Effect of vegetarian diet on systemic lupus erythematosus.
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Adolescent↗
Biomedical subjects
C Shigemasa
Publications and source records attributed to C Shigemasa.
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↗
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↗
Cardiac and plasma catecholamine responses to exercise in patients with hyperthyroidism.
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Adult↗
Effect of prednisolone on urate and oxypurine excretion.
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Female↗
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↗
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↗
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↗
Disappearance of thyroid-stimulation blocking antibody by glucocorticoid therapy in a patient with primary myxedema who developed aortitis syndrome during L-thyroxine supplementation.
A 39-year-old woman with primary myxedema, who had the potent activities of thyrotropin-binding inhibitory immunoglobulins (TBII) and thyroid-stimulation blocking antibodies (TSBAb), developed aortitis syndrome about 6 months after the initiation of L-thyroxine (L-T4) supplementation. A 35 mg daily dose of prednisolone for aortitis syndrome was initiated, and the dose was gradually reduced. TBII and TSBAb activities were gradually decreased, and both reached normal levels (7.7% and 10.1%, respectively) 3 months after the initiation of prednisolone. Therefore, dose of L-T4 was gradually reduced, and L-T4 supplementation was stopped. Subsequently, however, recurrence of hypothyroidism was not observed. These observations indicate the possibility that hypothyroidism remits with disappearance of TBII and TSBAb activities in not only neonatal cases but also adult cases.
Adult↗
Development of postpartum spontaneously resolving transient Graves' hyperthyroidism followed immediately by transient hypothyroidism.
A 25-year-old woman with a history of Graves' disease, in remission for 8.5 years following 6 months of methimazole therapy, first came to our attention 5 months after her first delivery with clinical and biochemical hypothyroidism, markedly elevated titre of anti-thyroid microsomal antibody (MCHA; 1:102400) and mildly elevated activity of thyrotropin-binding inhibitory immunoglobulins (TBII; 29.5%). After short-term (3 months) treatment with L-thyroxine therapy, the development of hyperthyroidism in the first trimester of the second pregnancy, which remitted through the second and third trimesters, was observed. TBII showed a peak value (93.1%) 1 month after the onset of hyperthyroidism, and a normal value (12.4%) 6 d after delivery. One month after the second delivery, the patient developed hyperthyroidism, with an elevation of 99mTc thyroid uptake (5.58%; normal range 0.5-2.5%), which was immediately followed by transient clinical and biochemical hypothyroidism. Concomitant increases in MCHA titre and TBII activity were observed after delivery, and both reached peak levels (1:409600 and 81.0%, respectively) one and a half months after the onset of hypothyroidism. Thyroid-stimulating antibody (TSAb), measured using FRTL-5 thyroid cells, was detected at a weakly positive level (161%) on initial examination, and the serial change in TSAb was almost identical to that in TBII. Patients with Graves' disease may develop Graves' type hyperthyroidism, followed immediately by transient hypothyroidism due to coexisting destructive autoimmune thyroiditis during the early postpartum period, despite increasing TSAb activity.
Adult↗
The mechanism involved in the conversion of thyrotropin receptor-bound blocking-type immunoglobulin G (IgG) to the stimulating-type by anti-human IgG antibodies.
It has been reported that the addition of antibody (Ab) against human immunoglobulin G (IgG) converts TSH receptor-bound blocking-type IgG to stimulating-type IgG. However, the detail of converting mechanism remains unclear. In this study we examined the mechanism involved in this conversion using FRTL-5 cells. Blocking-type IgG was obtained from a patient with hypothyroidism. FRTL-5 cells were first incubated with IgG solution, then washed with PBS and exposed to antihuman IgG Ab. The effect of antihuman IgG Ab on converting activity was dose dependent. Maximal stimulation of cAMP was achieved with an antiserum dilution of 1:75. It seems likely that antimicrosomal Ab does not interfere with cAMP production, since IgG with a high anti-hemagglutination antibody titer did not show converting activity. Of the several kinds of antibodies tested, Ab against human IgG-Fab fragment was the most effective in converting ability, while the least effective were those against human IgG-Fc fragment. Although the divalent F(ab')2 fragment of antihuman IgG was significantly more effective in its converting ability than the monovalent Fab fragment, the Fab fragment itself also converted blocking IgG to the stimulating type in a dose-dependent manner. Accordingly, receptor cross-linking or aggregation does not play a major role in promoting this converting phenomenon. When cells were first exposed to blocking-type IgG and then to both antihuman IgG Ab and bovine TSH, cAMP production was much greater than the sum of each alone. However, anti-IgG Ab alone did not affect the binding of blocking-type IgG to receptor. These results suggest that the addition of antihuman IgG Ab not only converts blocking-type IgG to the stimulating type but also recovers TSH activity via a postreceptor step. Forskolin, like TSH, showed an additive effect on cAMP stimulatory action with antihuman IgG. In contrast, cholera toxin and antihuman IgG Ab were not additive. The reason for this discrepancy remains unknown. In summary, our observation indicates that 1) the converting phenomenon is induced via IgG-TSH receptor complexes; 2) the mechanism aside from receptor aggregation, i.e. the recognition of a critical domain in TSH receptor molecule, seems necessary for promoting converting phenomenon; and 3) the addition of antihuman IgG Ab affects a postreceptor step via TSH receptor structures that differ from the TSH-binding site.
Adult↗
Chronic thyroiditis with painful tender thyroid enlargement and transient thyrotoxicosis.
Clinical and laboratory findings and long term outcome (1.5-9 yr) in 7 women and 1 man with chronic thyroiditis (CT) who had painful tender thyroid enlargement were evaluated and compared with those in 11 women with subacute thyroiditis (SAT). Histological features consistent with SAT were not demonstrable, and various forms of CT (fibrous variant, diffuse, or focal lymphocytic thyroiditis) were observed. There were no differences in mean age, duration of symptoms, erythrocyte sedimentation rate, and C-reactive protein values in the 2 diseases. Seven patients had a history of goiter, and none had a history of a preceding upper respiratory tract infection. The mean white blood cell count was significantly lower in CT than in SAT patients. Six CT patients had transient thyrotoxicosis with a marked depression of radioactive iodine uptake. Mean serum T4 and T3 levels and T3 to T4 ratio in these 6 patients did not differ from those in the SAT patients. Five (all with high antimicrosomal antibody titers) of 8 CT patients developed persistent hypothyroidism. In contrast, none of the SAT patients became permanently hypothyroid. TSH binding inhibitory immunoglobulins and thyroid stimulation-blocking antibody at recent examination were negative in these 5 patients. Patients with this disorder present with transient thyrotoxicosis, with a marked depression of the thyroid radioactive iodine uptake, and often develop goitrous or atropic persistent hypothyroidism. This disorder may represent acute exacerbation of an underlying immunological process during the course of CT. To differentiate this syndrome from SAT, thyroid biopsy is necessary.
Adult↗
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↗
Effect of luteinizing hormone-releasing hormone on the mechanical activity of the guinea-pig cardiac muscle.
1. The inotropic effect of physiological concentrations of luteinizing hormone-releasing hormone (LH-RH) in isolated guinea-pig cardiac muscles was studied. 2. LH-RH increased the contractile force elicited by either fast and slow responses in a dose-dependent manner. 3. These effects of LH-RH were affected by phentolamine and diltiazem but not by propranolol and cold condition. 4. This study showed the positive inotropic effect of LH-RH on myocardium through the affection to intracellular Ca, and the difference from the effect of cardiotonic steroids.
Animals↗
A case of paroxysmal ventricular tachycardia during pregnancy.
We report a case of a 37-year-old woman who had paroxysmal ventricular tachycardia (VT) during early pregnancy. She had severe hyperemesis, palpitation at 6 weeks of gestation and many episodes of paroxysmal VT, but no apparent organic heart disease. At that time she had a transient increase of thyroid hormone levels. With bed rest and without medication, her symptoms and episodes of VT disappeared in accordance with the improvement of hyperemesis and thyrotoxicosis. She demonstrated a rare course of arrhythmias in which the deterioration of VT was observed at transient thyrotoxicosis and hyperemesis.
Adult↗
The influence of diabetes mellitus on thyrotropin response to thyrotropin-releasing hormone in untreated acromegalic patients.
Impairment of thyrotropin (TSH) response to thyrotropin-releasing hormone (TRH) has been documented in patients with uncontrolled diabetes mellitus (DM). In acromegalic patients, however, there have been no data regarding TSH secretion studied taking the existence of DM into consideration. Therefore, we investigated the TSH response to TRH [expressed as TSH increment (delta TSH)] in 14 untreated acromegalic patients, who did not show the suprasellar extension of adenoma, divided into two groups on the basis of either presence or absence of uncontrolled DM, and in 28 normal subjects. The mean max delta TSH was significantly reduced (p less than 0.02) in acromegalic patients despite similar mean serum T4 and free T4 index (FT4l) levels. Furthermore, the mean basal and max delta TSH in 7 patients with DM (FBS, 120-300 mg/dl; HbA1, 8.8-15.2%) were significantly lower than those in 7 patients without DM (p less than 0.05 and p less than 0.02, respectively) despite similar the mean serum T3, T4, FT4l, growth hormone (GH) and prolactin (PRL) levels and sellar volume. In 4 patients with DM the TSH response to TRH 6-8 weeks after insulin therapy, when their HbA1 levels were normal, increased compared to that before insulin therapy. The mean max delta TSH after selective adenomectomy in 8 patients (3 in DM group and 5 in non-DM group), whose fasting basal GH fell to less than 5 ng/ml, was almost identical to that in normal subjects. In conclusion, the present study suggests that the abnormality in TSH secretion in acromegalic patients may be increased by the existence of uncontrolled DM.
Acromegaly↗
Sequential changes in serum thyroglobulin, triiodothyronine, and thyroxine following partial thyroidectomy for nontoxic nodular goiter.
The sequential changes in serum thyroglobulin (Tg), thyroxine (T4), free thyroxine (FT4), triiodothyronine (T3) and thyrotropin (TSH) were evaluated in ten patients on whom partial thyroidectomy for nontoxic nodular goiter had been performed. These changes were compared with those in ten patients who underwent upper abdominal surgery (cholecystectomy) under similar anesthesia, and whose calorie and fluid intake was similar until at least 48 hours after surgery. In agreement with previous reports, marked elevations in serum Tg that reached peak concentration (660 to 1350 ng/mL) at one or two hours after the thyroid incision (mean +/- SD; 787 +/- 304.0 ng/mL and 839 +/- 345.7 ng/mL, respectively) were observed. On the other hand, the significant but minimal increases in serum T4 and FT4 were observed at 24 hours (P less than .001 and P less than .001, respectively), 48 hours (P less than .01 and P less than .001, respectively), and 72 hours (P less than .01 and P less than .01, respectively) after the thyroid incision compared with the level just prior to the thyroid incision. Similarly, serum T3 also increased significantly at 6 to 168 hours after the thyroid incision (P less than .01, P less than .05, P less than .05, P less than .05, and P less than .05, respectively). These increases in serum T4, FT4 and T3 were not observed in the cholecystectomy patients. The mean serum TSH levels at 24 to 72 hours after thyroid incision and those at 6 to 48 hours after the abdominal incision were significantly decreased compared with those before thyroid and abdominal incision, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
In vivo effects of molybdate on activation of rat liver cytosol glucocorticoid receptor.
To clarify the in vivo events following administration of steroid hormones, the effect of molybdate on the cytoplasmic glucocorticoid receptor (GR) translocation in rat livers after administration of glucocorticoids was examined. After injection of hydrocortisone-succinate (Hydro) (200 micrograms/150 g rat) into the inferior vena cava of adrenalectomized rats, 3H-dexamethasone (3H-Dex) binding in liver cytosol rapidly decreased within 5 min, followed by a rapid replenishment. This decrease in binding was partially prevented by pre-treating the animals with 20 mg of sodium molybdate (Mo), which was considered to inhibit GR activation. Administration of 200 micrograms/150 g body weight of hydrocortisone caused a rapid replenishment of the binding sites following the depletion. Administration of molybdate 5 min after the hydrocortisone injection did not influence the replenishment. The GR content was increased significantly 20 min after the administration of molybdate in intact rats but not in adrenalectomized rat. It is concluded that activation of the hormone receptor complex observed in vitro also occurs in vivo after administration of glucocorticoid to animals.
Animals↗