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Biomedical subjects

F Escobar-Jimenez

Publications and source records attributed to F Escobar-Jimenez.

At least 19 recordsLinked to original sources
PubMed2001

The contribution of IGF-I to skeletal integrity in postmenopausal women.

OBJECTIVES: The pathogenic role of the decline in serum concentrations of IGF-I in postmenopausal osteoporosis is not fully elucidated. We investigated the associations among IGF-I, bone mineral density (BMD), ultrasound parameters and prevalence of vertebral fractures in postmenopausal women. DESIGN: A cross-sectional study. PATIENTS: One hundred and fifty-four ambulatory postmenopausal women (61 +/- 7 years) referred for osteoporosis screening. MEASUREMENTS: IGF-I was measured by radioimmunoassay and BMD using dual-energy X-ray absorptiometry. Broadband ultrasound attenuation (BUA) and speed of sound (SOS) at calcaneus were measured by a quantitative ultrasound system. RESULTS: IGF-I was significantly lower in osteoporotic subjects and correlated positively with BMD, BUA and SOS. After adjusting for age, years since menopause and body mass index, IGF-I accounted for 8.5% of the variance at lumbar spine BMD, 4.6% at femoral neck and 7.1% at calcaneal BUA. BUA was associated with IGF-I independently of BMD. IGF-I was lower in women with vertebral fractures (91 +/- 39 microg/l vs. 114 +/- 44 microg/l; P = 0.003). The osteoporosis densitometric criteria (t-score < or = -2.5 SD) was the most strongly independent associated variable with prevalent vertebral fractures [odds ratio (OR): 3.3 (1.4-7.6)], followed by IGF-I levels below 75th percentile [OR: 3 (1-8.8)]. CONCLUSIONS: Our study shows that IGF-I is strongly associated with bone mineral density and reflects aspects of bone quality. The contribution of IGF-I to skeletal integrity in postmenopausal women is clinically relevant.

Aged↗
PubMed1998

Increased risk of autoimmune thyroid disease in hepatitis C vs hepatitis B before, during, and after discontinuing interferon therapy.

BACKGROUND: Thyroid gland dysfunction has been reported to occur with variable frequency during interferon alfa (IFN-alpha) therapy in patients with the hepatitis C virus (HCV). We prospectively evaluated if the prevalence of autoimmune thyroid disease in patients with HCV differs from that in patients with the hepatitis B virus (HBV) before, at the end of, and 6 months after stopping treatment with IFN-alpha. METHODS: One hundred thirty-four patients with HCV and 41 patients with HBV were studied. Measurements of serum free thyroxine, free triiodothyronine, thyrotropin, thyroid peroxidase antibodies (TPOAbs), thyroglobulin antibodies (TgAbs), and thyrotropin-binding inhibitory immunoglobulin were performed. RESULTS: Positive levels of TPOAb and TgAb were found in 20% and 11% of patients with HCV compared with 5% and 3% of patients with HBV, respectively. At the end of IFN-alpha therapy, thyroid gland dysfunction was more prevalent in patients with HCV (12%) compared with those with HBV (3%), with thyrotropin levels significantly higher in the HCV group (P = .03). Titers of TPOAb, TgAb, and thyrotropin-binding inhibitory immunoglobulin increased significantly (P = .02, P = .04, and P = .02, respectively) at the end of IFN-alpha therapy in patients with HCV but not in those with HBV. Patients who developed thyroid gland dysfunction were predominantly female (P = .03), had decreased levels of free triiodothyronine (P<.001), and had a higher prevalence of TPOAb (P = .03) before treatment with IFN-alpha. Thyroid gland dysfunction was reversed in 60% of those with HCV 6 months after discontinuing treatment with IFN-alpha. CONCLUSIONS: Patients with HCV are more susceptible than patients with HBV to autoimmune thyroid disease. Systematic screening of thyroid gland function and TPOAb titers in all patients with HCV before, during, and after IFN-alpha therapy appears warranted. This precaution is not necessary for patients with HBV.

Adolescent↗
PubMed1998

Methimazole-induced aplastic anemia in third exposure: successful treatment with recombinant human granulocyte colony-stimulating factor.

The major adverse reactions of antithyroid drugs are hematologic; aplastic anemia (AA) is one of the rarest and most severe complications. Use of recombinant human hemopoietic colony-stimulating factor was reported to be of benefit in patients who developed agranulocytosis, although there is still some doubt regarding the efficacy in AA. We present a case of a 58-year-old female patient with Graves' disease who developed AA in the third exposure to methimazole (MMI). The withdrawal of MMI and early treatment with 5 microg/kg per day recombinant human granulocyte colony-stimulating factor (G-CSF) for 9 days, allowed a favorable recovery of peripheral blood cell count. We conclude that the use of hemopoietic colony stimulating factors might be a suitable means to achieve the correction of severe thionamide-induced hematologic adverse reactions.

Anemia, Aplastic↗
PubMed1995

Circulating alpha-actin in non-insulin-dependent diabetics with autonomic dysfunction.

Silent myocardial ischemia in non-insulin-dependent diabetic patients occurs frequently in association with autonomic dysfunction, suggesting that diabetic neuropathy may be involved in the development of this disorder. Repeated episodes of silent myocardial ischemia can induce myocardial necrosis. Recently, actin was detected with Western blotting in the serum of patients with acute myocardial infarction and angina pectoris. We found that a large proportion of non-insulin-dependent diabetic patients with neuropathy also have detectable circulating concentrations of alpha-actin, and therefore suggest that the determination by immunoblotting of serum alpha-actin in such patients is an effective method to detect myocardial cell suffering and to identify patients that may need special consideration.

Actins↗
PubMed1995

Increased plasma pancreastatin-like immunoreactivity levels in non-obese patients with essential hypertension.

DESIGN: Pancreastatin, a novel peptide, is known to inhibit insulin secretion and to have a glycogenolytic effect, and is present in many endocrine and chromaffin cells. Both the plasma insulin levels and the adrenergic activity accompanying insulin resistance have been shown to be increased in hypertensive subjects. Our working hypothesis was that pancreastatin might play a role in these pathological phenomena. METHODS: We studied the plasma pancreastatin level in non-obese essential hypertensive patients in response to an intravenous glucose load. We further measured the responses to the glucose challenge of insulin, glucagon, catecholamines and free fatty acids, as well as other factors related to insulin resistance (i.e. lipoproteins and apolipoproteins). We separated the hypertensive patients into three groups according to their response to an oral glucose-tolerance test: normoinsulinaemic, hyperinsulinaemic and glucose-intolerant. Matched normotensive control subjects were also studied. RESULTS: Pancreastatin levels did not change in the control group after the glucose challenge. However, all hypertensive patients showed an increase in plasma pancreastatin levels after glucose loading. The normoinsulinaemic hypertensive patients also had elevated basal pancreastatin levels. The increase in pancreastatin levels was in the ranking: normoinsulinaemic > hyperinsulinaemic > glucose-intolerant. The pancreastatin: insulin ratio showed that the secretion of pancreastatin and insulin may be regulated differently. Basal free fatty acid and glucagon levels were found to be elevated both in the hyperinsulinaemic and in the glucose-intolerant group. Fasting triglycerides levels were increased in all of the hypertensive patients. Other risk factors for coronary artery disease were also found to be altered: elevated very low-density lipoprotein-cholesterol and decreased high-density lipoprotein-cholesterol, with ranking: normoinsulinaemic < hyperinsulinaemic < glucose-intolerant. CONCLUSIONS: These results show an increase in pancreastatin levels in hypertensive patients, suggesting that pancreastatin might play a role in the pathophysiology of essential hypertension.

Adult↗
PubMed1991

Hyperthyroidism due to familial pituitary resistance to thyroid hormone: successful control with 3, 5, 3' triiodothyroacetic associated to propranolol.

We herein describe a family with thyroid hormone resistance. Thyroid hormones and basal TSH were elevated. Pituitary tumor or abnormality in thyroid hormone binding proteins were ruled out by appropriate tests. Mother and sister of the propositus presented similar abnormal hormonal features but no hyperthyroidism. Initially the patient was treated with carbimazole (30 mg/day): three months later a dramatic increase in the size of the thyroid gland and in TSH levels (12.5 to 28 mU/l) were noted. Thereafter, dextrothyroxine (D-T4) and 3, 5, 3'-triiodothyroacetic acid (TRIAC) were given consecutively and treatment was accompanied by a decrease of TSH levels (2 mU/l) but thyroid hormone remained elevated. The symptoms and signs of hyperthyroidism improved with the addition of propranolol (30-60 mg/day). In conclusion, the present report describes a new family with the syndrome of THR and variable degrees of involvement among relatives. We suggest the usefulness of TRIAC therapy to decrease TSH levels and propranolol to improve thyrotoxicosis due to pituitary resistance to thyroid hormone.

Adolescent↗
PubMed1988

Measurement of parathyrin in blood from thyroid veins: two radioimmunoassays compared in patients with primary hyperparathyroidism.

We measured parathyrin (PTH) in peripheral venous blood samples and in thyroid veins (both homolateral and contralateral to the lesion) in 13 patients with surgically confirmed parathyroid adenomas. Two different RIAs were used, one specific to the mid-region of the molecule (44-68, M-PTH), the other specific to the carboxy-terminal region (65-84, C-PTH). With the M-PTH assay we established a statistically significant multiple correlation (P less than 0.05) between the PTH concentrations in blood from the peripheral and thyroid veins; no significant correlation was found when we used the C-PTH assay. Our results confirm the superiority of the M-PTH RIA over the C-PTH RIA for study of hormonal secretion in primary hyperparathyroidism.

Adult↗
PubMed1980

Behavior of secretion in the hypoxia-immobilisation stress on the rat.

Secretin was determined radioimmunologically in portal vein blood and in duodenal mucosa biopsies in stressed male Wistar rats as compared to control animals. The stressed animals showd a significantly higher scretin content of the duodenalmucosa and no different levels of the portal vein blood. A stress ulcer-reducing cimetidine application does not demonstrate any influence of secretin content on duodenal mucosa. The obvious elevation of duodenal secrtin is not the result of an increased gastric acid production, but may be a consequence of a stress-reduced susceptibility of the pancreas to endogenous secretin.

Animals↗
PubMed1978

[A field study with the combination of Pindolol and Clopamid in antihpertensive therapy (author's transl)].

In a field study comprising 678 patients with arterial hypertension efficacy and tolerance of the stable combination VKB 105 consisting of 10 mg Pindolol (Visken) and 5 mg Clopamid (Brinaldix) were investigated. Treatment with 1--2 tablets of VKB per day resulted in a successful therapy in 94% of all patients corresponding on the average to a reduction in blood pressure to 145/85 mm Hg within 14 days. In mean arterial pressures ranging between 120 and 170 mm Hg a positive linear relationship between the individual initial value and the hypotensive effect of the combination could be observed. A controlled omission trial disclosed qualitatively the respective contribution to the effect of the two components Pindolol and Clopamid. With a systematic case control of the serum potassium under the combined therapy with VKB 105 and during a monotherapy with Clopamid and antihypokalaemic effect of Pindolol could be demonstrated diminishing the tendency for potassium loss. The result revealed a far-reaching potassium neutrality of diuresis-depending stimulation of renin by the beta-receptor blocker. In 61 patients altogether subjective side-effects could be recorded, such as vertigo (5%), palpitations (2.8%), fatigue (2%), insomina (1.9%), nausea (1.7%) and vomiting (0.8%). Laboratory controls gave no indication for clinically relevant changes.

Adrenergic beta-Antagonists↗
PubMed1977

Prevention by somatostatin of rise in blood pressure and plasma renin mediated by beta-receptor stimulation.

The interrelationships of increased plasma renin and elevated blood pressure following acute beta-stimulation by orcipernaline and its prevention by somatostatin was studied in normal man. During somatostatin infusion basal values of renin and blood pressure were unchanged. Following orciprenaline both variables increased significantly. Combination of somatostatin and orciprenaline reduced the rise in plasma renin activity by 49%, mean arterial blood pressure by 21% and heart rate by 19%, compared with beta-stimulation alone. The results indicate that the inhibitory action of somatostatin on plasma renin activity may be mediated via beta-receptors. The lesser increase of blood pressure under somatostatin plus orciprenaline also indicates a possible inhibitory effect of somatostatin on beta-adrenergic receptors.

Adult↗
PubMed1977

Somatostatin modulation of pancreatic glucagon, insulin, glucose and free fatty acids following beta-adrenergic stimulation.

This study was undertaken to determine the effect of somatostatin on acute, orciprenaline mediated, beta-adrenergic stimulation of free fatty acids, blood glucose, insulin, and glucagon in healthy subjects. After orciprenaline and somatostatin insulin and glucagon decreased, whereas blood glucose and free fatty acids increased, probably in part as a result of the lesser inhibition of glucagon (50%) than of insulin (83%). From these observations it is tentatively concluded that the inhibitory effects of somatostatin on insulin and glucagon release in man are a consequence of beta-adrenergic receptor involvement. These effects are possibly mediated through increased destruction of cAMP, blocking of camp dependent secretion or impairment of calcium uptake.

Adult↗
PubMed1977

The effect of somatostatin on platelets: in vivo and in vitro studies.

The influence of somatostatin on platelets was studied in healthy volunteers. After a bolus injection of 250 microgram somatostatin followed by a three hour infusion at a rate of 250 microgram somatostatin/hr a statistically significant fall of platelet count and impairment of platelet aggregation was observed. The aggregation inhibiting effect of somatostatin at the end of the three hour infusion is clinically unimportant as compared to the effect of aspirin. In vitro concentrations up to 10.0 microgram somatostatin per ml do not show any effect on platelet aggregation and platelet stickiness. Endocrinologically active doses of somatostatin in short term infusions are very unlikely to cause bleeding disorders.

Adolescent↗