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 37,932 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of dermal mucinosis and musculoskeletal symptoms simulating polymyositis as a presenting sign of hypothyroidism is presented. The patient presented muscle weakness and edema of the face including the eyelids. Laboratory examination revealed elevated creatinine phosphokinase, decreased free-T4, decreased free-T3, elevated TSH, positive anti-microsome antibody and positive anti-TSH receptor antibody. The skin biopsy specimen revealed swelling of the collagen bundles with the bundles splitting up into individual fibers, with some blue threads and granules of mucin interspersed. Alucian blue stain demonstrated vast amounts of mucin throughout the whole dermis, which was completely removed on incubation with Streptomyces hyaluronidase. The patient was diagnosed as having hypothyroidism due to Hashimoto's disease with possible polymyositis complications. After two months of thyroid hormone replacement therapy, she was euthyroidic and discharged. These results indicate that our case was a rare case of severe generalized myxoedema due to hypothyroidism of Hashimoto's disease simulating the musculoskeletal symptoms of polymyositis.
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PMID:Dermal mucinosis and musculoskeletal symptoms simulating polymyositis as a presenting sign of hypothyroidism. 1021 Jul 91

A 45-year-old woman had pyrexia, headaches, collapse and hyponatraemia. Intracerebral abscess, bacterial meningitis and subarachnoid haemorrhage were excluded. She was given intravenous antibiotics and gradually recovered. One month later she was readmitted with diplopia, headache and vomiting. Serum sodium was low (107 mmol/l) and a diagnosis of inappropriate ADH secretion was made. MRI scan showed a suprasellar tumour arising from the posterior pituitary gland. A skin rash gradually faded. Serum cortisol, prolactin, gonadotrophins and thyroid hormone levels were low. A pituitary tumour was removed trans-sphenoidally, she had external pituitary radiotherapy, and replacement hydrocortisone and thyroxine. She was well for 12 months when she developed progressive weakness and numbness of both legs. Examination suggested spinal cord compression at the level of T2 where MRI scanning showed an intradural enhancing mass. This spinal tumour was removed and her neurological symptoms disappeared. Nine months after this she developed facial pain and nasal obstruction. CT scan showed tumour growth into the sphenoid sinus and nasal cavities. A right Cauldwell-Luc operation was done and residual tumour in the nasal passages was treated by fractionated external radiotherapy and Prednisolone. Histological examination of the specimens from pituitary, spinal mass, and nasal sinuses showed Rosai-Dorfman disease, a rare entity characterized by histiocytic proliferation, emperipolesis (lymphophagocytosis) and lymphadenopathy. Aged 48 she developed cranial diabetes insipidus. Although Rosai-Dorfman syndrome is rare, it is being reported with increasing frequency, and should be borne in mind as a possible cause of a pituitary tumour.
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PMID:Rosai-Dorfman disease presenting as a pituitary tumour. 1034 67

Though proximal muscle weakness is characteristic of polymyositis, other agents may also lead to proximal muscle weakness, such as drugs, endocrine diseases, or infections. Here, we report a thirty year-old female suffering from proximal weakness which initially was thought to be a case of polymyositis with high serum creatine phosphokinase level. Very low thyroid hormone levels were found as the history inquiry revealed constipation, hoarseness and cold intolerance. The muscle biopsy showed no obvious inflammation. After thyroxine therapy, her muscle weakness recovered. Up to now, hypothyroid myopathy with muscle mitochondrial abnormalities shown by electron microscopic examination has not been reported in the medical literature in Taiwan. Hypothyroid myopathy, though it is rare, may be misdiagnosed as polymyositis clinically. Therefore, it is recommended that hypothyroid myopathy should be considered in the differential diagnosis of proximal muscle weakness.
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PMID:[Hypothyroid myopathy: a case report]. 1156 66

Thyrotropin (TSH)-secreting pituitary adenoma presenting with hypokalemic periodic paralysis is extraordinarily rare and may be misdiagnosed. We describe a 44-year-old man who suffered from acute muscle weakness and inability to ambulate upon awakening in the morning. Physical examination showed hypertension, tachycardia, and symmetrical flaccid paralysis of all extremities. The major biochemical abnormality was hypokalemia (K+, 2.0 mmol/L) with low urine K+ excretion. A thyroid function study revealed elevated thyroid hormone levels and inappropriately high TSH concentrations (2.10 microU/mL). Brain magnetic resonance imaging delineated a pituitary tumor with suprasellar extension. After trans-sphenoidal removal of tumor, he became clinically and biochemically euthyroid without any further attack of paralysis. Pathological findings confirmed a TSH-secreting adenoma with exclusive TSH immunostaining. TSH-secreting pituitary adenoma must be kept in the differential diagnosis in any thyrotoxic periodic paralysis patients with detectable TSH levels to avoid delaying diagnosis and management.
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PMID:Thyrotropin-secreting pituitary adenoma presenting as hypokalemic periodic paralysis. 1254 87

Primary hypothyroidism is a chronic and insidious disease caused by failure of thyroid hormone production. We observed a 38-year-old woman admitted to our hospital due to progressive proximal weakness, muscle pain and fatigue during mild exercise. Laboratory tests showed features of rhabdomyolysis and hypothyroidism. After examination of the thyroid, we reached a diagnosis of Hashimoto's thyroiditis and hypothyroid myopathy. Hypothyroidism should be considered as a differential diagnosis of creatine kinase elevation; actually, neuromuscular symptoms and signs occur in most newly diagnosed patients with thyroid diseases. Hypothyroidism presenting as muscle stiffness and pseudohypertrophy is called 'Hoffman's syndrome'.
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PMID:Hoffman's syndrome: muscle stiffness, pseudohypertrophy and hypothyroidism. 1258 16

Congenital hypothyroidism (CH) is a neonatal disorder that is caused by a prolonged loss of thyroid hormone, which is essential for early brain development. While CH was once the leading cause of mental retardation, newborn screening for CH now allows for early identification and treatment. As a result, affected children now show normal physical and psychological development. Nevertheless, because they still undergo a brief but circumscribed period of thyroid hormone insufficiency, they are at risk for subtle selective impairments. This paper examines several of the persisting deficits observed in children with CH that was identified early in life by newborn screening as well as the relevant disease- and treatment-related factors contributing to such deficits. Highlighted will be (a) a weakness in visuospatial processing, which is associated with prenatal thyroid hormone insufficiency, (b) selective memory deficits associated with postnatal thyroid hormone insufficiencies, (c) a weakness in sensorimotor abilities also reflecting postnatal thyroid hormone insufficiencies, and (d) attention deficits, which are due to abnormal thyroid hormone levels at time of testing. Because these four disabilities implicate different neural substrates, the findings described presently will provide insights as to the specific time windows when different brain structures in the human critically need thyroid hormone.
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PMID:Congenital hypothyroidism: an analysis of persisting deficits and associated factors. 1275 31

We reported a rare case with hypothyroid myopathy after interferon-alpha (IFN-alpha) therapy. A 59-year-old man complained of his weakness in proximal part of upper and lower extremities which started at 1 month and progressed during 6 months after IFN-alpha therapy for chronic hepatitis C, but he did not complain of any other symptoms. Blood chemistry showed an elevated level of CK (1,843 IU/l; normal range 43-170 IU/l) and increased myoglobin (250 ng/ml; normal range < 60 ng/ml). Thyroid function tests revealed an elevated level of TSH (148.7 microIU/ml; normal range, 0.4-4.1 microIU/ml), and decreased levels of free T3 (0.56 pg/ml; normal range, 2.27-3.90 pg/ml) and free T4 (0.24 ng/ml; normal range, 0.95-1.74 ng/ml). Blocking type TSH receptor antibody titer was elevated (75.4%; normal range < 15%) while other types of antithyroid antibody were not detected in his serum. Muscle biopsy from his quadriceps femoris muscle showed non-specific mild myopathic changes. His weakness was completely ameliorated and serum CK levels were normalized by thyroid hormone administration alone, confirming the diagnosis of hypothyroid myopathy. However, even after total amelioration of his hypothyroidism, blocking type TSH receptor antibody titer remained elevated. These findings may suggest that IFN-alpha fostered an autoreactivity arising from HCV infection to cause the autoimmune thyroid disease.
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PMID:[Hypothyroid myopathy caused by interferon-alpha therapy for chronic hepatitis C]. 1602 70

Multiple sclerosis (MS) occurs with immune-mediated mechanisms, but its pathogenesis is not accurately known. The coexistence of MS with other autoimmune diseases has been reported. The hypothesis that MS coexists with other autoimmune diseases has been supported by the reported association of MS with type I diabetes mellitus and inflammatory disorders. Even though there have been only rare reports of associations between Hashimoto thyroiditis and MS, this association is important for its clinical and therapeutic aspects. Proximal muscle weakness, myalgia, and fatigue are symptoms that are common in both MS and hypothyroidism. When MS patients demonstrate these symptoms, thyroid function tests should be performed. The thyroid hormone levels of MS patients being treated with interferon-beta and Campath-1H also should be monitored. The authors report the clinical data of 2 definite MS patients who also fulfilled criteria for Hashimoto thyroiditis.
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PMID:Multiple sclerosis and Hashimoto thyroiditis: two cases. 1614 37

Hypothyroidism is a frequently diagnosed endocrine disorder that has characteristic clinical signs and symptoms. Myopathy is one of the manifestations of hypothyroidism and relatively common. We report a case of Hoffmann's Syndrome due to hypothyroid myopathy documented by clinical features, laboratory findings and positive response to thyroid hormone replacement therapy. A man, age of 22, was diagnosed as having primary hypothyroidism at the age of five, had been describing progressive weakness in his arms and legs for two months and complained about generalized muscle cramps and pain. He was diagnosed with Hoffmann's syndrome with low levels of thyroid hormones and high levels of muscle enzymes. After six months of thyroid hormone replacement therapy, both the clinical picture and laboratory findings were remarkably improved.
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PMID:Early diagnosis and treatment reverse clinical features in Hoffmann's syndrome due to hypothyroid myophaty: a case report. 1648 71

Symptomatic ascites as a presenting symptom of hypothyroidism is quite rare. In most of the case reports, patients with ascites requiring therapeutic abdominal paracentesis have long-standing hypothyroidism. We present a case of symptomatic ascites in a subject with hypothyroidism following radioiodine therapy for Graves disease. A 70-year-old African-American man presented with increasing weakness, shortness of breath, weight gain, constipation, and abdominal distention. Past history was significant for coronary artery disease, diabetes, hypertension and history of radioiodine therapy for Graves disease 9 months prior to the presentation. He was taking levothyroxine at 50 microg per day for 3 months prior to the presentation. Physical examination findings were significant for puffiness around the eyes, decreased breath sounds at the lung bases, and distended abdomen with free fluid, hung-up reflexes, and cold extremities. The thyroid-stimulating hormone level at the time was 64 with a free T4 less than 0.4 ng/dL. Analysis of the ascitic fluid revealed an exudative effusion with a serum to ascitic fluid albumin gradient of 1.2. The patient required therapeutic abdominal paracentesis twice, with 4 L each time, to relieve the symptoms. Work-up to rule out other causes did not reveal any other relevant abnormality. After initiation of thyroid hormone replacement, the patient responded very well and the ascites resolved within 2 months. We conclude that ascites associated with hypothyroidism is rare but must be recognized early, since thyroid replacement is the definitive therapy.
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PMID:Symptomatic ascites in a patient with hypothyroidism of short duration. 1722 Jun 93


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