Cases reported "Hypothyroidism"

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11/77. 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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12/77. Intra-uterine treatment of a hypothyroid fetus.

    A woman in her 24th week of gestation was referred for treatment of hypothyroidism, after she underwent radioablation of the thyroid during the 13th week of gestation. Because of the high risk of hypothyroidism in the fetus, prenatal administration of intramuscular T-4 to the fetus was begun at 32 weeks. The last dose of T-4 was given 2 weeks before delivery; cord blood levels of T-4 and T-3 were undetectable and the TSH concentration was markedly elevated. The case illustrates several important physiological concepts regarding thyroid hormone and TSH metabolism in the fetal-placental unit, including the minimal placental permeability to iodothyronines and TSH, independent function (including feedback control) of the fetal hypothalamic-pituitary-thyroid axis, and the TSH response at parturition. In addition we suggest that administration of T-4 to the hypothyroid fetus in utero is an acceptable modality of treatment and may help to minimize irreversible mental retardation in known high risk infants. However, further studies are necessary to assess the effectiveness and safety of this approach.
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keywords = gestation
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13/77. Maternal isodisomy for chromosome 2p causing severe congenital hypothyroidism.

    Severe congenital hypothyroidism (CH) due to a total iodide organification defect (TIOD) is usually due to mutations in the thyroid peroxidase (TPO) gene located at chromosome 2p25. A homozygous deletion [DeltaT2512 (codon 808)] in exon 14 was identified in a patient with classical TIOD. The transmission pattern of the TPO gene in this family was anomalous; the mother was heterozygous for the deletion; and the mutation was absent in the father. Polymorphic short tandem repeat (STR) markers confirmed paternity and demonstrated on chromosome 2 that the propositus was homozygous for most markers on chromosome 2p and that these were identical to one of the maternal 2p homologs. A normal karyotype was found in the propositus, his parents and sister. We conclude that the homozygosity in the patient is due to partial maternal isodisomy of the short arm of chromosome 2, carrying a defective TPO gene. The patient, born small for gestational age, develops and grows well and appears healthy (while being treated with thyroxine) and has a normal phenotype except for a unilateral preauricular skin tag. This shows that partial maternal isodisomy for chromosome 2p (2pter - 2p12) is compatible with a minimal influence on normal development.
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14/77. Short-term hyperthyroidism followed by transient pituitary hypothyroidism in a very low birth weight infant born to a mother with uncontrolled Graves' disease.

    Transient hypothyroxinemia in infants born to mothers with poorly controlled Graves' disease was first reported in 1988. We report that short-term hyperthyroidism followed by hypothyroidism with low basal thyroid-stimulating hormone (TSH) levels developed in a very low birth weight infant born at 27 weeks of gestation to a noncompliant mother with thyrotoxicosis attributable to Graves' disease. We performed serial thyrotropin-releasing hormone (TRH) tests in this infant and demonstrated that TSH unresponsiveness to TRH disappeared at 6.5 months of age. The maternal thyroid function was free triiodothyronine (FT(3)), 21.1 pg/mL; free thyroxine (FT(4)), 8.1 ng/dL; TSH, <0.03 microU/mL; thyroid-stimulating hormone receptor antibody, 52% (normal: <15%); thyroid-stimulating antibody, 294% (normal: <180%); and thyroid-stimulation blocking antibody, 9% (normal: <25%) on the day of delivery. A nonstress test revealed fetal tachycardia >200 beats per minute, and a male infant weighing 1152 g was born by emergency cesarean section. Thyroid-stimulating hormone receptor antibody was 16% and thyroid-stimulating antibody was 370% in the cord blood. We administered 10 mg/kg per day of oral propylthiouracil from day 1. tachycardia along with elevated FT(4) and FT(3) levels in the infant decreased from 200/minute to 170/minute, 4.7 ng/dL to 2.9 ng/dL, 7.0 pg/mL to 4.8 pg/mL, respectively, in the first 33 hours. At 5 days, FT(4) and FT(3) were 1.1 ng/dL and 2.9 pg/mL, respectively, and we stopped propylthiouracil administration. Although FT(4) decreased to 0.4 ng/dL, TSH was quite low and did not respond to intravenous TRH by 14 days of age. We began daily levothyroxine 5-micro/kg supplementation. The responsiveness of TSH to TRH did not become significant until 4 months old and normalized at 6.5 months old. At this time, levothyroxine was stopped. We conclude that placental transfer of thyroid hormones may cause hyperthyroidism in the fetal and early neonatal periods and lead to transient pituitary hypothyroidism in an infant born to a mother with uncontrolled Graves' disease.
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15/77. Changing thyroid status related to pregnancy.

    A case of post-thyroidectomy hypothyroidism is reported. The patient became euthyroid in three consecutive pregnancies, reverting to hypothyroid within three months of delivery on each occasion. The alteration in thyroid status is attributed to pregnancy related changes in antibody titres, though the laboratory data to confirm this are not available.
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keywords = pregnancy
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16/77. Neonatal hyperthyroidism following intrauterine hypothyroidism.

    An infant, whose mother was treated for thyrotoxicosis during pregnancy, appeared normal at birth, but laboratory data were indicative of hypothyroidism. On the sixth day of life the infant had clinical and laboratory evidence of hyperthyroidism. A plan of management is proposed for infants born to thyrotoxic mothers.
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17/77. Anovulatory infertility: a report of four cases and literature review.

    Four cases of anovulatory/dysovulatory infertility encountered in Ilorin, nigeria are presented and the literature extensively reviewed on the up-to-date management of this aspect of infertility. All the patients had bilateral tubal patency on hysterosalpingography (HSG) and their husbands had normal seminal fluid analysis. The first case, 30 years of age, had hyperprolactinaemia with galactorrhoea, treated with bromocriptine given 2.5 mg twice daily. Another case, aged 27 years, had polycystic ovarian syndrome with hyperprolactinaemia but no galactorrhea This was treated with clomiphene citrate 100 mg daily. The third case, 34 years old, had hypothyroidism with hyperprolactinaemia and galactorrhea and was treated with thyroxine. The last case, aged 32 years, had hyperprolactinaemia and was treated with bromocriptine and clomiphene citrate. None of the patients had demonstrable pituitary adenoma. After the appropriate treatment, ovulatory menses were restored in all the patients; two have been pregnant, while the other two have not yet achieved pregnancy but have having regular ovulatory menses. All the patients are Nigerians.
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keywords = pregnancy
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18/77. 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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keywords = pregnancy
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19/77. 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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keywords = gestation
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20/77. 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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