Browsing by Author "Arteaga, E"

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    Bilateral oophorectomy in a pregnant woman
    (2005) Villaseca, P; Campino, C; Oestreicher, E; Mayerson, D; Serón-Ferré, M; Arteaga, E
    Background: A 16 week pregnant woman presented with massive theca-lutein cysts requiring bilateral oophorectomy. Pregnancy progressed uneventfully and spontaneous lactation ensued after delivery. Methods: To study the role of the ovary on the hormonal profile at the end of gestation and in post-partum, we measured FSH, estradiol (E-2), unconjugated estrone (E-1), unconjugated estriol (E-3), sex hormone-binding globulin, progesterone, dehydroepiandrosterone sulphate and prolactin at 37 weeks gestation and at 8 h, 4 days, 5 weeks, and 2 months post-partum. Results: These hormones were within the range expected for ovary-intact pregnant and puerperal women until 4 days post-partum. At 5 weeks post-partum, FSH increased to a peri-menopausal range (31.4 IU/l) while estrogens remained within the normal puerperal range (E-2=239 pmol/l; E-1=102 pmol/l), contrasting with their rapid changes in non-pregnant women after bilateral oophorectomy. At 2 months, while partially breastfeeding, FSH, E-2 and E-1 were closer to menopausal range (68 IU/l, 136 and 70.2 pmol/l respectively), and hormone replacement was started. Conclusions: We conclude that the ovary is not required to maintain a normal hormonal profile in late pregnancy and early puerperium. However, the increase in FSH to peri-menopausal levels at 5 weeks post-partum, despite breastfeeding, suggests that the ovary is needed to maintain low FSH concentrations during lactation.
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    Ethinylestradiol/cyproterone acetate in polycystic ovary syndrome: lipid and carbohydrate changes
    (PARTHENON PUBLISHING GROUP, 2004) Villaseca, P; Hormaza, P; Cardenas, C; Oestreicher, E; Arteaga, E
    Objective Ethinylestradiol (EE) combined with the antiandrogenic progestin cyproterone acetate (CPA) is a possible treatment in polycystic ovary syndrome (PCOS). We investigated the impact of EE/CPA on lipid and carbohydrate metabolism in women with PCOS,who were otherwise healthy.
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    Novel intronic mutation of MEN1 gene causing familial isolated primary hyperparathyroidism
    (ENDOCRINE SOC, 2004) Carrasco, CA; Gonzalez, AA; Carvajal, CA; Campusano, C; Oestreicher, E; Arteaga, E; Wohllk, N; Fardella, CE
    Primary hyperparathyroidism may occur as part of hereditary syndromes, including multiple endocrine neoplasia types 1 and 2A (MEN1 and MEN2A), hyperparathyroidism-jaw tumor syndrome, and the familial isolated hyperparathyroidism (FIHP). It is unclear whether FIHP corresponds to a different genetic entity or a variant of MEN1 ( or hyperparathyroidism-jaw tumor syndrome). We report a patient and 11 family members with FIHP in whom we identified a heterozygous G-to-A mutation at nucleotide 7361 of tumor suppressor MEN1 gene. This mutation is located in the first base of intron 9 (IVS9 + 1 G>A). All the family members with hyperparathyroidism were heterozygous for the intronic mutation. In vitro studies were performed in COS cells transfected with minigenes carrying the coding regions spanning exon-intron 9 and 10 with the mutant and the wild-type sequences. RT-PCR analyses showed an abnormal mRNA of greater size ( 829 bp) in the mutated MEN1 gene than the normal transcript ( 629 bp). The longer PCR product includes the exon 9, the unspliced intron 9, and part of exon 10. RT-PCR of MEN1 mRNA from patient's blood confirmed the existence of unspliced intron 9 in mature mRNA. In summary, we report a case of FIHP associated with a new intronic heterozygous germline mutation (IVS9 + 1 G> A) of MEN1 gene. This mutation produces an aberrant splicing of mRNA that could lead to a truncated protein, without activity, explaining the clinical picture of this patient and his family.
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    Pathological characteristics of thyroid microcarcinoma. A review of 402 biopsies
    (2005) Fardella, C; Jimenez, M; Gonzalez, H; Leon, A; Goni, I; Cruz, F; Solar, A; Torres, J; Mosso, L; Gonzalez, G; Rodriguez, JA; Campusano, C; Lopez, JM; Arteaga, E
    Background: Thyroid microcarcinoma is a tumor of 10 mm or less. that should have a low risk of mortality. However a subgroup of these carcinomas is as aggressive as bigger tumors. Aim To describe the pathological presentation of these tumors.. and compare them with larger tumors. Material and methods. All Pathological samples of thyroid carcinoma that were obtained between 1992 and 2003, were studied. In all biopsies, the pathological type, tumor size. the focal or multifocal character the presence of lymph node involvement and the presence of lymphocytic thyroiditis or thyroid hyperplasia, were recorded. Results: One hundred eighteen microcarcinomas and 284 larger tumors were studied. The mean age of patients with microcarcinoma and larger tumors was 42.7 +/- 14 and 49.3 +/- 16 years respectively (p < 0,00.1) and 83% were female. without gender differences between tumor types. klean size of microcarcinomas was 8.6 mm and 116 (98%) were papillary carcinomas. Of these. 109 (94% were well differentiated and seven (6%) were moderatly differentiated. Thirty six(31%) were multifocal and in 10 (8,6%), there was lymph node involvement. The mean size of larger tumors was 23.8 mm and 241 (85%) were papillary carcinomas. Of these, 200 (83%) were well differentiated, and 41 (17%) were moderately differentiated.Eighty five (35%) were multifocal and in 44 (18%) there was lymph node involvement. The prevalence of thyroiditis and hyperplasia was significantly higher among microcardinomas than in larger tumors (15 and 2.5%, respectively, p < 0.001, for the former; 32.4 and 1.7%, respectively, p < 0.001, for the latter. Conclusions. In this series. one third of microcarcinomas were multifocal and 10% had lymph node involvement. Therefore, aggresiveness of these tumors is higher than what is reported in the literature and they should be treated with total thyroidectomy.
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    Persistent hypokalemia after successful adrenalectomy in a patient with Cushing's syndrome due to ectopic ACTH secretion
    (1999) Arteaga, E; Fardella, C; Campusano, C; Cárdenas, I; Martinez, P
    Ectopic ACTH secretion is characterized by a high incidence of hypokalemia. The pathophysiology of hypokalemia has not been totally clarified, although it has been postulated that excessive amounts of adrenal steroids may play a role, as well as a possible role of the inhibition of the enzyme 11 beta-hydroxysteroid dehydrogenase (11 beta-OHSD). This enzyme normally converts cortisol to cortisone avoiding the mineralocorticoid action of cortisol. We present a patient with ectopic ACTH secretion due to a metastatic carcinoid tumor. The clinical picture was characterized by maintained hypokalemia (1.4 mmol/l) resistant to potassium, spironolactone and ketoconazole administration. A bilateral adrenalectomy was performed but the hypokalemia persisted while he was receiving a physiological dose of cortisol. Eight days after adrenalectomy cortisol was replaced by an equivalent dose of dexamethasone. This change was followed by a rapid and persistent normalization of hypokalemia suggesting a mineralocorticoid effect of cortisol. In conclusion, the origin of hypokalemia in our patient with ectopic ACTH secretion was secondary to cortisol. We postulate that this peculiar effect of cortisol could have happened if an inhibition of 11 beta-OHSD occurred. (J. Endocrinol. Invest. 22: 857-859, 1999) (C) 1999, Editrice Kurtis.
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    Sequential estrogen-progestin replacement therapy in healthy postmenopausal women: Effects on cholesterol efflux capacity and key proteins regulating high-density lipoprotein levels
    (W B SAUNDERS CO-ELSEVIER INC, 2002) Ulloa, N; Arteaga, E; Bustos, P; Duran Sandoval, D; Schulze, K; Castro, G; Jauhiainen, M; Fruchart, JC; Calvo, C
    Thirty healthy postmenopausal women were randomized into 2 groups that received a sequential combined hormone-replacement therapy (HRT) (n = 18; conjugated equine estrogen 0.625 mg/d for 28 days and 5 mg of medroxyprogesterone acetate during the last 14 days) or placebo (n = 12). Plasma samples were collected before and during treatment (days 0, 15, 43, 71). High-density lipoprotein (HDL) lipid content, lipoprotein (Lp)A-I and LpA-I:LpA-II concentration, lecithin:cholesterol acyl transferase activity (LCAT), phospholipid transfer protein (PLTP) activity, and the plasma capacity to carry out cholesterol efflux from Fu5AH cells were measured. Most significant changes were found within the first 15 days after HRT. After 71 days of HRT, we found an increase in LpA-I lipoparticles (27%) and the following HDL lipids: phospholipids (21%), triglycerides (45%), and free cholesterol (43%), as well as an increase in cholesterol efflux (12.5%). PLTP activity, on the other hand, decreased 21% after 71 days of treatment. No significant changes in LCAT activity, HDL-cholesterol ester or LpA-I:LpA-II particles were found. Positive correlation between cholesterol efflux and the variables LpA-I and HDL-phospholipids were observed. PLTP was negatively correlated with apolipoprotein (apo) A-1, LpA-I, and LpA-I:LpA-II. In summary, our study, performed during 3 hormonal cycles, shows that HRT not only modifies HDL-cholesterol level, but also its lipid composition and HDL lipoparticle distribution. HRT enhances the plasma capacity to carry out cholesterol efflux from the Fu5AH system and decreases the activity of PLTP, a key protein regulating HDL levels. Considering the protocol sampling, these results represent mainly the estrogenic effect of HRT. Copyright 2002, Elsevier Science (USA). All rights reserved.
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    Successful treatment of hyperthyroidism with amiodarone in a patient with propylthiouracil-induced acute hepatic failure
    (MARY ANN LIEBERT, INC, 2004) Brusco, F; Gonzalez, G; Soto, N; Arteaga, E
    Acute hepatic failure is a rare and potentially lethal complication of propylthiouracil (PTU) use for hyperthyroidism. We present a 20-year-old woman with Basedow-Graves' disease who developed PTU-induced fulminant hepatitis, which progressed to acute hepatic failure with grade III hepatic encephalopathy. Laboratory evaluation ruled out the most common causes of fulminant hepatitis. We treated her hyperthyroidism with amiodarone (average daily dose, 200 mg) for 3 weeks, achieving rapid and persistent euthyroidism, (triiodothyronine [T-3] levels ranged between 64 and 109 ng/dL) without side effects. Amiodarone treatment did not abolish the thyroid radioactive iodine uptake (RAIU), allowing for subsequent treatment with radioactive iodine. The clinical course was favorable and the patient achieved full hepatic recovery 3 months after the hepatic failure was detected. After an extensive review of the literature, we believe that this is the first communication of the successful use of amiodarone to control hyperthyroidism in a patient with PTU-induced fulminant hepatitis.