Case Report of Graves' Disease in a 45-Year-Old Woman Secondary to Herceptin Treatment for Breast Cancer.

Graves' disease is the most common cause of thyrotoxicosis and is characterized by ophthalmopathy with proptosis, chemosis, or conjunctival injection; pretibial myxedema; and thyroid acropachy. It is an autoimmune disease that can be genetic or influenced by coexisting environmental factors such as exposure to anticancer drugs, including immune checkpoint inhibitors. The incidence rate of breast cancer is increasing due to rising awareness of risk factors and screening for breast cancer, and the mortality rate is decreasing due to recent advances in cancer treatment. However, there are side effects that are attributed to these treatment modalities, manifesting in various forms in breast cancer survivors, which are reflected in the patient in this case study.

Localized alopecic myxedema of the scalp.

Myxedema is a rare, cutaneous complication of autoimmune thyroid diseases that most often affects the anterior shins. Herein, we report a patient with a history of Graves disease and Hashimoto thyroiditis who presented with boggy, alopecic patches associated with scalp pruritus. Punch biopsies from these lesions showed increased interstitial mucin in the reticular dermis, consistent with localized myxedema. This report showcases a rare presentation of localized myxedema of the scalp, highlighting the diverse cutaneous manifestations of autoimmune thyroid diseases.

A unique case of concurrent cutaneous lichen amyloidosis and myxedema.

Lichen amyloidosis is believed to be caused by damage to keratinocytes, often by chronic scratching. It has also been associated with autoimmune conditions, including thyroid disease. Dermatologic manifestations of poorly controlled thyroid disease are well described within the medical literature, within both hypothyroid and hyperthyroid states. Myxedema is a rare complication of Graves disease. We report a unique case of concurrent myxedema and lichen amyloidosis in a 63-year-old patient with uncontrolled hypothyroidism in the setting of post-ablative Graves disease.

An Unusual Presentation of ST Elevation Myocardial Infarction Complicated with Cardiogenic Shock Due to Myxedema Coma: A Case Report.

BACKGROUND Myxedema coma is an endocrine emergency with a high mortality rate, defined as a severe hypothyroidism leading to hypotension, bradycardia, decreased mental status, hyponatremia, hypoglycemia, and cardiogenic shock. Although hypothyroidism and cardiac disease has been interlinked, ST elevation myocardial infarction in the setting of myxedema coma have not been reported previously. CASE REPORT We report the case of a 70-year-old man who presented to the Emergency Department with chest pain and confusion. He also reported fatigue for the past week, which was progressively worsening. His past medical history was significant for renal cell carcinoma with metastatic bone disease being treated with chemotherapy (axitinib and pembrolizumab). In the Emergency Department, an ECG revealed inferior ST elevations. Shortly after presentation, the patient's blood pressure was decreasing, he became bradycardic (sinus), and his mental status was getting worse, so he was intubated for airway protection and was taken emergently for a cardiac catheterization, which failed to reveal an acute coronary occlusion. TSH was 60.6 mIU/L (0.465-4.680) mIU/ML, and free T4 0.3 ng/dL (0.8-2.2) ng/dL. The cardiac index was calculated to be 0.8 L/min/m² (normal range 2.6-4.2 L/min/m²), which confirmed cardiogenic shock due to myxedema coma. He was treated with levothyroxine (T4), liothyronine (T3), hydrocortisone, and multiple vasopressors but failed to respond and died 13 h after admission to the hospital. CONCLUSIONS Because of its rarity and high mortality, early diagnosis of myxedema coma and initiation of treatment by cardiologists requires a high level of suspicion, especially when patients with a history of hypothyroidism present with a cardiac complaint (ie, acute coronary syndrome, or bradycardia) that does not completely fit the clinical picture. It is of utmost importance for physicians to keep a wide differential diagnosis of other causes of ST elevation and/or persistent cardiogenic shock.

Myxedema ascites complicated by ischemic colitis.

Myxedema Ascites is a rare finding of primary hypothyroidism, thereby leading to delayed diagnosis. However, prompt treatment with levothyroxine leads to complete resolution of the condition. We present a rare case of myxedema ascites in an elderly female and highlight the importance of early diagnosis and management. We also present ischemic colitis in the same patient, which has not been reported thus far in literature as a complication of myxedema ascites.

Unusual Case of a Massive Macroglossia Secondary to Myxedema: A Case Report and Literature Review.

Macroglossia is classified as true macroglossia, which exhibits abnormal histology with clinical findings, and relative macroglossia, in which normal histology does not correlate with pathologic enlargement. This report describes an atypical case of morbidity with massive macroglossia secondary to myxedema; the macroglossia enlarged over a 3-month period before being presented to the Department of Oral and Maxillofacial Surgery, University of Texas Health Science Center at Houston (Houston, TX). Substantial enlargement of the tongue (16 cm long × 10 cm wide) was first attributed to angioedema, which was refractory to the discontinuation of lisinopril and a C1 esterase inhibitor. A core tongue biopsy examination was performed to rule out angioedema, amyloidosis, myxedema, and idiopathic muscular hypertrophy. Interstitial tissue was positive for Alcian blue and weakly positive for colloidal iron, which are correlated with hypothyroidism and a diagnosis of myxedema. However, the macroglossia did not resolve after correcting for hypothyroidism. The patient required a wedge glossectomy for definitive treatment. She recovered unremarkably, with excellent cosmesis and preservation of lingual and hypoglossal function. There are some case reports of massive macroglossia but none with myxedema as the primary etiology.

Myasthenic Crisis Complicated with Myxedema, Positive for Both Anti-acetylcholine Receptor and Anti-muscle-specific Tyrosine Kinase Antibodies.

We herein report the case of myasthenic crisis occurring in a 51-year-old man. He had experienced ptosis, increased body weight with edema, and fatigue with dyspnea. He presented at our emergency department with disturbed consciousness. He was originally diagnosed with myxedema coma, and he required artificial respiration. Because his weakness persisted and he was positive for anti-acetylcholine receptor antibodies and anti-muscle-specific tyrosine kinase antibodies, we diagnosed myasthenic crisis after various examinations. His clinical response to treatment was good and he was discharged in an ambulatory status 3 months after admission. This case demonstrates that myasthenic crisis may occur in association with myxedema.

Coma mixedematoso e trombo de veia cava superior. Relato de caso e revisão da literatura / Myxedema coma and superior vena cava thrombus: case report and literature review

O coma mixedematoso é uma emergência endocrinológica rara e consiste na máxima expressão do hipotireoidismo, com alta mortalidade por suas complicações hemodinâmicas e ventilatórias, podendo ser agravadas por distúrbios da coagulação. Relatamos o caso de uma paciente diagnosticada com coma mixedematoso e trombo de veia cava superior. Buscamos salientar os distúrbios de coagulação frequentes no hipotireoidismo grave, que contribuem para o aumento da mortalidade deste grupo de pacientes. O diagnóstico e o tratamento precoce do coma mixedematoso, aliados à instituição imediata da terapia para o fenômeno trombótico encontrado, permitiram a evolução favorável do quadro. O relato, juntamente da bibliografia pesquisada, orientou o raciocínio sobre a relação dos distúrbios de coagulação, que ocorrem no hipotireoidismo descompensado. Apesar de poucos relatos, estes distúrbios podem ser frequentes e devem ser pesquisados, pois contribuem com o aumento da mortalidade.(AU)

Myxedema coma is a rare endocrinological emergency, consisting of the highest expression of hypothyroidism with high mortality due to hemodynamic and ventilatory complications, which may be aggravated by coagulation disorders. We report the case of a patient diagnosed with myxedema coma and superior vena cava thrombus. We sought to emphasize the frequent coagulation disorders in severe hypothyroidism, which contribute to increased mortality in this group of patients. The diagnosis and early treatment of myxedema coma, together with the immediate institution of therapy for the thrombotic phenomenon found, allowed the favorable evolution of the condition. The report, together with the literature, has guided the rationale for the influence of coagulation disorders that occur in decompensated hypothyroidism. Despite the few number of reports, these disorders can be frequent and should be investigated because they contribute to the increase in mortality.(AU)

Myxedema coma: A case report of pediatric emergency care.

RAIONALE: Myxedema coma (MC) is extremely rare but lethal in pediatric patients with hypothyroidism leading to altered mental status and hypothermia. But there is no clinical guideline for such cases. PATIENT CONCERNS: A 6-year-old Chinese girl presented with coma and hypothermia preceded by pneumonia. Her lab results were: free thyroxin (T4) 4.18 pmol/L and thyroid-stimulating hormone (TSH) > 150 µIU/mL with extremely elevated anti-thyroid peroxidase (TPO-Ab) and anti-thyroglobulin. Pneumonia, mild pleural, and pericardial effusion were seen on computed tomographic (CT) scan. DIAGNOSES: MC, autoimmune hypothyroidism, pneumonia and sepsis were diagnosed. INTERVENTION: Gastric levothyroxine, intravenous dexamethasone and antibiotics were administered. OUTCOME: Her consciousness was restored and temperature returned to normal 2 days after starting levothyroxine. She was discharged two weeks later. CONCLUSION: MC is rare but may be the initial presentation in pediatric patients with prolonged untreated hypothyroidism. Autoimmune thyroiditis could cause hypothyroidism in children. MC should be suspected in pediatric patients with altered mental status, hypothermia and cardiovascular instability. Treatment with 100 mg/m of gastric levothyroxine is an option for pediatric patients with MC.

'Myxoedema madness' with Capgras syndrome and catatonic features responsive to combination olanzapine and levothyroxine.

We present the case of an elderly woman with hypothyroidism and no psychiatric history who presented with new onset of psychosis, paranoia, catatonic features and Capgras syndrome (CS). This case illustrates the spectrum of neuropsychiatric symptoms that may accompany hypothyroidism and the importance of considering thyroid dysfunction as a primary contributor to severe psychiatric symptoms, especially in previously stable patients. We demonstrate the effectiveness of combination levothyroxine and olanzapine, with its favourable cardiac profile, in the treatment of myxoedema madness. Antipsychotics can be weaned once psychiatric symptoms resolve and hormone levels are stabilised.

A rabbit model of fatal hypothyroidism mimicking "myxedema coma" established by microscopic total thyroidectomy.

Myxedema coma (MC) is a life-threatening endocrine crisis caused by severe hypothyroidism. However, validated diagnostic criteria and treatment guidelines for MC have not been established owing to its rarity. Therefore, a valid animal model is required to investigate the pathologic and therapeutic aspects of MC. The aim of the present study was to establish an animal model of MC induced by total thyroidectomy. We utilized 14 male New Zealand White rabbits anesthetized via intramuscular ketamine and xylazine administration. A total of 7 rabbits were completely thyroidectomized under a surgical microscope (thyroidectomized group) and the remainder underwent sham operations (control group). The animals in both groups were monitored without thyroid hormone replacement for 15 weeks. Pulse rate, blood pressure, body temperature, and electrocardiograms (ECG) were recorded and blood samples were taken from the jugular vein immediately prior to the thyroidectomy and 2 and 4 weeks after surgery. The thyroidectomized rabbits showed a marked reduction of serum thyroxine levels at 4 weeks after the surgical procedure vs. controls (0.50±0.10 vs. 3.32±0.68 µg/dL, p<0.001). Additionally, thyroidectomized rabbits exhibited several signs of hypothyroidism such as hypothermia, systolic hypotension, bradycardia, and low voltage on ECGs, compared with controls. Of the 7 rabbits with severe hypothyroidism, 6 died from 4 to 14 weeks after the thyroidectomy possibly owing to heart failure, because histopathologic examinations revealed a myxedema heart. In summary, we have established a rabbit model of fatal hypothyroidism mimicking MC, which may facilitate pathophysiological and molecular investigations of MC and evaluations of new therapeutic interventions.

Myxedema madness complicating postoperative follow-up of thyroid cancer.

Although hypothyroidism is associated with an increased prevalence of psychiatric manifestations, myxedema madness is rarely observed. We report the case of a 62-year-old woman with no prior history of psychiatric disorders, who presented to the emergency department with psychomotor agitation 6 weeks after total thyroidectomy for papillary thyroid cancer. Serum thyroid stimulating hormone (TSH) on admission was 62.9 mIU/L and free T4 was < 0.35 ng/dL, indicating severe hypothyroidism. After ruling out other possible causes, the diagnosis of myxedema madness was considered; hence, antipsychotic drug treatment and intravenous levothyroxine were prescribed. Behavioral symptoms returned to normal within 4 days of presentation, while levels of thyroid hormones attained normal values 1 week after admission. Recombinant TSH (Thyrogen®) was used successfully to prevent new episodes of mania due to thyroid hormone withdrawal in further controls for her thyroid cancer. This case illustrates that myxedema madness can occur in the setting of acute hypothyroidism, completely reverting with levothyroxine and antipsychotic treatment. Recombinant TSH may be a useful tool to prevent myxedema madness or any severe manifestation of levothyroxine withdrawal for the follow-up of thyroid cancer.

Myxedema madness complicating postoperative follow-up of thyroid cancer

Although hypothyroidism is associated with an increased prevalence of psychiatric manifestations, myxedema madness is rarely observed. We report the case of a 62-year-old woman with no prior history of psychiatric disorders, who presented to the emergency department with psychomotor agitation 6 weeks after total thyroidectomy for papillary thyroid cancer. Serum thyroid stimulating hormone (TSH) on admission was 62.9 mIU/L and free T4 was < 0.35 ng/dL, indicating severe hypothyroidism. After ruling out other possible causes, the diagnosis of myxedema madness was considered; hence, antipsychotic drug treatment and intravenous levothyroxine were prescribed. Behavioral symptoms returned to normal within 4 days of presentation, while levels of thyroid hormones attained normal values 1 week after admission. Recombinant TSH (Thyrogen®) was used successfully to prevent new episodes of mania due to thyroid hormone withdrawal in further controls for her thyroid cancer. This case illustrates that myxedema madness can occur in the setting of acute hypothyroidism, completely reverting with levothyroxine and antipsychotic treatment. Recombinant TSH may be a useful tool to prevent myxedema madness or any severe manifestation of levothyroxine withdrawal for the follow-up of thyroid cancer.

Development of an objective tool for the diagnosis of myxedema coma.

Myxedema coma, a rare entity, with a reported 25%-65% mortality had no objective criteria for making the diagnosis when we began our study. We developed an objective screening tool for myxedema coma to more easily identify patients and examine the best treatment method in future prospective studies to reduce the mortality of this entity. We conducted a retrospective chart review to find all patients aged ≥18 years admitted with myxedema coma from January 1, 2005 through June 13, 2010 at Indiana University Health Methodist Hospital. On the basis of both our retrospective chart review and on literature accounts, we identified 6 criteria to diagnose myxedema coma. We identified 10 patients initially diagnosed with myxedema coma and established a control group consisting of 13 patients identified with altered mental status and increased thyroid-stimulating hormone (TSH) levels. The 6 variables we created for the screening tool were heart rate, temperature, Glasgow coma scale, TSH, free thyroxine, and precipitating factors. The screening tool has a sensitivity and specificity of about 80%. We ran a logistic regression model using the 10 study patients and 13 controls with the 6 variables. No variables alone significantly contributed to the model. However, the overall model was highly significant (P = 0.012), providing strong support for a scoring system that uses these variables simultaneously. This screening tool enables physicians to rapidly diagnose myxedema coma to expedite treatment. A more refined diagnostic tool may be used in future clinical studies designed to determine the optimal treatment.

Postoperative myxoedema coma.

Hypothyroidism is a commonly diagnosed endocrine disorder in medicine. Hyponatraemia is reported in up to 10% of hypothyroid patients, although it is usually mild and rarely causes symptoms. Myxoedema coma is a rare manifestation of hypothyroidism and it can be lethal if it goes undiagnosed and untreated. Our patient presented with an acute manifestation of probable long-standing, but undiagnosed, hypothyroidism. She was asymptomatic but when subjected to surgery (identifiable stress factor) it precipitated as myxoedema coma. Stressful situations such as surgery or infection are the usual precipitating factors for myxoedema coma. The patient responded well to treatment with levothyroxin, 0.9% saline infusion and other general supportive measures. Judicious use of intravenous saline to correct hyponatraemia is important. Correction with 3% normal saline should be carried out with great caution, as rapid correction with 3% normal saline can lead to central pontine demyelination.

Coma mixedematoso en hombre de 74 años: reporte de caso con revisión narrativa / Myxedema coma in a 74 year old man: case report and narrative review

Las células foliculares de la glándula tiroides producen las hormonas tiroxina y triyodotironina, reguladas por la hormona tirotrópica de la hipófisis anterior o tiroestimulante. El coma mixedematoso es definido como un hipotiroidismo profundo que se caracteriza por alteraciones de la conciencia que van desde letargia, estupor y coma al cual se asocia hipotermia, hipoglucemia, convulsiones, hipotensión arterial y manifestaciones de un hipotiroidismo descompensado. La causa o factor desencadenante puede prevenirse si existe diagnóstico previo de hipotiroidismo primario con tratamiento sustitutivo de hormonas tiroideas bien establecido o bien, si en ausencia de diagnóstico éste se sospecha y se trata adecuadamente. Constituye una urgencia médica de mortalidad elevada, donde los factores medioambientales como el frío, infecciones severas e intoxicaciones medicamentosas son importantes factores desencadenantes. Se presenta el caso de un adulto mayor de 74 años, de sexo masculino, sin antecedentes de enfermedad tiroidea que ingresó en Sala de Medicina Interna del Hospital Enrique Cabrera, Habana, Cuba, en el mes de diciembre de 2011, con signología clínica y de laboratorio propias de la hipofunción tiroidea, siendo confirmado coma mixedematoso y con evolución desfavorable.

The follicular cells of the thyroid gland produce thyroxine and triiodothyronine hormones, as regulated by the thyrotropic hormone of the anterior pituitary, also called thyroid stimulating hormone. Myxedema coma is defined as profound hypothyroidism characterized by impairment of consciousness ranging from lethargy to stupor and coma, associated with hypothermia, hypoglycemia, seizures, hypotension, and manifestations of uncompensated hypothyroidism. The condition can be prevented if diagnosis of primary hypothyroidism is established and thyroid hormone replacement therapy is instituted. It is considered a medical emergency with high mortality rates, where environmental factors such as cold, severe infections and drug poisoning are important triggering factors. We report the case of a 74 year old male adult with no history of thyroid disease who was admitted to the Internal Medicine Ward of the “Enrique Cabrera” Hospital, Havana, Cuba, in December 2011, with clinical and laboratory signs of thyroid hypofunction. Myxedema coma was confirmed and patient course was untoward.