Preradial myxedema in a euthyroid male: A distinct rarity.

Localized or pretibial myxedema is one of the signs of Graves disease (along with goiter, exophthalmus, thyroid acropathy, and high circulating levels of long-acting thyroid-stimulating hormone) and usually tends to occur at a later stage of the disease or even after the patient becomes euthyroid post treatment. Very rarely has it been reported in euthyroid patients. We report a euthyroid man presenting with localized myxedema on the extensor surface of his forearm with clinical and histopathological features consistent with pretibial myxedema. He responded partially to topical clobetasol propionate cream and tacrolimus ointment 0.1 percent for about 7 months. To the best of our knowledge, this is the first case of preradial myxedema in a euthyroid patient in the English international dermatological literature.

Heart failure presenting as myxedema coma: case report and review article.

Hypothyroidism is a common medical problem easily treated when diagnosed but requiring regular follow-up and patient medication compliance. At times, this diagnosis can go untreated resulting in the development of severe consequences such as Myxedema Coma. Of all the clinical symptoms, cardiovascular manifestations tend to be especially severe and often life threatening.

[Predisposition to autoimmune thyroid diseases within a Tunisian multiplex family]. / Prédisposition aux maladies auto-immunes thyroïdiennes au sein d'une famille tunisienne multiplexe.

The autoimmune thyroid diseases (AITDs) are multifactorial diseases which result from interplays between predisposing genes and triggering environmental factors. In order to study the genetic susceptibility factors to AITDs, we have followed up 115 control members belonging to a large Tunisian family with a high prevalence of AITDs (Akr family) during 15 years between 1990 to 2005. The follow-up of these control members have showed that 13 subjects (11.3%) developed AITDs (G2). The Hashimoto thyroiditis was the most frequently seen in 77% of the cases, whereas the Graves's disease was present in 23% of the cases. One hundred and two members remained controls (G1). High female predominance was noted in the two groups. The mean age of the G1 subjects group was slightly higher than that of G2. The prevalence of positive antithyroglobulin antibody (TgAb) and antithyroperoxydase antibody (TPOAb) was more frequent in G2 group (P=0.27 and P=0.23) respectively. The HLA haplotypes was realized in 42% of control members. The most frequent HLA haplotypes that were found were B37, DRB11 and A1. HLA B37 and DRB11 were significantly more frequent for the patients of G2 (P=0.0001 and P=0.034) respectively. Our study confirms the contribution of the genetic factors in the development of AITDs in 'Akr' family and suggested that the members of this family share the same genetic inheritance.

Postoperative myxedema coma in patients undergoing major surgery: Case series.

OBJECTIVE: Myxedema coma is a serious complication of hypothyroidism that can be precipitated by major surgery. It is extremely rare, with only a few reports in the literature. This study aims to present a relatively large case series of post-surgical myxedema coma and to analyze medical and surgical risk factors. METHODS: Analysis of the patients' surgical records and medical charts. RESULTS: Four patients developed postoperative myxedema coma and were evaluated for risk factors. Three had known hypothyroidism. Two had undergone large head and neck composite resections necessitating a free flap repair for malignant disease. One had undergone coronary artery bypass graft for ischemic heart disease, and another had undergone endoscopic cholecystectomy for complicated cholecystitis. All four patients required prolonged hospitalization, including treatment in the intensive care unit. One patient had undergone full cardiopulmonary resuscitation directly related to the myxedema coma state. CONCLUSION: We present a series of four patients who developed myxedema coma following major surgery. We recommend that patients with known hypothyroidism who are scheduled for major surgery should be tested for thyroid function status and assessed for postoperative risk of hypothyroidism. Those who develop complications following major surgery, should be immediately tested for thyroid function to rule out myxedema coma.

Myxedema coma precipitated by diabetic ketoacidosis after total thyroidectomy: a case report.

BACKGROUND: Myxedema coma is profound decompensated hypothyroidism usually precipitated by stressors, and its occurrence in association with total thyroidectomy or metabolic disorders, such as diabetic ketoacidosis, is unusual. CASE PRESENTATION: A 43-year-old Asian man with history of total thyroidectomy who was scheduled for a second radioactive iodine therapy presented to our hospital with decreased mental status and hyperglycemia. He had a history of thyroid cancer but did not have diabetes mellitus. He was in a hypothermic state and had a Glasgow Coma Scale score of 10 out of 15 at presentation; arterial blood gas analysis revealed a state of metabolic acidosis and laboratory findings suggested hyperglycemia with glycosuria, ketoacidosis, and severe hypothyroidism. A thyroid function test showed thyroid-stimulating hormone of 34.126 uIU/mL, free thyroxine of 1.02 ng/dL, and triiodothyronine of 1.04 ng/mL. The glycated hemoglobin of this patient was checked due to hyperglycemia and the value of glycated hemoglobin was 16.5% which met the criteria for a diagnosis of diabetes. After treatment for myxedema with liothyronine 5 mcg two times per day and levothyroxine 175 mcg once daily via a nasogastric tube and diabetic ketoacidosis with intravenously administered fluid and insulin, his clinical condition rapidly improved including mental status, hyperglycemia, and acidosis. During the hospitalization, a workup for diabetes mellitus was performed and the results suggested that a diagnosis of type 2 diabetes mellitus would be appropriate. CONCLUSIONS: This case demonstrated that diabetic ketoacidosis not only could be a potential contributor to myxedema coma but also mask typical clinical features, making diagnosis more difficult. Considering the possibility of an increasing number of potential patients with hypothyroidism developed after thyroidectomy, constant vigilance is required for a better clinical outcome, including early recognition and management in critical care in advance for unusual diabetic ketoacidosis which could precipitate decompensated hypothyroidism.

Pretibial myxedema in a euthyroid patient.

Pretibial myxedema (PM) is a rare extrathyroidal manifestation of Graves' disease (GD), usually during the hyperthyroid state, coexisting with orbitopathy. We describe a rare case of a biopsy-proven PM in a euthyroid patient, without history of GD or Hashimoto's thyroiditis. Assessment of commonly reported thyroid autoantibodies, such as thyroid peroxidase and thyroglobulin autoantibodies, thyroid stimulating immunoglobulins and thyroid binding inhibitory immunoglobulins, was negative. Resolution of skin pathology was achieved after topical application of corticosteroids and was sustained 1 year later.

Challenges in the Management of a Patient with Myxoedema Coma in Ghana: A Case Report.

Myxoedema coma is a rare life-threatening disease, and it is essential that it is managed appropriately to reduce the associated high mortality. However, in the setting where efficient healthcare delivery is hampered by inadequacies, the management of such cases may pose a significant challenge. We present the case of a middle-aged woman diagnosed with myxoedema coma and severe hyponatremia. The case report highlights some of the challenges that may be encountered during the management of myxoedema coma in similar settings and outlines the management strategies undertaken to overcome them in the absence of national guidelines. It also brings to the fore the need for clinicians to look out for clinical features suggestive of hypothyroidism particularly among high risk individuals for early diagnosis and treatment. FUNDING: None declared.

Myxedema coma.

Myxedema coma is the term given to the most severe presentation of profound hypothyroidism and is often fatal in spite of therapy. Decompensation of the hypothyroid patient into a coma may be precipitated by a number of drugs, systemic illnesses (eg, pneumonia), and other causes. It typically presents in older women in the winter months and is associated with signs of hypothyroidism, hypothermia, hyponatremia, hypercarbia, and hypoxemia. Treatment must be initiated promptly in an intensive care unit setting. Although thyroid hormone therapy is critical to survival, it remains uncertain whether it should be administered as thyroxine, triiodothyronine, or both. Adjunctive measures, such as ventilation, warming, fluids, antibiotics, pressors, and corticosteroids, may be essential for survival.

Myxedema ascites with elevated serum CA 125 concentration.

We report a case of myxedema ascites and markedly elevated serum CA 125 concentration. The cause of ascites and elevated tumor markers in hypothyroidism remains unknown. Diagnosis was characterized by no evidence of malignancy seen by transvaginal ultrasonography or abdominal computed tomography and ascites resolution with serum CA 125 normalization after adequate hormonal treatment. Our data suggest that hypothyroidism should be considered in patients with ascites and elevated serum CA 125.

Myxedema coma in a patient with Down's syndrome.

INTRODUCTION: hyroid dysfunction is common in Down's syndrome, most common being hypothyroidism. Longstanding, untreated hypothyroidism can lead to myxedema coma. METHODS: Here we report a patient with Down's syndrome who presented with myxedema coma. DISCUSSION: The three essential elements for the diagnosis of myxedema coma include altered mental status, defective thermoregulation and a precipitating event or illness; all of these were present in our patient. Also, very high TSH, low T3 and T4, and the rapid response to the treatment with levothyroxine confirmed the diagnosis. CONCLUSION: Patients with Down's syndrome should have regular screening for thyroid dysfunction.

Hyperprolactinemia--a review of recent clinical advances.

Since the radioimmunoassay for serum prolactin became available eight years ago, prolactin has become a hormone of considerable clinical interest. An elevated serum prolactin concentration is the most frequent hormone marker for pituitary tumors. Secreted in excess, prolactin causes dysfunction of the hypothalamic-pituitary axis, the gonads, and the adrenal cortex. In women, menstrual disturbances, galactorrhea, infertility, and hirsutism result. Impotence, oligospermia, and decreased libido are common in men. These metabolic abnormalities attributed to prolactin excess are corrected when prolactin concentrations are lowered by either medical or surgical therapy. The availability of effective therapy mandates early recognition and proper management of the patient with hyperprolactinemia.

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.

Serum markers of type I collagen formation and degradation in metabolic bone disease: correlation with bone histomorphometry.

Type I collagen makes up more than 90% of bone matrix. Therefore, analysis of antigens related to collagen formation and degradation in bone should provide good and specific estimates of both bone resorption and bone formation rates. In this study we measured serum levels of the pyridinoline cross-linked telopeptide domain of type I collagen (ICTP) as a marker of bone resorption and serum carboxy-terminal propeptide of type I procollagen (PICP) as a marker of bone formation. Serum levels of the two antigens were correlated to histomorphometric indices of bone resorption and bone formation calculated from iliac crest bone biopsies in a group of 18 individuals with high- and low-turnover bone disease (myxedema, primary hyperparathyroidism, and thyrotoxicosis). After logarithmic transformation the regression of S-ICTP on volume-referent resorption rate (BRs/R/BV) was significant (r = 0.61, p < 0.01, SEM/Y = 56%). S-ICTP also showed a significant regression on the volume-referent cancellous bone balance (r = -0.45, p < 0.05, SEM/Y = 412%). S-PICP was significantly correlated to the mineral appositional rate (r = 0.53, p < 0.05) and volume-referent bone formation rate (r = 0.61, p < 0.01, SEM/Y = 48%). The correlation to bone turnover as expressed in the activation frequency was also highly significant (r = 0.61, p < 0.01, SEM/Y = 51%). No significant correlation with wall thickness or bone balance was demonstrable per remodeling cycle. Thus, assays employing antigens that reflect collagen formation and degradation are useful instruments for the evaluation of rates of bone remodeling in metabolic bone disease.

Stimulation of fibroblast biosynthetic activity by serum of patients with pretibial myxedema.

Skin fibroblasts from the shoulder and lower extremities of normal individuals, as well as from patients with pretibial myxedema (PTM) were grown in culture. When cells reached the monolayer stage, they were labeled with 3H-glucosamine and tested for hyaluronic acid synthesis in the presence of either serum from PTM patients or normal human serum. All the fibroblasts from the pretibial area synthesized 2 to 3 times more hyaluronic acid when incubated with PTM sera than when incubated in normal human serum. Fibroblasts cultured from skin of the back or prepuce did not respond to PTM sera. This heat-stable, protease-sensitive, and dialyzable, fibroblast-stimulating factor is not a 7S gamma-globulin. The enhanced sensitivity to PTM sera exhibited by fibroblasts from the lower extremities may explain why the lesions in this disease are restricted primarily to that area.

Osmoregulation of plasma vasopressin in myxedema.

We studied osmoregulation of plasma vasopressin (AVP) in eight patients with untreated myxedema due to primary hypothyroidism. All patients had severe thyroid hormone deficiency due to chronic thyroiditis and had been receiving no medication at the time of this study. AVP release was defined by 5% hypertonic saline infusion test in all patients, and urinary diluting capacity was estimated by the iv water-loading tests in five patients. Plasma AVP was measured by sensitive and specific RIA. The mean basal plasma AVP level in the patients (0.5 +/- 0.1 pmol/L) was significantly lower (P less than 0.01) than that in normal adults (2.5 +/- 0.5 pmol/L). During hypertonic saline infusion, the rise in plasma AVP was normal or subnormal in all patients. In two patients who showed mild to moderate hyponatremia in the basal state and mild urinary diluting defect during water loading, plasma AVP was appropriately suppressed in each case. These results indicate that inappropriate elevation of plasma AVP is not common in myxedema, and that impaired water excretion is due mainly to AVP-independent mechanisms.

Thyroperoxidase, but not the thyrotropin receptor, contains sequential epitopes recognized by autoantibodies in recombinant peptides expressed in the pUEX vector.

The sequential epitopes on the human thyroperoxidase (TPO) recognized by antibodies in the sera of patients with autoimmune thyroid disease were investigated using a recombinant DNA technique. Previous studies led to the isolation of two overlapping cDNA clones that encode polypeptides of TPO (85 residues, C2; 100 residues, C21) recognized by sera from several patients with autoimmune disease that contained antimicrosomal autoantibodies. In this report the vector pUEX1 was used to clone and express small random fragments of TPO cDNA in Escherichia coli as a beta-galactosidase fusion protein. Colonies were screened with a serum from a patient with Hashimoto's thyroiditis, and immunoreactive peptides were identified by sequencing the corresponding DNA inserts. Two linear epitopes of human TPO (amino acids 590-622 and 710-722) were recognized by the autoantibodies. This confirmed our previous results and provide a more precise localization of the antigenic determinants involved. The same approach has been applied in an attempt to identify the binding site(s) for autoantibodies on the human TSH receptor. In contrast to the data obtained with TPO, sera from patients with blocking (from idiopathic myxoedema) or stimulating (from Graves' disease) activity did not recognize the linear TSH receptor peptide fragments generated in our libraries.