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Key Clinical Message
High‐dose intravenous thyroxine (T4) is the preferable treatment for myxedema coma. We describe the clinical course of a 69‐year‐old man who presented with myxedema coma and received oral levothyroxine (LT4) therapy (1 mg) in a split dose. This suggests split high‐dose oral LT4 as a therapeutic option in myxedema coma.
Similar publications
Myxedema coma and pituitary apoplexy are well-known life-threatening endocrine emergencies. The coincidence of these entities is exceedingly rare. Myxedema coma occurring as a result of pituitary lesion is a much less seen entity. A high index of suspicion is often required for early diagnosis as it is of particular importance in improving survival...
Severe untreated hypothyroidism has been shown to affect cardiovascular function. While there have been a few reports of life-threatening arrhythmias occurring as a direct result of the hypothyroid state, very few cases of cardiac arrest have been reported in the literature. We report one such case of a middle-aged man who suffered a cardiac arrest...
Introduction: The COVID-19 pandemic was a major challenge for all health care employees, but it was also difficult for patients to gain access to health care services. Myxedema coma (MC) is an exteremely rare but potentially fatal endocrine emergency.
Objectives: The aim of the study was to report an increased incidence of life-threatening myxedema...
Myxedema coma is a grave medical condition that warrants emergent medical management to avoid adverse effects and unfavorable outcomes. Intravenous thyroid hormones (T3 and T4), along with intravenous hydrocortisone and frequent vital monitoring, are the mainstays of the management of myxedema coma. The interplay between CKD and hypothyroidism is f...
Citations
... By our knowledge, this is the first case report showing that oral treatment, with both T4 and T3, of hypothyroid crisis is possible in Caucasian patients [4] . Recent publications have demonstrated that oral treatment is possible in Asian patients with oral levothyroxine alone [5,6] . European guidelines recommend intravenous substitution therapy because of assumed reduced intestinal absorption with oral treatment [7] . ...
... Guidelines recommend intravenous substitution despite the potential disadvantages, because more data are available on intravenous treatment. Our and other [4][5][6] cases show that oral substitution is an appropriate alternative. ...
Background: Hypothyroid crisis, or myxoedema coma, is a rare condition with high mortality and must be treated promptly. Even though it may be unfavourable, most guidelines only focus on intravenous drug administration due to lack of data on oral treatment.
Methods/Results: The course of oral treatment in two patients admitted in our hospital is described. Patients were treated with levothyroxine 1.3 µg/kg and liothyronine 25 µg twice daily, followed after 1 week with only levothyroxine 1.3 µg/kg daily. Oral treatment was successful in both patients without complications or side-effects.
Conclusions: Oral substitution is an appropriate alternative to intravenous substitution, which has potential disadvantages and is associated with higher mortality.
... Empiric treatment of coexisting adrenal crisis and possibly infection should be maintained unless they have been excluded [25]. Patients should be admitted to an intensive care unit under close monitoring, and interventions such as mechanical ventilation, passive warming, and intravenous fluid resuscitation should be administered as necessary [26]. While pericardial effusion was identified in our patient, echocardiography did not suggest that it contributed to her cardiogenic shock. ...
Hypothyroidism is a common pathological condition of thyroid hormone deficiency that varies widely in relation to both the acuity with which the deficiency develops and the clinical manifestations of the disease. While hypothyroidism is commonly mild or even subclinical, one rare complication of hypothyroidism that can cause multiorgan dysfunction is myxedema coma. Myxedema coma is precipitated by an acute stressor such as infection, surgery, or trauma, which disrupts the otherwise compensatory mechanisms present in severe hypothyroidism. Swift diagnosis and treatment of the condition is vital to improving patient outcomes as mortality from myxedema coma ranges from 40 to 60%. The mainstay of treatment includes IV levothyroxine (LT4) with or without the use of liothyronine (LT3). Here we present a case of a patient who presented with presyncope in the setting of generalized fatigue, poor appetite, anhedonia, and slowed speech and movement. Full workup revealed hypotension, hyponatremia, hypoglycemia, respiratory acidosis, undetectable cortisol, free T4, total T4 and an inappropriately normal TSH level. A diagnosis of myxedema coma and adrenal crisis due to pituitary dysfunction was made. A combination of 300 mcg IV LT4 and 5 mcg IV LT3 every 8 hours was used with successful resolution of the patient's symptoms. The patient is currently well maintained on a combination of oral LT4 and hydrocortisone replacement with no further endocrinological complications. This case underscores the need for physicians to maintain a high index of suspicion for secondary adrenal insufficiency and central hypothyroidism in patients with compatible symptoms or risk factors. Furthermore, it also highlights the successful treatment of adrenal crisis and myxedema coma with severe cardiogenic shock with a combination of hydrocortisone, levothyroxine, and liothyronine therapy.
... doi: bioRxiv preprint first posted online Nov. 17, 2019; myxedema coma, estimation based on case reports, e.g. (90), and physiological distribution of FT4 levels in (91)). ...
Many endocrine organs show prevalent autoimmune diseases (AID) such as type-1-diabetes and Hashimoto's-thyroiditis. The fundamental origins of these diseases is unclear. Here we address AID from the viewpoint of feedback control. Endocrine tissues maintain their mass by feedback-loops that balance cell proliferation and removal according to input signals related to the hormone function. Such feedback is unstable to mutant cells that mis-sense the signal, and therefore hyper-proliferate and hyper-secrete the hormone. We hypothesize that in order to prevent these mutants from expanding, each organ has a dedicated 'autoimmune surveillance of hyper-secreting mutants' (ASHM), in which hyper-secreting cells are preferentially eliminated, at the cost of a fragility to AID. ASHM correctly predicts the identity of the self-antigens and the presence of T-cells against these self-antigens in healthy individuals. It offers a predictive theory for which tissues get frequent AID, and which do not and instead show frequent mutant-expansion disease (e.g. hyperparathyroidism).
Myxedema coma (MC) develops from a long-standing, unrecognized, or untreated hypothyroidism. This article discusses the pathophysiology, clinical manifestations, treatment, and nursing considerations for patients with MC.
Introduction:
Myxedema coma is an endocrine emergency with a very high mortality rate. As per the American Thyroid Association, initial thyroid hormone replacement for myxedema coma should be intravenous levothyroxine (LT4). However, in India, the availability of intravenous LT4 is limited. Often, crushed LT4 tablets are given through the enteral route when parenteral therapy is unavailable. No data or protocol is available for the administration of oral LT4 in myxedema coma. The aim of this study was to assess the effectiveness of oral LT4 in patients diagnosed with myxedema coma and to formulate a protocol for oral LT4 that can be used to guide the treatment of patients when intravenous LT4 is unavailable.
Methods:
This retrospective observational study included patients diagnosed with myxedema coma between January 2010 and December 2019. The diagnosis of myxedema coma was based on the diagnostic scoring system for myxedema coma proposed by Popoveniuc et al. [Endocr Pract. 2014 Aug;20(8):808-17]. Dosing of oral LT4 was decided as per our institutional protocol.
Results:
Fourteen patients (11 males and 3 females) with a median age of 67.5 years (range 11-82) with myxedema coma were included. All patients had central nervous system manifestations, and sepsis was the most common precipitating factor. The median myxedema score was 72.5 (normal ≤25), and the median length of hospital stay was 12 days (range 3-18). The oral LT4 regimen consisted of a loading dose of 300-500 μg, followed by taper over the next 3-5 days. With this regimen, 13 patients survived, and only 1 patient died.
Conclusion:
Oral LT4 is an effective treatment option for myxedema coma when intravenous LT4 is unavailable.
Sudden unexpected death (SUD) refers to the sudden (usually occurs within 24 h from the onset of the initial symptoms) and unexpected (not caused by obvious reasons like trauma, poisoning, violent asphyxia, etc.) death of a person. It may be the result of one or several serious underlying diseases, while the initial symptoms may be totally different from the common manifestations of those diseases. Disorders of many endocrine organs can cause SUD, and some of these conditions are reviewed in this article.
Some endocrine organs are frequent targets of autoimmune attack. Here, we addressed the origin of autoimmune disease from the viewpoint of feedback control. Endocrine tissues maintain mass through feedback loops that balance cell proliferation and removal according to hormone-driven regulatory signals. We hypothesized the existence of a dedicated mechanism that detects and removes mutant cells that missense the signal and therefore hyperproliferate and hypersecrete with potential to disrupt organismal homeostasis. In this mechanism, hypersecreting cells are preferentially eliminated by autoreactive T cells at the cost of a fragility to autoimmune disease. The “autoimmune surveillance of hypersecreting mutants” (ASHM) hypothesis predicts the presence of autoreactive T cells in healthy individuals and the nature of self-antigens as peptides from hormone secretion pathway. It explains why some tissues get prevalent autoimmune disease, whereas others do not and instead show prevalent mutant-expansion disease (e.g., hyperparathyroidism). The ASHM hypothesis is testable, and we discuss experimental follow-up.
We induced hypothyroidism (HT) in male rats through chronic oral administration of carbimazole and then tested whether an i.v. injection of rat bone marrow-derived mesenchymal stem cells (BM-MSCs) could ameliorate the HT-induced changes in pancreatic structure and function. The thyroid and pancreatic function tests, as well as total antioxidant capacity (TAC) and malondialdehyde (MDA) were estimated. The pancreatic structure was evaluated by hematoxylin and eosin (H&E) stain. Insulin protein and cleaved caspase-3 were detected immunohistochemically. The degree of apoptosis was assessed by TUNEL assay. The morphometric measurements were done by an image analyzer system and the obtained data were statistically analyzed. HT rats showed hyperglycemia associated with insulin deficiency, decreased TAC and increased MDA levels. H&E-stained sections showed that the pancreatic septa were infiltrated with acidophilic material. Some acini were vacuolated while others showed depleted acidophilia and dilated lumina. Spindle-shaped cells were accumulated within deformed islets in HT rats. The positive reaction with anti-cleaved caspase-3 was exclusively noted in the cytoplasm of islet cells with no immunostaining reaction in the acinar and ductal cells, whereas the positively stained nuclei with TUNEL were demonstrated in the islet and acinar cells. A significant increase in the apoptotic index % of both markers was detected. Injection of BM-MSCs in HT rats restored all biochemical indicators of disturbed pancreatic function to normal level and improved pancreatic structure, resulting in a clear septa and normal appearance of acini and islets. In conclusion, many of the significant structural and func tional pancreatic alterations detected in HT rats were ameliorated after the injection of BM-MSCs. These data demonstrate the ability of BM-MSCs to repair pancreatic disturbances. Further studies on humans are necessary to determine the potential clinical applications of BM-MSCs.
