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Biomedical subjects

N Momotani

Publications and source records attributed to N Momotani.

At least 37 records · Page 2Linked to original sources
PubMed1994

Relationship between silent thyroiditis and recurrent Graves' disease in the postpartum period.

We carried out a close follow-up study of 96 episodes of postpartum hyperthyroidism, which developed in women with a history of Graves' disease. Hyperthyroidism had developed 1-6 months (mean +/- SD, 2.3 +/- 1.4) after delivery. Radioiodine uptake (RAIU) values during the thyrotoxic phase, determined after a 1-week restriction of iodine-rich diet, ranged from very low to very high (1-70%). The group with low RAIU values (group L: < 10%, n = 26) and the normal group (group N: 10-40%, n = 33) showed significantly higher urinary excretion of iodine (UI) than the high group (group H: > 40%, n = 37), and UI in group L was comparable to that in patients with silent thyroiditis. TSH binding inhibiting antibody (TBIAb) values were determined in 87 patients at the RAIU testing, and were above normal in most of them: all in group H, 68% in group N, and 52% in group L. The mean TBIAb value in group H was significantly higher than that in group N or L (P < 0.0001 for both). Fifty-one patients in group L and group N were observed without treatment. Of these, hyperthyroidism resolved spontaneously in 39 patients (76%), in whom transient hypothyroidism developed with substantial frequency. Hyperthyroidism subsequently resumed in 18 (46%) of these 39 between 4 and 9 months (mean +/- SD, 7.1 +/- 2.1) after delivery and did not resume in the other 21. RAIU values, determined again during this later phase of hyperthyroidism, were high enough to indicate Graves' hyperthyroidism in all but one patient. During the postpartum period, TBIAb values increased and then declined in the majority of the patients irrespective of the course of hyperthyroidism. Of the 21 patients who maintained euthyroidism after spontaneous resolution of hyperthyroidism, transient increase in TBIAb was observed in 14. These findings suggest that silent thyroiditis commonly develops concomitantly with the activation of Graves' disease and delays or masks the development of Graves' hyperthyroidism.

Autoantibodies↗
PubMed1993

[Cases of Graves' disease with falsely high TSH values due to interfering substances which cross-link with mouse monoclonal antibodies in the TSH assay kits].

It has been reported that highly sensitive two-site immunometric assays occasionally indicate falsely high serum TSH values. A possible reason for this is that heterophilic antibodies interfere with these assays. Recently we had a patient in whom the Delfia TSH kit falsely indicated an elevated serum TSH value. A 29-year-old female was diagnosed as having Graves' disease and was referred to Ito Hospital for surgical treatment. Her thyroid hormone values were distinctly high two months before admission (FT3: 20.7pmol/L, FT4: 42.3pmol/L), but her serum TSH level was normal (1.1mU/l). She was clinically hyperthyroid, and T3 and T4 values determined after ethanol extraction and T3 or T4 analog binding rates did not indicate the presence of T3 or T4 antibodies. Her TSH value became undetectable when mouse IgG was added to the assay. These results suggested that the "normal" serum TSH value was caused by interfering substances such as anti-mouse IgG antibodies which had cross-linked with mouse monoclonal antibodies in the Delfia TSH kit. Another 12 patients who were suspected of having the interfering substances were examined because of the discordance between TSH values and thyroid hormone values. All of the serum TSH values measured using the DELFIA TSH kit decreased when mouse IgG was added. In another case, the presence of serum TSH could not be detected using the Delfia TSH kit but could be measured using the RIABEAD II TSH kit.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1993

[A case of subacute thyroiditis with highly positive thyrotropin receptor antibodies and normal radioiodine uptake].

In this paper, we report on a 40-year-old female with subacute thyroiditis (SAT) who showed high levels of TSH-binding inhibitory immunoglobulins (TBII) and thyroid-stimulation blocking antibodies (TSBAb) from the early stage of the disease. Thyrotoxicosis continued for 2 months and it was subsequently followed by severe hypothyroidism. Levothyroxine was then started. At that time, both TBII and TSBAb were still positive, but they disappeared 6 months later and she remained euthyroid thereafter without treatment. When she was in a thyrotoxic phase and had a suppressed TSH level, her 24-hour radioiodine uptake was not suppressed (11%), and thyroid scan showed partial suppression of uptake in the right lobe. These observations indicate that the presence of TSH receptor antibodies (TRAb) may have modified the changes in thyroid state and the course of SAT.

Adult↗
PubMed1992

Deceptively high thyroid hormone levels in a neonate due to autoantibodies against thyroid hormones transferred from a mother with Graves' disease.

At birth, a clinically euthyroid male neonate was found to have unexpectedly high levels of free T3 and T4 concurrent with a high TSH level. The mother was treated with propylthiouracil for Graves' disease during and after pregnancy. The neonate also had an extremely high titer of TSH receptor antibodies. He soon became clinically thyrotoxic as TSH levels were suppressed and thyroid hormone levels rose. After instituting antithyroid therapy, TSH levels became elevated again, while thyroid hormone levels decreased but were still above normal. Around 3 months after birth, both TSH receptor antibodies and discordance, between the levels of thyroid hormones and TSH, disappeared. Because of high maternal TSH levels in conjunction with an elevated free T3 level at 7 months postpartum, we suspected the presence of autoantibodies against thyroid hormones (AAb). Maternal and infant blood samples were then examined retrospectively for AAb and were detected in all the samples except those of the infant taken more than 3 months after birth. The authors, therefore, suggest that physicians be aware of the presence of AAb in pregnant women with Graves' disease, in order to avoid inappropriate treatment which could lead to fetal and neonatal hypothyroidism.

Autoantibodies↗
PubMed1992

Effects of iodine on thyroid status of fetus versus mother in treatment of Graves' disease complicated by pregnancy.

To investigate the effect of maternal iodine therapy for Graves' disease on fetal thyroid, we examined serum free T4 (FT4) and TSH levels in the fetus vs. those in the mother. Patients who were severely thyrotoxic were not included. Cord and maternal sera were tested at delivery in 35 patients with Graves' disease treated with iodine alone during pregnancy (6-40 mg daily). At the initiation of therapy, the mothers were at 11-37 weeks gestation, and FT4 levels ranged from 28.3-65.8 pmol/L. At delivery, maternal FT4 values ranged from 9.3-42.0 pmol/L, slightly above normal in 22 of the 35 mothers and normal in the other 13. Fetal FT4 levels were above the normal range occurred significantly less often than maternal levels (2 in 35; P less than 0.001), and no fetus had FT4 below normal. In the 13 mothers with normal FT4 levels, all fetal FT4 levels were normal; the fetal TSH level was above normal in 1 and normal in the remainder. A significant correlation was found between cord and maternal FT4 levels (P less than 0.05). In 12 of the 35 mothers, FT4 levels rose after a transient fall during iodine administration. The correlation of cord FT4 and maternal FT4 was closer when these 12 cases were excluded (P less than 0.001). Neither the dose of iodine nor the duration of therapy correlated with thyroid function in fetuses or mothers. Fetal TSH binding inhibitory antibody values strongly correlated with maternal TSH binding inhibitory antibody values (P less than 0.001). These findings indicate that 1) in the treatment of hyperthyroidism due to Graves' disease, iodine seldom if ever exposes the fetus to the risk of hypothyroidism; 2) the fetal thyroid is influenced by the same stimulatory and inhibitory factors as the maternal thyroid; and 3) escape from the inhibitory effects of iodine occurs less often in fetuses than in mothers, which may account at least in part for the lower thyroid status in the fetus compared to that in the mother.

Adult↗
PubMed1991

A case of Graves' disease with false hyperthyrotropinemia who developed silent thyroiditis.

We encountered a patient who developed silent thyroiditis during the course of Graves' disease. The diagnosis of silent thyroiditis was made on the basis of a low thyroidal 131I uptake, no response to the thyrotropin releasing hormone (TRH) test, and subsequent hypothyroidism despite the presence of high titers of thyrotropin (TSH) receptor antibody (TRAb) and thyroid stimulating antibody (TSAb). The patient, in addition, had a discrepancy between serum TSH and thyroid hormone values. This was due to the presence of interfering substances that react to mouse IgG in the sera since serum TSH levels were decreased in a dose dependent manner by the addition of increasing amounts of mouse IgG to the sera. It should therefore be noted that silent thyroiditis can develop in patients with Graves' disease. Furthermore, clinicians should be aware that two-site immunoassay kits that use mouse monoclonal antibodies are subject to interference by some substances, possibly antibodies which react to mouse IgG.

Adult↗
PubMed1989

Recovery from foetal hypothyroidism: evidence for the safety of breast-feeding while taking propylthiouracil.

We assessed the post-natal thyroid function in eight infants of mothers with Graves' disease whose thyroid function at birth was suppressed by maternal ingestion of propylthiouracil during pregnancy. These mothers continued taking propylthiouracil after delivery and breast-fed exclusively (two mothers supplemented their breast milk with a small amount of baby food). The cord free T4 level was slightly but uniformly below the normal range in all eight infants, and the cord TSH level was above the normal in seven infants. The dose of propylthiouracil after delivery ranged from 50 to 300 mg daily, which was equal to, or higher than, that before delivery. All these abnormal values normalized in the infant after birth. Serum samples, from seven of the eight mothers, taken at delivery were examined for TSH receptor antibodies; all were positive. The antibody titre, however, was too low, and/or free T4 and TSH levels were examined too long after delivery, for the antibodies to be the cause of the restoration of the infants' thyroid function. These results assure the safety of breast-feeding for the infants of mothers with Graves' disease taking propylthiouracil.

Adult↗
PubMed1989

Evidence against the importance in the disease process of antibodies to bovine thyroid-stimulating hormone found in some patients with Graves' disease.

The antibody to TSH (TSH-Ab) found in some patients with Graves' disease may be either an antiidiotype (anti-id-Ab) to the TSH receptor antibody (TRAb) or the antigen (idiotype) for which the anti-id-Ab is in fact TRAb. Four groups have found antibodies to bovine TSH (bTSH-Ab) in Graves' disease patients in a TSH binding-inhibiting immunoglobulin (TBII) RRA that uses [125I]bTSH. In this assay serum samples containing bTSH-Ab give highly negative TBII values. The purpose of this study was to look for any clinical significance of potential idiotypic-antiidiotypic network regulation related to bTSH-Ab. Twenty-one (0.49%) of 4285 Graves' disease patients had TBII values less than the mean -4 SD of normal subjects. In all 21, bTSH-Ab was found by incubation of [125I]bTSH with the patient's serum, and significant inhibition of binding of bTSH-Ab to bTSH by human TSH was found in only 3 of these serum samples. We investigated next whether the binding site of the anti-TSH-Ab mimicked the TSH receptor-binding site. Binding of [125I]bTSH to bTSH-Ab-positive serum was not inhibited by bTSH-Ab-negative, thyroid-stimulating immunoglobulin-positive [(+)], and/or TBII(+) immunoglobulin G. In one patient with human TSH-Ab, TSH-Ab appeared and disappeared, and when TSH-Ab was negative, TBII was positive. Inhibition of [125I]bTSH binding to TSH-Ab by the same patient's serum when that patient was serum thyroid-stimulating immunoglobulin(+), TBII(+), and TSH-Ab-negative was sought but not found. Changes in serum TSH-Ab activity and disease activity were not correlated in this patient. In six untreated patients with Graves' hyperthyroidism with bTSH-Ab, the serum T3 and T4 concentrations and the time required to become euthyroid during antithyroid drug treatment were not significantly different from those in 52 such patients without bTSH-Ab. These data suggest that bTSH-Ab is not an anti-id-Ab to TRAb and that TSH-Ab does not directly modulate the activity of Graves' disease.

Animals↗
PubMed1989

[Ga-67 scintigram in evaluation of malignant lymphoma of the thyroid originating from chronic thyroiditis].

At the Itoh Hospital, 27 patients with primary malignant lymphoma of the thyroid gland have been diagnosed from April 1985 to April 1988. Within the 27 patients, 8 patients were treated with a diagnosis of chronic thyroiditis during 1 year to 7 years at Itoh Hospital. Ga-67 scintigraphy was performed in the 8 patients as suspected malignant lymphoma. Of the 8 patients, 6 were very strong positive, 1 was strong positive and 1 was weak positive. All patients with Ga-67 strong positive scans should have a biopsy and the scans are helpful to direct the biopsy. Ga-67 scintigraphy is useful in the diagnosis of malignant lymphoma of the thyroid gland.

Aged↗
PubMed1987

Retrospective reevaluation of the significance of thyroid microsomal antibody in the treatment of Graves' disease.

The results of treatment were analyzed in relation to serum microsomal antibody (MCAb) titre before treatment in 1185 patients with Graves' disease. The percentage of patients who had ablative therapy because of poor response to antithyroid drug treatment was significantly greater in those with MCAb haemagglutination test (MCHA) titres greater than 1:25,000. With 131I treatment, the patients with MCHA titres greater than 1:6400 responded significantly less to therapy, although the analysis was done in 146 selected patients with certain defined radiation doses and small goitres. With surgical treatment, the percentage of the patients entering into remission was significantly smaller for patients with MCHA titres greater than 1:25,000, because of an increase in both hypothyroidism and relapses. The incidence of hypothyroidism was significantly higher in patients with marked lymphocyte infiltration and/or lymphoid follicles. The degree of these histological findings in Graves' disease was not marked in spite of high MCAb titre and it was significantly different from that in Hashimoto's disease when analyzed in relation to the MCHA titre. These data indicate that in Graves' patients with high MCAb titre, remission is difficult to obtain by treatment, and suggest that the significance of MCAb is different in Graves' disease and Hashimoto's disease. The titre in Graves' disease may be one expression of the activity of this disease.

Adolescent↗
PubMed1986

Antithyroid drug therapy for Graves' disease during pregnancy. Optimal regimen for fetal thyroid status.

We compared fetal and maternal serum indexes of thyroid status at delivery in 70 patients with Graves' disease who required therapy with thionamides (such as propylthiouracil) during pregnancy. Forty-three mothers required thionamides until delivery (Group 1), whereas the drugs were discontinued during pregnancy after remission in 27 mothers (Group 2). Maternal free thyroxine levels were closely correlated with cord levels in both groups, being essentially identical in Group 2 but slightly lower in fetuses than in mothers in Group 1. Normal maternal free thyroxine levels did not preclude fetal hypothyroidism. The mothers and fetuses in Group 1 had a significantly higher incidence of antibodies that inhibit thyrotropin binding than did those of Group 2. However, a significant correlation between maternal levels of these antibodies and cord levels of free thyroxine or triiodothyronine was found only in Group 2, in which some maternal and cord thyroxine levels were in the thyrotoxic range at delivery, presumably because therapy was discontinued. These findings indicate that high free thyroxine levels and the presence of antibodies that inhibit binding of thyrotropin are useful indexes of the fetal need for antithyroid treatment, and that the thionamide dosage that maintains maternal free thyroxine levels in a mildly thyrotoxic range seems appropriate for maintaining euthyroid status in the fetus.

Antibodies↗
PubMed1986

Factors predicting the course of diabetes mellitus in hyperthyroid patients.

The relationship between changes in glucose tolerance with treatment of hyperthyroidism and various factors that might be relevant to carbohydrate metabolism were investigated in 64 hyperthyroid patients with abnormal glucose tolerance, including 35 cases with fasting plasma glucose (FPG) levels of 140 mg/dl or more. All patients had diffuse toxic goiter. After correction of the hyperthyroidism, glucose intolerance improved in almost all cases, even in cases with fasting hyperglycemia, but diabetes mellitus in patients with FPG above 140 mg/dl and/or delta IRI/delta PG X 30' during a 50-g oral glucose tolerance test below 0.10, persisted. Patients who showed diabetic glucose tolerance even after remission from thyroid dysfunction had significantly lower delta IRI/delta PG X 30' values and a higher incidence of family histories of diabetes mellitus than those not showing diabetic glucose tolerance. There were no significant differences in serum T3 and T4 levels between these two groups of patients. The findings suggest that predisposition to diabetes may be an important factor in persistent glucose intolerance in the hyperthyroidism of Graves' disease. The FPG and delta IRI/delta PG X 30' values may be useful in predicting which patients with hyperthyroidism will have permanent diabetes.

Adolescent↗
PubMed1985

Blocking type antithyrotropin receptor antibody in patients with nongoitrous hypothyroidism: its incidence and characteristics of action.

The incidence, characteristics of action, and pathogenetic importance of blocking type anti-TSH receptor antibody were examined in patients with autoimmune thyroiditis. Serum immunoglobulin G (IgG) from 8 of 20 patients with nongoitrous hypothyroidism contained substantial amounts of TSH binding inhibitor immunoglobulin (TBII) activity. Newborn infants of a patient with the greatest TBII activity had neonatal transient hypothyroidism. In sera of patients with goitrous hypothyroidism and euthryoid chronic thyroiditis, only weakly positive or negative TBII activity was found. IgGs of these patients and those of nongoitrous hypothyroid patients without strongly positive TBII activity did not inhibit TSH stimulation of thyroid adenylate cyclase activity. Seven of 8 IgGs which had strongly positive TBII activity significantly inhibited cAMP generation induced by 9.1 mU/ml TSH, and the eighth IgG inhibited stimulation with 0.5 mU/ml TSH. Although the modes of TSH binding inhibition were variable, markedly close correlation was found between TSH binding- and TSH stimulation-inhibiting activities of these 8 IgGs (r = 0.90; P less than 0.01). These IgGs may exert their inhibitory effects on adenylate cyclase activity by inhibiting TSH binding to its receptor.

Adenylyl Cyclases↗
PubMed1984

[An improved method for plasma methimazole assay and its clinical application].

An improved method for plasma methimazole assay using high performance liquid chromatography is described. The plasma samples were treated with sodium bisulfite and ammonium sulfate prior to extraction with chloroform. This pretreatment of the samples raised the extraction coefficient to 90%, while simple extraction yielded only 55%. The minimal detection limit was 0.02 microgram/ml, and the coefficient of variation at the level of 0.2 and 1.0 microgram/ml was less than 5%. Pharmacokinetics of methimazole was studied after a single oral dose (20 mg/m2) in six subjects including two healthy adults and four thyrotoxic children. Plasma levels of methimazole showed a peak concentration of 1.03 +/- 0.25 microgram/ml approximately one hour after the drug administration. Plasma half-life, area under the curve and distribution volume were 4.56 +/- 0.71 hr, 7.05 +/- 0.95 microgram/ml X hr, and 630 +/- 110 ml/kg respectively.

Adolescent↗
PubMed1984

Maternal hyperthyroidism and congenital malformation in the offspring.

Six hundred and forty-three neonates from mothers with Graves' disease were examined for major malformations of external organs to compare the influence of maternal hyperthyroidism vs. ingestion of methimazole (MMI) during the first trimester on the incidence of congenital malformations. The subjects were divided into four groups according to maternal therapy and thyroid status during the first trimester as follows: (1) infants whose mothers did not receive MMI and were hyperthyroid (Group 1), (2) infants whose mothers did not receive MMI and were euthyroid (Group 2), (3) infants whose mothers received MMI and were hyperthyroid (Group 3) and (4) infants whose mothers received MMI and were euthyroid (Group 4). The prevalence of malformed infants in these four groups was 6.0% (three of 50), 0.3% (one of 350), 1.7% (two of 117) and 0.0% (none of 126), respectively. The incidence in Group 1 was significantly higher than that in Group 2 (P less than 0.01). There was no discernible dose dependency of MMI on the occurrence of malformations. These findings suggest that maternal uncontrolled hyperthyroidism may cause congenital malformations and that the beneficial role of MMI treatment outweighs its teratogenic effect, if any.

Abnormalities, Drug-Induced↗
PubMed1983

Sequential serum measurements of thyrotropin binding inhibitor immunoglobulin G in transient familial neonatal hypothyroidism.

Infants with transient neonatal hypothyroidism, in whom TSH binding inhibitor immunoglobulin G (IgG) (TBII) were sequentially measured, are described. Their mother had been taking thyroid replacement for hypothyroidism due to nongoitrous autoimmune thyroiditis. IgGs inhibiting TSH binding were detected in maternal sera by radioreceptor assay. These IgGs also inhibited the adenylate cyclase response to TSH in human thyroid membranes. Three infants had frank hypothyroidism immediately after birth, and TBII were detected in two of them. In the two surviving infants, hypothyroidism was transient and improved when TBII disappeared from their sera. The profile of TBII in one patient corresponded to the IgG disappearance curve. These findings suggest that the transient neonatal hypothyroidism reported was caused by transplacental transfer of TBII.

Adenylyl Cyclase Inhibitors↗