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E Takazakura

Publications and source records attributed to E Takazakura.

At least 37 records · Page 2Linked to original sources
PubMed1995

Histological features of the thyroid gland in a patient with lithium induced thyrotoxicosis.

A 26 year old woman with lithium induced thyrotoxicosis is reported. The thyrotoxicosis was associated with a non-tender diffuse goitre and a low radioiodine uptake by the gland. The thyrotoxicosis was reversible and remitted on withdrawal of the drug. The histopathological alterations of the thyroid glad were characterised by extensive follicular cell disruption with no lymphocytic infiltration. It is postulated that lithium might directly damage thyroid follicular cells and that subsequent release of thyroglobulin into the circulation might be a cause of transient thyrotoxicosis.

Adult↗
PubMed1995

Tubulointerstitial nephritis in a patient with eosinophilic fasciitis and IgA nephropathy.

We report a tubulointerstitial nephritis in a patient with eosinophilic fasciitis and IgA nephropathy. Urinalysis revealed mild proteinuria and microscopic hematuria, and renal biopsy disclosed diffuse interstitial infiltrations of lymphocytes and plasma cells with few eosinophils in spite of mild mesangial proliferation with IgA deposits, indistinguishable from those of primary tubulointerstitial nephritis. Immunohistochemical examination showed a predominance of helper/inducer T cells infiltrating the renal interstitium and the fascia. Corticosteroid treatment led to a decrease of infiltrating cells in both tissues. Therefore, eosinophilic fasciitis and tubulointerstitial nephritis in our patient seemed to be interdependent phenomena.

Adult↗
PubMed1995

I-123 metaiodobenzylguanidine cardiac scintigraphy in patients with an implanted permanent pacemaker.

T1 scintigraphic abnormalities have been reported in patients with an implanted permanent pacemaker, but little is known about the MIBG scintigraphic findings in such patients. This study was performed to assess the MIBG scintigraphic findings in patients with an implanted permanent pacemaker, and to test the hypothesis that imaging characteristics of MIBG scintigraphy differ according to its mode. Twelve patients (4 men and 8 women, mean age: 72.4 +/- 9.5 years), who had undergone the implantation of a permanent pacemaker for bradyarrhythmias, underwent MIBG scintigraphy. The patients were divided into VVI pacemaker and DDD pacemaker groups. The tomograms were divided into nine segments and the MIBG defect in each segment scored on a scale ranging from 0 (normal uptake) to 3 (no uptake). Total MIBG defect scores were generated by summing the scores for the nine segments in each patient. MIBG scintigraphic abnormalities were found in ten of the twelve patients. The six patients with the VVI pacemaker manifested MIBG scintigraphic abnormalities. These MIBG scintigraphic abnormalities were observed in all segments, particularly in the posterior segments. The mean total defect score of the VVI group was higher than that of the DDD group (14.8 +/- 9.8 vs 3.0 +/- 3.5, respectively p < 0.05). Therefore, we conclude that despite several limitations of the study, MIBG scintigraphic abnormalities occur in patients with implanted permanent pacemakers, and that such abnormalities are more prominent with the VVI than DDD pacemaker.

3-Iodobenzylguanidine↗
PubMed1994

[A case of unilateral primary adrenal nodular hyperplasia with elevated plasma adrenocorticotropin (ACTH)].

A 57-year-old woman was admitted to our hospital with occipital headache and nausea. She had severe hypertension (192/122mmHg), hypokalemia (2.8mEq/l) and fasting hyperglycemia (127 mg/dl). Further examination revealed elevated plasma ACTH (124pg/ml) and cortisol (26.5 mu g/dl) with a lack of diurnal rhythm. Plasma ACTH or cortisol did not increase by injection of corticotropin releasing hormone (CRH). Rapid ACTH test resulted in an exaggerated response of plasma cortisol. Abdominal MRI scan showed a left adrenal tumor. Since the bilateral adrenal venous blood sampling revealed a significant increase of cortisol on the left, left adrenalectomy was performed. Histological examination of the resected adrenal gland revealed marked cortical hyperplasia. Postoperative investigations revealed that despite a small dose of steroid replacement for only 20 days, plasma ACTH level was decreased for a period of 6 months. Both plasma ACTH and cortisol increased by a CRH injection 38 days after surgery. CRH test during bilateral inferior petrosal sinus sampling indicated that this patient had no functioning pituitary tumor. Although the exact mechanism of high plasma ACTH level in this case was unknown, these findings suggest that any substance secreted from primary adrenal nodular hyperplasia adrenal nodular hyperplasia may stimulate pituitary ACTH production. This is a very rare case of Cushing's syndrome due to unilateral primary adrenal nodular hyperplasia with elevated plasma ACTH.

Adrenal Glands↗
PubMed1994

An autopsy case of pyruvate kinase deficiency anemia associated with severe hemochromatosis.

We report an autopsy case of pyruvate kinase deficiency anemia with severe hemochromatosis. This anemia is rarely associated with hemochromatosis. In this case, the autopsy findings showed hemochromatosis of the heart, pancreas, liver, kidneys, thyroid gland, adrenal glands, testes and skin. Microscopic examination showed iron depositions in these organs, but not in the bone marrow. A family study showed negative data for iron overload and no known HLA type suggestive of idiopathic hemochromatosis. To explain this rare association, we suggest that this patient's iron overload was an acquired type, which might have mainly been caused by increased iron absorption due to the severe hemolytic anemia.

Adult↗
PubMed1994

[A case of atelectasis of the middle lobe associated with congestive heart failure].

A 74-year-old man was admitted to our hospital for work up of a shadow in the right middle lobe on chest X-ray film. He had hypertension, aortic regurgitation, and atrial fibrillation on admission. Bronchoscopy demonstrated total obstruction of the right B4 orifice, but the etiology of obstruction was unknown. He was discharged and followed up. The shadow in the middle lobe disappeared spontaneously and the cardiac silhouette was slightly smaller than that on the first admission. The shadow in the middle lobe reappeared again with the progression of cardiomegaly. Because hypertension became uncontrolled and pretibial edema developed, he was readmitted. Bronchoscopy showed the same findings as on the first admission. After treatment of heart failure for one month, bronchoscopy demonstrated partial patency of the right B4 orifice. As cardiomegaly improved, the shadow in the middle lobe diminished and then disappeared, and chest CT scan showed patency of the right B4. These findings suggest that congestive heart failure caused the atelectasis of the right middle lobe, so-called middle lobe syndrome. A possible mechanism of the right B4 obstruction is that the right B4 was compressed between the middle lobe artery and the dilated middle lobe vein due to heart failure.

Aged↗
PubMed1993

Postpartum thyroiditis. A clinical, histologic, and immunopathologic study of 15 cases.

Fifteen specimens from 15 patients with clinically and laboratory-proven postpartum thyroiditis were examined histologically; 8 specimens were obtained during the hypothyroid phase and the other 7 during the recovery euthyroid phase. All specimens showed focal or diffuse chronic thyroiditis. In the eight specimens taken during the hypothyroid phase and four specimens during the early recovery phase, follicular disruption and hyperplastic change of the follicle were common and characteristic histologic features. In the three specimens taken during the late recovery phase, only focal infiltration of lymphocytes was observed. This histologic change resembled that in spontaneous silent thyroiditis, as shown in the authors' previous study. The authors believe that postpartum thyroiditis and spontaneous silent thyroiditis may fit the same category clinically and histologically. In addition to performing the histologic examination, the authors examined the intrathyroidal lymphocyte subsets and HLA-DR antigen expression in the follicular cells immunohistochemically and compared them with those in chronic thyroiditis (usual type). In postpartum thyroiditis, a significant increase of helper-T-cell numbers and increased expression of HLA-DR antigen in the follicular cells were observed, suggesting an enhancement of autoimmune reactivity.

Adult↗
PubMed1993

Iodine-induced hypothyroidism in patients on regular dialysis treatment.

Hypothyroidism with a serum concentration of thyroid-stimulating hormone (TSH) above 40 microU/ml was noted in 3 (3.2%) of 93 patients on regular hemodialysis or continuous ambulatory peritoneal dialysis. These 3 patients had no history of thyroid disease and were receiving no medication known to influence thyroid function. They had habitually eaten iodine-rich foods and showed an enlarged thyroid gland with a preserved radioactive iodine uptake and a markedly elevated serum inorganic iodine (II) level. In all 3 patients, both thyroidal microsomal antibody and thyroglobulin antibody titers measured by hemagglutination methods were less than 100, and TSH-binding inhibitory immunoglobulin was negative. Moreover, histologically no lymphocytic infiltrations were observed. With only iodine restriction, serum TSH level markedly decreased from 44.6 to 3.6 microU/ml in case 1, from 90.6 to 3.2 microU/ml in case 2 and from 43.2 to 9.4 microU/ml in case 3 in parallel with decreases in the serum II level. These results suggest that at least in an area like Japan, where the daily intake of iodine is high, iodine-induced hypothyroidism may be induced in patients undergoing regular dialysis treatment even in the absence of apparent underlying thyroid disease.

Adult↗
PubMed1993

Iodine-induced hypothyroidism: a clinical and histological study of 28 patients.

Thirty-three thyroid specimens obtained from 28 patients with clinically and laboratory-proven iodine-induced hypothyroidism were examined clinically, histologically, immunohistochemically, and ultrastructurally. Twenty-eight specimens obtained during the hypothyroid phase showed common histological changes in the thyroid thought to be specific for this disease; hyperplastic change in the follicles with some papillary folding, cuboidal to columnar change of follicular cells with clear and vesicular cytoplasm, scanty or absent colloid material in the large distended follicles, and occasional dilatation of capillary vessels. Lymphocytic infiltration was present in about half of the specimens. No specimens showed either stromal fibrosis or parenchymal atrophy. Immunohistochemical and electron microscopic examination revealed that severe interference with thyroid hormone biosynthesis occurs in the follicular cells. In two patients who had a follow-up biopsy in the recovery (euthyroid) phase after iodine restriction, the histological involvement seen in the hypothyroid phase was no longer present. The histological changes in the thyroid gland seen in patients with iodine-induced hypothyroidism are characteristic. This disease can be diagnosed from laboratory tests, but thyroid biopsy is also a useful tool to differentiate this condition from other diseases causing hypothyroidism. Not only clinicians, but also pathologists, must pay attention to this type of hypothyroidism, because thyroid function may revert to normal by iodine restriction alone.

Adult↗
PubMed1992

Successful ultrasonically guided percutaneous ethanol injection for secondary hyperparathyroidism.

Ultrasonically guided percutaneous ethanol injection to all of four enlarged parathyroid glands, which were confirmed by fine-needle aspiration biopsy, was successfully performed in a hemodialysis patient with secondary hyperparathyroidism. In addition to marked reduction of serum parathyroid hormone, the size of parathyroid glands was significantly decreased after the procedure. As an adverse effect, the patient experienced a transient self-limiting dysphonia due to right recurrent nerve palsy after the first injection. This procedure may be an effective alternative to surgical treatment or administration of high-dose 1,25(OH)2 vitamin D3 in uremic patients with sonographically verified multiple enlarged parathyroid glands.

Adult↗
PubMed1991

The role of peripheral capacitance and resistance vessels in hypotension following hemodialysis.

The arterial pressure (AP) response to hemodialysis was studied with echocardiography and strain gauge plethysmography in 17 patients with end-stage renal disease; mean AP was unchanged in seven (group A) and was reduced by more than 10 mm Hg in 10 patients (group B). Following dialysis, body weight decreased and heart rate increased equally in both groups. Ejection fraction did not change in the two groups. Left ventricular end-diastolic volume fell by 13 +/- 10% in group A and by 24 +/- 16% in group B. Cardiac index (CI) fell in group B, but remained unchanged in group A. Systemic vascular resistance (SVR) did not change in both groups. The change in mean AP before and after dialysis was significantly correlated with that in Cl (r = 0.49, p less than 0.05), but not with that in SVR. Calf venous pressure-volume curves were not different between the two groups before dialysis. Hemodialysis shifted the curve toward the volume axis for group B but not for group A. These results suggest that hypotension following dialysis is mainly due to the fall in cardiac output, in which increases in venous distensibility play an important role.

Blood Volume↗
PubMed1991

Exonic point mutations in NADH-cytochrome B5 reductase genes of homozygotes for hereditary methemoglobinemia, types I and III: putative mechanisms of tissue-dependent enzyme deficiency.

We analyzed the NADH-cytochrome b5 reductase gene of hereditary methemoglobinemia type I and type III, by using PCR-related techniques. The mutation in type I is a guanine-to-adenine substitution in codon 57 of exon 3 of the NADH-cytochrome b5 reductase gene, and the sense of this codon is changed from arginine to glutamine. In type III the mutation is a thymine-to-cytosine transition in codon 148 of exon 5, causing leucine-to-proline replacement in type III. The former mutation abolishes the MspI recognition site. Homozygosity for the former mutation in a patient with type I was confirmed by restriction analysis of PCR-amplified fragments and by dot blot hybridization of amplified products with allele-specific oligonucleotide probes. The latter mutation generates a recognition site for MspI. Amplification of exon 5 by PCR followed by digestion with MspI revealed homozygosity for this mutation in patients with type-III. Putative mechanisms of tissue-dependent enzyme defects in hereditary methemoglobinemia are discussed.

Adult↗
PubMed1990

Reduction in microalbuminuria in diabetics by eicosapentaenoic acid ethyl ester.

Eicosapentaenoic acid (EPA) ethyl ester (1.8 g/d) was administered to 16 diabetic patients (5 insulin-dependent and 11 noninsulin-dependent diabetics) for 6 mon. EPA in total plasma fatty acids increased from 4.0 +/- 2.4 mol% (mean +/- SD) to 7.5 +/- 3.1 mol% (p less than 0.001). Albumin excretion, measured with spot urine, was significantly reduced from 65 to 36 mg/g creatinine (geometric means, p less than 0.001). Fasting blood sugar levels, glycohemogloblin, body weight and blood pressure did not change significantly during the study. There were also no significant changes in serum levels of creatinine, urea nitrogen, total cholesterol and triglycerides. Although no overt hemorrhage was observed in the patients, hematocrit was reduced from 42.6 +/- 2.8% to 41.0 +/- 3.9% (p less than 0.02). Ten other similar diabetic patients (4 insulin-dependent and 6 noninsulin-dependent diabetics) were followed as a reference group, not concomitantly, for 6 mon with neither EPA ethyl ester nor placebo. The parameters mentioned above were not changed significantly in this group during 6 mon. EPA administration might retard the appearance of overt diabetic nephropathy.

Aged↗