Bilirubin blood test: MedlinePlus Medical Encyclopedia
Bilirubin blood test: MedlinePlus Medical Encyclopedia
What are normal bilirubin levels? - WebMD
Normal serum bilirubin levels in the newborn and the
What are normal bilirubin levels? - Medscape
Elevated or Abnormal Conjugated Bilirubin
Bilirubin (conjugated/direct)
Normal Bilirubin Levels in Blood: Conjugated, Unconjugated
Bilirubin - Lab Tests Online UK
Conjugated & unconjugated bilirubin, causes & treatment of
Bilirubin blood test Information | Mount Sinai - New York
normal conjugated bilirubin level
normal conjugated bilirubin level - win
Was this a gallbladder attack?? What are the next steps?
Hi! So about two weeks ago, I woke up feeling extremely nauseous. In an attempt to make myself feel better, I made some homemade chicken noodle soup, but after eating I felt ridiculously and uncomfortably full. I assumed I just ate a lot and then went to bed. The next day, I woke up with the same uncomfortable feeling, but I assumed I was just very bloated. My stomach felt extremely heavy to the point where I felt like I had chicken noodle soup in my lungs. I spent the day doing things to help with bloating, but nothing really seemed to help. I called some family members who work in healthcare and one of them asked me if my urine was dark, but it wasn't at that point. The next day, I woke up and my pee was bright orange, so I was obviously concerned. I waited one more day to be sure, but then decided I should go to the ER. While I was there, they took my blood and urine samples and told me my bilirubin levels were elevated (3.0, conjugated). They thought it was a gallstone but after an ultrasound and a CT scan, they found nothing. They sent me home with some Tylenol and Motrin for the pain and told me to come back if I noticed my eyes turning yellow. Two days later, the pain was still pretty awful. I couldn't eat anything without feeling horrible nausea and was losing weight like crazy. The few times I was able to eat I would throw it back up. I decided to go to the ER again after vomiting and seeing blood in there, in addition to my eyes looking a little yellow. So I went back to the ER for them to tell me they thought I had a virus, and tested me for mono. It came back negative and my lab results were pretty much the same. They told me to see a GI so I flew home to see one ASAP. By the time I went to see the GI, the pain was gone and everything was normal except my urine was still dark. GI ordered some more lab tests (which I am going to do tomorrow) and an endoscopy scheduled for December 19th. That was on the 4th of December. Now, my urine is back to a normal color and I feel none of the symptoms. I've been eating normally and have been completely fine. What I'm wondering is how worried I should be exactly? I feel completely fine, and I'm worried that the tests are going to come back with no information, and I'm just going to have to be doing additional tests which I cannot afford. Is it worth going through with the endoscopy? Was this even a gallbladder attack? I've read that they last from 15minutes to a couple hours, but I had this abdominal pain and jaundice for about a week and a half. Any information would be helpful! Thanks, and sorry for the long read!
[Discussion] Hepatic Metabolism of Oral AAS, Hepatotoxicity, and Liver Support
I know this is a long write up, the first half is biochemistry and what happens on a cellular level. The second half is more pertaining to the average AAS user, including a deeper dive into liver functioning tests and liver support. I highly recommend at least reading the second half, especially the Liver Support section. Hepatotoxicity is a word that is frequently thrown around, everyone’s heard it, everyone thinks they know what it is, but once you ask something beyond surface level, you get a whole lot of conflicting answers. Let’s dive into it. Overview/Background/General Information/What the fuck actually happens? Drug Metabolism: The human body identifies almost all drugs as foreign substances and subjects them to various chemical processes to make them suitable for elimination. Drug metabolism is typically split into two phases: Phase 1 (oxidation via Cytochrome P450, reduction, and hydrolysis) tends to increase water solubility of the drug and can generate metabolites. Phase 2 further increases water solubility of the drug, inactivating metabolites, thus preparing it for excretion.
Aside: There has been a lot of questions regarding using high dose psoralens (from grapefruit juice/extract) to inhibit the activity of Cyp3A4 (and the Cyp450 family in general) or consuming large quantities of chargrilled meat to induce the activity Cyp450. DO NOT purposely do this in an attempt to increase the bioavailability of oral steroids. The Cyp450 family is incredibly important enzyme family that is involved in the metabolism (both activation and degradation depending) of statins, oral contraceptives, acetaminophen, anti-depressants, beta-blockers, antiarrhythmic agents, and many, many more. This can cause SEVERE adverse effects.
Example: Acetaminophen (Tylenol) is often seen as hepatotoxic, it is not. One of the metabolites, NAPQI, is. Under normal conditions, NAPQI is produced in incredibly minor amounts. Alcohol induces Cyp450 enzyme family, which increases the breakdown of Tylenol into NAPQI, causing intensive acute liver damage which can often be fatal in high doses. In short, don’t nurse your hangover with Tylenol, use Advil instead… or better of just don’t drink alcohol.
17α-Alkylated Anabolic Steroids. These AAS contain a methyl or ethyl group on the C17α position, allowing for oral activation. This modification allows the drug to survive hepatic metabolism, limiting the amount of steroid that is broken down, allowing for more drug to reach the bloodstream. Without this modification, the drug is completely broken down by the liver, never reaching systemic circulation. This initial process is called First Pass Metabolism. First pass metabolism: After a drug is swallowed, it is absorbed by the digestive system and enters the hepatic portal system. It is carried through the portal vein into the liver before it reaches the rest of the body. The liver metabolizes many drugs, sometimes to such an extent that only a small amount of active drug emerges from the liver to the rest of the circulatory system. This first pass through the liver may greatly reduce the bioavailability of the drug. Some oral steroids have a very low bioavailability due to first pass metabolism, thus injectable versions may be used to prevent the initial breakdown, effectively increase bioavailability and reducing liver stress.
Aside: There have been questions regarding sublingual administration of oral AAS in order to bypass first pass metabolism. In short, very few drugs can be properly absorbed sublingually, Nitroglycerin is a prime example. AAS, although can be manufactured for sublingual absorption it requires a specific method of delivery (sublingual tablets, strips, or sprays for example), which are difficult to obtain and manufacture; it’s not as simple as placing some powder under your tongue. Other drawbacks exist of sublingual administration such as tooth decay and difficulty in dose management.
Anavar: The exception to the rule: The oral bioavailability of oxandrolone is 97%. The drug is metabolized primarily by the kidneys and to a lesser extent by the liver. Oxandrolone is the only AAS that is not primarily or extensively metabolized by the liver, and this is thought to be related to its diminished hepatotoxicity relative to other AAS. For this reason, there is no reason to ever use injectable anavar (unless poking yourself that often is your kink, no judgement).
[aside: not all drugs are orally active, in fact the majority are inactive. For example, codeine (inactive) will be converted into the active form, Morphine, within the liver via Cyp450 enzymes]
In the case of oral AAS, hepatic metabolism can convert an active drug into its inactive form; C17α methylation prevents this. Why is this modification known to be hepatotoxic? The primary enzyme that normally breaks down hormonal steroids (such as endogenous DHEA, testosterone, estradiol, etc) is 17β-Hydroxysteroid dehydrogenase, 17β-HSD, (and to a minor extent the Cyp450 family) which can no longer break down the methylated drug, thus the liver finds an alternative route for metabolism. The actual specific process is still relatively unknown, but involves a variety of oxidation reactions, inducing an increase of free oxygen radicals within the hepatocytes (liver cells), causing cell death due to oxidative stress. There is another hypothesis which involves the presence of androgen receptors within the liver. The C17α methylated oral steroid, that is no longer properly broken down, will bind to these receptors, causing a drastic increase of androgenic activity within the liver, leading to hepatoxicity. In my opinion, it is a mixture of both. Many studies show a direct correlation between the androgenic effect of the oral steroid and the amount of hepatoxicity. The exact link between the two is yet to be determined. In general, the greater the affinity of C17α methylated oral steroid for the androgen receptor, the more hepatoxicity occurs.
Hepatotoxicity is an overlying term: the specifics related to AAS use are Cholestasis (blockage of biliary flow), Steatosis (accumulation of fatty lipids within the liver), Zonal Necrosis (hepatocyte death within a specific zone of the liver), and Peliosis Hepatitis (vascular lesions leading to liver enlargement).
Aside: Steatosis (fatty liver) has been an observed adverse effect of Nolvadex and Raloxifene
Cholestasis is a condition where bile cannot flow from the liver to the duodenum. It is the most common condition resulting from oral AAS use. In short, bile is continuously produced but cannot leave the liver, causing build up, backflow, and eventually hepatocyte death. Differential symptoms of cholestasis include but are not limited to pruritus (itchiness), jaundice (yellowing of the skin and whites of the eyes), pale stool, and dark urine. Liver Functioning Tests: What do they mean and why are they relevant? AST: Aspartate Transaminase: This alone is not a good indication of liver damage. AST is found in abundance within both cardiac and skeletal muscle. An elevated AST value can be caused by something as minor as weightlifting. ALT: Alanine Transaminase: ALT is found specifically within the liver and is released into the plasma when significant liver stress, including hepatocyte death, occurs. An elevated value is of concern.
Aside: general rule of thumb (not always true) if both elevated are elevated and if AST>ALT in a ratio of 2:1, suspect alcohol/drug induced damage. If both values are elevated and if ALT>AST in a ratio of 2:1, suspect viral hepatitis.
ALP: Alkaline Phosphatase: ALP is found within the hepatobiliary ducts. An elevated value is commonly indicative of obstruction and bile buildup, signifying cholestasis. GGT: Gamma-glutamyl Transferase: GGT is an enzyme that is found in many organs throughout the body, with the highest concentrations found in the liver. GGT is elevated in the blood in most diseases that cause damage to the liver or bile ducts. 5’-nucleotidase: The concentration of 5’-nucleotidase protein in the blood is often used as a liver function test in individuals that show signs of liver problems. ALP can be elevated due to both skeletal disorders and hepatic disorders. 5’-nucleosidase is elevated ONLY with hepatic stress, not skeletal, thus allowing for differentiation.
Putting it all together: Cholestasis can be suspected when there is an elevation of both 5'-nucleotidase and ALP enzymes. Normally GGT and ALP are anchored to membranes of hepatocytes and are released in small amounts in hepatocellular damage. In cholestasis, synthesis of these enzymes is induced, and they are made soluble. GGT is elevated because it leaks out from the bile duct cells due to pressure from inside bile ducts. As hepatocyte damage continues, ALT, AST, and unconjugated bilirubin will begin to rise. In short: Initial liver stress causes 5’-nucleiotidase and ALP to rise, shortly after GGT rises, then finally AST and ALT rise. Thus, with only AST and ALT values, it is difficult to determine the cause and extent of hepatic damage. Liver Support: NAC/TUDCA/Liv52 NAC: N-Acetyl Cystein NAC is a prodrug of L-cysteine, a precursor of the biological antioxidant glutathione which is able to reduce free radicals within the body. Free radicals, which as discussed above, are associated with causing extensive hepatocyte damage due to the oxidative breakdown of C17α methylated AAS. In addition to its antioxidant action, NAC acts as a vasodilator by facilitating the production and action of nitric oxide. This property is an important mechanism of action in the prophylaxis of contrast-induced nephropathy and the potentiation of nitrate-induced vasodilation.
Aside: NAC has been constantly used as an adjunct to multiple neurological disorders including Parkinson’s, Huntington’s, Multiple Sclerosis, Cerebral Ischemia, Alzheimer’s and MANY more due to the potent free radical trapping effect which prevent mitochondrial dysfunction.
Multiple studies have constantly showed NAC decreasing liver functioning tests and improving liver function and mitigating cholestasis. NAC had the ability to vastly improve markers of kidney function and was actually able to even double the rate of sodium excretion, indicating that NAC is may be useful in preventing water retention. In short, NAC has a vast number of benefits, including hepatoprotective (liver), nephroprotective (kidney), and neuroprotective (neural), and anti-inflammatory effects that have been constantly demonstrated thru literature. Moreover, NAC can and should be used for year-round support since the adverse effects are incredibly mild. There is absolutely NO reason to not be taking NAC.
TUDCA: Tauroursodeoxycholic acid TUDCA is a bile acid taurine conjugate form of UDCA. As discussed above, during cholestasis, bile builds up, creating backflow and inducing hepatocyte death thru apoptosis. Apoptosis, or programmed cell death, is largely influenced by the mitochondria. If the mitochondria are distressed, they release the molecule cytochrome C. Cytochrome C initiates enzymes called caspases to propagate a cascade of cellular mechanisms to cause apoptosis. TUDCA prevents apoptosis with its role in the BAX pathway. BAX, a molecule that is translocated to the mitochondria to release cytochrome C, initiates the cellular pathway of apoptosis. TUDCA prevents BAX from being transported to the mitochondria, effectively inhibiting hepatocyte death. Furthermore, TUDCA aids in the processing of toxic bile acids into less toxic forms, resulting in decreased liver stress, further preventing hepatocyte death. Moreover, TUDCA aids in the transport of bile from the liver into the duodenum, effectively unblocking the build up causing cholestasis. Finally, TUDCA has been proven to be an effective treatment for the necro-inflammatory effects of Hepatitis. Study after study has shown that TUDCA greatly improves liver enzyme values. Why do we recommend only using TUDCA with hepatotoxic oral steroids? The idea is that TUDCA induces liver damage when there is no hepatotoxicity present… but after reading the above, does that make sense? It does not. I could not find any literature showing that TUDCA induces liver toxicity. The recommendation instead is due to the negative effects of TUDCA on cholesterol values. TUDCA has been shown to greatly decrease HDL levels when taken for extended periods of time. The idea is, if you have a healthy functioning liver, there is no reason to take TUDCA for long periods of time since all you’re doing is decreasing HDL values. That being said, after doing the research and seeing the vast benefits of TUDCA (included bellow, not a comprehensive list), I am beginning to change my perspective on TUDCA use with only hepatotoxic oral AAS. In short, TUDCA prevents hepatocyte death, enhances hepatocyte function, exhibits anti-inflammatory effects on the liver, neutralizes toxic bile, and prevents bile build up that was caused by the alternative metabolism of C17α methylated AAS. ***THERE IS NO EVIDENCE THAT I HAVE COME ACROSS THAT SHOWS THAT TUDCA ITSELF INDUCES LIVER DAMAGE WHEN USED WITHOUT HEPATOTOXIC DRUGS**\* TUDCA has a variety of other benefits outside the liver, but I will not go into them this time. In short:
Increasing glucose-induced insulin release via the cAMP/PKA pathway, increasing insulin sensitivity.
Relieving endoplasmic reticulum (ER) stress. The ER makes sure proteins are folded properly.
Reducing programmed cell death (apoptosis) in healthy cells. TUDCA prevents the molecule BAX from reaching the mitochondria. BAX causes mitochondria to release cytochrome C, which causes enzymes (caspases) to initiate apoptosis.
Inactivating Bcl-2-associated death promoter (BAD), a molecule involved in apoptosis.
Removing toxic bile acids from the liver and preventing them from damaging liver cells
Exhibits neuroprotective effects via the inhibition of NF-kB
Preserve photoreceptor function and increases retinal health by increasing rd10
Liv52 Liv52 is an herbal liver support. There have been medical studies conducted on Liv.52 in recent years, many of which involve its ability to protect the liver from damage by alcohol or other toxins. Liv52 has been shown to exhibit antiperoxidative function, antioxidant effects, anti-inflammatory, diuretic effects and neutralization of toxic products within the liver. “The results demonstrated that the patients treated with Liv-52 for 6 months had significantly better child-pugh score, decreased ascites, decreased serum ALT and AST. We conclude that Liv-52 possess hepatoprotective effect in cirrhotic patients. This protective effect of Liv-52 can be attributed to the diuretic, anti-inflammatory, anti-oxidative, and immunomodulating properties of the component herbs.”
“Liv.52 enhanced the rate of absorption of ethanol and rapidly reduced acetaldehyde levels, which may explain its hepatoprotective effect on ethanol-induced liver damage.”
“Liv.52 administration reduced the deleterious effects of ethanol. The concentration of acetaldehyde in the amniotic fluid of ethanol-consuming animals was 0.727 microgram/ml. Liv.52 administration lowered it to 0.244 microgram/ml. The protective effect of Liv.52 could be due to the rapid elimination of acetaldehyde.”
That being said, there is conflicting research on Liv52. The studies either show hepatoprotective function or no effect, positive or negative. “There was no significant difference in clinical outcome and liver chemistry between the two groups at any time point. There were no reports of adverse effects attributable to the drug. Our results suggest that Liv.52 may not be useful in the management of patients with alcohol induced liver disease.”
In short, Liv52 can be used if you have the additional funds, it is not the end-all-be-all but can be used as an adjunct. It is an incredibly cheap drug thatmayimprove liver function and exhibit hepatoprotective effects. IT SHOULD IN NO WAY YOUR ONLY LIVER SUPPORT MEDICATION, but there is nothing wrong with using it.
Age : 18 Sex : F Race : Caucasian Weight : 65.5kg/144lbs Height : 164cm/5.5ft Existing conditions : ADHD Current medication : Concerta LP 54mg Drug use : none Smoking : no Hello, I am about to start isotretinoin so my dermatologist prescribed a routine blood test to check my cholesterol, my bilirubin and my hormones. It was the first time in my life that I had a bilirubin check. When the results came back this afternoon, everything was normal (cholesterol, ASAT, ALAT) except my bilirubin levels which were abnormally high :
total bilirubin (plasma) : 17.7 mg/L or 30.3 μmol/L
conjugated bilirubin (plasma) : 4.3 mg/L or 7.4 μmol/L
un-conjugated bilirubin (calculated) : 13.4 mg/L or 22.9 μmol/L
The thing is, I have absolutely no symptoms other than fatigue, and sometimes when i don't sleep or eat well, the corners of my eyes get slightly yellowish. This usually disappears in 2-3 days. I don't have a fever, no pain, no nausea, no migraines, nothing ! I was told it could possibly be Gilbert syndrome, but I have no idea if it adds up or not... I just want to know if this is a possibility. Thank you for reading
Hi all! I recently had my yearly check-up and my total bilirubin was 3.2 mg/dL. Since it was elevated, my doctor ordered another blood test last week to get a breakdown of the bilirubin (I'm assuming to see the direct/indirect bilirubin levels). I'm still waiting on the results of that blood test, but I was doing some reading about elevated bilirubin levels and I came across some info that said if bilirubin is present in the urine then the elevation is probably caused by direct (conjugated) bilirubin. That means the absence of bilirubin in the urine points to the total bilirubin being made up of indirect (unconjugated) bilirubin. It also said that the absence of urobilinogen points to direct bilirubin levels being high, while normal urobilinogen levels are a characteristic of high levels of indirect bilirubin. I was wondering if this was true for those of you who have been diagnosed with Gilbert Syndrome. My urine was negative for bilirubin and the urobilinogen was normal, so I'm leaning towards the breakdown probably showing mostly unconjugated bilirubin and being Gilbert Syndrome.
So lately I’ve been having some weird symptoms. I want to know which of these are not normal and which could be related to anxiety. I am a male, 21 years old, Brazilian. The question I put here: how often does glycemic level change? I made two blood tests in a period of 2 weeks that measured my glycemic levels and they all showed different results. The first showed 87, then 80 and whenever I measure it at home it’s always around 70/73. One day it was 65 (in the morning). I know all of these values are still within the limit of normal, but I want to know if these changes are that quick. Other symptoms: - My blood pressure has been a bit lower than usual but still within the normal. - One of these days I went for a run at night and when I got home my body temperature was around 34,5ºC and sometimes it’s around that value when I wake up in the morning too (I know temperature is lower in the morning but is it that low?). Along the day its normal. - Occasional dizziness when I stand up - GI symptoms: I lost 5kg from march up til now; explosive diarrhea at times (which I thought could be IBS, but I will be tested for that this week); really fatty and weird green colored stools, sometimes with food in them like beans (never seen that before in them); distended abdomen; - Heart rate feels lower than usual; - Sensation of poor circulation, sometimes hands go pale and cold; - Occasional muscular pain; Other important info: Vitamin D deficiency (taking supplements for that); Have recently got tested for autoimmune diseases (because mom has lupus) and it all came back negative; Blood tests mostly normal besides very irrelevant liver alterations (conjugated bilirubin a bit higher than normal and GGT lower); I was thinking if this could be the beginning of adrenal insufficiency? I don’t even know which doctor to report to. I’m having an upper endoscopy, colonoscopy and MRI this week. Have done cardiac routine tests and they came back normal. Anxiety is really bad over these small things. Any help will be deeply appreciated. Thank you.
Apologies if this is too much unnecessary information. ME: 29M, 290lbs, 5' 9, mix black/hispanic; palpitations with trouble breathing; on and off 2 years; cause unknown; 3.6cm liver lesion detected with CT scan with contrast declared most likely benign, ALT 79; No drugs/drinking/smoking/vaping; Prescribed metoprolol Part 1: Weight loss and initial heart problems Had a huge weight loss few years back 250lbs -> 185lbs, started gaining it back in a year and at the end of 2017, ~250lbs again, I was suffering from palpitations and sudden shortness of breath. I went in and out ERs and everything was more or less normal except for an elevated heart rate that hit 150-160 while just lying in the hospital bed. At the end of the journey I had several ekgs, an echocardiogram, and was given a ZIO patch to monitor my heart rate. EKGs and echo normal, no reason for tachycardia epsiodes found but there were abnormal events while wearing the ZIO patch. I had an episode of an extremely low HR (for me who usually sits in the 80s) when it plummeted to 34bpm the pulse ox i had at the time read an extremely low oxygen level (I feel like it was in the 70s but it's been a while) which freaked me out and then my heart rate sky rocketed to compensate. I had a few more episodes of my heart rate hitting 150-160 with no obvious cause. I was prescribed metoprolol and told to see if it continues or gets worse. Part 2: Intermediate period, weight gain It got a lot better I stopped taking metoprolol, I carry baby aspirin all the time and take it if I feel wonky which happened rather sparingly. Regrettably did not pursue follow up with cardio. I developed what I assume is a tick during this period, I inhale air suddenly and belch it out looked it up and it seems I'm swallowing air suddenly and immediately burping it out, usually happens infrequently but when nervous or sitting for long periods it becomes more frequent. Does not occur when sleeping, occurs less when talking, occurs very frequently while anxious/nervous. I feel down on myself and dieting and end up gaining 40lbs (290lbs current weight) which I didn't discover until last night because I don't use the scale anymore. Part 3: No heart answers, Liver lesion One or two more high HR episodes and I've been taking more baby aspirin over the past month or two and then last night I get a big one while eating, I feel like my face is tight and like I'm not getting enough oxygen I use my pulse ox and my oxygen is dropping and hits the high 80s and then my HR skyrockets to compensate and I hit 180 bpm. Double whammy of a high heart rate, being nervous because of a high HR, and being home alone so I call an ambulance. EMT says my blood pressure was ~150/~110 (i feel like it was 153/109 but I cannot remember exactly) but blood pressure after I left ER settled down to 109/71. Battery of tests to find out what's going on again and everything comes out normal just like it usually does, this time my heart rate never got lower than 99bpm even though I stayed there from 8PM ~ 3AM. Oxygen is intermittently a little low, at least from looking at my pulse ox, I get 91-93 oxsat in my worst moments during my stay otherwise it's normal at 94-98. They order a CT scan with contrast of my chest, everything looks fine but they noticed a lesion on my liver the doctor said he thinks it's benign but that I need to follow up with my PCP and cardiologist since they still don't know why I get these heart episodes. He says it may simply be anxiety, prescribes metoprolol but tells me to wait a day or two before I start taking it to see if my heart finally settles below 100. When resting in bed I check my heart rate and I've successfully hit 83. I read my bloodwork and their report and now I can't help being anxious about the state of my liver, the lesion is 3.6cm and one of them noted hepatic steatosis. Now I'm worried about my follow up and I feel like I compounded my health problems by eating myself fatter than when I was already too fat, I cannot help but contemplate the possibility of liver cancer despite how the doctor seemed unconcerned. And now I realize if I don't lose weight I'll destroy my liver, I've never felt guiltier for breaking my diet. In fact ever since gaining all the weight back I've never physically felt so miserable. Liver tests: ALBUMIN 4.4 g/dL BILIRUBIN TOTAL .3 mg/dL BILIRUBIN, CONJUGATED <.2 mg/dL ALKALINE PHOSPHATE 113 u/L ALANINE AMINOTRANSFERASE (ALT) 79 u/LNOTED AS HIGH ASPARTATE AMINOTRANSFERASE (AST) 43 u/L PROTEIN TOTAL 8.2 g/dL NOTED AS HIGH Everything else in bloodwork came back as in normal ranges except for MONOCYTE COUNT 0.8 k/uL NOTED AS HIGH Quotes from imaging: "3.6 cm hypervascular lesion in the right lobe of the liver, incompletely characterized on this exam. A benign etiology is favored, but the lesion is ultimately indeterminate. Nonemergent MRI can be obtained for definitive characterization." "There are no enlarged mediastinal, hilar or axillary lymph nodes.The visualized portion of the thyroid gland is unremarkable. Anterior mediastinal soft tissue density likely represents benign thymic tissue.Images of the upper abdomen demonstrate hepatic steatosis There is a 3.6 cm a prevascular lesion in the right hepatic lobe." Per recommendation I've already scheduled a meeting with my PCP on the 12th, I want to try and schedule another visit earlier (if possible) with another doctor that accepts my insurance. Also per recommendation I want to schedule a meeting with my cardiologist although if possible I'll take any appointment that's earlier (in addition to the one who knows me). I would like any advice or analysis. On doctor visits and testing: Is it pointless to visit a doctor that can fit me in (if i can find such a doctor) before my pcp? I feel like I need to schedule an MRI asap to get this lesion verified. What should I be asking my doctors? What tests should I get or not get? How concerned should I be? What should I ask my cardiologist? What's the best thing for me to do as a patient? Is there anything I should look for when picking a doctor? On weight loss: I cannot do what I first did to lose weight over concerns with my heart, my restriction to 1000 calories per day when I first lost weight was too strict and in that weight loss period I had scheduled a month for fasting which I view as impossible with my current heart. On mental state: I don't consider myself an anxious person but I may just lack perspective on that, however I can't help but think any kind of lesion is cause for concern and fevered investigation. I definitely am not in my best mental state right now but I'm not freaking out either. However I am feeling low especially when I consider that I may have put myself in an irreversible situation, however remote that possibility may or may not be, which leads me to my desire to get as accurate of a picture of what's going on as I possibly can. I've definitely had an upset stomach and discomfort over this and for now am chalking it all up to hyper awareness of my body, like feeling itchy because you see someone else scratching I have no severe pains only slight discomforts. tl;dr 3.6cm liver lesion detected with CT scan with contrast declared most likely benign, ALT 79, and persistent palpitations with sustained elevated heart rate, no history of drug use or smoking (no vaping either), no stds. Apologies for the long submission and thank you for your time.
12-yo girl has a 2-month history of intermittent jaundice. She has both unconjugated and conjugated bilirubinemia. Also - normal haptoglobin, AST, ALT levels. There is no evidence of injury/toxins. Which additional finding is most likely?
So, obviously I ruled out hemolysis immediately (hemolysis would have ↓ haptoglobin) Then I ruled out "decreased activity of UDP gluronysyltransferase" because of the direct bilirubinemia. That left me with: A. Ineffective erythropoiesis → didn't seem to be a likely cause of jaundice B. Increased alkaline phosphatase → I forget what this even means C. Gallstones I chose gallstones because I was thinking ↑ bilirubin would lead to gallstones. The answer ended up being "decreased activity of UDP gluconysyltransferase" because I guess since the jaundice was intermittent/mostly asymptomatic that automatically points you to Gilbert's syndrome? Just seems pretty bullshit to me. Anyway, can someone please explain the right answer and why it's not the 3 answers I was left with? Thanks.
Conjugated bilirubin literally off the charts! 70+ mg/dcl.
My father had a liver xplant two weeks ago and was literally signing papers to be transferred to an occupational therapy center after day 6. It's now day 13 and his conjugated bilirubin score is >70.4, higher than the instrument can even measure. The perplexing issue for the doctors is the enzymes and other liver numbers have remained within normal levels the entire time. Two endoscopy procedures of the biliary system were done and no obstructions were found. A biopsy was done from 2 locations, and the results showed a ”healthy liver." Potentially related issues: The doctors postulate the abnormal liver function is a result of infection. He has e coli sepsis and his latest white blood cell count had it's first drop from 40.6 to 26; encouraging. He is not on anti rejection because of the immuno suppression, of course. Interestingly, twice he's had unanticipated bleeding from surgeries. As a consequence, he's getting a lot of blood and I wonder if this is exasperating the high bilirubin issue as these extra red blood cells die. My father has obviously regressed to the point I'm not sure he makes it through the weekend. I need your help medical. You could very well save my dad...
Conjugated bilirubin literally off the charts: >70.4!
65M, 6'0", 225 lbs, caucasian, non-drinker, non-smoker, NASH Liver sufferer, diabetic, with multiple medications including insulin. My father had a liver xplant two weeks ago and was literally signing papers to be transferred to an occupational therapy center on day 6. It's now day 13 and his conjugated bilirubin score is >70.4 mg/dcl, higher than the instrument can even measure. The perplexing issue for the doctors is the enzymes and other liver numbers have remained within normal levels the entire time. Two endoscopy procedures of the biliary system were done and no obstructions were found. A biopsy was done from 2 locations, and the results showed a ”healthy liver." The doctors postulate the abnormal liver function is a result of infection. He has e coli sepsis and his latest white blood cell count had it's first drop from 40.6 to 26; encouraging. He is not on anti rejection because of the immuno suppression. They got the biopsy when they cleaned out the infection. Twice he's had unanticipated bleeding from the surgeries. As a consequence, he's getting a lot of blood. My father has obviously regressed to the point where I'm fearful for his life. I need your help, AskDocs. You could very well save my dad...
I am 24 Male, suffering from jaundice with bilirubin level as follows Serum bilirubin (Normal : 0.2 - 1.2 mg/100 ml) (mine 1.75 mg/100 ml) conjugated (Normal 0.0 - 0.2 mg/100 ml) (mine 1.40 mg/100 ml) unconjugated (0.2 - 1.0 mg/100 ml) (mine 1.35 mg/100 ml) I tried medicine but still i don't feel like its gone. Unable to eat anything in the morning. Feels like vomiting. Lost so much weight. Please help
Hello everyone, this will by my last big post for a little while. I wanted to address hepatotoxicity since it seems to be this big grey area for a lot of people. Drug metabolism is a very complicated processes, so I have tried to condense it into a readable format. I wanted to address how drugs are metabolized, how drug metabolism can affect the liver, how to determine liver damage, and how to prevent it. Please feel free to ask questions! Drug Metabolism When it comes to drug metabolism, the liver’s primary function is to metabolize the drug into a form that is suitable for elimination by the kidneys. The main goals of this metabolism is to reduce fat solubility, make the drug water soluble, and to decrease its biological activity so that it stops working. This occurs for not only foreign substances (known as xenobiotics, which drugs are considered), but also endogenous chemicals. Drug metabolism in the liver exists in two main phases, phase I and phase II.
Phase I: Phase I metabolism happens primarily in the smooth endoplasmic reticulum of hepatocytes. The main purpose of this phase is to make lipid soluble compounds water soluble. This typically renders the metabolites of the drug to be inactive, but not always.
Phase II: Phase II metabolism takes place in the cytosol of hepatocytes. In this phase, the products from phase I will undergo conjugation to increase their water solubility.
The efficacy of the enzymes used in drug metabolism are age-dependent. In newborns and the geriatric, the ability to metabolize drugs is greatly decreased. Smoking can increase the efficacy of drug metabolism through the inhalation of polycyclic aromatic hydrocarbons. This is most noticeably manifested in the increased metabolic activity of caffeine. Drug Induced Hepatotoxicity Drug induced hepatotoxicity can have many causes. Some medications cause direct damage to hepatocytes while others block certain metabolic processes. As an example, acetaminophen itself is not the source of hepatotoxicity, but rather one of its metabolites. When taken in extreme quantities, this metabolite accumulates because the enzymes required are unable to keep up in phase II metabolism and cell damage occurs. Likewise, mitochondrial damage can increase oxidative stress which can damage hepatocytes. These causes are categorized in seven general categories based on the mechanism of hepatotoxicity. The main categories where AAS and ancillaries are implicated are:
Steatosis: Steatosis is the accumulation of triglycerides in the liver. Liver function tests (LFTs) are unreliable when it comes to the diagnosis of hepatic steatosis. Often will have an AST/ALT ratio < 1. Imaging and possible biopsy is required to make an accurate diagnosis. AST and ALT both upwards of 4 times ULN. Tamoxifen and raloxifene have been shown to induce hepatic steatosis.
Zonal Necrosis: Zonal necrosis is essentially the death of cells in a specific zone of the liver. This is the most common manifestation of hepatotoxicity. This will cause an increase in ALT with normal ALP levels. This can be caused by C-17-alpha-alkylated (C17aa) steroids.
Cholestasis: Cholestasis is the impediment of biliary flow from the liver through the biliary tract. This is the cause of jaundice. The increase in bilirubin causes a yellowing of the skin and that is occurs with itching. C17aa steroids may cause hepatotoxic cholestasis. This can be seen on labs as normal levels of ALT and > 2 times ULN ALP. The mechanism of this is not well known. Testosterone and 19-nortestosterone compounds have been implicated in cases of hyperbilirubinemia, but rarely to the point of jaundice.
Hyperplasia and Neoplasia: C17aa compounds have been implicated in cases of hepatic hyperplasia and neoplasia, essentially cancer. However, non-C17aa steroids have also been noted as a cause of liver cancer in medical case reports.
Vascular Lesions: These vascular lesions are known as Peliosis Hepatis. These lesions are present on endothelial cells of hepatic vasculature and is typically asymptomatic. This can eventually lead to hepatomegaly (enlarged liver) and frequently death if untreated.
Effects of liver damage include jaundice, ankle edema, gynecomastia, increased bleeding due to decrease in clotting factor synthesis. Most of these effects come from deficiencies in synthesis of their respective plasma proteins. For example, damage to hepatocytes that are responsible for synthesis of SHBG will result in a decrease in SHBG. This will alter the free estrogen/free androgen ratio, potentially inducing gynecomasta. Likewise, a decrease in plasma proteins will change the blood colloid osmotic pressure, causing a change in capillary net filtration pressure leading to edema in the lower extremities. Liver Function Tests LFTs can be done to assess hepatic function. These are not exactly conclusive and require some sort of follow up to assess the degree of severity. Often this will be some sort of imaging or biopsy. Most of these biomarkers are assessed in a multiplication of the upper limit of normal (ULN), which is the top end of the normal range. Aminotransferases: Aminotransferases are enzymes that are used in the synthesis of amino acids. There are two aminotransferases that are checked as part of an LFT.
Aspartate Transaminase (AST): Reference range: 8 - 40 IU/L. While AST is found in the liver, this enzyme is also found in great quantities in cardiac and skeletal muscle. Because of these other sources, AST alone is not a good indicator of liver damage. Essentially, AST does not require the entire cell to be damaged for it to enter the plasma, where ALT does. This is due to its location within the cell. If AST is elevated then there is a good possibility that the source of the AST is from muscle damage. This can be caused by myocardial infarction (heart attack), rhadomyolysis, and even resistance training. This is why slightly elevated AST levels should not be of concern if you lift frequently.
Alanine Transaminase (ALT): Reference range: ≤ 52 IU/L. Much like AST, ALT is an enzyme used to catalyze the synthesis of amino acids. Unlike AST, ALT is found predominantly in the liver and requires significant damage to hepatocytes for it to be released in to the plasma.
AST to Platelet Ratio Index (APRI): This typically won’t be included in lab tests, but it is easy to figure out. An online calculator can be found here. APRI has been shown to be a predictor of liver cirrhosis. Alkaline Phosphatase (ALP): Reference rage: 30 - 120 IU/L. ALP is an enzyme that is located within hepatic biliary ducts. Elevations in plasma concentrations of this enzyme are indicative of either cholestasis or biliary obstruction. In these pathologies, ALT and AST may remain unaffected. Total Bilirubin: Reference range: 0.1-1.0 mg/dL. Bilirubin is a byproduct of hemoglobin catabolism. The heme group of hemoglobin is broken down into biliverdin, then bilirubin, which is transported to the liver for the production of bile salts along with urobilin (the pigment that makes urine yellow) and stercobilin (the pigment that makes feces brown). High hepatic sources of bilirubin are indicative of cirrhosis or hepatitis. 5'-nucleotidase (5'NTD): Another biomarker used int he diagnosis of cholestasis. Liver Protection
Cessation: Hepatotoxic drug withdrawal is the widely accepted treatment for drug induced liver damage.
Tauroursodeoxycholate (TUDCA): TUDCA is a bile acid that was found in bears. It is currently being researched in the treatment of ophthalmologic and neurologic conditions. TUDCA has been shown to reduce cholestasis, hepatic steatosis, cirrhosis, and transient liver enzyme levels. The extent of this efficacy still needs more research and clinical trials. No research exists to support its use in zonal necrosis, peliosis hepatis, or hyperplasia.
Milk Thistle: This is bullshit, don't waste your money
[Personal Medical Question/ Health Advice] Should I Be Worried?
I am 24 Male, suffering from jaundice with bilirubin level as follows Serum bilirubin (Normal : 0.2 - 1.2 mg/100 ml) (mine 1.75 mg/100 ml) conjugated (Normal 0.0 - 0.2 mg/100 ml) (mine 1.40 mg/100 ml) unconjugated (0.2 - 1.0 mg/100 ml) (mine 1.35 mg/100 ml) I tried medicine as prescribed by the doctor but still i don't feel like its gone. Unable to eat anything in the morning. Feels like vomiting. Lost so much weight. Please help
[Personal Medical Question/ Health Advice] Should I Be Worried?
I am 24 Male, suffering from jaundice with bilirubin level as follows Serum bilirubin (Normal : 0.2 - 1.2 mg/100 ml) (mine 1.75 mg/100 ml) conjugated (Normal 0.0 - 0.2 mg/100 ml) (mine 1.40 mg/100 ml) unconjugated (0.2 - 1.0 mg/100 ml) (mine 1.35 mg/100 ml) I tried medicine as prescribed by the doctor but still i don't feel like its gone. Unable to eat anything in the morning. Feels like vomiting. Lost so much weight. Please help
[Personal Medical Question/ Health Advice] Should I Be Worried?
I am 24 Male, suffering from jaundice with bilirubin level as follows Serum bilirubin (Normal : 0.2 - 1.2 mg/100 ml) (mine 1.75 mg/100 ml) conjugated (Normal 0.0 - 0.2 mg/100 ml) (mine 1.40 mg/100 ml) unconjugated (0.2 - 1.0 mg/100 ml) (mine 1.35 mg/100 ml) I tried medicine as prescribed by the doctor but still i don't feel like its gone. Unable to eat anything in the morning. Feels like vomiting. Lost so much weight. Please help
Normal results for conjugated (direct) bilirubin should be less than 0.3 mg/dl. Men tend to have slightly higher bilirubin levels than women. African-Americans tend to have lower bilirubin levels... The 95th percentile for bottle-fed infants is a serum bilirubin level of 11.4 mg/dL v 14.5 mg/dL for the breast-fed population, and the 97th percentiles are 12.4 and 14.8 mg/dL, respectively. Of the formula-fed infants, 2.24% had serum bilirubin levels greater than 12.9 mg/dL v 8.97% of breast-fed infants (P less than .000001). It is normal to have some bilirubin in the blood. A normal level is: Direct (also called conjugated) bilirubin: less than 0.3 mg/dL (less than 5.1 µmol/L) Total bilirubin: 0.1 to 1.2 mg/dL (1.71 to 20.5 µmol/L) Normal value ranges may vary slightly among different laboratories. Some labs use different measurements or may test different samples. A small amount (approximately 250 to 350 milligrams) of bilirubin is produced daily in a normal, healthy adult. Normally, small amounts of unconjugated bilirubin are found in the blood, but virtually no conjugated bilirubin is present. Both forms can be measured by the laboratory tests but total bilirubin result (a sum of these) is usually It is normal to have some bilirubin in the blood. A normal level is: Direct bilirubin or conjugated bilirubin: less than 0.3 mg/dL (less than 5.1 µmol/L) Total serum bilirubin: 0.1 to 1.2 mg/dL (1.71 to 20.5 µmol/L) Normal value ranges may vary slightly among different laboratories. Some labs use different measurements or may test different samples. The normal value for direct bilirubin or conjugated bilirubin is 0.1 - 0.3 mg/dL or 1.7-5.1 mmol/L. For indirect or unconjugated bilirubin, the normal values are 0.2-0.8 mg/dL or 3.4-12.0 mmol/L. Consult your medical practitioner to help understand your bilirubin tests. Elevated conjugated bilirubin should lead to increased total bilirubin. If the patient has normal conjugated bilirubin levels and elevated indirect bilirubin levels, it is a sign either of excessive hemolysis or of a failure of the liver as it struggles to cope with the normal rate of hemolysis. The level of direct, indirect and total bilirubin will be measured as part of a standard liver panel test. Answer. Normal serum values of total bilirubin typically are 0.2-1 mg/dL (3.4-17.1 µmol/L), of which no more than 0.2 mg/dL (3.4 µmol/L) are directly reacting. For patient education resources It is normal to have some bilirubin in the blood. A normal level is: Direct (also called conjugated) bilirubin: less than 0.3 mg/dL (less than 5.1 µmol/L) Total bilirubin: 0.1 to 1.2 mg/dL (1.71 to 20.5 µmol/L) Normal value ranges may vary slightly among different laboratories. Some labs use different measurements or may test different samples. concentration of conjugated bilirubin in the sample. Biological reference range or cut off: Neonates 1‐13 µmol/L Older children (up to 18 years) 1‐8 µmol/L Adult <5 µmol/L A ‘normal’ level in a very young baby could be an artefact of poor conjugating ability and be falsely reassuring.
GET LECTURE HANDOUTS and other DOWNLOADABLE CONTENT FROM THIS VIDEOSUPPORT US ON PATREON OR JOIN HERE ON YOUTUBE.https://www.patreon.com/medsimplifiedBilirub... Bilirubin is produced from the destruction of Red Blood Cells. It is a highly toxic molecule and there is 0.2 - 0.3g of it produced every day in the body. Yet, a normal Bilirubin level is ... In this video you will learn about liver function test results normal range, alt blood test, ast test, bilirubin test, ggt test, ld test, pt test and total pro... Enjoy the videos and music you love, upload original content, and share it all with friends, family, and the world on YouTube. https://www.facebook.com/ArmandoHasudunganSupport me: http://www.patreon.com/armandoInstagram:http://instagram.com/armandohasudunganTwitter:https://twitter.c... Bilirubin is the terminal product of heme metabolism. Heme is present in hemoglobin and in other oxidative compounds such as hepatic mitochondrial and microsomal cytochromes (P-450). Thus plasma ... A mild elevated number in a liver function test, may not be significant clinically. Most of the time, it is just an incidental finding or it may some intercu... Generally, the Bilirubin Test is used to screen or monitor liver disorders or hemolytic anemia. To learn all it needs about this test and to interpret your t... #Bilirubin Test Total and Direct Test #Procedure and Normal Range Hi,I Am #PremBhatiawelcome to our you tube channel.in this video there are bilirubin test ...
