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Biomedical subjects

F Y Tseng

Publications and source records attributed to F Y Tseng.

10 recordsLinked to original sources

Prognostic factors of anaplastic thyroid carcinoma.

BACKGROUND AND PURPOSE: Anaplastic thyroid carcinoma (ATC) is one of the most aggressive malignancies. We tried to elucidate the possible prognostic factors. METHODS: A retrospective review was conducted of ATC patients in National Taiwan University Hospital from 1978 to 2003. Their demographic characteristics, clinical presentations, laboratory data and treatment modalities were reviewed. Possible prognostic factors for survival were evaluated. RESULTS: Forty-five patients (14 males and 31 females) of mean age 61.9 +/- 12.6 yr were included in this study. The median survival time was 94 days (range 6 to 776 days). The overall survival rate was 27% at 6 months and 10% at 1 yr. Thirty-two patients receiving intervention regimens had a median survival of 106 days, while 13 patients receiving palliative therapy had a median survival of 39 days. The difference in survival is statistically significant (logrank test, p = 0.017). Adjusted with sex and age, increment in white blood cell count (per 10(9)/l) and serum albumin (per 1.0 g/l) had a hazard ratio of 1.12 (Cox regression, p < 0.001) and 0.92 (p = 0.041), respectively. Patients with leukocytosis [white blood cell (WBC) count > 10(10)/l] or hypoalbuminemia (serum albumin < 35 g/l) had significant shorter survival than patients without leukocytosis or hypoalbuminemia (logrank test p = 0.008 and p = 0.032, respectively). Patients with serum T4 levels lower than 64.35 nmol/l had significantly shorter survival than patients without hypothyroxinemia (median survival 24 vs 128 days, logrank test, p = 0.004). CONCLUSIONS: ATC is an aggressive malignancy. Leukocytosis, hypoalbuminemia and hypothyroxinemia indicated poor prognosis. Survival time might be prolonged if intervention treatment is tolerable.

Adult↗

A case of extraadrenal pheochromocytoma associated with adrenal cortical nodular hyperplasia and papillary thyroid carcinoma.

A 64-year-old woman was admitted in November, 1996 for fluctuating blood pressure. There was multinodular goiter in her neck. High urine VMA and serum aldosterone were noted. Computed tomography showed an oval lesion in the left adrenal gland. Left adrenalectomy was performed and the pathology was proved to be adrenal cortical nodular hyperplasia. Fluctuating blood pressure and high urine VMA persisted after the operation. CT scan of the abdomen revealed a soft tissue mass in lower abdomen. The patient was admitted again in September, 1997. Laboratory examinations showed normal serum aldosterone, normal plasma renin activity and high urine VMA. Aspiration cytology of the thyroid gland disclosed papillary thyroid carcinoma. [131I]-metaiodobenzylguanidine image revealed a high uptake lesion in the right L-3 paravertebral area. Tumor excision and thyroidectomy were performed. The pathology was reported as extraadrenal pheochromocytoma and papillary thyroid carcinoma. Papillary thyroid carcinoma is rarely associated with pheochromocytoma. To our knowledge, this paper is the first report of a patient with extraadrenal pheochromocytoma associated with papillary thyroid carcinoma and adrenal cortical nodular hyperplasia.

Adrenal Cortex↗

Quality of medical care for noninsulin-dependent diabetic patients in a community teaching hospital in Taiwan.

To evaluate the quality of diabetes management provided by a community teaching hospital in Taipei County, the medical records of 208 noninsulin-dependent diabetes mellitus (NIDDM) patients who attended the Department of Internal Medicine, Taiwan Provincial Taipei Hospital, from July to December 1994, were selected at random and reviewed. First visit examination results were compared to the practice guidelines established by the Diabetes Association, Taiwan ROC. The frequency of biochemical tests within the last 3 years was traced for 142 NIDDM patients who had been treated regularly in the hospital. Physicians knowledge and attitudes towards diabetes management were assessed by a questionnaire. The results revealed that the practice guidelines were not followed closely by the physicians. Urinalysis, glycosylated hemoglobin A1c and high-density lipoprotein-cholesterol were the items most frequently neglected. Chest x-rays, electrocardiograms, hemograms and serum electrolytes were seldom arranged for patients without specific symptoms. Although not recommended in the guidelines, most of the physicians arranged liver function tests for their patients. Factors such as physicians knowledge and attitudes, medical insurance, high patient loads and educational levels of patients influenced medical behavior in this study. The results of the study showed that the quality of medical care for diabetes mellitus patients in this community hospital should be improved.

Adult↗

[Thyroid function tests in acute drug intoxication].

It is well known that thyroid function tests may be changed in non-thyroidal illnesses. To understand the influence of acute drug intoxication on thyroid function tests, 31 drug intoxicated patients without previous thyroid disorders and systemic diseases were included in our study. T3, T4, TSH, and resin T3 uptake were checked as soon as they arrived at our emergency service and were compared to that of 58 healthy volunteers. Within 31 patients, 14 were intoxicated by organophosphorous compounds, 6 by sedatives and hypnotics, 3 by strong acid, 2 by paraquet, 2 by rodenticides (warfarin), 2 by lysol and the other 2 were intoxicated by acetaminophen. The mean T3 and TSH levels were significantly lower in the drug intoxicated group. Among the 31 patients, 14 (45.2%) had a low T3, 2 (6.5%) had a low T3 and T4, and 6 (19.3%) had an elevated T4. All of the patients with an elevated T4 were intoxicated by organophosphates. If we divided the 31 patients into 2 subgroups: organophosphate intoxicated group and non-organophosphate intoxicated group, T4 and FT4I were significantly higher in the former group. Thyroid function tests became normal after treatment in 27 patients, discharged in good general condition. T3 and T4 became extremely low in 4 patients before they expired. The present study confirms that acute drug intoxication, like other non-thyroidal illnesses, affects thyroid function tests. Acute organophosphate intoxication may cause transient hyperthyroxinemia.

Acute Disease↗

Acute relapsing pancreatitis in primary hyperparathyroidism with hypercalcemia aggravated after aspiration cytology: report of a case.

In 1957, Cope and his associates first noted 2 cases of pancreatitis associated with primary hyperparathyroidism. They emphasized the association of hyperparathyroidism and pancreatitis. Since then pancreatitis has become a diagnostic clue to primary hyperparathyroidism. We report herein a 39-year-old woman who had suffered from acute relapsing pancreatitis 3 times in the past 2 years. Hypercalcemia persisted throughout the course. A movable mass 3 x 3 cm in diameter was noted over the right thyroid area on physical examination. A hypoechogenic mass 3.5 x 2.7 x 1.4 cm was found between the right lobe of the thyroid and the carotid artery. Because of a persistently high serum level of Ca2+, normal saline and furosemide were infused; the serum Ca2+ decreased gradually. After aspiration of the suspected mass, the serum level of Ca2+ increased from 8.7 mg/dL to 18 mg/dL. Because of the impression of parathyroid adenoma, surgery was performed and a 3 x 2.5 x 1.5 cm well-encapsulated mass was excised without difficulty. Pathologic examination revealed a well-encapsulated parathyroid adenoma. This case reveals that primary hyperparathyroidism maybe one of the causes of pancreatitis, and aspiration cytology, although it may be helpful for the diagnosis, can aggravate the hypercalcemia.

Acute Disease↗

Inhibition of intermediary metabolism by amiodarone in dog thyroid slices.

Amiodarone, an iodine-containing antiarrhythmic drug, has been reported to interfere with thyroid function and thyroid hormone metabolism. We studied the effects of amiodarone on basal and agonist [thyroid-stimulating hormone (TSH), phorbol ester, or carbachol]-stimulated glucose oxidation, 32PO4 incorporation into phospholipids, and adenosine 3',5'-cyclic monophosphate (cAMP) concentration in dog thyroid slices. Slices were preincubated with amiodarone at 37 degrees C for 1 h before the addition of agonist and the appropriate radioisotope. cAMP stimulation was measured after 20 min, glucose oxidation for 45 min, and 32PO4 incorporation into phospholipids for 2 h. Amiodarone (0.5 mM) had no effect on basal 14CO2 formation or 32PO4 incorporation into phospholipids but significantly inhibited TSH, phorbol ester, and carbachol stimulation of these parameters. It also inhibited cAMP stimulation by TSH. Inhibition of TSH-stimulated [14C]glucose oxidation was also obtained with another iodide-containing compound, iopanoic acid (0.5 mM), but not with iothalamate (up to 10 mM). Inhibition by amiodarone was still present, but to a lesser extent, when it was added at the same time as the agonist. Inhibition of stimulated [14C]glucose oxidation persisted even after the slices were incubated without amiodarone for 6 h. Inhibition by amiodarone, in contrast to that by inorganic iodide, was not prevented by 1 mM methimazole added at the same time as amiodarone. These results indicate that the inhibitory effects of amiodarone on thyroid function are not due to dissociation of iodide from the molecule.

Amiodarone↗

Effect of iodide on glucose oxidation and 32P incorporation into phospholipids stimulated by different agents in dog thyroid slices.

Since iodide (I-) inhibits TSH stimulation of cAMP formation, which mediates most of the effects of the hormone, it has been assumed that this accounts for the inhibitory action of iodide on the thyroid. However, TSH stimulation of 32P incorporation into phospholipids and stimulation of thyroid metabolism by other agonists, such as carbachol, phorbol esters, and ionophore A23187, is not cAMP mediated. The present studies examined the effect of iodide on stimulation of glucose oxidation and 32P incorporation into phospholipids by TSH and other agonists to determine if the inhibition of cAMP formation was responsible for the action of iodide. Preincubation of dog thyroid slices for 1 h with iodide (10(-4) M) inhibited TSH-, (Bu)2cAMP-, carbachol-, methylene blue-, 12-O-tetradecanoyl phorbol-13-acetate-, ionophore A23187-, prostaglandin E1-, and cholera toxin-stimulated glucose oxidation. I- also inhibited the stimulation by TSH, 12-O-tetradecanoyl phorbol-13-acetate, carbachol, and ionophore A23187 of 32P incorporation into phospholipids. The inhibition was similar whether iodide was added 2 h before or simultaneously with the agonist. I- itself sometimes stimulated basal glucose oxidation, but had no effect on basal 32P incorporation into phospholipids. The effects of iodide on basal and agonist-stimulated thyroid metabolism were blocked by methimazole (10(-3) M). When dog thyroid slices were preloaded with 32PO4 or [1-14C]glucose, the iodide inhibition of agonist stimulation disappeared, suggesting that the effect of iodide involves the transport process. In conclusion, I- inhibited stimulation of glucose oxidation and 32P incorporation into phospholipids by all agonists, indicating that the effect is independent of the cAMP system and that iodide autoregulation does not only involve this system. Oxidation and organification of iodide are necessary for the inhibition. The ability of iodide to decrease glucose and 32PO4 transport may play an important role in thyroid autoregulation.

Alprostadil↗

Effects of lithium on stimulated metabolic parameters in dog thyroid slices.

Thyroid abnormalities may develop during chronic lithium therapy for affective disorders. Lithium, like iodide, inhibits TSH stimulation of adenylate cyclase and thyroid hormone release. The present study examined the effect of lithium on stimulation of intrathyroidal intermediary metabolism by several agonists. LiCl (5 mmol/l) did not inhibit basal cAMP, glucose oxidation or 32P incorporation into phospholipids in dog thyroid slices. Although LiCl inhibited TSH stimulation of cAMP, it did not abolish the hormone's effect on cAMP-dependent protein kinase. The stimulation of iodide organification, glucose oxidation or 32P incorporation into phospholipids by TSH, carbachol and phorbol esters was not inhibited by lithium. This is in contrast to the effects of iodide, which inhibited stimulation of glucose oxidation and 32P incorporation into phospholipids by various agonists. Thus, although both lithium and iodide inhibited TSH-stimulated cAMP formation, they act differently on intrathyroidal intermediary metabolism.

Animals↗

The changes of serum titers of thyroid antibodies in patients of Graves' disease with hyperthyroidism after treatments with antithyroid drugs.

In order to investigate the effect of antithyroid drugs on serum titers of antithyroglobulin and anti-thyroid microsomal antibody, these two antibody levels were studied in 38 patients of Graves' disease with hyperthyroidism before and after treatments with carbimazole or methimazole. The results showed no consistent changes in their titers. To explain the inconsistent findings as compared with other authors' studies, lower doses of antithyroid drugs were postulated as one of the causes.

Adolescent↗