Cases reported "Myxedema"

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1/12. sweat gland proliferations in scleromyxedema.

    Eccrine sweat duct proliferations may be found in various inflammatory and neoplastic skin lesions. We report a patient with scleromyxedema with extensive proliferations of intradermal sweat ducts. Three-dimensional reconstruction demonstrated extensive coiling and branching of the sweat ducts leading into cystic lacunae. In contrast to the basal cell carcinoma that had grown within the scleromyxedematous skin, the ducts close to the lumen stained positive for carcinoembryonic antigen and could therefore be differentiated from basal cell carcinoma. In micrographically controlled surgery of cutaneous epithelial tumors that are located in chronically inflamed skin, such sweat gland proliferations have to be considered as differential diagnosis.
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2/12. Graves' disease presenting as elephantiasic pretibial myxedema and nodules of the hands.

    A 67-year-old man presented with a 2-year history of asymptomatic, firm, multiple nodules and plaques and cerebriform hypertrophy of both lower legs and feet, and well-defined, skin-colored, firm nodules and tumors on both hands. He had been diagnosed as having Graves' disease 3 years previously, and had been treated with 10 mg of methimazole and 100 microg of thyroxin (T4) daily for 2 years. Physical examination revealed nonpitting edema, flesh-colored to erythematous, firm, confluent, polypoid nodules and fissured plaques extending from the shins to the dorsa of both feet (Fig. 1), and round to oval, firm, skin-colored, walnut-to-egg-sized tumors on all 10 fingers and the ulnar side of the dorsum of the right hand (Fig. 2). The thyroid gland was diffusely enlarged; however, there was no exophthalmos, and extraocular movements were normal. There was no weight loss, loss of appetite, tremor, heat intolerance, diarrhea, or fatigue. On laboratory evaluation, thyroid-stimulating hormone (TSH) had a markedly low titer of < 0.05 microU/mL (normal: 0.4-5.0), and the TSH receptor antibody was extremely high at 73.8% (normal: < 15%). serum free triiodothyronine (T3), T4, antimicrosome, and antithyroglobulin antibodies were normal or negative. skin biopsy samples from the shin and hand disclosed extensive mucin deposition throughout the dermis.
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3/12. Triad of exophthalmos, pretibial myxedema, and acropachy in a patient with Graves' disease.

    Graves' disease is an autoimmune disorder of the thyroid gland with characteristic peripheral manifestations. The most common clinical findings include ophthalmopathy in 30% of patients, dermopathy (pretibial myxedema) in 4% of patients, and thyroid acropachy in 1% of patients. The triad of exophthalmos, pretibial myxedema, and acropachy occurs in less than 1% of patients. We present a case of Graves' disease with the clinical triad of eye disease, dermopathy, and acropachy.
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4/12. The rare presentation to the cosmetic and plastic surgeon of a patient with myxedema.

    Myxedema results from hypofunction of the thyroid gland. Symptoms include dry skin, loss of and dryness of hair, mental apathy, drowsiness, and sensitivity to cold. Ocular complications associated with myxedema may be the symptoms that first prompt patients to seek a physician or cosmetic surgeon, however, though other symptoms may be present before eyelid myxedema occurs. The case reported here illustrates the value of a correct diagnosis and appropriate medical treatment, and demonstrates how surgical intervention to correct remaining eyelid problems can succeed when it is part of a comprehensive treatment plan.
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5/12. Localized hyperhidrosis in pretibial myxedema.

    Two cases of spontaneous hyperhidrosis limited to pretibial myxedema lesions were studied. Quantitative measurements of stimulated eccrine sweat were made after the intradermal injection of methacholine. The sweat rate was two to four times greater in the lesional skin than in perilesional skin. Eccrine secretory glands in excisional biopsy specimens from the pretibial lesions were significantly larger than those in perilesional skin. To our knowledge, hyperhidrosis localized to areas of pretibial myxedema has not been reported.
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6/12. Pouting sublinguals: enlarged salivary glands in myxoedema.

    Enlarged salivary glands are common in patients with hypothyroidism but this finding is not widely appreciated. Although chronic painless enlargement of the salivary glands was reported in papers published 50-60 years ago, mainly in German, it is not mentioned in current textbooks on the thyroid. Along with the parotids, the submandibular and especially the sublingual glands may be quite enlarged, and the enlargement can be a useful clue to the diagnosis of hypothyroidism. The gland enlargement regresses at least partly after thyroid replacement therapy.
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7/12. Myxoedema presenting with chiasmal compression: resolution after thyroxine replacement.

    A 60-year-old woman presented with deteriorating vision. A computed tomography (CT) scan showed pituitary enlargement with chiasmal compression. serum prolactin levels were normal but assessment of thyroid function showed a serum thyroxine level of 25 nmol/l (normal range 76-160 nmol/l) and a thyroid-stimulating hormone (TSH) level of 60 mU/l (normal range 0.5-5.0 mU/l). After 8 weeks of thyroxine replacement therapy (0.05 mg daily increasing to 0.1 mg daily after 3 weeks) the visual defects had resolved, serum TSH had fallen to 0.7 mU/l, and the CT scan showed pronounced reduction in the size of the pituitary gland. Measurement of TSH as well as prolactin is essential in all patients with pituitary enlargement, to avoid unnecessary pituitary surgery.
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8/12. Euthyroid pretibial myxedema.

    Pretibial myxedema is typically associated with clinical hyperthyroidism, diffuse goiter, and ophthalmopathy in patients with Graves' disease. A case of biopsy-proved pretibial myxedema was encountered in a clinically euthyroid woman who had neither diffuse goiter nor exophthalmos. Although serum total and free thyroxine hormone concentrations were normal, the thyroid-stimulating hormone response to thyrotropin-releasing hormone was absent. This case illustrates that pretibial myxedema may present without other more common manifestations of Graves' disease. In patients with suspect pretibial skin lesions, the thyrotropin-releasing hormone stimulation test may be required to establish the presence of subtle underlying thyroid gland autonomy and the diagnosis of euthyroid pretibial myxedema.
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9/12. multiple sclerosis co-existent with myxedema. An autopsy case report.

    A 64-year-old woman developed impaired consciousness and vision, sensorimotor paresis, hypothermia, bradycardia, and edema. Symptoms fluctuated with seasonal exacerbations in winter and terminated in coma with respiratory insufficiency at age 69. High CSF protein content and low serum T4 and TSH levels were noted. Treatment with prednisolone and thyroxin considerably improved her consciousness and edema. The patient suddenly expired of pulmonary embolism. Postmortem examination revealed a marked atrophy of pituitary and thyroid glands, while multiple demyelinating plaques were disclosed in the optic tract and cervical cord. A review of the literature indicates that this is the first report of the co-existence of two such disorders.
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10/12. The advantage of the use of echocardiographic evaluation in hypothyroid patients.

    Authors examined 10 patients with untreated myxoedema. The disease lasted at least one year in seven cases. The etiology of disease was autoaggressive thyroiditis in 9 cases and was diagnosed by a high titre of antibodies against thyroglobulin. The levels of T4 and T3 were low in all cases, level of TSH was elevated. The mean level of T4 was 0.91 microgram/dl, of T3 43.5 ng/dl. The level of TSH was over 96 microU/ml in 7 cases, in rest over 54 microU/ml. In all cases ECHO examination was done: pericardial effusion was proved in 80%. 5 patients were followed during substitutional therapy. Clinical signs and laboratory test normalised in all 5 cases. ECHO finding improved: left ventricular SEF from 54.4 /- 7.4% to 67.9 /- 10.3%, Vcf 0.82 /- 16 circ/sec to 1.32 /- 0.37 circ/sec max PWVs from 43.8 /- 6.8 mm/sec to 63.2 /- 9.9 mm/sec. The etiology of myxoedema may play a role in the incidence of pericardial effusion either by influence of autoaggressive disease or, which seems more probable, by a complete failure of thyroid gland secretion with low not only T4 but T3, too. T3 receptors are supposed to play an important role in the myxoedema heart disease.
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