Lack of elevated serum carcinoembryonic antigen and calcitonin in medullary thyroid carcinoma.
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Biomedical subjects
Publications and source records attributed to J J Diez.
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Thyroid hormones play a role in the regulation of insulin-like growth factor type 1 (IGF-1) and insulin-like growth factor-binding protein-3 (IGFBP-3) expression, and both IGF-1 and IGFBPs have been shown to be related to the function and growth of the thyroid. Our aim was to evaluate serum concentrations of IGF-1, IGFBP-1, and IGFBP-3 in patients with thyroid dysfunction before and after normalization of thyroid function. The study was performed in 86 patients with thyroid dysfunction (43 hyperthyroid and 43 hypothyroid patients) and 17 euthyroid subjects. Serum growth hormone (GH), insulin, IGF-1, IGFBP-1, and IGFBP-3 were measured in all patients before and after normalizing serum thyroid hormone concentrations. Hyperthyroid patients showed IGF-1 (198.8 +/- 17.0 microg/L) and IGFBP-3 levels (4.2 +/- 0.2 mg/L) similar to those found in the control group (217.9 +/- 20.3 microg/L and 4.2 +/- 0.3 mg/L, respectively). After therapy these levels significantly decreased to 156.6 + 11.1 microg/L (p < 0.01) and 3.3 +/- 0.1 mg/L (p < 0.001), respectively. IGFBP-1 concentrations were clearly higher than those found in controls (22.7+/- 2.6 vs. 5.7 +/- 1.5 microg/L, p < 0.001) and exhibited a significant reduction after therapy for thyroid hyperfunction (11.0 +/- 1.7 microg/L, p < 0.001). Patients with hypothyroidism showed serum concentrations of IGF-1 (161.5 +/- 13.1 microg/L, p < 0.05) and IGFBP-3 (3.2 +/- 0.3 microg/L, p < 0.05) significantly lower than those found in healthy volunteers. However, replacement therapy with levothyroxine did not induce any significant modification of these concentrations (152.6 +/- 10.6 microg/L and 3.2 +/- 0.2 mg/L, respectively). Similarly, patients with thyroid hypofunction exhibited raised levels of IGFBP-1 (15.5 +/- 0.9 microg/L, p < 0.05 vs. control group) that were significantly decreased after therapy (8.8 +/- 1.4 microg/L, p < 0.01). The results of the present study show that thyroid status affects GH/IGF axis. Hypothyroidism is associated with significant reductions of IGF-1 and IGFBP-3, and IGFBP-1 is elevated in both hypothyroidism and hyperthyroidism.
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Subungual hemorrhages may be observed in a variety of systemic diseases and in some otherwise healthy persons. We describe three male patients who were referred because of toenail hemorrhages. Analytical investigations showed hyperglycemia in all the patients. Toenail bilateral hemorrhages were the first manifestation of previously undiagnosed type II diabetes mellitus in all cases. Ophthalmologic examination showed signs of background diabetic retinopathy in all three patients. The existence of retinopathy suggests that subungual hemorrhages might be due to microvascular involvement and could herald the presence of diabetes mellitus.
Recovery of the pituitary function from post-traumatic hypopituitarism is an exceptional event. We present the case of a 32 year-old man who was involved in a road traffic accident in which he suffered a severe head injury. Four days following the trauma the patient developed post-traumatic central diabetes insipidus and desmopressin was started. At discharge of the intensive care unit, the patient was referred to us for endocrine assessment. Three months after the head injury, the hormonal evaluation of the hypothalamic-pituitary axis by means of insulin stress test with the simultaneous administration of TRH and GnRH resulted in reduced responses of GH, cortisol, TSH, FSH, and LH with low baseline serum concentrations of free T4 and testosterone. Both serum basal and stimulated PRL concentrations were normal. Magnetic resonance imaging demonstrated deformity of the sella turcica with displacement of the pituitary gland by a post-traumatic retention cyst. A new evaluation of the pituitary function performed 6 months after the trauma showed spontaneous recovery of the gonadal, thyroid and adrenal function. However, GH response was reduced both to insulin-induced hypoglycemia, clonidine and GHRH tests. Presence of normal serum PRL levels, normal PRL response to TRH and reduced GH responses to pituitary and hypothalamic stimuli suggests both hypothalamic and pituitary damage. The present case shows an unusual case of partial spontaneous resolution of a post-traumatic hypopituitarism. Based on this clinical observation we recommend periodic evaluation of the pituitary function in these kind of patients.
Correction of anemia with recombinant human erythropoietin (rHuEPO) in patients with end-stage renal disease (ESRD) has been associated with improvement of several endocrine abnormalities. However, long-term effects of this therapy on pituitary secretion in patients undergoing continuous ambulatory peritoneal dialysis (CAPD) is not known. The aim of the present work was to assess the growth hormone (GH) and cortisol responses to insulin-induced hypoglycemia before and after the correction of anemia with rHuEPO therapy in CAPD patients. Five well-nourished and clinically stable patients were studied before and after 12-24 weeks of rHuEPO treatment. Seven normal volunteers were studied as controls. Insulin-induced hypoglycemia tests were performed prior to starting rHuEPO therapy and again after partial correction of anemia. Blood samples for GH, cortisol, and glucose were collected between -30 and 120 min after insulin (0.1 U/kg bw) administration. GH responses to hypoglycemic stress were characterized by marked differences in single patients when compared with the control group. However, the GH peak and the area under the secretory curves (AUC) of GH responses in CAPD patients (10.6 +/- 4.8 micrograms/L and 15.4 +/- 6.1 micrograms h/L, respectively) did not differ from those obtained in control subjects (14.3 +/- 4.1 micrograms/L and 19.4 +/- 3.5 micrograms h/L, respectively). The study, after correction of anemia, showed an evident decrease of GH values at each time point on the response curve in 4 patients, and no modification in 1 patient. Mean values of GH peak and AUC were 8.8 +/- 2.8 micrograms/L and 9.6 +/- 2.3 micrograms h/L.(ABSTRACT TRUNCATED AT 250 WORDS)
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CAPD has been considered an appropriate method for treatment of diabetics in renal failure. Up to now the choice of route for insulin administration in these patients has not been definitely defined, although there is a general consensus for employing the intraperitoneal route for this purpose. However, contradictory data have appeared on this subject. Our aim has been to investigate whether the subcutaneous or intraperitoneal route makes any difference to metabolic control, and if so what is the price in terms of the incidence of peritonitis. Two groups of diabetic patients from three different hospitals with a similar peritonitis incidence and training protocols were studied. Of the 30 patients, 15 were treated with subcutaneous insulin (sc group) and in the other 15 the intraperitoneal route was employed (ip. group). The average follow-up period was 20.8 +/- 7.5 months for sc group and 18.7 +/- 8 months for ip. group. Insulin requirements were 30 +/- 11 u./day in the sc. and 110 +/- 60 u/day in the i.p. group (p less than 0.05) and remained constant during the study period. Metabolic controls (home glucose levels, HbA1C, hospital fasting glucose levels) were similar for both groups. However, the incidence of peritonitis was 4 times greater in the ip. group. In the ip. group 18 peritonitis episodes were registered in 280 patient-months vs 5 episodes in sc. group in 312 patient-months. We conclude that the intraperitoneal route for insulin administration in diabetic CAPD patients produces a higher risk of suffering peritonitis with no real metabolic improvement in the medium term.
The effects of pincainide, a new beta-amino anilide, on contractile responses and 45Ca fluxes were studied in rat aorta and on spontaneous mechanical activity in rat portal veins. Pincainide (10(-5) to 10(-2) M) produced a dose-dependent inhibition of noradrenaline (NA) and high K+ -induced contractions. These inhibitory effects were observed with pincainide added either before or after the induced contractions. The Ca2+ -induced contractions of K+ -depolarized aorta as well as the spontaneous mechanical activity of portal veins were also inhibited by pincainide. Pincainide (5 X 10(-3) M) inhibited the 45Ca influx stimulated by 10(-6) M NA and increased 45Ca efflux. It was concluded that in isolated rat aorta, pincainide not only inhibited the influx of Ca2+ reducing the contractile responses to NA and high K+ but it also inhibited other effects related to NA-induced release of intracellular Ca2+ stores.