Introduction
Thyroid hormones play a central role in regulating thermogenesis and human metabolism, with these processes mediated through the regulation of various cell types, including hepatocytes, which significantly influence hepatic function. Notably, liver cells are pivotal in both regulating thyroid hormone levels and modulating their metabolism, transport, activation, and inactivation. A remarkable 85% of thyroxine (T4) is metabolically transformed into its more active form, triiodothyronine (T3), primarily by liver cells. Furthermore, liver cells are responsible for synthesizing plasma proteins that bind nearly 99% of the thyroid hormones circulating in the plasma.
Thyrotoxicosis is characterized by an excess of circulating thyroid hormones, irrespective of the underlying etiology. The global prevalence of thyrotoxicosis is estimated to be around 0.2% to 1.3% in iodine-replete regions, notably with a higher incidence among females. The most prevalent cause of hyperthyroidism is Graves’ disease, affecting a significant number of young to middle-aged individuals, particularly women, with a female-to-male incidence ratio that reaches approximately 7 to 10:1.
In this study, we set out to characterize hepatic dysfunction and identify potential causes of hepatic dysfunction in Thai patients who were recently diagnosed with thyrotoxicosis.
Materials and Methods
Study Patients
This research involved a retrospective review of patients diagnosed with liver test abnormalities within six months following the diagnosis of thyrotoxicosis at Siriraj Hospital in Bangkok, Thailand, between January 1, 2015, and January 31, 2021. Diagnoses were made per the ICD-10-CM codes E05, which were associated with liver-related conditions. The Siriraj Institutional Review Board approved the study protocol under certificate of approval number Si 029/2020, and the necessity for informed consent was waived due to the study’s retrospective nature.
Medical Data Collection
Patient medical data were retrieved from electronic medical records. Collected demographic data encompassed the age at the time of thyrotoxicosis diagnosis and gender. Comorbidities such as atrial fibrillation, heart failure, dyslipidemia, diabetes mellitus, renal disease, and chronic liver status were recorded as well. Data included clinical history and laboratory test results, encompassing TSH, T3 (or free T3), T4 (or free T4), and comprehensive liver function tests (ALT, AST, ALP, total bilirubin, direct bilirubin, albumin, and globulin).
Statistical Analysis
The age of patients is presented as mean ± standard deviation. Comorbidities, chronic liver status, and hyperthyroidism diagnoses are expressed as percentage values. Laboratory test results including initial, peak, and resolution levels are summarized as median values. Univariate analysis was employed to identify predictive factors for thyroid storm in patients with thyrotoxicosis. Multivariate analysis was conducted to ascertain independent factors that significantly predict thyroid storm using forward stepwise logistic regression. A significance threshold of p < 0.05 was adopted for statistical computations.
Results
Among the 771 patients diagnosed with thyrotoxicosis, 43 (5.58%) exhibited abnormal liver function tests within a six-month window following their diagnosis, as recorded at Siriraj Hospital from January 1, 2015, to January 31, 2021. The baseline characteristics are summarized in Table 1. The mean age of patients was 53.16 ± 15.10 years, with a significant female predominance of 60.5%. A total of 35 patients (81.4%) had comorbidities, including atrial fibrillation (25.6%), heart failure (23.3%), dyslipidemia (23.3%), diabetes (18.6%), and renal disease (4.7%). Chronic liver diseases were present in 18 patients (41.9%), with chronic hepatitis C being the most common etiology, followed by chronic hepatitis B, autoimmune hepatitis, and nonalcoholic fatty liver disease (NAFLD). Only two patients (4.7%) had cirrhosis.
Most patients with thyrotoxicosis were diagnosed with Graves’ disease (97.7%), with only one case attributed to amiodarone-induced thyrotoxicosis. At the initial presentation, 9 of 43 patients (20.9%) were clinically diagnosed with thyroid storm. Additionally, 23 patients (53.5%) had at least one abnormal liver test at the time of thyrotoxicosis diagnosis, while others displayed abnormal liver tests at a median of 5.79 weeks following the diagnosis.
Elevations in liver biomarkers were classified following R factor criteria for liver injury based on ALT and alkaline phosphatase levels. Cholestatic patterns were most prevalent (46.5%), succeeded by mixed (30.2%) and hepatocellular (20.9%) patterns. Although most hepatic outcomes after thyrotoxicosis treatment indicated resolution, nearly one-fourth of patients retained persistent abnormal liver tests.
Discussion
A systematic review indicated the prevalence of liver test abnormalities among hyperthyroid patients: 23% for AST, 33% for ALT, 44% for ALP, and 12% for bilirubin. Our findings classified patients with abnormal liver tests according to the liver injury R factor. A notable portion exhibited cholestatic liver injury (46.5%), though elevated alkaline phosphatase can overestimate liver dysfunction due to its nonspecific nature.
In thyroid storm cases, diagnosing relies on clinical presentation and results aligning with established scoring protocols. This study confirmed factors differentiating clinical thyroid storm from uncomplicated thyrotoxicosis, such as congestive heart failure and hyperbilirubinemia with total bilirubin levels ≥ 3 mg/dL.
Conclusion
This study sheds light on the critical interplay between hepatic dysfunction and thyrotoxicosis, reinforcing the necessity for careful monitoring of liver function in patients diagnosed with thyroid disorders. The identification of predictive factors also aids in recognizing thyroid storm in thyrotoxic patients.
Abbreviations
ALP, alkaline phosphatase; ALT, alanine aminotransferase; AST, aspartate aminotransferase; CNS, central nervous system; FT3, free triiodothyronine; FT4, free thyroxine; IFN-α, interferon-α; MMI, methimazole; NAFLD, nonalcoholic fatty liver disease; T3, triiodothyronine; T4, thyroxine; TSH, thyroid-stimulating hormone.
The study was approved by the Siriraj Institutional Review Board. The informed consent requirement was waived, ensuring data confidentiality. All methods complied with the Declaration of Helsinki.
All authors report no conflict of interest.
Thyroid Hormones, Liver Dysfunction, and Thyrotoxicosis: A Comedic Analysis
By Your Favourite Comedic Blend: Jimmy Carr, Rowan Atkinson, Ricky Gervais, and Lee Evans
Introduction: A Laughing Matter?
Ah, thyroid hormones! Those nifty little chemicals that manage our body’s thermostat. Think of them like the remote that’s always gone missing – you know, the one that controls what you wear on hot or cold days. But in a twist worthy of a sitcom, they also pull some major tricks on our trusty liver. Who knew the liver could be such a drama queen? Calculating hormone levels while trying to keep its cool is classic liver behavior! This article dives into the correlation between these hormones, liver dysfunction, and that mean old gremlin known as thyrotoxicosis—so grab your popcorn!
The Dynamics of Thyroid Hormones and Liver Function
Here’s the deal: thyroid hormones, specifically thyroxine (T4) and triiodothyronine (T3), are essential for thermogenesis—essentially keeping you from freezing into a human popsicle. But when T4 gets too cozy, it converts to T3 like a chameleon changing colors at a disco party. This conversion predominantly happens in the liver, which tickles our fancy by also binding 99% of these hormones. One could say the liver is the bouncer at the exclusive club of hormones!
However, when thyroxine becomes an overbearing parent at this party, we run into problems like thyrotoxicosis, which occurs when we have excess thyroid hormones. Unfortunately, this isn’t a dance-off; it’s where your body literally starts throwing tantrums.
Diagnosing the Drama: Thyrotoxicosis in Thai Patients
Now, this splendid study retreads old ground, focusing on Thai patients diagnosed with thyrotoxicosis paired with abnormal liver tests at Siriraj Hospital. Imagine a room full of future Liver Function Test (LFT) award winners juggling health complications. It turns out that of the 771 patients with thyrotoxicosis, just under 6% decided their liver had too many party favors – abnormal liver function tests. And guess what? Most were women! It’s like a ladies’ night gone rogue.
Unpacking the Statistics
The researchers enlisted a hefty number of players in this comedy of errors: age demographics, comorbidities, liver status—like chronic hepatitis hanging around like the friend nobody invited to the party. This study revealed a plethora of comorbidities, including heart failure and diabetes! Talk about stacking the odds against your liver! Poor thing can’t catch a break…
Among our protagonists, 81.4% had some medical baggage. A staggering 97.7% of diagnosed cases were from Graves’ disease, which is like the leading actress in this bizarre play. And did you know the liver dysfunction exhibited a cholestatic pattern for 46%? They must have an affinity for vibrant cocktails!
Results: The Climax of Chaos
Fast forward to the grand reveal: treatment of thyrotoxicosis means many of these unfortunate failed liver functions started settling down. Almost 76.7% got their liver tests straightened out, but 23.3% said, “Not so fast!” This is like the to-be-continued moment in a Netflix series where viewers question their life choices. What were they doing this whole time? Bingeing on thyroid hormones?
Conclusion: The Final Bow
As we wrap up this journey, it’s clear that thyroid hormones aren’t just interesting in a biochemistry lecture; they throw some serious kicks in the liver department too! The interplay between the liver and thyroid is about as complicated as your relationships on social media. But rest assured, every bit of data, every sour note in our health performance, brings us one step closer to understanding how to mitigate these chaotic events. So here’s to our livers—may they continue to function splendidly while we laugh along the way!
Er! And let’s not forget the 81.4% with some form of comorbidity—clearly, they weren’t just sitting at home knitting! They were lively participants in the grand circus of health complications.
Cholestatic Patterns: The Liver’s Way of Saying “Help!”
Now, as the liver started displaying its version of a melodramatic monologue, around 46.5% of the patients presented cholestatic patterns. It’s as if the liver put on a theatrical performance, waving its hands and crying “Look at me, I’m not okay!” Meanwhile, 20.9% were practicing mixed styles, and only a smidge showed classic hepatocellular patterns—because why stick to one act when you can have an entire repertoire?
And while many patients returned to normal after thyrotoxicosis treatment, about one-fourth of them remained in the abnormal camp. Talk about a stubborn cast member who won’t leave the stage!
Conclusions: A Call for Caution and Comedy
To wrap it all up, this study isn’t just a dry rundown of statistics—it’s a call to pay attention to the liver while diagnosing thyrotoxicosis. We learned that comorbidities are not just statistical phenomena; they’re Martha and Tom from the dinner party you never invited! So, proper monitoring of liver function in thyroid disorder patients is essential. Who knew that the interplay between hormones and livers could be this entertaining? But seriously, folks, let’s look out for those warning signs before it gets too chaotic!
