Thyrotoxicosis associated with severe hypoalbuminemia and hyperbilirubinemia

Evlice, Mert; Aksöz, Zekeriya

doi:10.4103/ejim.ejim_7_17

Cited by 3 publications

(4 citation statements)

References 15 publications

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“…There has been reported nonspecific changes on the liver from cases with thyrotoxicosis including intrahepatic cholestasis, lobular inflammation and Kupffer cell hyperplasia. 24 Cholestatic liver injury in patients with thyrotoxicosis has been associated with autoimmune hepatitis or primary biliary cirrhosis. It may occur due to liver congestion from HF, side effects of ATDs or hepatic necrosis from systemic embolisation from AF.…”

Section: Discussionmentioning

confidence: 99%

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Challenges in the Management of Thyrotoxicosis Associated with Atrial Fibrillation and Heart Failure: Two Case Reports

Sadiq

Chamba

2021

Clin Med Insights Case Rep

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Background: Thyrotoxicosis is a clinical syndrome with high amounts of free thyroid hormone levels causing elevated thyroid hormone function in body tissues. Prolonged effects of free thyroid hormones may lead to cardiac complications such as atrial fibrillation (AF) and heart failure (HF). Case 1: A 31-year-old female, was admitted due to difficulty in breathing, generalised body swelling and jaundice. She was dyspnoeic with an irregular heart rate, and presented with abnormal vitals, liver and thyroid function tests which were diagnostic for thyroid storm. She was managed over 32 days in-hospital stay with carbimazole, propranolol, hydrocortisone, digoxin and furosemide. Unfortunately, she was readmitted 6 months later with worsened HF symptoms and passed away. Case 2: A 57-year-old female, was admitted due to difficulty in breathing, bilateral lower limb swelling and jaundice. She was tachypnoeic with an irregular heart rate, and presented with abnormal liver enzymes and thyroid function tests which were diagnostic for thyrotoxicosis. She was managed with carbimazole, propranolol, digoxin and furosemide, and was discharged on the 6th hospital day. Conclusion: Prolonged untreated thyrotoxicosis increases the risk of AF and HF. Early and monitored treatment and follow-up of hyperthyroidism is key to the management of AF and HF in achieving a better outcome.

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Section: Discussionmentioning

confidence: 99%

“…Most of these cases normalising following adequate treatment. 24 Follow up is crucial in all patients with hyperthyroidism, mainly because of treatment options and complications. 2 Lifethreatening thyrotoxicosis or thyroid storm characterised by multisystem involvement has mortality rates between 8% and 25%.…”

Section: Discussionmentioning

confidence: 99%

Challenges in the Management of Thyrotoxicosis Associated with Atrial Fibrillation and Heart Failure: Two Case Reports

Sadiq

Chamba

2021

Clin Med Insights Case Rep

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“…Serum RBP4 concentrations in patients with overt hypothyroidism (median: 1.76 mmol/L) were significantly higher than in patients with overt hyperthyroidism (median: 1.23 mmol/L). Cases with an overactive thyroid (fT4 .40.0 pmol/L) (11,12) relating to protein breakdown (i.e., severely low serum RBP4 and albumin) were not included in our patients.…”

Section: Serum Rbp4 Concentrations In Patients With Hypothyroidismmentioning

confidence: 99%

“…Thyroid hormones stimulate metabolic cycles involving fat, glucose, and protein catabolism and anabolism (10). Thyroid hormones secreted at higher than normal levels facilitate protein catabolism rather than anabolism (11)(12)(13). On the contrary, because hypothyroidism causes a low BMR, we hypothesized that the serum levels of RBP4 (holo-and apo-RBP4) in hypothyroidism would increase or remain constant, but this prediction has not been fully investigated.…”

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confidence: 99%

Does Retinol-Binding Protein 4 (<i>holo</i>- and <i>apo</i>-RBP4) Increase or Remain Constant in Sera from Patients with Hypothyroidism?

KIUCHI,

IHARA,

SEGA

et al. 2023

J Nutr Sci Vitaminol

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Retinol-binding protein 4 (RBP4) is a retinol transporter in the blood plasma. Many diseases alter the plasma or serum levels of RBP4. Since serum RBP4 concentrations have been reported to decrease in hyperthyroidism, this study investigated whether serum RBP4 concentrations increased or remained constant in hypothyroidism. In sera from patients with hypothyroidism (n571), hyperthyroidism (n530), and healthy subjects (n520), serum concentrations of RBP4 (sum of holo-and apo-RBP4), retinol, albumin, creatinine, and related constituents were measured, and RBP4/retinol molar ratio (as an index of apo-RBP4) and estimated glomerular filtration rate (eGFR) were calculated. The results showed that serum RBP4 concentrations tended to increase with decreasing free thyroxine concentrations, but there were no significant differences among patients with hypothyroidism, hyperthyroidism, and healthy subjects. When patients with hypothyroidism were subdivided by serum RBP4 level using 2.1 mmol/L cut-off value, patients with .2.1 mmol/L were revealed to be patients with older age having lower tri-iodothyronine, higher holo-RBP4, higher apo-RBP4, higher retinol, higher RBP4/retinol molar ratio, and lower eGFR than those in patients with ,2.1 mmol/L. Multiple regression analysis showed significant associations between serum RBP4 levels and explanatory variables (retinol and eGFR). Although serum levels of RBP4 prior to the onset of renal dysfunction may affect the present concentrations, we conclude that the increase of serum RBP4 (both holo-and apo-RBP4) in patients with hypothyroidism was attributed to the decline in eGFR. In contrast, serum RBP4 concentration remained constant without renal dysfunction.

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Unusual Presentations of Thyrotoxic Tricuspid and Mitral Regurgitations in 62 Adults: A Systematic Review of Case Reports with In-depth Pathophysiological Review

Witarto,

Pramudito

et al. 2024

Eur Cardiol

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Background: Thyrotoxicosis is related to cardiovascular mortality. This can be caused by several clinical manifestations involving the rare provocation of tricuspid regurgitation (TR) and mitral regurgitation (MR). However, there are still no clear data on thyrotoxic TR and/or MR. This study examines the progression of TR, MR, heart failure (HF) and pulmonary hypertension (PH) in response to the thyrotoxic heart manifestations, clinical characteristics and treatment approaches. Methods: A PRISMA-based systematic search was conducted using PubMed and other databases up to 17 June 2023. The outcomes of this study were TR, MR, HF and PH with their progression on follow-up, clinical characteristics and treatment approaches. Results: A total of 57 case reports involving 62 patients (45.77 ± 13.41 years) were included in this study. They were predominantly women (n=50; 80.65%) and diagnosed with Graves’ disease (n=41; 75.81%). All patients were diagnosed with thyrotoxicosis, and this included 23 (37.10%) cases of thyroid storm. From echocardiographic studies, several patients improved clinically within the first 6 months of follow-up, including 20 TR patients (83.33%) in 6 months, nine MR patients (69.23%) in 3 months, eight HF patients (66.67%) in 2 months and 16 PH patients (76.19%) in 6 months. Conclusion: Several mechanisms are involved in thyrotoxic TR and/or MR, including the direct thyroid hormone effect and the indirect effect of other hyperthyroidism-associated factors. Patients with thyrotoxic TR and/or MR, including those with HF and PH, can experience clinical and structural improvements following hyperthyroidism treatment in the first 6 months.

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Thyrotoxicosis associated with severe hypoalbuminemia and hyperbilirubinemia

Cited by 3 publications

References 15 publications

Challenges in the Management of Thyrotoxicosis Associated with Atrial Fibrillation and Heart Failure: Two Case Reports

Challenges in the Management of Thyrotoxicosis Associated with Atrial Fibrillation and Heart Failure: Two Case Reports

Does Retinol-Binding Protein 4 (<i>holo</i>- and <i>apo</i>-RBP4) Increase or Remain Constant in Sera from Patients with Hypothyroidism?

Unusual Presentations of Thyrotoxic Tricuspid and Mitral Regurgitations in 62 Adults: A Systematic Review of Case Reports with In-depth Pathophysiological Review

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