Cases reported "Hypothyroidism"

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1/282. Development of primary hypothyroidism with the appearance of blocking-type antibody to thyrotropin receptor in Graves' disease in late pregnancy.

    Spontaneous remission of Graves' disease with a decrease of thyroid stimulating antibody (TSAb) activity is commonly observed in pregnancy. In this article, however, a Graves' patient who developed primary hypothyroidism with an appearance of thyroid stimulation-blocking antibody (TSBAb) activity in late pregnancy is reported. A 25-year-old woman presented with clinical and biochemical hyperthyroidism with an elevation of 99mTcO4- thyroid uptake (4.7%; normal range, 0.7%-3.0%) and mildly elevated activity of thyrotropin-binding inhibitory immunoglobulin (TBII; 30.4%). She was euthyroid with normal TBII (8.0%) and TSAb (126%) before pregnancy, when the patient was taking a 5-mg daily dose of methimazole (MMI). MMI was stopped by the patient when she became pregnant. Subsequently, the patient progressed into primary hypothyroidism with a marked elevation of TBII activity (78.4%) in the third trimester of the pregnancy (at that time, TSAb activity was not detected). TSBAb measured 2 weeks later was detected at the activity of 85.0%. Replacement therapy was initiated with levothyroxine (LT4) (0.05-0.1 mg/day), which was discontinued on the 55th day postpartum because of the onset of mild thyrotoxicosis followed by short-term euthyroid state despite high TSBAb activity. Subsequently, because the patient developed primary hypothyroidism 5 months after delivery, replacement therapy with LT4 (0.1-0.125 mg/day) was readministered. Thus, it is suggested that the development of hypothyroidism with the appearance of TSBAb in Graves' patients can occur even in late pregnancy.
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2/282. Dermal mucinosis and musculoskeletal symptoms simulating polymyositis as a presenting sign of hypothyroidism.

    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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3/282. A case of congenital hypopituitarism: difficulty in the diagnosis of ACTH deficiency due to high serum cortisol levels from a hypothyroid state.

    A three-month-old boy presented congenital hypopituitarism in which the hypothyroid state masked ACTH deficiency. Multiple anterior pituitary hormone deficiencies, including ACTH, were finally confirmed. High basal serum cortisol levels (up to 45.1 microg/dl) were observed during a stressful episode before L-thyroxine replacement therapy was started. Decreased morning serum cortisol levels (5.0 microg/dl or below) were observed on the sixth day of L-thyroxine replacement therapy despite mild hypoglycemia (lowest serum glucose level of 50 mg/dl). ACTH deficiency was then confirmed by insulin-induced hypoglycemia test (peak serum cortisol level of 4.9 microg/dl). The present findings showed that serum cortisol levels can be high during a stressful episode in an infant with ACTH deficiency and a coexisting hypothyroid state. Thus, the diagnostic evaluation of adrenal function soon after L-thyroxine replacement therapy is important in order to verify a possible subclinical ACTH deficiency, even in the presence of high serum cortisol levels before L-thyroxine replacement therapy.
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4/282. Primary hypothyroidism-associated TSH-secreting pituitary adenoma/hyperplasia presenting as a bleeding nasal mass and extremely elevated TSH level.

    A 41-year-old male with primary hypothyroidism and a huge TSH-secreting pituitary tumor presented with a bleeding nasal mass that was initially misdiagnosed as a paraganglioma. Other unique features of the case include lack of complaints related to hypothyroidism, an extremely elevated TSH level of 3474 mU/l, and a low prolactin level. The presence of primary hypothyroidism made differentiating TSH-secreting pituitary adenoma from secondary thyrotroph hyperplasia difficult. A low molar ratio of alpha-subunit to TSH on presentation, together with normalization of TSH level and a 50% reduction in the size of the tumor after 6 weeks of thyroxine replacement therapy, suggested the presence of thyrotroph hyperplasia. However, the lack of further decrease in the size of the tumor that was associated with increased metabolic activity on 18-FDG PET scan, intense uptake on octreotide scan, and an elevated alpha-subunit to TSH molar ratio despite the normalization of free T4 and TSH levels for 16 months suggested the coexistence of thyrotroph adenoma. Together, the findings support the view that thyrotroph adenoma/irreversible hyperplasia can result from long standing primary hypothyroidism.
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5/282. Increased sensitivity to thyroid hormone replacement therapy followed by hyponatremia and eosinophilia in a patient with long-standing young-onset primary hypothyroidism.

    We describe a 51-year-old woman with long-standing young-onset primary hypothyroidism. serum cortisol, adrenocorticotropin, and arginine vasopressin levels were normal, but urinary excretion of 17-hydroxycorticosteroid was decreased. Administration of a very small initial dose of thyroid hormone induced severe acute complications including fever, palpitation, and sweating associated with a rapid decrease in serum thyrotropin level, a dramatic increase in serum alkaline-phosphatase level, and a decrease in serum total cholesterol level. A week later, the late complications of nausea, severe hyponatremia, and eosinophilia occurred. serum cortisol level decreased slightly but remained within normal limits during this hyponatremic period. This rare case suggests that increased sensitivity to thyroid hormone can occur in long-standing primary hypothyroidism with biphasic clinical course of acute thyrotoxic complications followed by severe hyponatremia resembling hypoadrenocorticism.
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keywords = replacement therapy, replacement
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6/282. Outcome of a baby born from a mother with acquired juvenile hypothyroidism having undetectable thyroid hormone concentrations.

    We report a baby born from a mother with strongly positive thyroid stimulation blocking antibody (TSBAB) and nearly undetectable T4 level. This case is a unique model of nearly complete absence of thyroid hormones during fetal and early neonatal life in humans. The infant girl was born by cesarean section, because of fetal bradycardia, after 41 weeks gestation and received mechanical ventilation for 3 days. The TSH level was more than 120 microU/mL in the neonatal thyroid screening. At age 17 days, the results of a thyroid function study showed undetectable free T3 and free T4 concentrations, TSH 550 microU/mL, and TSH receptor antibody (TRAB) 87%. thyroxine at a dose of 30 microg/day was started at age 17 days. The patient required thyroxine treatment until age 8 months. The brain magnetic resonance image at age 2 months revealed reduced brain size. Her auditory brain stem response was absent at age 2 months. The audiogram at age 4 yr revealed sensorineural deafness of 70 dB. When she was 6 yr of age, motor development remained the same as that at age 4 months. Her height was 106 cm (- 1.5 SD). The results of thyroid function study of the mother 23 days after delivery showed undetectable free T3 and free T4, TRAB 84%, and TSBAB 83%. In conclusion, the outcome of severe thyroid hormone deficiency in utero and early in human neonatal life was normal physical growth, fetal distress resulting in cesarean section, difficulty in the onset of breathing, permanent deficit in auditory function, brain atrophy, and severely impaired neuromotor development despite the start of an adequate dose of thyroxine replacement during the neonatal period.
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keywords = replacement
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7/282. Raynaud's phenomenon in hypothyroidism.

    Two patients with Raynaud's phenomenon were found to be hypothyroid and their symptoms disappeared with thyroid replacement therapy. Vascular reactivity studies in one patient demonstrated decreased vasomotor tone after therapy. Raynaud's phenomenon may be an expression of altered autonomic function in hypothyroidism.
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8/282. Successful outcome of pregnancy in a thyroidectomized-parathyroidectomized young woman affected by severe hypothyroidism.

    Severe hypothyroidism was discovered in a young woman in her 29th week of pregnancy. Previously, at the age of 12 years, she had undergone thyroid surgery for Graves' disease that resulted in persistent hypothyroidism and hypoparathyroidism. After surgical excision, the patient started levothyroxine replacement therapy and had regular control of thyroid function with normal findings throughout the years. The dose of levothyroxine had not been adjusted when the pregnancy started, and at the 29th week of gestation the patient had a thyrotropin (TSH) of 72.4 microU/mL. Ultrasound studies were performed in order to monitor fetal development. The fetal parameters analyzed before the adjustment of levothyroxine therapy showed growth retardation of various degrees. All analyzed fetal parameters (biparietal diameter, cranial and abdominal circumference, humerus and femur length) improved during the last 6 weeks of gestation, showing a good correlation with the newly achieved euthyroid state of the mother. The infant was clinically euthyroid at birth and was found normal at all evaluations of the neonatal hypothyroidism screening program (1, 5, 30 days).
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keywords = replacement therapy, replacement
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9/282. Pituitary hyperplasia resulting from primary hypothyroidism mimicking macroadenomas.

    Three patients presented with clinical and imaging features suggestive of a primary functional pituitary adenoma. Surprisingly, thyroid function testing revealed co-existing primary hypothyroidism. The pituitary tumours represented hyperplasia of anterior pituitary thyrotrophs secondary to hypothyroidism. Complete regression was achieved with thyroxine replacement therapy. Careful attention should be paid to differentiating this condition from prolactinoma or the rare TSH producing adenoma.
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keywords = replacement therapy, replacement
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10/282. hypothyroidism in primary hyperoxaluria type 1.

    We describe 4 patients, aged 3 months to 23 years, with end-stage renal disease and severe, symptomatic hypothyroidism. All 4 had primary hyperoxaluria type 1 (PH1) with diffuse tissue (kidneys, skeleton, eyes, heart) calcium-oxalate deposition, a condition known as oxalosis. The hypothyroidism responded to thyroid hormone replacement therapy. Clinical hypothyroidism within the framework of PH1/oxalosis was probably caused by thyroid tissue damage from an abundance of calcium oxalate. We recommend that thyroid function be monitored in patients with PH1 and oxalosis.
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