This systematic review found that high blood liver function tests are common in patients with newly diagnosed and untreated hyperthyroidism, with a frequency of having at least one abnormal test. Common causes of elevated liver enzymes include nonprescription pain medicines, such as acetaminophen (Tylenol), and certain prescription medicines. Elevated liver enzymes may be related to impaired lipid metabolism, hepatic steatosis, or hypothyroidism-induced myopathy. Severe hypothyroidism can also cause mild serum enzyme elevations when given in high doses. Standard doses of levothyroxine have been linked to rare instances of mild, immunoallergic liver injury.
Elevated liver enzyme levels can be a sign of serious liver disease, but they can also occur with mild, temporary illnesses. Symptoms of liver disease may not be present until later stages of severe liver disease. Elevated liver enzymes often indicate inflamed or damaged cells in the liver, which leak higher levels of certain chemicals into the bloodstream.
Fluoxetine has been noted to cause asymptomatic liver enzyme elevations in about 0.5 of patients. Liver test abnormalities have been reported rarely in patients on fluoxetine (less than 1), and elevations are usually modest and minimal. Medsafe is highlighting a potential interaction between fluoxetine and levothyroxine leading to reduced serum levels of levothyroxine and increased thyroid-related issues.
Levothyroxine is used primarily to treat hypothyroidism, a condition where the thyroid gland is no longer able to produce sufficient quantities of the thyroid hormone. Thyroid medication interactions include coffee, certain foods, supplements, and other medications. In most cases, taking these drugs as prescribed will not lead to liver damage.
Article | Description | Site |
---|---|---|
Fluoxetine – LiverTox | It has been observed that fluoxetine therapy may be associated with transient asymptomatic elevations in serum aminotransferase levels. Additionally, there have been reports of rare instances where this therapy has been linked to adverse effects. | www.ncbi.nlm.nih.gov |
Thyroid Hormone – LiverTox | Additionally, high doses of thyroxine and hyperthyroidism may exacerbate underlying liver disease, including drug-induced liver injury, as evidenced by previous research. | www.ncbi.nlm.nih.gov |
Potential interaction between fluoxetine and levothyroxine | Medsafe is drawing attention to a potential interaction between fluoxetine and levothyroxine, which may result in decreased serum levels of levothyroxine. | www.medsafe.govt.nz |
📹 Rapid Weight Gain in Hypothyroidism? Here’s Why
It’s well known that your thyroid controls and regulates your weight through its impact on your metabolism. As a result, it’s actually …
Which SSRI is safest for liver disease?
This class of antidepressants is generally believed to be safe for use in CLD. However, sertraline has been associated with fatal liver injury in uncontrolled observations. Selective serotonin reuptake inhibitors (SSRIs) with a lower risk of liver injury include fluoxetine, paroxetine, citalopram, and escitalopram. One concern when using SSRI in patients with liver disease is its association with GI bleeding, and the extent of risk of bleeding in those with liver disease. Encouragingly, evidence from published reviews suggests that an increased risk of bleeding events with SSRIs in liver disease occurs only when co-prescribed with antiplatelet agents; this aligns well with recommendations in routine practice.
Typical pharmacokinetic changes seen in CLD prolong the half-life and reduces drug elimination. The usual recommendation is to keep the maintenance dosage at 50% of that used for healthy individuals. However, no change is needed for the starting/initial doses.
There is evidence for efficacy of SSRIs in treating symptoms of depression in chronic hepatitis C infection. Paroxetine, dosed at 20 mg/day for 4 weeks, was found to be effective in the reduction of depression scores among patients with IFN-induced depression. Similarly, in a randomized controlled trial comparing the efficacy of citalopram versus placebo in IFN-induced depression, citalopram dosed at 20 mg daily, separated from placebo at 2 and 4 weeks. Also, no major adverse effects were noted in therapeutic open-label trials of SSRIs in hepatitis C patients. Dosing suggestions for major antidepressants in liver disease are shown in Table 1.
What antidepressants are good for high liver enzymes?
This class of antidepressants is generally believed to be safe for use in CLD. However, sertraline has been associated with fatal liver injury in uncontrolled observations. Selective serotonin reuptake inhibitors (SSRIs) with a lower risk of liver injury include fluoxetine, paroxetine, citalopram, and escitalopram. One concern when using SSRI in patients with liver disease is its association with GI bleeding, and the extent of risk of bleeding in those with liver disease. Encouragingly, evidence from published reviews suggests that an increased risk of bleeding events with SSRIs in liver disease occurs only when co-prescribed with antiplatelet agents; this aligns well with recommendations in routine practice.
Typical pharmacokinetic changes seen in CLD prolong the half-life and reduces drug elimination. The usual recommendation is to keep the maintenance dosage at 50% of that used for healthy individuals. However, no change is needed for the starting/initial doses.
There is evidence for efficacy of SSRIs in treating symptoms of depression in chronic hepatitis C infection. Paroxetine, dosed at 20 mg/day for 4 weeks, was found to be effective in the reduction of depression scores among patients with IFN-induced depression. Similarly, in a randomized controlled trial comparing the efficacy of citalopram versus placebo in IFN-induced depression, citalopram dosed at 20 mg daily, separated from placebo at 2 and 4 weeks. Also, no major adverse effects were noted in therapeutic open-label trials of SSRIs in hepatitis C patients. Dosing suggestions for major antidepressants in liver disease are shown in Table 1.
Can levothyroxine raise liver enzymes?
Finally, there have been rare reports of immunoallergic hepatitis or hypersensitivity reactions due to levothyroxine which was associated with enzyme elevations and even mild jaundice. The time to onset ranged from 1 to 8 weeks and symptoms typically included fever and fatigue. The enzyme pattern was usually hepatocellular or mixed. Autoantibodies were not detected, but eosinophilia was common. The fever resolved rapidly upon stopping the thyroid preparation, but liver test abnormalities generally required one to two months to fall into the normal range. In at least one case, switching to another form of thyroid hormone was associated with persistence of fever and a worsening of liver tests. In contrast, waiting until recovery from the liver injury and starting triiodothyronine at a low dose with gradual increase to therapeutic levels was generally tolerated without recurrence. Strikingly, the case reports of liver injury due to levothyroxine and thyroid extract were all reported from Asia and Japan, which suggests a racial and possibly genetic predisposition to this idiosyncratic hypersensitivity reaction. Another possibility, however, was that the cases were due to a locally contaminated commercial preparation of levothyroxine.
Likelihood score: C (probable rare cause of clinically apparent liver injury).
Mechanism of Injury. The mechanism of injury accounting for serum enzyme elevations and jaundice during levothyroxine induced liver injury is likely due to hypersensitivity and is possibly genetically determined.
Can you take Prozac and levothyroxine together?
Highly clinically significant. Avoid combinations; the risk of the interaction outweighs the benefit.
This report displays the potential drug interactions for the following 2 drugs:
Alcohol can increase the nervous system side effects of FLUoxetine such as dizziness, drowsiness, and difficulty concentrating. Some people may also experience impairment in thinking and judgment. You should avoid or limit the use of alcohol while being treated with FLUoxetine. Do not use more than the recommended dose of FLUoxetine, and avoid activities requiring mental alertness such as driving or operating hazardous machinery until you know how the medication affects you. Talk to your doctor or pharmacist if you have any questions or concerns.
The timing of meals relative to your oral levothyroxine dose can affect the absorption of the medication. Therefore, levothyroxine should be taken on a consistent schedule with regard to time of day and relation to meals to avoid large fluctuations in blood levels, which may alter its effects. In addition, absorption of levothyroxine may be decreased and/or delayed by foods such as soybean flour, cotton seed meal, walnuts, dietary fiber, calcium, calcium fortified juices and grapefruit or grapefruit juice. These foods should be avoided within several hours of dosing if possible. It is important to tell your doctor about all other medications you use, including vitamins and herbs. Do not stop using any medications without first talking to your doctor.
Can Prozac cause elevated liver enzymes?
Fluoxetine-induced hepatotoxicity is generally considered of minimal clinical importance and is not well recognized. Asymptomatic increases in liver enzyme values have been observed in 0. 5% of patients who take long-term fluoxetine therapy.
Does fluoxetine cause fatty liver?
Fluoxetine, a selective serotonin reuptake inhibitor antidepressant, has been found to increase hepatic lipid accumulation, a key factor in the development of nonalcoholic fatty liver disease. Fluoxetine has also been reported to increase peripheral serotonin synthesis. The study aimed to determine if fluoxetine-induced hepatic lipid accumulation is mediated via altered serotonin production. Fluoxetine treatment increased lipid accumulation in association with increased mRNA expression of tryptophan hydroxylase 1 (Tph1) and intracellular serotonin content. Serotonin alone had a similar effect to increase lipid accumulation. Blocking serotonin synthesis reversed the fluoxetine-induced increases in lipid accumulation. These data suggest that fluoxetine-induced lipid accumulation can be mediated, in part, by elevated serotonin production. These results suggest a potential therapeutic target to ameliorate the adverse metabolic effects of fluoxetine exposure.
The study also reported that fluoxetine increases the production of sérotonine, which could play a role in the appearance of nonalcoholic fatty liver disease. The administration of fluoxetine induced an increase in lipid accumulation in association with increased mRNA expression of tryptophan hydroxylase 1 (Tph1) and intracellular sérotonine levels. Serotonine alone had a similar effect on lipid accumulation. Inhibiting sérotonine synthesis allowed for a reversed increase in lipid accumulation. These findings suggest that sérotonine production could contribute to the mediation of lipid accumulation induced by fluoxetine, potentially acting as a therapeutic target to mitigate the metabolic effects of fluoxetine exposure.
Which antidepressant is hardest on the liver?
Drug-induced liver injury (DILI) is a significant concern in the context of increasing drug availability and prescription. 0. 5-3 of patients treated with antidepressants may develop mild elevation of serum aminotransferase levels, and all antidepressants can induce hepatotoxicity, especially in elderly patients and those with polypharmacy. Liver damage is idiosyncratic and unpredictable, and the interval between treatment initiation and onset of liver injury is typically between several days and 6 months. Life-threatening DILI has been described involving fulminant liver failure or death. The underlying lesions are often of the hepatocellular type, with citalopram, escitalopram, paroxetine, and fluvoxamine having the least potential for hepatotoxicity. Cross-toxicity has been described, mainly for tricyclic and tetracyclic antidepressants. Aminotransferase surveillance is the most useful tool for detecting DILI, and prompt discontinuation of the drug responsible is essential. Results of antidepressant liver toxicity in all clinical trials should be available and published, and further research is needed before any new and rigorously founded recommendations can be made.
Can Prozac affect thyroid function?
In contrast, clinically silent SSRI-induced abnormalities in thyroid function tests have been widely documented. 2, 10 After paroxetine treatment in severely depressed patients, for example, T 4 level has been reported to decrease by 11. 2%. Fluoxetine has been reported to reduce T 3 and T 4 levels in otherwise euthyroid depressed patients. 11 Similarly, sertraline and fluoxetine have been reported to reduce hypothalamic thyrotropin-releasing hormone secretion, which would reduce secretion of TSH from the pituitary gland and thyroid hormones from the thyroid. 12.
As a potent serotonin-specific reuptake inhibitor, fluoxetine can increase the concentration of serotonin in cerebrospinal fluid and other serotonergic tissues. Therefore, serotonin acting at 5-HT 2 receptors on the thyroid follicular cells may promote the production and release of thyroid hormones. 13 As evident in our depressed patient with hyperthyroidism, we speculate that in susceptible patients, fluoxetine can have a more potent stimulatory effect on the thyroid than inhibitory effects on the hypothalamus and pituitary gland, which ultimately demonstrates as hyperthyroidism.
This case indicates that monitoring of thyroid hormone levels during treatment with SSRIs is warranted, particularly when clinical response is insufficient or otherwise atypical or complicated.
Can antidepressants raise ALT?
Results: Although data on antidepressant- induced liver injury are scarce, 0. 5%23% of patients treated with antidepressants may develop asymptomatic mild elevation of serum aminotransferase levels. All antide- pressants can induce hepatotoxicity, espe- cially in elderly patients and those with polypharmacy.
Can you take antidepressants and levothyroxine?
Taking levothyroxine with certain drugs may result in an increase in adverse effects. Examples of these drugs include:
- Antidepressants such as amitriptyline and maprotiline. The side effects of both of these antidepressants and levothyroxine may increase when you take these drugs together. This may put you at risk for irregular heart rhythms ( arrhythmias ).
- Sympathomimetic drugs such as pseudoephedrine and albuterol. The effects of both the sympathomimetic drugs and levothyroxine may increase when you take these drugs together. This may put you at risk of serious heart problems.
- Blood thinners such as warfarin. Taking these drugs with levothyroxine may increase your risk of bleeding. Your doctor may need to decrease the dosage of your blood thinner if you’re also taking levothyroxine.
- Ketamine. Taking this drug with levothyroxine may increase your risk of high blood pressure and fast heart rate.
Interactions that can make your drugs less effective.
When levothyroxine is less effective: When you take levothyroxine with certain drugs, it may not work as well to treat your condition. This is because the amount of levothyroxine in your body may be decreased. Examples of these drugs include:
Can thyroid issues cause elevated liver enzymes?
WHAT ARE THE IMPLICATIONS OF THIS STUDY? This systematic review showed that high blood liver function tests are common in patients with newly diagnosed and untreated hyperthyroidism. Frequency of having at least one abnormal liver function test in patients was 55%, much higher than 32% as reported in previous studies. In most cases, liver function tests were only mildly elevated, up to 5 times the normal range. However, high liver function tests became normal in most of these patients after they were treated with antithyroid drugs and thyroid hormone levels became normal.
The American Thyroid Association currently recommends checking baseline liver function tests in patients with newly diagnosed hyperthyroidism. These studies show that antithyroid drugs can be safely used in patients with mild liver function test increases and will usually result in resolution of the liver abnormalities. However, these patients should be monitored carefully to make sure liver function tests improve with improvement of hyperthyroidism.
📹 These Supplements Block Thyroid Medication Absorption
These supplements block thyroid medication absorption and function. These supplements should be AVOIDED if you are taking …
When my labs are crazy out of wack, I feel great. When my labs are ‘normal’, I feel terrible and gain weight and fatigued. Why can’t my labs ever match my body? 😢 I’m on a higher dose and I am gaining like crazy. Maybe it’s bc I’m perimenopausal? If that’s the case, do I see a female hormone specialist instead of an endocrinologist?
Omg! This is exactly what’s happening with me with exception of constipation. I have had IBS for most my life. I have whole body edema especially my legs and im gaining weight at a rapid speed. First it was 7 pds in nine days the 5 pds in less than 24 hours. The doctors can’t figure it out and thought it was heart failure and I said no it’s something else and sure enough all four doctors found out from my blood work that it’s not related to the heart. I have Hashimotos. I take dessicated thyroid but not enough. Most Drs don’t know about what to check for besides TSH levels. They don’t know to check for T4, T3 free T4 thyroid antibodies and one other. Luckily one Dr. Checked them all and told me I had the autoimmune form of hypothroid. Before that I was diagnosed with just hypothyroid. I’m so happy your article showed up as I was surfing YouTube. Your a blessing Dr. 👏🤗
I had a thyroidectomy in 2009 and weight slowly started adding on. Finally in 2017 I had enough, and I released 60 pounds and kept it off now for almost 6 years. I would suggest to look at the program Brightline Eating. I liked it because the creator has thyroid issues and she kept it off for over 10years! Also there is a maintenance piece as many weight loss plans don’t offer. The creator is also a Neuro doctor and she studied why we eat the way we do!
I have had a 2 inch increase on my hip despite an average 3 hours exercise of 3 hours daily i intake 600′ to 900 calories daily. I now have high blood pressure and reduced heart rate. If it gets worse ill obviously present to ED Dept. Id been taking my meds with food in care setting. Im very thin and wanted to gain muscle. It stayed at 900 as i noted massive fat gain. Im 5st. My goal is lean gains not massive fat accumulation.
I don’t know what to do, i eat two small meals a day, no processed food i make everything from scratch, but i’ve been struggling with this disease for 10+ years, ever since i was in fifth grade i gained weight and i cant lose it. My doctor tells me to try harder and he doesn’t believe me, i even gained 10kgs from DOING NOTHING JUST EXISTING. As long as i can remeber i was always dieting and struggling to lose weight 😭😭😭😭
I’ve been diagnosed with Graves disease (HYPERthyroidism) for about 7 years and the only consistent symptom I’ve had before and during treatment – have been stable on the lowest dose of carbimazole for a few years now) – is weight gain. I was 74kg pre illness and now struggle to get below 89kg, no matter diet, calorie counting, low carb, exercise etc and it’s making me so miserable. So much advice is for hypo but I’m definitely hyper and still struggling with weight gain
Pls help me I get test and my tsh was 1mg H t3t4normal dc give me 50 thyroxine After 20 day dc told me get off pils After 3 day i feel horrible I get test again my tsh was 0.2H I start medicine again and i feel Worse I have no energy, I hardly walk i cant sleep I try to take 25mg but make it Worse Now I have heart palpitations Completely empty of energy I am a man, twenty-three years old, thin I dont have access to any specialist doctor Please help me
Mine has been removed for more than 29yrs. I have been with same endo. Radiation fallouts in southwestern Idaho, ” Down winders,” is the name given to people who were down wind of the nuclear bombs tested in the deserts and ocean. We ate the food. Drank the milk. Played in the dirt. Plagued with benign, fast growing tumors. Mass on one adrenal, rapid advanced osteoarthritis. Mother and siblings are similar. Brother died of glioblastoma. I am 63 yrs old . Real tired of seeing Dr’s and loosing body parts. Whew! Keep up the articles 👍
You are AMAZING!! Just when I start thinking about thyroid questions I have— and could NEVER expect to be answered by a DOC–(what, you usually get 10 minutes)—you come up with the subject/answers that I didn’t even contemplate!! This supplement talk is one of the subjects that would NEVER get covered. Many thanks! John L
Thank you Dr Childs for this informative article . Been on levothyroxine for 10 years now and have been taking it first thing in the morning . Once taking it I don’t take any food for the next 6 hours but I do take apple cider vinegar mixed with 500ml of water say like 30 mins before taking levothyroxine to enhance absorption. Is this safe doctor ?
This is wonderful information as always. And enjoying your 60 day metabolism reset also, priceless information you have provided for us. What about supplements that can be taken safely with thyroid/T3, Bvitamins? Bioidentical Progesterone? Msm? Vit e? I usually wait an hour or so with these ones, I hope this is enough time? Thanks again for putting all these articles together. Greatly appreciated!
I have panhypopituitarism, Adrenal insufficiency, diabetes insipidus and growth hormone deficiency and damage to the hypothalamus making it very hard to loose weight. When’s the best time to take my thyroid medication with other medication? And what’s your advice on how I can loose weight and feel less hungry?
My body needs magnesium. So when I learned this, and I’d been taking mag for about 9 months, mag at bedtime and med in the morning, I ve decided to experiment and have stopped taking the med which no longer made me feel better as it did 10 yrs ago. Plus I had an aggressive gastric bypass 25 years ago which blocks absorption of nutrients (had the procedure b4 I learned i was hypo, they missed it completely). I also have learned my BRAIN needs acetyl L carnitine. I was feeling intense frustration and anger at the smallest trigger. Im doing my best to build my health and strength back, im 64. It’s a shame doctors are so ignorant and don’t care, don’t listen to what the patient learns (from experience), and therefore won’t help or observe an experiment like mine. When I expressed i felt my anger was too easily triggered, the go to thinking was needing a psych medication, and if not, a helpless what do u expect shrug….
Does any of this apply if you are on tirosint? I switched to tirosint because I drink coffee with oat milk which has added calcium. I take progesterone and magnesium and 5-htp at night. I also take other supplements different times of the day. I was told by my Dr that I can drink coffee 5 minutes after the tirosint. Please let me know your thoughts. Thanks. 🙏🏻
Great post as always…i have a question about Irish sea moss. I make a daily smoothie out of it every morning but i tend to try to wait 4 hours after levothyroxine because of the iodine in the moss. Will sea moss effect the levothyroxine absorption also even though its naturally sourced iodine and not synthetic?
You stated in another article that magnesium, zinc and selenium are crucial for T4 to T3 conversion. Now you are saying they block it! I am now confused. I now take 90 mg of Armour at 6AM. If I take it at night won’t it keep me awake? If I can take at night how long after my last meal, before bedtime is best to take it?
Hi I been taking my t4 in the evening and t3 in the am. I take my supplements mid afternoon and a probiotic after dinner ( my Dr advised the probiotic at that time). since then I have been able to reduce my t4 from 137 mcg to 112 mcg Dr feels bc I am absorbing my. meds better with the probiotic. I am due for a follow up this week did bloodwork already but I have noticed the past few weeks I have been getting more palpitations . Could this lead to more med adjustments? I have not lost any weight and my hair still thinning, 49 year old female begining menopause and has Hashimotos and Hypothyriodism. supplements are vitamin D,B12,biotin, collagen powder. any advise be appreciated. thank you