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Biomedical subjects

O Mizuno

Publications and source records attributed to O Mizuno.

At least 37 records · Page 2Linked to original sources

Multiple saccular aneurysm formation in a patient with bilateral coronary artery fistula: a case report and review of the literature.

We describe a case of bilateral coronary artery fistula originating from the left anterior descending and right coronary arteries which showed multiple saccular aneurysm formation. Although saccular aneurysm formation in patients with bilateral coronary artery fistula is extremely rare, only 3 similar cases having been reported before, it shows two distinctive features upon coronary angiography: multiplicity and origin in the left fistulous coronary artery.

Adult↗

[A case of malignant pheochromocytoma treated with a combination of cyclophosphamide, vincristine, and dacarbazine (CVD). A review of the Japanese literature of malignant pheochromocytoma treated with a combination of CVD].

A 49-year-old woman had a right adrenalectomy for pheochromocytoma in April 1989. In May 1990 she underwent an operation to remove paraaortic lymph nodes, and the lymph nodes showed pheochromocytoma. Twenty-two months after the first operation, metastases to the left cervical nodes, lung, and liver occurred. Her blood pressure was 172/104 mmHg; fasting plasma glucose (FPG), 342 mg/dl; urinary noradrenaline (NA), more than 2000 micrograms/day; and plasma NA, 17.28 ng/ml. Treatment with the CVD regimen (cyclophosphamide, 750 mg/m2 on day 1; vincristine, 1.4 mg/m2 on day 1; dacarbazine, 600 mg/m2 on days 1 and 2, every 21 days) was begun on February 14, 1991. After 3 cycles of the CVD regimen her blood pressure was 140/82 mmHg; FPG, 157 mg/dl; urinary NA, 917 micrograms/day 1; and plasma NA, 4.54 ng/ml. The size of the metastatic lesions in the liver had decreased. Treatment with the CVD regimen was continued until May 1992. After that she did not go to the hospital for about 2 months. Metastatic lesions progressed gradually and treatment with the CVD regimen was repeated again. She was admitted to the hospital on February 17, 1993 because of appetite loss and nausea. Her blood pressure was 188/94 mmHg; FPG, 197 mg/dl; HbA1c, 9.5%; urinary NA, 18265.3 micrograms/day; and plasma NA, 47.20 ng/ml. She was treated with the CVD regimen in 2 repeated cycles (28th cycle of treatment with the CVD regimen) but there was no effect. She died following hemoptysis on March 15, 1993.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Gland Neoplasms↗

[Increased plasma antidiuretic hormone in the presence of hyponatremia in primary hypothyroidism].

A 70-year-old woman was admitted because of disturbance of her consciousness. Physical examinations and laboratory data suggested hypothyroidism. Primary hypothyroidism was subsequently confirmed with endocrinological examinations. Antidiuretic hormone (ADH) levels were elevated despite severe hyponatremia. On admission, urinary sodium concentration was 10mEq/l. The patient was treated with saline intravenously; serum sodium level increased from 120 to 125mEq/l and urinary sodium concentration increased from 10 to 54mEq/l. Mental confusion developed and serum sodium level dropped with urinary sodium concentration above 20mEq/l when thyroid replacement was started with the cessation of saline infusion. The patient's state of consciousness, elevated ADH levels, decreased serum sodium level and urinary sodium concentration were improved by thyroid replacement together with hydrocortisone therapy. Effects of acute water loading were abnormal with the administration of iodothyronine (T3) alone but were normalized with the administration of hydrocortisone together with T3. On discharge she was treated with the oral administration of levothyroxine alone. Pituitary hormones were normal. These results suggest that the patient was in a state of hypoadrenocorticism. Impaired water excretion in a state of hypoadrenocorticism due to hypothyroidism may give rise to an inappropriate secretion of ADH thereby resulting in hyponatremia, which in turn leads to hypotonic dehydration induced by water intoxication.

Adrenal Cortex↗

Vascular responses to angiotensin II in anorexia nervosa.

Anorexia nervosa (AN) patients have a tendency to develop renin-angiotensin-aldosterone (RAA) abnormalities caused by abnormal behaviors expressed over long periods of time. Short-term dietary sodium intake is a known modulator of blood pressure response to infused angiotensin II (A II) in normal subjects. Therefore AN patients and normal gender-matched and age-matched controls were studied for vascular responses to exogenous A II. Untreated AN patients needed significantly greater quantities of exogenous A II to raise diastolic blood pressure (DBP) to over 20 mmHg for 30 min compared with controls (12.1 +/- 0.47 versus 7.6 +/- 0.69 ng/kg/min, p < 0.01). The amount of A II required to raise DBP to over 20 mmHg in AN patients in tests before and after completion of treatment (4.2 +/- 0.33 months later) was significantly different (12.1 +/- 0.47 versus 8.1 +/- 0.25 ng/kg/min, p < 0.01). There was no significant difference between AN patients following treatment and controls. Our results indicate that it requires long time before decreased A II responsiveness caused by chronic sodium depletion normalizes in AN patients.

Adolescent↗

An autopsy case of intracranial hemorrhage during tissue plasminogen activator infusion.

We describe an autopsy case of severe intracranial hemorrhage which occurred during the infusion of tissue plasminogen activator (t-PA) for acute myocardial infarction. A 75-year-old man was admitted with substernal chest pain of 3-h duration and electrocardiographic changes consistent with an acute inferior myocardial infarction. Physical examination was unremarkable, except for an initial blood pressure reading of 160/96 mmHg. The patient received 3,000 IU intravenous heparin followed by a 2.4 x 10(6) IU bolus dose of tissue plasminogen activator (t-PA) (Alteplase). This was followed by a drip infusion of 21.6 x 10(6) IU of t-PA over 1 h (total dose 41 mg). Thirty minutes after the infusion of t-PA was initiated, the patient suddenly lost consciousness and began to have violent convulsions, followed by cardiac arrest. Autopsy revealed massive hemorrhage in the bilateral cerebrum and brain stem. To our knowledge, this is the first case of sudden death during t-PA infusion therapy.

Aged↗

Aldosterone responses to angiotensin II in anorexia nervosa.

Patients with anorexia nervosa (AN) tend to have renin-angiotensin-aldosterone (RAA) abnormalities caused by abnormal behaviors such as strict dieting, fasting, vigorous exercise, self-induced vomiting and abuse of laxatives and/or diuretics. Adrenal responsiveness to angiotensin II (A II) was studied in 13 AN patients before and after therapy and in 6 normal sex- and age-matched controls: adrenal responses to postural change (1 h of walking following 1 h in a supine position) and to exogenous A II injection (A II: 10 ng/kg/min intravenous infusion for 30 min). The 24-h urine sodium concentration was significantly lower in AN patients before therapy than after therapy. Plasma aldosterone secretory response to A II was significantly higher in AN patients before therapy in both postural change and exogenous A II injection tests compared with after therapy response and that of controls. On the other hand, there was no significant difference in adrenal response to postural change or to exogenous A II between AN patients after therapy and controls. In conclusion, increased A II sensitivity caused by chronic sodium deficiency in AN patients normalized over time as the patients recovered.

Adult↗

Secretory function of the renin-aldosterone system in patients with anorexia nervosa.

Patients with anorexia nervosa frequently demonstrate dehydration, electrolyte imbalance and low blood pressure that are secondary to starvation. Hyperactivity of the Renin-Aldosterone system and insensitivity to the pressor effects of exogenous angiotensin II are observed in Pseudo-Bartter syndrome caused by the abuse of diuretics or laxatives and self-induced vomiting, however, little information about the Renin-Aldosterone system has been reported in patients with anorexia nervosa. This study was designed to investigate the secretory function of the Renin-Aldosterone system in anorexia nervosa. The subjects were 13 patients with anorexia nervosa and 6 normal controls. Experiment 1: Angiotensin II infusion test was performed. Blood pressure was measured every 5 minutes, and the samples for plasma renin and serum aldosterone analysis were taken every 15 minutes during infusion test. Experiment 2: Plasma renin activity and serum aldosterone concentration were measured before and after one-hour walking. The results were as follows; (1) Basal plasma renin activity and serum aldosterone concentration in patients were not significantly higher than those in normal subjects. (2) Hypertensive response with elevation of the diastolic pressure during angiotensin II infusion in patients similar to that of normal subjects was observed. (3) Responses of plasma renin activity and serum aldosterone concentration after one-hour walking were significantly greater in patients than in normal subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Heterogeneity of serum prolactin in patients with menstrual disorder in conjunction with hyperthyroxinemia.

Since the secretion of PRL is regulated by the hypothalamic-pituitary axis, an increase in large molecular size PRL in the serum is most likely due to secretion by the pituitary itself. The present study was performed to investigate the possible occurrence of PRL heterogeneity in 128 subjects with menstrual disorder in conjunction with hyperthyroxinemia (88 with untreated Graves' disease, 40 with subacute thyroiditis) and 50 age- and sex-matched healthy controls. All 128 patients in this study were suffering from amenorrhea or oligomenorrhea at the time of their initial visit. PRL heterogeneity was found in the sera of 5 of 88 (5.7%) patients with untreated Graves' disease, in 2 of 40 (5.0%) patients with subacute thyroiditis, but in none of the normal controls. PRL heterogeneity remained essentially unchanged in patients with Graves' disease over 6 months of treatment; however, in patients with subacute thyroiditis, either big-big PRL or big PRL decreased significantly along with a corresponding increase in little PRL associated with recovery from the illness within 6 months. The menstrual disorders in all patients were restored to normal after restoration to a euthyroid state. The underlying cause of the occurrence of PRL heterogeneity in patients with menstrual disorder in conjunction with hyperthyroxinemia is not known.

Adolescent↗

Thyroid-stimulating antibody and thyrotropin-binding inhibitory immunoglobulin activity in hypothyroid patients who subsequently developed thyrotoxicosis.

Although abnormal thyroid-stimulating and -blocking antibodies have been demonstrated in hyperthyroid and hypothyroid patients with autoimmune thyroid disorders, a direct correlation is not always observed. Thyroid-stimulating antibody, thyrotropin-binding inhibitory immunoglobulin, and thyroid-stimulating blocking antibody levels were determined in three hypothyroid patients who subsequently developed hyperthyroidism. Thyroid-stimulating antibodies levels were normal in one, elevated in another, and unmeasured in the third hypothyroid patient, but became elevated in all patients with the onset of hyperthyroidism. There was discordance, however, in one patient who had markedly elevated thyroid-stimulating antibodies and TSH-binding inhibitory immunoglobulin levels when she was hypothyroid. The data indicate that thyroidal responses to the abnormal stimulating antibodies may differ among patients with autoimmune thyroid disease.

Adult↗

Transient nephrogenic diabetes insipidus associated with acute hepatic failure in pregnancy.

A 29-year-old nullipara was admitted at 31 weeks' gestation because of toxemia. She noted gradually polyuria, severe thirst, malaise, nausea and anorexia. A water-deprivation test and administration of aqueous vasopressin confirmed the diagnosis of nephrogenic diabetes insipidus. At 33 weeks' gestation, blood chemistry studies revealed moderately elevated transaminase levels and hyperuricemia. Male twins were delivered by vacuum extraction at 35 weeks' gestation. After delivery, she became drousy and icterus appeared. Acute hepatic failure with marked hyperuricemia was diagnosed. She was treated with glucose solution with glucagon and soluble insulin, branched chain amino acids, gabexate mesilate, lactulose and famotidine. Her consciousness cleared rapidly and all laboratory data became normal by 15 days postpartum. The urine volume was about 5 liters per day from the first to sixth postpartum day. The diuresis decreased after the eighth postpartum day. Rare pregnancy complicated by transient nephrogenic diabetes insipidus and acute hepatic failure is discussed.

Adult↗

[The changes of serum total cholesterol, HDL-cholesterol and atherogenic index in postpartum].

The changes of serum total cholesterol (TC), HDL-cholesterol (HDL-C), Atherogenic Index [TC-HDL-C)/HDL-C, AI) and body weight in postpartum were studied in 58 normal women with obvious hypercholesterolemia (TC greater than or equal to 300 mg/dl) during pregnancy. They were divided into two groups: Groups A (n = 33) and B (n = 25), according to the maximal levels of TC (TCmax) in pregnancy, (Group A: TCmax less than 350mg/dl, Group B: TCmax greater than or equal to 350mg/dl). These groups were divided into four subgroups according to the length of time during which TC was below 250mg/dl) after delivery. In Groups A1 (n = 20) and B1 (n = 12) TC reached 250mg/dl within 10 weeks postpartum, and in Groups A2 (n = 13) and B2 (n = 13) after more than 11 weeks postpartum. TC in Group A was significantly higher than in Group B within 6 weeks postpartum. In Group A AI was significantly lower than in Group B at the same period. HDL-C in Group B1 was significantly higher than in Group B2. AI in Group B1 was significantly lower than in Group B2. In Group A TC reached 250mg/dl more rapidly than in Group B. The average weekly weight loss in postpartum in each Group A1 or B1 was significantly greater than each Group A2 or B2. The degree of hypercholesterolemia in pregnancy might influence the changes of serum lipids in postpartum. Rapid weight loss in postpartum might bring rapid recovery from abnormal metabolism of serum lipids in pregnancy.

Adult↗

[The influence of weight changes in pregnancy and postpartum on serum total cholesterol and triglyceride].

We measured total cholesterol (TC) and triglyceride (TG) in 78 pregnant women with obvious hypercholesterolemia (TC greater than or equal to 300 mg/dl) in pregnancy, measuring the concomitant effects of age, grade of obesity prior to pregnancy, total weight gain and degree of weight gain during pregnancy. After delivery the body weight was measured until TC was below 250 mg/dl, and then the average weekly weight loss was calculated. Age, the grade of obesity prior to pregnancy, total weight gain or degree of weight gain during pregnancy did not influence TC or TG in pregnancy. TC or TG in pregnancy had no effects on the birth weight of the newborn. There was significantly positive correlation between TC or TG at the 13th-16th week of pregnancy and the maximal level of TC or TG in pregnancy. In 22 of the 25 subjects, whose average weekly weight loss was 1.0 kg or over, TC was below 250 mg/dl by the 8th week postpartum. In pregnancy many factors including weight changes might influence TC or TG; however, the effects of weight changes postpartum on TC or TG such as weight reduction in obesity might appear.

Adult↗

Maturation of ovarian follicles after inhibition of ovulation in rats.

The present investigation was performed to elucidate the mechanism of the initiation of follicular maturation after inhibition of ovulation in rats treated with pentobarbitone sodium at 13.30 h and progesterone at 14.00 h on the day of pro-oestrus (day 0 denotes the day of these treatments). Ovulation was completely inhibited and the next spontaneous ovulation occurred on day 5, the expected day of the next oestrus. Follicular responsiveness to injection of human chorionic gonadotrophin (hCG) indicated that preovulatory follicles at the time of treatment with pentobarbitone and progesterone regressed by 05.00 h on day 2. Maturation of a new set of follicles began from 17.00 h on day 2 and all rats were induced to ovulate by hCG injection by 17.00 h on day 3, the number of oocytes ovulated being comparable to normal ovulation. In the animals receiving pentobarbitone sodium and progesterone treatment, two selective rises in plasma FSH, which had peak levels at 05.00 h on day 1 and 11.00 h on day 2, were observed without a rise in LH. Preovulatory surges of FSH and LH occurred on the afternoon of day 4. These results suggest that the second rise in FSH was induced by regression of Graafian follicles present at the time of treatment with pentobarbitone sodium and progesterone and that this surge of FSH was responsible for initiation of maturation of a new set of follicles destined to ovulate in the subsequent cycle. The mechanism of induction and the role of the first rise of FSH from the night of day 0 to the morning of day 1 cannot be explained at present.

Animals↗

Transient thyrotoxicosis occurred after cessation of steroid therapy in a patient with autoimmune thyroiditis and rheumatoid arthritis.

A 51-year-old woman with chronic lymphocytic thyroiditis showed transient thyrotoxicosis at seven weeks after cessation of steroid therapy for treatment of rheumatoid arthritis. Radioactive iodine uptake was only 3% even in the thyrotoxic state. Aspiration biopsy, performed just before the development of hypothyroidism, revealed histological features compatible with chronic lymphocytic thyroiditis. At two months after the onset of thyrotoxicosis, hypothyroidism developed, and she was kept in a euthyroid state by 1-thyroxine replacement therapy. Irreversible hypothyroidism was confirmed by the recurrence of hypothyroidism after cessation of thyroid replacement therapy at one year after the onset of thyrotoxicosis. The causal relationship between the cessation of steroid therapy and the occurrence of transient thyrotoxicosis is discussed.

Arthritis, Rheumatoid↗