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Biomedical subjects

C Shigemasa

Publications and source records attributed to C Shigemasa.

13 recordsLinked to original sources
PubMed1992

Evaluation of thyroid function in patients with isolated adrenocorticotropin deficiency.

Thyroid hormone and thyrotropin (TSH) levels were evaluated before and after adrenal replacement in eight patients (six men and two women, 35-62 years old) with isolated adrenocorticotropin (ACTH) deficiency. Six patients (cases 1-6) showed TSH excess before treatment. Four patients (cases 1-4), who initially had subnormal thyroid hormone levels, showed resolution of biochemical features of primary hypothyroidism after treatment, although TSH excess has persisted in two patients (cases 1 and 2). Case 1 had an extremely high titer of antimicrosomal antibody (MCHA), and cases 2 and 3 showed histologically and cytologically chronic thyroiditis, despite negative results for MCHA and antithyroglobulin antibody, respectively. Two patients (cases 5 and 6), who had had normal thyroid hormone levels and did not show the significant rise in serum T3 in TSH releasing hormone testing, showed TSH normalization without changes in serum thyroid hormone levels after treatment. The other two patients (cases 7 and 8), who initially had normal TSH and thyroid hormone levels, did not show the significant changes in serum TSH and thyroid hormone levels after treatment. The prevalence of chronic thyroiditis coexistence in isolated ACTH deficiency may be higher than predicted. Therefore, TSH excess before adrenal replacement may be attributed to not only direct enhancement of TSH release due to chronic cortisol deficiency but also to thyroid dysfunction due to chronic thyroiditis. It is possible that hypothyroidism due to chronic thyroiditis can be improved only by adrenal supplementation.

Adrenocorticotropic Hormone↗
PubMed1992

Detection of thyroid-stimulating antibody in patients with inflammatory thyrotoxicosis.

The detection of thyrotropin-binding inhibitory immunoglobulins (TBII) and/or thyroid-stimulating antibody (TSAb) has been reported in some patients with painless thyroiditis (PT) or subacute thyroiditis (SAT). However, its mechanism is unknown. TBII and TSAb measured using cultured FRTL-5 thyroid cells were evaluated in 18 patients with PT, 11 patients with SAT and a patient with SAT-like symptoms. In PT, we detected both TBII and TSAb activities in only 1 patient. This case had first come to our attention with subclinical hypothyroidism and had already had weakly positive TSAb activity (205.9%) 1 year before the present onset of PT. This patient had a transient thyrotoxicosis with a low uptake (24 h) of 123I (4.3%) and 821.0% TSAb activity, and subsequently developed a transient subclinical hypothyroidism. Even after 2 years, she still had positive TSAb activity (382.3%). In SAT, TBII and TSAb activities were not detected during the courses of any patients. A patient with transient thyrotoxicosis, who had a high uptake (30 min) of 99mTc (5.6%) and SAT-like symptoms (painful tenderness on right thyroid lobe and markedly accelerated erythrocyte sedimentation rate), showed positive activities of TBII (34.9%) and TSAb activity (1,366.9%). Histological findings by thyroid needle biopsy performed in the thyrotoxic phase showed coexistence of granulomatous inflammatory changes and hyperplasia with papillary folds of some residual follicular cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1991

Onset of subacute aggravation of chronic thyroiditis followed immediately by transient hypothyroidism during antithyroid drug therapy for Graves' hyperthyroidism.

A 56-year-old man presented with clinical and biochemical hyperthyroidism with high thyroid 99mTc uptake, positive result for antimicrosomal antibody (MCHA; 1:8,100) and markedly high activities of thyrotropin-binding inhibitory immunoglobulin (TBII; 90.0%) and thyroid-stimulating antibody (TSAb; 2,400%). Fifty days after the initiation of antithyroid drug therapy, he developed a painful tender enlarged thyroid and an accelerated erythrocyte sedimentation rate (ESR), which were followed immediately by hypothyroidism with a transient increase in MCHA titer (peak; 1:218,700) despite of maintenance of high TBII and TSAb activities. Two and a half months after the recovery from hypothyroidism, recurrent hyperfunction was observed with further elevation of TSAb activity (4,643%). After about 2 weeks, recurrences of a painful tender enlarged thyroid and an accelerated ESR, which were followed by abrupt progression to hypothyroidism, were found. Specimens obtained when he had still slightly tender goiter after the first and second episodes of neck pain showed microscopically extremely extended interstitial fibrosis with collapsed follicles and moderate lymphocytic infiltration. Thyroid-stimulation-blocking antibody was not detected at either onset of hypothyroidism. Thus, it is possible that Graves' disease, subacute aggravation of chronic thyroiditis and hypothyroidism coexist in the same individual. In such patients, thyroid status may be determined by the degree of each of the stimulating factors (TSH, TSAb and/or unknown factors) and suppressive or destructive factors (humoral and/or cellular) and may be changed in a very short interval.

Autoantibodies↗
PubMed1991

Autoimmune thyroiditis with transient thyrotoxicosis: comparison between painful thyroiditis and painless thyroiditis.

Clinical and laboratory findings and long-term outcomes in 8 patients (7 women) with autoimmune thyroiditis (AT), aged 34-59 years, who had a painful tender goiter and a transient thyrotoxicosis with a low thyroid radioactive iodine uptake (RAIU), were compared with those in 15 patients (13 women) with painless thyroiditis (PT), aged 23-69 years. Six painful AT and 6 PT patients had a history of prior awareness of goiter. All patients with painful AT had a moderate or marked elevation of erythrocyte sedimentation rate and a positive result for C-reactive protein, while only 3 PT patients (group B) did. There were no significant differences between the mean age, duration of symptoms, white blood cell count, serum triiodothyronine (T3) and thyroxine (T4) concentrations, serum T3/T4 ratio and duration of thyrotoxicosis after the initial examination and prevalences of positive results for antithyroglobulin and -microsomal antibodies in the two diseases. Two of 8 painful AT patients showed a histologically chronic fibrous variant and 6 others showed chronic lymphocytic thyroiditis. All PT patients examined also showed lymphocytic thyroiditis. Two and 5 painful AT patients developed transient and persistent hypothyroidism, respectively, while 8 [7 in group A (normal ESR), 1 in group B] and 3 PT patients (1 in group A, 2 in group B) did, respectively. The mean serum thyroid-stimulating hormone level in the hypothyroid phase in painful AT patients was higher than that in PT patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

An unexpected rise in plasma aldosterone to furosemide-upright test in primary aldosteronism due to aldosterone producing adenoma.

This paper documents an unexpected rise in plasma aldosterone concentration (PAC) to the furosemide-upright test despite a decrease in adrenocorticotropin (ACTH) by dexamethasone, and an unresponsiveness in plasma renin activity to this stimulus in a patient with aldosterone producing adenoma. Furthermore, this patient showed an appropriate response in PAC to a rapid ACTH test, and an insensitivity in PAC to angiotensin-II (Ang-II) infusion. Other factor(s) besides ACTH or Ang-II may play a role in the plasma aldosterone response to ambulation after intravenous furosemide administration in patients with primary aldosteronism.

Adenoma↗
PubMed1990

Three patients who spontaneously developed persistent hypothyroidism during or following treatment with antithyroid drugs for Graves' hyperthyroidism.

Three patients with Graves' disease who spontaneously developed hypothyroidism after treatment with antithyroid drugs are described herein. Patient 1 developed a painful tender thyroid enlargement with a fever and accelerated erythrocyte sedimentation rate when she was receiving maintenance therapy with methimazole, and she progressed to persistent hypothyroidism with increased titers of antithyroglobulin and antimicrosomal antibodies and marked reduction of goiter size within the subsequent 2 months. Thyroid-stimulating hormone-binding inhibitory immunoglobulins (TBIIs) and thyroid stimulation-blocking antibody (TSBAb) were absent when she was hypothyroid. Hypothyroidism probably resulted from autoimmune thyroid destruction due to subacute aggravation of Hashimoto's thyroiditis. During the clinical course of patient 2, accelerated erythrocyte sedimentation rate and later transient increases of antimicrosomal and antithyroglobulin antibody titers were observed repeatedly (four times), and she finally fell into overt hypothyroidism. She also had negative results of tests for TBII and TSBAb. Her hypothyroidism appeared to result from repeated thyroid destruction due to aggravation of Hashimoto's thyroiditis. Patient 3 fell into hypothyroidism when receiving a small dosage of methimazole. The TBII and TSBAb were strongly active when she developed hypothyroidism, which thus seemed to be due to blocking antibody. Patients with Graves' hyperthyroidism may eventually progress to hypothyroidism later by several different mechanisms. Severe and sudden or slowly repeated thyroid destruction due to aggravation of Hashimoto's thyroiditis is one mechanism. Another may be the appearance of a blocking antibody to the TSH receptor.

Adult↗