A Case Report of Hypothyroidism and Pericardial Effusion

The pericardial sac is made of two layers: the visceral and parietal pericardium. Located between these two layers, the pericardial cavity is found. It contains around 15 to 50 mL of a liquid secreted by mesothelial cells. Pericardial effusion is described as the accumulation of liquid within the pericardial cavity, exceeding the previous mentioned quantity. It has multiple causes, such as malignancy, infectious origins, inflammation, and others, such as hypothyroidism. One of the multiple clinical manifestations associated with hypothyroidism is pericardial effusion. It is related to the severity and duration of the disease, being more frequent in congenital hypothyroidism or cases of a long history of hypothyroidism, as well as clinical hypothyroidism. It can present a clinical challenge mainly due to the discordance between the total volume of the effusion and the clinical symptoms shown by the patient. male with hypothyroidism-associated pericardial effusion which resolved satisfactorily with hormone replacement therapy.


Introduction
In 1656, English anatomist Thomas Warton names "thyroid", which means "shieldlike", to a bilobulated gland located under the larynx and in front and both sides of the trachea [1].
Zondek, in 1918, described a patient with some characteristics matching a mix edematous heart: dilated cardiac silhouette, low cardiac voltage and slowed cardiac activity. Triiodothyronine was discovered by Pitt-Rivers and Gross in 1952, while its endogenous production was described by Ingbar, Sterling, and Braverman in 1970. Conliffe isolated thyroxine in 1963. In 1971, Mayberry and Hershman simultaneously described the tyrotrophin to diagnose hypothyroidism [2].
T4 is the main product of such synthesis, having no biological effect. T4 to T3 conversion does not happen within the myocyte. About 85% of the total concentration of T3, which is biologically active, is derived from peripherical conversion of T4 by an enzyme named 5'-monodeiodinase, mainly occurring within the liver, kidneys, and skeletal muscle. Both T4 and T3 circulate almost entirely (90%) bound to proteins. The remaining 5% circulates freely. T3 is the biologically active hormone within the cardiac myocyte [1] [2].
Thyroid hormone synthesis is regulated by a negative feedback mechanism in which the hypothalamus-hypophisis-thyroid axis is involved. The hypothalamus secretes thyrotrophin releasing hormone (TRH), which stimulates the hypophysis to secrete thyrotrophin (thyroid stimulating hormone, TSH). TSH stimulates the thyroid gland toi produce and secretes thyroid hormones (TH). Concentration changes of TH are detected by the hypophysis. If there are los levels of TH, it secretes TSH. On the contrary, if the levels are elevated, it lowers secretion.
Iodine itself intervenes on TH regulation through a negative feedback mechanism (Wolff-Chokoff effect) with a biphasic effect: on iodine ingestion, synthesis is increased; with increased consumption, synthesis is lowered [2].
Evidence shows that cell membranes contain specific transporting proteins for active hormone. T3 is the main effector of biological actions of thyroid hormones, tissue thermogenesis, effects on diverse cellular proteins' expression, direct effects on the hear, and effects on smooth muscle cells on blood vessels. T3 enters the cell through a facilitated diffusion process, and it seems to penetrate directly into the nucleus without binding to any other protein within the cell.
Most of the observations indicate cardiac myocytes can metabolize neither T3 nor T4, so all nuclear effects and genic expressions are due to changes on blood concentrations of T3. All the biological effects of T3 are due to genic and extragenic transcription [1].
Once within the myocyte, T34 interacts with molecules highly associated to chromatin, known as "thyroid hormone nuclear receptors" (RT3). These proteins belong to one of the super family of nuclear receptors. Each of them is a nuclear transcription factor, ligand-dependent, which regulates transcription speed of target genes by binding to a specific sequence of deoxyribonucleic acid (DNA) located on the 5' region flanking said genes. They bind to DNA as monomers, although most of them do so as homodimers or heterodimers made of nuclear receptors of T3 and another thyroid hormone target. These genes code  Three months later, a new echocardiogram was performed, but there was no evidence of pericardial effusion (Figures 1-3). Currently, the patient is found asymptomatic and on a 150 mcg/day levothyroxine prescription.

Discussion
Pericardial effusion is described as the abnormal accumulation of fluid within the pericardial cavity. Such liquid can be either exudate, transudate, pyopericardium, or hemopericardium [5].
A fibroelastic sac contains the heart and proximal great vessels. The pericardium anchors the heart to the mediastinum, provides lubrication, and acts against infection and acute distention of the heart chambers. It is made of two fine leaf- patients presented pericardial effusion [11]. It is associated with disease severity, being more frequent in congenital hypothyroidism or long-evolution hypothy-  [8]. In the reported case, despite the effusion's volume was estimated to be more than 1000 cc, cardiovascular physical examination did not provide relevant data.
Due to patients suffering of pericardial effusion might report thoracic pain or dyspnea, chest X-rays must be obtained. However, they might show no abnormalities. In large-volume effusions, cardiac silhouette might be rounded, usually described as a bottle. In the reported case, cardiomegaly and bottle sign could be observed. Chest X-ray findings, though, lack sensibility and specificity. Cardiothoracic index is higher in 55% of 70% of all patients, but only in 67% of patients is higher than 75% [5] [6].
Echocardiogram is the preferred diagnostic tool, being sensible to diagnose pericardial effusion and cardiac tamponade. It provides useful information about the volume, localization, and hemodynamic effects of the effusion. Located between the epicardium and pericardium, many effusions are anechoic, but a complex effusion may present with a more heterogeneous appearance. Pericardial fat is more hyperechoic and moves along the myocardium during cardiac cycle.
Sometimes, it is difficult to distinguish between pleural and pericardial effusion.
Using the descending aorta on a parasternal long axis might serve as a reference point. Pericardial effusion normally is located anteriorly, between the aorta and the myocardium, whereas pleural effusion remains posteriorly to the aorta [6] [7].

Conclusion
Pericardial effusion on hypothyroidism is an infrequent entity. Hypothyroid patients might develop a progressive effusion. It is more frequent in clinical hypothyroidism; clinical manifestations are those caused by the underlying disease which caused the effusion. The best diagnostic method is echocardiography. Thyroid hormone replacement therapy is the best option for treatment. With it, the effusion resolves in one to 15 months after being initiated. Pericardiocentesis is only performed if cardiac tamponade is present.