Browsing by Author "Campino, C"

Now showing 1 - 3 of 3
  • No Thumbnail Available
    Item
    11 beta-hydroxysteroid dehydrogenase activity in patients with hypertension and low plasma renin activity
    (2002) Mosso, L; Carvajal, C; Campino, C; Rojas, A; Gonzalez, A; Barraza, A; Montero, J; Fardella, C; NCD Risk Factor Collaboration (NCD-RisC)
    Background: Half of hypertensive patients with, low plasma renin activity have a primary hyperaldosteronism. Among the remaining half 11beta-hydroxysteroid dehydrogenase type 2 (11betaHSD2) deficiency plays all important role. This enzyme catalyzes the conversion of cortisol to cortisone, avoiding the interaction of cortisol with, the mineralocorticoid receptor. If the enzyme fails, cortisol will stimulate sodium and water reabsorption and increase blood pressure. Aim: To determine biochemical alterations, suggestive of 11betaSHSD2 deficiency, in low-renin hypertensive patients. Patients and Methods: Twenty eight hypertensive patients with a plasma renin activity of less than 0.5 ug/ml/h and with a plasma aldosterone of less than 5 ng/dl were studied. Twenty eight normotensive patients were studied as controls. Serum. cortisol (RIA), cortisone (ELISA) and the serum cortisol/cortisone ratio were determined in all of them, between, 9 and 10 AM. Measurements were confirmed by high pressure liquid chromatography. The serum cortisol/cortisone ratio was considered abnormal when its Ln (cortisol/cortisone) value was over 2 standard deviations of the mean. Results: Serum cortisol was higher in hypertensive subjects than in controls (11.1 +/- 3.3 and 9.2 +/- 2.8 mug/dl, respectively; p <0.05). No differences were observed in serum cortisone (3.4 +/- 1.3 and 3.7 +/- 1.2 μg/dl, respectively). Four hypertensive subjects bad all abnormally high Ln (cortisol/cortisone) value (1.86; 1.73; 2.07 and 2.01, considering a normal value of less than 1.61). Conclusions: Four of 28 hypertensive subjects with, low plasma renin activity and aldosterone had biochemical alterations suggestive of 11.1βHSD2 deficiency.
  • Thumbnail Image
    Item
    Biochemical and genetic characterization of 11 beta- hydroxysteroid dehydrogenase type 2 in low-renin essential hypertensives
    (LIPPINCOTT WILLIAMS & WILKINS, 2005) Carvajal, CA; Romero, DG; Mosso, LM; Gonzalez, AA; Campino, C; Montero, J; Fardella, CE
    Background The 11beta-hydroxysteroid dehydrogenase type 2 (11betaHSD2) catalyzes the conversion of cortisol M to cortisone (E), avoiding the interaction of cortisol with the mineralocorticoid receptor. If it fails, cortisol will stimulate sodium and water reabsorption, increasing the intravascular volume that suppresses renin and secondarily increase the blood pressure.
  • No Thumbnail Available
    Item
    Hyperthyroxinemia and clinical euthyroidism. Report of one case
    (1999) Lopez, JM; Mosso, L; Campino, C
    The association of hyperthyroxinemia and euthyroidism is frequent and characterized by high plasma thyroxin concentrations, normal TSH values and absence of clinical signs of hyperthyroidism. We report an asymptomatic 28 years old male presenting with a serum total plasma thyroxin of 18.5 mu g.gl (N 6.1-12.5), a free thyroxin of 2.9 ng/dl (N 0.8-1.4) a TSH of 3.4 mu IU/ml (N 0.5-5), and a triiodothyronine of 128 ng/dl (N 80-180). Laboratory assessment did not find high thyroxin binding globulin, albumin or prealbumin concentrations or antithyroxin antibodies. The thyroxin binding capacity of albumin was elevated to 58.2 mu g/dl (N 11.5-34.1). TSH responded normally to TRH stimulus and was suppressed with exogenous triiodothyronine, which caused an hyperthyroid syndrome. We concluded that this patient had a familial dysalbuminemia.