Biomedical subjects
H Hosojima
Publications and source records attributed to H Hosojima.
[Erythrocyte sorbitol, sorbitol dehydrogenase (SDH) and glyceraldehyde reductase (GAR) in diabetes mellitus].
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[Intrarenal resistive index (RI) from renal duplex Doppler sonography in diabetic patients with nephropathy].
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Urinary angiotensin-converting enzyme activity in type 2 diabetes mellitus: its relationship to diabetic nephropathy.
Urinary angiotensin-converting enzyme (ACE) and urinary N-acetyl-beta-D-glucosaminidase (NAG) were measured after a 5-year interval in 38 non-azotemic type 2 diabetic patients. Of these patients at baseline, 16 had nil nephropathy, 15 had incipient nephropathy, and 7 had overt nephropathy. During the follow-up, 6 and 1 of the 16 patients with nil nephropathy developed incipient and overt nephropathy, respectively. Four of the 15 patients with incipient nephropathy progressed to overt nephropathy. The 7 patients with overt nephropathy continued to have overt nephropathy, with slight azotemia in one. Urinary ACE and NAG levels were normal at baseline and showed no significant elevations at follow-up in the patients with nil nephropathy, no significant changes in baseline and modest elevations at follow-up in the patients with incipient nephropathy, and high at baseline and marked elevations at follow-up in the patients with overt nephropathy. In all patients, urinary ACE during the follow-up was positively correlated with urinary albumin or NAG, but not with glomerular filtration rate. Urinary ACE may be of poor prognostic value for the follow-up of diabetic patients, which is at variance with urinary albumin.
Rhabdomyolysis accompanying thyroid crisis: an autopsy case report.
Rhabdomyolysis is occasionally associated with metabolic disorders such as diabetic coma, severe electrolyte disturbances and myxedema coma. We describe rhabdomyolysis accompanying thyroid crisis. A 50-year-old man with Graves' disease developed rhabdomyolysis, congestive heart failure and hepatic failure during the course of thyroid crisis and then died of acute renal failure. Postmortem examination revealed rhabdomyolysis in the cardiac and psoas muscles, old myocardial infarction, hepatic centrilobular necrosis, renal cortical necrosis, and follicular hyperplasia in the thyroid. Circulatory collapse and dehydration under excessive hypermetabolic state presumably suppressed the source of energy and oxygen for muscle cells, leading to cellular damage.
[HLA-antigens in thyrotoxic patients with overt diabetes mellitus].
The incidence of thyrotoxicosis accompanied by overt diabetes has been reported to be 2 to 3%. Several workers have suggested the possible role of immunological and inherited factors in the occurrence of thyrotoxic patients with overt diabetes. We investigated, therefore, the clinical characteristics, backgrounds, and HLA antigens in thyrotoxic patients with overt diabetes. In nine thyrotoxic patients with overt diabetes (group DM) (3 men and 6 females, average age of 45.8 +/- 2.9 yr), mean levels of free-triiodothyronine (FT3) and free thyroxine (FT4) were 8.2 +/- 0.8 pg/ml and 4.9 +/- 0.4 ng/dl, respectively. Although these levels were extremely high, they were significantly lower than those levels in forty thyrotoxic patients without overt diabetes (group ND) (8 men and 32 females, average age 35.1 +/- 4.5 yr). Mean levels of both thyrotrophin receptor-antibody (TR-Ab) and thyroid simulating antibody (TS-Ab) in group DM were relatively lower than those in group ND. Mean titers of both antithyroid antibody (TGHA) and antimicrosomal antibody (MCHA) in group DM were also relatively lower than those in group ND, respectively. Regarding the clinical features in thyrotoxic patients with overt diabetes, mean duration of diabetes mellitus was 4.1 +/- 2.5 years with mean levels of fasting plasma glucose (FPG), HbA1c, and serum fructosamine 208.1 +/- 34.0 mg/dl, 10.6 +/- 0.6%, and 3.9 +/- 0.9 mmol/L, respectively. Seven patients in group DM frequently had ketosis or ketoacidosis in their histories, and they had been treated with insulin injection. However, the diabetic complications in group DM were moderate or severe.(ABSTRACT TRUNCATED AT 250 WORDS)
[Erythrocyte sorbitol levels in patients with thyrotoxicosis].
Hyperglycemia and impaired glucose tolerance are frequently observed in patients with hyperthyroidism. However, little is known about whether altered polyol metabolism in hyperthyroidism is present or not. To examine changes in polyol metabolism in hyperthyroidism, we investigated changes in erythrocyte sorbitol, glyceraldehyde reductase (GAR) and sorbitol dehydrogenase (SDH) activities during hyperthyroid and euthyroid states in patients with thyrotoxicosis. Mean levels of erythrocyte sorbitol and GAR were 32.0 +/- 1.6nM/g.Hb and 147.1 +/- 0.3mU/g.Hb, respectively. In thyrotoxic patients in a hyperthyroid state, these values were significantly higher than those in euthyroid controls. Mean level of erythrocyte SDH in thyrotoxic patients was weak but was significantly increased in comparison with that of euthyroid controls. However, mean levels of erythrocyte sorbitol and GAR were remarkably reduced to 23.6 +/- 1.4nM/g.Hb and 125.3 +/- 4.6mU/g.Hb in thyrotoxic patients in a euthyroid state after treatment with anti-thyroid drugs or by subtotal thyroidectomy. Mean level of SDH, on the other hand, was increased after the treatment. In addition, positive correlations were observed between the level of erythrocyte sorbitol or GAR, and the level of free thyroxine(FT4) or free triiodothyronine(FT3). A negative correlation was observed between the level of erythrocyte SDH and the level of FT4 or FT3. These results suggest that the level of erythrocyte sorbitol may be increased through direct acceleration of erythrocyte GAR activity by increased thyroid hormone levels in patients with thyrotoxicosis.
[Changes in TSH-receptor antibody (TR-AB) and thyroid stimulating antibody (TS-AB) after thyroidectomy in thyrotoxic patients].
Changes in TSH-receptor antibody (TR-Ab) and thyroid stimulating antibody (TS-Ab) after thyroidectomy were examined in seventeen thyrotoxic patients (3 males and 14 females, 40.0 +/- 3.4 yr) with positive TR-Ab and TS-Ab. They were subjected to thyroid surgery because of suspected malignancy, methymazol induced agranulocytosis, cardiac failure, recurrent gastric ulcer or emotional instability. Of these patients, 3 were totally thyroidectomized, 11 were subtotally thyroidectomized and 3 were unilaterally lobectomized. Histological findings in these patients showed diffuse hyperplasia in 8 cases, an adenomatous goiter in 3, diffuse hyperplasia plus follicular adenomas in 5, and Hashitoxicosis in one. Their thyroid function before surgery was as follows: T3 level, 3.9 +/- 0.7 ng/ml; T4, 19.5 +/- 3.3 micrograms/dl; free T3, 11.9 +/- 1.2 pg/ml; free T4, 4.9 +/- 1.0 ng/dl; and TSH, 0.9 +/- 0.1 microU/ml. Mean levels of TR-Ab and TS-Ab before surgery were 56.8 +/- 4.6% and 1,218.6 +/- 262.4%, respectively. Positive anti-thyroid antibody (TGHA) was 47.0%, positive anti-microsomal antibody (MCHA) was 88.2% in these thyrotoxic patients, and mean levels of TGHA and MCHA were 1,688 +/- 715 and 89,280 +/- 34,717 times, respectively. After the operation, these parameters were decreased and their thyroid functions became an euthyroid or a hypothyroid state one month later. The incidence of post-operative hypothyroidism was 45.5% in subtotally thyroidectomized patients, 33.3% in unilaterally lobectomized patients and 100% in totally thyroidectomized patients. TR-Ab levels decreased from 56.2 +/- 6.5% before surgery to 24.5 +/- 12.2% 12 months after surgery, but increased again to 35.0 +/- 15.7% 24 months after surgery in subtotally thyroidectomized patients. These levels also decreased from 50.4 +/- 11.0% before surgery to 37.8 +/- 11.4% 12 months after surgery, and remained unchanged to 38.2 +/- 10.4% 24 months after surgery in unilaterally lobectomized patients. On the other hand, in totally thyroidectomized patients, TR-Ab levels decreased and normalized 12 months after surgery. One of subtotally thyroidectomized or unilaterally lobectomized patients developed recurrent thyrotoxicosis with an increased positive TR-Ab. Mean levels of TS-Ab decreased to 28.3 +/- 181.3% and 152.5 +/- 47.9% 12 and 24 months after surgery, respectively, in subtotally thyroidectomized patients. These levels decreased 12 months after surgery and then increased again to 303.6 +/- 130.6% in unilaterally lobectomized patients. On the other hand, TS-Ab levels decreased and normalized to 94.3 +/- 3.9% 6 months after surgery in totally thyroidectomized patients.(ABSTRACT TRUNCATED AT 400 WORDS)
[Clinical significance of erythrocyte sorbitol, sorbitol dehydrogenase and glyceraldehyde reductase in diabetic complications].
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[Primary plasmacytoma of the thyroid--report of an autopsy case and review of the literature in Japan].
Primary extramedullary plasmacytoma (PEMP) of the thyroid is rare. Only nine patients with PEMP of the thyroid have been reported in Japan to date. We describe an additional autopsy case with PEMP of the thyroid and review of the literature in Japan. A 67-year-old women complaining of swelling of the anterior neck exhibited thin scalp hair, edematous face and a giant, hard, nodular goiter. Laboratory examination showed elevated levels of ESR, collagenous reaction, gammaglobulin, and a M-bow of the IgG-k type in immunoelectrophoresis. No Bence-Jones protein was found in the urine. Thyroid function test revealed a subclinically hypothyroid state, showing a T3 of 1.32 ng/ml, a T4 of 10.0 micrograms/dl, a TSH of 23.4 microU/ml and positive thyroid antibodies. The scintigram and the CT scan of the thyroid showed deviation of the trachea by the thyroid tumor and calcification within homogeneous thyroid gland. She underwent total thyroidectomy because of suspected malignancy. The histological examination of the removed thyroid weighing 117gr revealed a proliferation of plasma cells and lymphocytes and small amounts of atrophied thyroid follicles. The immunohistological examination of the removed thyroid showed the monoclonality to IgG-k chain. Plasma cells were stainable with methylgreenpyronine. Twenty-six months after thyroidectomy, she died due to progressive emaciation, anemia, hypoalbuminemia and ascites. Postmortem examination revealed widespread metastasized plasma cell tumors in the liver, intestine, spleen and mesentery with ischemic changes in heart and kidney. Based on our autopsy case and the nine cases reported in Japan, clinical and histological characteristics of PEMP of the thyroid were discussed.
Urinary excretion of angiotensin-converting enzyme in NIDDM patients with nephropathy.
Twenty-four-hour urinary excretion of angiotensin-converting enzyme (ACE) was investigated in relation to that of albumin and beta 2-microglobulin (beta 2M) in 25 non-insulin-dependent diabetes mellitus (NIDDM) patients without nephropathy, 13 NIDDM patients with incipient nephropathy, 18 NIDDM patients with overt nephropathy, and 14 nondiabetic subjects. NIDDM patients without nephropathy and nondiabetic subjects were similar in albumin, beta 2M, and ACE excretion. NIDDM patients with incipient nephropathy had elevated albumin excretion (P less than .01) and similar beta 2M and ACE excretion compared with nondiabetic subjects. On the other hand, NIDDM patients with overt nephropathy had elevated albumin, beta 2M, and ACE excretion compared with nondiabetic subjects (P less than .01). In all NIDDM patients studied, a positive correlation was found between ACE excretion and albumin excretion (r = 0.76, P less than .001) or beta 2M excretion (r = 0.52, P less than .01). These data suggest that elevated ACE excretion in NIDDM patients with overt nephropathy may be reflective of renal tubular damage.
Effect of altered sodium intake on circadian rhythm of plasma 18-hydroxycorticosterone in conscious rats.
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High-performance liquid chromatographic separation of corticosteroids in plasma of rats. Its application to the determination of the circadian rhythm of 18-hydroxycorticosterone related to aldosterone and corticosterone.
An efficient separation of corticosteroids in plasma of rats was obtained by reversed-phase high-performance liquid chromatography (HPLC). Plasma corticosteroid assays with HPLC separation were used to determine the circadian rhythm of 18-hydroxycorticosterone (18-OHB) and its possible relationship to aldosterone or corticosterone in conscious rats under standard conditions (regular diet; 12-hour light and 12-hour dark cycle). Significant circadian rhythms of plasma corticosterone, 18-OHB and aldosterone were observed with peak values at 20.00 h and nadir values at 08.00 h. The mean ratio of plasma 18-OHB to aldosterone during 24 h was 2.4. The circadian rhythm of 18-OHB was also correlated with that of plasma aldosterone or corticosterone.
Effect of atrial natriuretic factor on aldosterone and its precursor steroid production in adrenal zona glomerulosa cells from spontaneously hypertensive rats.
The effect of alpha-human atrial natriuretic factor (alpha-hANP, 10(-6) M- 10(-8) M) on basal, and maximum angiotensin II (AII, 4.8 X 10(-8) M)-, ACTH (4.3 X 10(-9) M)-, and potassium (8mM)-stimulated levels of corticosterone, 18-hydroxycorticosterone (18-OHB) and aldosterone production were studied in adrenal glomerulosa cells from spontaneously hypertensive rats (SHR) at 14 weeks of age as compared to those in the age-matched Wistar-Kyoto rats (WKY) on a normal sodium diet. Plasma corticosterone, 18-OHB and aldosterone levels and the aldosterone response in vitro to the graded doses of AII were similar in SHR and WKY. Basal, and maximum AII-, ACTH-, and potassium-stimulated levels of corticosterone, 18-OHB and aldosterone also were similar in the cells from SHR and WKY. alpha-hANP similarly inhibited basal and stimulated levels of these corticosteroids in the cells from SHR and WKY. These results indicate that the inhibitory effect of alpha-hANP on aldosteronogenesis is unaltered in SHR at 14 weeks of age on a normal sodium diet.
Direct effects of heparin on basal and stimulated aldosterone production in rat adrenal glomerulosa cells.
Direct effects of heparin (0.1-10 IU/ml) on basal and stimulated aldosterone production have been studied using intact rat adrenal glomerulosa cells. Heparin at any dose did not affect basal aldosterone production when added to the incubation medium. Heparin at a 0.01 IU/ml dose had no effect on aldosterone production maximally stimulated by angiotensin II (AII, 4.8 X 10(-8) M), ACTH (4.3 X 10(-9) M) or potassium (8.0 mM). However, heparin at 0.1 and 0.3 IU/ml doses selectively blocked aldosterone production maximally stimulated by AII but not by ACTH or potassium, while the compound at 1 and 10 IU/ml doses inhibited aldosterone production maximally stimulated by these three stimuli. In addition, the inhibitory effect of 0.3 IU/ml heparin occurred as early as 30 min after incubation with heparin. These data suggest that heparin at 0.1 and 0.3 IU/ml doses acts directly on adrenal zona glomerulosa to selectively block the stimulatory action of AII, while the compound at 1 and 10 IU/ml doses inhibits all the stimulatory actions of AII, ACTH and potassium.
Effect of angiotensin II on aldosterone and its precursor steroid production in adrenal zona glomerulosa cells from heparin-treated rats.
To assess the nature of the heparin-induced aldosterone deficiency, we investigated the stimulatory effect of angiotensin II (AII) on aldosterone and its precursor steroids in adrenal zona glomerulosa cells from heparin-treated rats compared with those in the cells from vehicle-treated rats. Heparin-treated rats had low plasma aldosterone levels, high plasma renin activity and plasma AII levels, and normal plasma corticosterone level 6 weeks after the treatment (1500 IU/kg, twice daily). Basal aldosterone production, when corrected to a uniform number of cells per group, was similar in the cells from heparin- and vehicle-treated rats. The cells from heparin-treated rats had a less sensitive and lower response of aldosterone production to AII; an increase by 4 orders of magnitude in the threshold dose for AII and a decrease in the maximum AII-stimulated level. The maximum AII-stimulated levels, but not the basal levels, of pregnenolone, corticosterone and 18-OHB production were low in the cells from heparin-treated rats. ACTH caused a similar stimulatory effect on aldosterone production in the cells from heparin- and vehicle-treated rats. The cells from heparin-treated rats had a less sensitive and lower response of aldosterone production to potassium; an increase by one order of magnitude in the threshold dose for potassium and a decrease in the maximum potassium-stimulated level, presumably because of the glomerulosa hyporesponsiveness to AII. These results suggest that our heparin-treated rats have selective impairment of adrenal zona glomerulosa cells, involving the specific receptors and the aldosterone biosynthesis, to AII.
[Production of aldosterone and its precursor steroids by the adrenal zona glomerulosa in dextran sulfate-treated rats].
Heparin and heparinoids are known to produce selective aldosterone deficiency in man and experimental animals. To assess the nature of the hypoaldosteronism caused by heparin and heparinoids, we investigated the production of aldosterone and its precursor steroids in response to angiotensin II (AII), ACTH or potassium in adrenal zona glomerulosa cells from dextran sulfate-treated rats compared with that in the cells from vehicle-treated rats. Dextran sulfate-treated rats had a decrease in plasma aldosterone and a reduction in the width of the zona glomerulosa 4 weeks after the treatment (40 mg/day, intramuscularly). In these rats, PRA and plasma AII tended to be high, and plasma corticosterone was normal. Basal aldosterone production, when corrected to a uniform number of cells per group, was similar in cells from dextran sulfate- and vehicle-treated rats. The cells from dextran sulfate-treated rats had a less sensitive and lower response of aldosterone production to AII; an increase by 4 orders of magnitude in the threshold dose for AII and a decrease in the maximal AII-stimulated level. The maximal AII-stimulated levels, but not the basal levels, of pregnenolone, corticosterone and 18-hydroxycorticosterone production were low in the cells from dextran sulfate-treated rats. ACTH produced a similar stimulatory effect on aldosterone production in the cells from dextran sulfate- and vehicle-treated rats. The cells from dextran sulfate-treated rats had a less sensitive and lower response of aldosterone production to potassium; an increase by one order of magnitude in the threshold dose for potassium and a decrease in the maximum potassium-stimulated level, presumably because of the glomerulosa hyporesponsiveness to AII. These results suggest that long-term treatment with dextran sulfate in rats produces selective impairment of adrenal zona glomerulosa cells, involving the specific receptors and the aldosterone biosynthesis, to AII in addition to a reduction in the glomerulosa width.
Prolactin control of growth and prolactin autoregulation in cultured human pituitary cells.
A human pituitary cell line (18-54,SF) grows in serum-free medium and secretes prolactin (PRL). Autoregulation of pituitary cell growth and PRL production by exogenously supplied ovine PRL (oPRL) was investigated. Human PRL (hPRL) and oPRL stimulated pituitary cell growth up to 92% and 85%, respectively, at hPRL and oPRL additions of 100-1,000 ng/ml. Short-term (1 h) incubation of the cells with oPRL decreased hPRL secretion from the cells by 72% at 10 ng/ml addition. Intracellular hPRL was stimulated under the same conditions by 50-275% at oPRL concentrations of 10-1,000 ng/ml. Long-term (10 days) incubation of the cells with oPRL had no significant effect on extracellular or intracellular hPRL production. These data suggest that the pituitary gland can serve as a primary feedback site and that PRL can autoregulate its own production as well as affect the growth of pituitary cells.