Cases reported "Goiter"

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1/28. Management of a pregnant patient with airway obstruction secondary to goitre.

    A case of airway obstruction in advanced pregnancy is presented. The patient was successfully managed with an awake fibreoptic intubation performed orally followed by a caesarean section and thyroidectomy as a combined procedure. On resection, a thyroid gland weighing 370 g was removed. The patient made an uneventful recovery.
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ranking = 1
keywords = pregnancy
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2/28. Efficacy of oral iodide therapy on neonatal hyperthyroidism caused by maternal Graves' disease.

    OBJECTIVE: To verify the efficacy of oral iodide therapy in treating a case of early neonatal hyperthyroidism due to maternal Graves' disease. methods: We report a case of neonatal hyperthyroidism which occurred in a 2,650-gram, female baby, born at 39 weeks' gestational age (GA) to a 30-year-old mother affected by Graves' disease and treated with thionamides (propylthiouracil) from the 20th week of gestation. A fetal goiter, due to maternal therapy, had been observed by ultrasound scan at 31 and 35 weeks of gestation, with contemporary low cord thyroid hormone levels. Two intra-amniotic injections of levothyroxine were then performed at 34 and 36 weeks of gestation, which led to a significant reduction of fetal goiter and to normalization of cord thyroid hormone levels. The neonatal clinical course was characterized by symptoms of hyperthyroidism from the 2nd to 3rd days of life (irritability, tachycardia, tachypnea, hyperphagia), mostly during feeding. Oral treatment with potassium iodide (KI, 8 mg x 3 times a day) was started at 23 days of life. RESULTS: Treatment with KI led to a significant reduction of neonatal clinical symptoms and to a normalization of hormone levels within 4 days of therapy. The treatment was discontinued in 13th week of life because of neonatal well-being and normal hormone levels. CONCLUSIONS: We believe that KI therapy is effective in treating neonatal hyperthyroidism and does not cause suppression of neonatal thyroid activity, which is possible using antithyroid drugs like thionamides.
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ranking = 11.2359647041
keywords = gestation
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3/28. Intrauterine treatment of fetal goitrous hypothyroidism controlled by determination of thyroid-stimulating hormone in fetal serum. A case report and review of the literature.

    We report a rare case of fetal goitrous hypothyroidism complicated by polyhydramnios and preterm labor in a mother without thyroid gland pathology. The diagnosis was made in the 26th week by ultrasound and cordocentesis [TSH 170 microU/ml, free T(4) 0.2 ng/dl]. The therapeutic regime required repeated fetal blood sampling for determination of thyroid hormones. Five intra-amniotic administrations of 250 microg levothyroxine (LT4) weekly were initiated. Because of the persisting goiter and the elevated level of TSH (128 microU/ml in 32 weeks) in the fetal serum the dosage had to be adjusted to 500 microg LT4 in the next five injections. TSH in fetal serum declined to 49.2 microU/ml in 36 weeks. Normal fetal growth and an uncomplicated course of pregnancy between the 27th and 37th week of gestation were observed. Monitoring of intrauterine therapy by determination of TSH in fetal serum may provide more reliable data than measuring TSH in amniotic fluid. A review of 15 cases of fetal goitrous hypothyroidism in the English literature is presented.
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ranking = 3.808991176025
keywords = gestation, pregnancy
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4/28. prenatal diagnosis and early in utero management of fetal dyshormonogenetic goiter.

    We present a case of a fetal dyshormonogenetic goiter diagnosed by ultrasound examination at 24 weeks of gestation, in a woman with no past history of thyroid disease or goitrogen treatment and with normal thyroid tests, including absence of auto-antibodies. In this situation, fetal goiter may only be associated with fetal hypothyroidism, therefore cord blood sampling was not performed but early treatment was initiated. amniotic fluid instillation of thyroid hormone led to a rapid decrease in amniotic fluid volume and a clear reduction in thyroid goiter. However, fetal thyroid volume did not totally normalise, and cord blood analysis at birth showed elevated fetal TSH level. As prenatal treatment of fetal hypothyroidism remains controversial in euthyroid mothers, the main objective is to prevent obstetrical complications of large goiters. Therefore, in some selected cases with no maternal history of thyroid disease and normal thyroid function tests, cordocentesis is not necessary to confirm fetal thyroid status or to adjust fetal treatment.
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ranking = 2.808991176025
keywords = gestation
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5/28. Neonatal goiter caused by expectorant usage.

    A female newborn was admitted with the symptoms of mild respiratory distress, protruding tongue, hypotonicity, cutis marmorata, sclerema, myxedema, abdominal distension, and feeding problems on the first day of life. She had a huge neck mass, a large anterior and posterior fontanel, and hoarse cry. She had no umbilical hernia or jaundice. A history of maternal potassium iodine (expectorant) usage without doctor's advice was obtained; the mother had not attended a clinic throughout the pregnancy. On ultrasonographic examination, the thyroid right lobe was 53 x 31 mm and the left lobe was 34 x 31 mm. The results of thyroid hormone tests on the first day were as follows: T3 20 ng/dl (normal: 32-216 ng/dl), T4 0.9 microg/dl (11.8-22.6 microg/dl), TSH 120 mIU/l (2.5-13.3 mIU/l). This patient is presented to emphasize the role of hypothyroidism in drug-induced neonatal goiter and to discuss the possibility of a life-threatening effect of congenital goiter, i.e. respiratory tract obstruction.
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ranking = 1
keywords = pregnancy
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6/28. A remission of goitrous hypothyroidism during pregnancy.

    A 21-yr-old female with a diffuse goiter, hypothyroidism, elevated thyroid autoantibodies, and chronic lymphocytic thyroiditis on needle biopsy, was subsequently nongoitrous and euthyroid with normal antibody titers during pregnancy. Following deliver, the goiter reappeared, autoantibody titers rose and hypothyroidism recurred. Chronic lymphocytic thyroiditis may undergo spontaneous remission during pregnancy.
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ranking = 6
keywords = pregnancy
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7/28. Intrauterine diagnosis and management of congenital goitrous hypothyroidism.

    The intrauterine recognition and treatment of congenital goitrous hypothyroidism may not only reduce the obstetric complications associated with large goiters, but possibly improve the prognosis for normal growth and mental development of affected fetuses. We present a case of fetal goiter diagnosed at 29 weeks of gestation following routine ultrasound examination. fetal blood sampling performed at this time confirmed the presence of fetal hypothyroidism. Treatment was performed using a series of intra-amniotic injections between 31 and 36 weeks, initially with tri-iodothyronine (T3) and subsequently with thyroxine. During this period, shrinkage of the fetal goiter, increasing neck flexion and resolution of the polyhydramnios was observed. Following birth, neonatal serum thyroid-stimulating hormone levels were within the normal range but thyroxine was reduced. The baby was started on daily oral thyroxine and, on examination 7 weeks following birth, he appeared clinically and chemically euthyroid. In the absence of maternal thyroid disease, fetal goiter is extremely rare, with only seven cases previously reported in the English literature to have used intra-amniotic thyroxine injections as a form of treatment. This report reviews the current literature regarding the diagnosis and intrauterine management of fetal goiter and considers the possibility of T3 therapy in future cases of congenital hypothyroidism.
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ranking = 2.808991176025
keywords = gestation
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8/28. Antenatal diagnosis and treatment of a case of fetal goitrous hypothyroidism associated with high-output cardiac failure.

    A case of fetal goitrous hypothyroidism associated with high-output cardiac failure is presented. At 32 weeks of gestation, the antenatal diagnosis of goiter was made based on ultrasound examination, and the fetal thyroid function was examined by amniocentesis and cordocentesis. color and pulsed Doppler examinations demonstrated a high vascular flow pattern in the goiter and marked elevation of the maximum velocity in the common carotid artery at the level of the neck. It was suspected that arteriovenous shunting through the large goiter resulted in high-output cardiac failure with cardiomegaly and pleural effusion. The fetus was treated by injection of levothyroxine sodium into the amniotic fluid at 33 weeks of gestation and the goiter thereafter decreased in size, with subsequent improvement of the high-output cardiac failure. The maximum velocity in the common carotid artery fell rapidly before the shrinkage of the fetal goiter and in parallel with the fetal level of thyroid stimulating hormone.
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ranking = 5.6179823520501
keywords = gestation
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9/28. goiter in a newborn exposed to lithium in utero.

    OBJECTIVE: To report a case of neonatal goiter and biological hypothyroidism in a newborn exposed to lithium in utero resulting from therapy given to the mother before and during her pregnancy. CASE SUMMARY: A male neonate, born at 37 weeks' gestation, presented with a goiter without other signs of hypothyroidism. His serum thyroid-stimulating hormone concentration was high and unbound tetrathyroxine concentration was low, indicating that chronic exposure to lithium was present. Oral thyroxine treatment was initiated when the infant was 3 days old and continued for 11 weeks. Treatment was effective in reducing the goiter and hormone concentrations, and allowing normal growth and psychomotor development during the following 3.5 months. Other drugs taken by the mother during pregnancy are not known to induce thyroid abnormalities. DISCUSSION: lithium is used for prophylaxis and treatment of bipolar disorder. goiter and hypothyroidism in adults have been described in patients treated with lithium; thyroid disorders are reversible if lithium is discontinued. Few cases of goiter and hypothyroidism have been reported in newborns exposed to lithium in utero. In our patient, congenital hypothyroidism required longer thyroxine treatment than lithium-induced thyroid disorders. The delay before improvement seems to be similar to that observed in adults. The Naranjo probability scale indicated that lithium was the probable cause of hypothyroidism resulting from in utero exposure. CONCLUSIONS: lithium is a well-known goitrogenic agent. Thus, if lithium treatment needs to be continued during pregnancy in women with bipolar disorder, adequate screening for morphology by ultrasonography and systematic hormonal biological control in newborns are recommended.
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ranking = 5.808991176025
keywords = gestation, pregnancy
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10/28. Compound heterozygous mutations in the thyroglobulin gene (1143delC and 6725G-->A [R2223H]) resulting in fetal goitrous hypothyroidism.

    In a 22-yr-old healthy woman, a fetal goiter was diagnosed coincidentally by ultrasound during the sixth month of gestation, and hypothyroidism was affirmed by a high TSH (336 mU/liter) concentration after cordocentesis. A second ultrasound examination at 27 wk gestation showed further enlargement of the goiter (34/21 mm). Two intraamniotic injections of 200 microg levothyroxine were performed during the seventh month of pregnancy. Ultrasound studies revealed a fetal goiter size of 30/18 mm during the eighth month of gestation. The woman delivered at term a female infant with an apgar score of 10 at 1 and 5 min. Cord blood analysis indicated elevated TSH (284 mU/liter) and low free T(4) (5.5 pmol/liter) levels. The serum thyroglobulin (Tg) concentration was low (0.8 ng/ml), whereas ultrasound of the neonate indicated an enlarged thyroid gland (32/15/14 mm). During the second pregnancy, ultrasound examination revealed a goiter, and fetal hypothyroidism was also confirmed after umbilical vein blood sampling (TSH, 472 mU/liter). After two intraamniotic injections of 500 microg levothyroxine, the woman delivered a male infant at 37 wk of pregnancy. In cord blood the serum TSH concentration was 39 mU/liter, and the serum Tg level was low (0.7 ng/ml). The parents were nonconsanguineous. After birth of the two affected siblings, genomic dna sequencing identified the presence of compound heterozygous mutations of the Tg gene: the paternal mutation consists of a cytosine deletion at nucleotide 1143 in exon 9 (1143delC), resulting in a frameshift that generates a stop codon at position 382, and the maternal mutation is a guanine to adenine substitution at position 6725 in exon 38, creating the R2223H missense mutation in the acetylcholinesterase homology domain of Tg. In conclusion, we report two siblings with congenital goiter and hypothyroidism caused by compound heterozygous mutations of the Tg gene.
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ranking = 11.426973528075
keywords = gestation, pregnancy
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