT, ALP, GGT and a total or conjugated bili. I’ll briefly try to explain each component of the LFT:

ALT (alanine aminotransferase) aka “Serum glutamic pyruvic transaminase”, and AST (aspartate aminotransferese) aka SGOT “Serum glutamic oxaloacetic transaminase” are two enzymes that are necessary for the metabolism of amino acids and protein within the liver. In the event that the liver receives any potential insults, these amino acids matriculate into the blood stream thus elevating their lab values. Now remember… these elevated liver enzyme levels can be due to oral anabolic steroid use, excessive ETOH or other drugs. In contrast, ALT and AST enzymes aren’t entirely specific to the liver. They are also present in other tissues such as cardiac and skeletal muscle. That being said, any type of mass injury to muscle including intense weight training can cause an elevation of those enzymes. This little caveat can easily trigger a false positive leading one to think that their liver is indeed being compromised. If you plan on having a LFT done, it’s best to take a day or two off of the gym prior to blood draw. The same could be said for any blood work. If ALT and/or AST are markedly elevated,  measuring enzymes such as creatine kinase and GGT would provide a more definitive picture of existing liver function, as would liver imaging tests.

Elevations in ALP ( alkaline phosphatase) and GGT (gamma-glutamyl-transpeptidase) can be indicative of bile duct obstruction. In case you didn’t know, bile is a green liquid created and released by the liver. It contains cholesterol, bile salts, and waste products such as bilirubin. Bile salts help your body break down (digest) fats. Bile passes out of the liver through the bile ducts and is stored in the gallbladder. After a meal, it is released into the small intestine. When the bile ducts become blocked, bile builds up in the liver, and jaundice (yellow color of the skin) develops due to the increasing levels of bilirubin in the blood. If you start to turn yellow…STOP the cycle!! I hope I didn’t really have to say that! lol

 

Values found to be WNL:

 ALP: 25-150 iu/l 

 GGT: <50 mol/l

 Bilirubin: 0.08-1.3 mg/dl

ALT aka “SGPT”: 0-55 iu/l

AST aka “SGOT”: 0-40 iu/l

 

OTC liver supps

Liv-52 (available in double strength) 

NAC (N-acetylcysteine) and gluthionine  

Essentiale Forte N (enteral/parenterl): I believe this is proprietary blend of vitamins, Linoleic, Linolenic and Oleic Acids.  

Silymarin (milk thistle)

 

If anybody has something to add, or finds something incorrect, please contribute. I'm always open to learn! 

 

 

Bash

New member

+1 for that science apex! What is ur thoughts on multiple orals used throughout a cycle. And is Proviron a 17aa?i know dbol is what about tbol? 

Feed me the knowledge 

 

Apex Peptides

New member

1. Do they really "work"? Honestly, I think you're going to have a hard time finding any SOLID PEER REVIEWED data supporting either argument. Think about it...any hospitalized patient that actually is in need of treatment wouldn't simply be given an OTC liver sup in lieu of actual pharmaceutical. On the other hand, most people who use OTC sups wouldn't go get serum levels drawn to see if they had actually worked.

Does anyone here have any experience in using OTC liver sups and then followed up with BW to validate efficacy?

2. Multiple orals? I have friends and know guys who've done it/do it. Would I? No....I've never been mad enough at my liver to do so. :) I guess if LFTs show everything is ok and WNL, then....

 

 

livinlife

New member

Damn good post! very acurate information for sure. My pops just underwent a liver transplant a little over a month ago. So the last couple years leading up to the transplant, I was doing my fair share of research on the liver, supporting organs and their functions. Interesting stuff. 

 

solidsnake

New member

 

I’ve been trying to learn more about liver values lately mainly for personal knowledge. I’m having a hard time understanding the differeces between Pt, aPTT, INR. Can anyone here help? You guys seem to know everything about anything. Any help would be great!

 

 

SemperFi

Well-known member

PT is a panel used to help diagnose bleeding or clotting disorders.

aPTT is similar to PT and is used to monitor heparin anticoagulant therapy.

INR is calculated from a PT result and is used to monitor how well the blood-thinning medicatio is working to prevent blood clots.

SEMPER FI

 

Apex Peptides

New member

 

Geesh…that’s kind of a tough one. I’ve worked with acute/chronic liver patients, pre/post transplant, even scrub in on transplants themselves and, I still have troubles knowing exactly when to give and hold anticoags, or which ones to give and how much. All the different pathways and factors, ect, ect.

SEMPER FI nailed it!!  If he doesn't mind, maybe I can add my .02 as well??

 

Without getting in over my head, I’ll try to explain it the best I can with my limited knowledge.  

Exactly like SEMPER FI stated; PT/PTT are lab tests that quantity ones clotting time. INR is a proportion devised from the PT. Your liver makes many proteins or clotting factors (amongst other things) that facilitate blood clotting (coagulation). With the help of vitamin K, Prothrombin aka factor II is one of them.

 

Prothrombin time (PT)

Prothrombin time (PT) measures the existence and action of the five main clotting factors ( I, 2, 5, 7, 10). In short, this test directly determines the integrity of both the extrinsic and common pathways of coagulation potential. In addition, it measures clotting time from the initiation of factor 7 through the creation of a fibrin clot.

 

Partial thromboplastin time (PTT)/Activated partial thromboplastin time (aPTT)

From my understanding, partial thromboplastin time (PTT) and activated partial thromboplastin time (aPTT) is basically the same thing….I could be wrong though. For the most part, aPTT has essentially succeeded the older PTT test. I think this was largely due to its inability to reliably incorporate variables in contact time. The activated partial thromboplastin time (aPTT) measures the function of various other clotting factors, throughout common and intrinsic pathways. aPTT evaluates the clotting time from the activation of factor 12 through the creation of the fibrin clot.

 

International normalized ratio

This one is much easier to explain and understand. INR is devised directly from the PT and was created to allow for more effective comparisons amongst labs values regardless of the type of PT reagent used amongst different laboratories. I guess labs were having a hard time communicating values, so someone came up with a way to standardize them. Before standardizing, there was likely a very wide range for PT values. It’s also so easy to calculate, even I can do it. Check it out…INR = patient’s PT / normal PT. An INR of 1 means the blood clots "normally" for that pt. The greater the INR, the longer it takes the blood to clot. An INR of 3 means the blood takes about three times as long to clot compared with the normal value for that pt. This is therapeutic range for most patients I’ve seen that are RX’d Coumadin for stroke precaution or Afib.

Meds and other stuff

 aPTT/PTT elongations are likely due to factors VIII, IX, XI, and/or XII deficiencies, or inhibitors. In most cases, heparin is used. Heparin prevents clotting by blocking certain factors in the intrinsic pathway. The aPTT/PTT test allows reassurance that there is enough heparin in the blood to preclude clotting, but not so much as to cause uncontrolled bleeding. Once heparin is withdrawn, its blood-thinning effects last merely a few hours.

PT is utilized to screen treatment with Warfarin aka “Coumadin”. When warfarin is dropped, it typically takes several days for it to clear the patient’s system.  Warfarin is often prescribed as a "blood thinner" because it is an effective vitamin K antagonist (blocks the formation of vitamin K)….remember when we talked about how vitamin K formed prothrombin??

 Warfarin dosage for patients undergoing treatment to prevent the formation of blood clots is usually titrated so that PT is about 2.5 < X >1.5 times the normal value. or has an “INR of 2-3”.

 The greater the PT/PTT values, the longer it takes for the blood to form a clot. Just remember; HIGH PT/PTT = BLEEDING. LOW PT/PTT = CLOTS/STROKE/EMBOLI.

 

 
Top