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Browsing by Author "Mosso, L"

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Evidences for mineralocorticoid excess in essential hypertension
(2000) Cortes, P; Fardella, C; Oestreicher, E; Gac, H; Mosso, L; Soto, J; Foradori, A; Claverie, X; Ahuad, J; Montero, J
Background: Primary hyperaldosteronism is more frequent among subjects with essential hypertension than previously thought. The prevalence, according to local and international evidence could fluctuate between 9 and 10%. Aim: To investigate if subjects with essential hypertension have different aldosterone and renin plasma levels than normotensive subjects. Patients and methods: One hundred twenty five subjects with essential hypertension, not receiving medications for a least two weeks prior to the study and 168 age and sex matched normotensive controls were studied. Blood was drawn between 9 and 10 AM during a sodium free diet to determine plasma aldosterone, plasma renin activity and potassium. Results: Plasma aldosterone was higher in hypertensive subjects than controls (11.6 +/- 7.6 and 9.9 +/- 5.1 ng/dl respectively; p = 0.04). Plasma renin activity was lower in hypertensives than controls (1.42 +/- 1.28 and 1.88 +/- 1.39 ng/ml/h respectively; p < 0.001). Thus, plasma aldosterone/plasma renin activity ratio was higher in hypertensives (13.8 +/- 13.5 and 8.3 +/- 7.8; p < 0.001), A pathological ratio was defined as over 25, corresponding to the mean plus two standard deviations of the control group. Primary hyperaldosteronism was found in 5/125 hypertensives (4%) and 1/168 normotensive subject (0.6%). None had hypokalemia. Conclusions: Subjects with essential hypertension have higher plasma aldosterone and lower plasma renin activity than normal controls. A plasma aldosterone/plasma renin activity over 25 was defined as abnormal.
Extensive personal experience - Increased diagnosis of primary aldosteronism, including surgically correctable forms, in centers from five continents
(ENDOCRINE SOC, 2004) Mulatero, P; Stowasser, M; Loh, KC; Fardella, CE; Gordon, RD; Mosso, L; Gomez Sanchez, CE; Veglio, F; Young, WF
Primary aldosteronism (PA) is a common form of endocrine hypertension previously believed to account for less than 1% of hypertensive patients. Hypokalemia was considered a prerequisite for pursuing diagnostic tests for PA. Recent studies applying the plasma aldosterone/plasma renin activity ratio (ARR) as a screening test have reported a higher prevalence. This study is a retrospective evaluation of the diagnosis of PA from clinical centers in five continents before and after the widespread use of the ARR as a screening test. The application of this strategy to a greater number of hypertensives led to a 5- to 15-fold increase in the identification of patients affected by PA. Only a small proportion of patients ( between 9 and 37%) were hypokalemic. The annual detection rate of aldosterone-producing adenoma (APA) increased in all centers ( by 1.3-6.3 times) after the wide application of ARR. Aldosterone-producing adenomas constituted a much higher proportion of patients with PA in the four centers that employed adrenal venous sampling ( 28 - 50%) than in the center that did not (9%). In conclusion, the wide use of the ARR as a screening test in hypertensive patients led to a marked increase in the detection rate of PA.
Free urinary cortisol is elevated in patients with low-renin essential hypertension
(2004) Krall, P; Mosso, L; Carvajal, C; Rojas, A; Fardella, C
Background: Glucocorticoids play a key role in blood pressure (BP) control and are associated with hypertension in patients with Cushing's syndrome. A number of reports indicate that cortisol (F) may be involved in etiology of essential hypertension (EH). F can bind to the mineralocorticoid receptor, triggering both sodium and water reabsorption in kidney, increase BP and cause renin suppression. Aim: To evaluate urinary free cortisol (UFF) excretion as a potential intermediate phenotype of essential hypertension and correlate F level with plasma renin activity (PRA) and serum aldosterone (SA). Patients and Methods: We recruited 132 EH patients and 16 normotensive healthy controls. Blood samples and 24 hours urine were collected for PRA, SA and UFF analysis. Differences in UFF excretion between sexes were normalized by urinary creatinine (Creat) excretion. The upper limit of UFF/Creat was determined in normotensives considering the mean value plus 2 standard deviations. According to this value, subjects were classified as having high or normal UFF. Results: In EH patients and in normotensives, the UFF/Creat was 36.9 +/- 17.0 mug/gr and 30.9 +/- 8.8 mug/gr, respectively. The upper limit was set at 48.5 mug/gr. A high UFF/Creat was found in 20/132 EH (15%) patients and 0/16 normotensive subjects. EH patients with high UFF showed lower PRA levels than patients with normal cortisol levels (0.78 +/- 0.47 vs 1.13 +/- 0.66 ng/ml*h, respectively, p = 0.027) and lower SA values (4.52 +/- 1.65 vs 6.34 +/- 3.37 ng/dl, respectively, p = 0.018). There was a negative correlation between UFF and PRA (r = -0.176, p = 0.044) and between UFF and SA (r = -0.183, p = 0.036). Conclusions: We have identified a subgroup of EH patients with increased UFF excretion. Patients with the highest UFF showed lower renin and aldosterone levels. These data suggest a potential influence of cortisol in the genesis of hypertension.
Functioning and non functioning parathyroid cysts. Report of two cases
(1997) Mosso, L; Lopez, JM; Trincado, P; Olea, E; Talesnik, E; Verdugo, C
We report two women presenting with parathyroid cysts. A 20 years old woman presented with goiter and a cystic lesion in the left thyroid lobe was identified on ultrasound examination and CAT scan. The patient had hypercalcemia and elevated PTH levels. The content of the cyst, obtained by needle aspiration, had an extremely high PTH concentration. The patient was operated, removing the cyst and a remaining thymus. Pathological study confirmed the diagnosis of a parathyroid cyst. An 11 years old girl presented with a mass in the left thyroid lobe. An ultrasound examination disclosed the presence of a cystic nodule. The patient was otherwise asymptomatic and laboratory work up was normal. The patient was operated and pathological examination of the surgical piece revealed a parathyroid cyst.
Genetic studies in dexamethasone supressible aldosteronism.
(2001) Fardella, C; Pinto, M; Mosso, L; Oestreicher, E; Montero, J
We report two women presenting with parathyroid cysts. A 20 years old woman presented with goiter and a cystic lesion in the left thyroid lobe was identified on ultrasound examination and CAT scan. The patient had hypercalcemia and elevated PTH levels. The content of the cyst, obtained by needle aspiration, had an extremely high PTH concentration. The patient was operated, removing the cyst and a remaining thymus. Pathological study confirmed the diagnosis of a parathyroid cyst. An 11 years old girl presented with a mass in the left thyroid lobe. An ultrasound examination disclosed the presence of a cystic nodule. The patient was otherwise asymptomatic and laboratory work up was normal. The patient was operated and pathological examination of the surgical piece revealed a parathyroid cyst.
Genetic study of patients with dexamethasone-suppressible aldosteronism without the chimeric CYP11B1/CYP11B2 gene
(ENDOCRINE SOC, 2001) Fardella, CE; Pinto, M; Mosso, L; Gomez Sanchez, C; Jalil, J; Montero, J
Glucocorticoid-remediable aldosteronism is an inherited disorder caused by a chimeric gene duplication between the CYP11B1 (11 beta -hydroxylase) and CYP11B2 (aldosterone synthase) genes. The disorder is characterized by hyperaldosteronism and high levels of 18-hydroxycortisol and 18-oxocortisol, which are under ACTH control. The diagnosis of glucocorticoid-remediable aldosteronism had been traditionally made using the dexamethasone suppression test; however, recent studies have shown that several patients with primary aldosteronism and a positive dexamethasone suppression test do not have the chimeric CYP11B1/CYP11B2 gene. The aim of this work was to evaluate whether other genetic alterations exist in CYP11B genes (gene conversion in the coding region of CYP11B1 or in the promoter of CYP11B2) that could explain a positive dexamethasone suppression test and to determine another genetic cause of glucocorticoid-remediable aldosteronism. We also evaluated the role of 18-hydroxycortisol. as a specific biochemical marker of glucocorticoid-remediable aldosteronism. We studied eight patients with idiopathic hyperaldosteronism, a positive dexamethasone suppression test, and a negative genetic test for the chimeric gene. In all patients we amplified the CYP11B1 gene by PCR and sequenced exons 3-9 of CYP11B1 and a specific region (-138 to -284) of CYP11B2 promoter. We also measured the levels of 18-hydroxycortisol, and we compared the results with those found in four subjects with the chimeric gene. None of eight cases showed abnormalities in exons 3-9 of CYP11B1, disproving a gene conversion phenomenon. In all patients a fragment of 393 bp corresponding to a specific region of the promoter of CYP11B2 gene was amplified. The sequence of the fragment did not differ from that of the wild-type promoter of the CYP11B2 gene. The 18-hydroxycortisol levels in the eight idiopathic hyperaldosteronism patients and four controls with chimeric gene were 3.9 +/- 2.3 and 21.9 +/- 3.5 nmol/liter, respectively (P < 0.01). In summary, we did not find other genetic alterations or high levels of 18-hydroxycortisol that could explain a positive dexamethasone suppression test in idiopathic hyperaldosteronism. We suggest that the dexamethasone suppression test could lead to an incorrect diagnosis of glucocorticoid-remediable aldosteronism.
Glucocorticoid treatable hypertension. Report of one case
(1997) Montero, J; Fardella, C; Mosso, L
Lately, a series of hypertensive syndromes of unknown etiology that respond to new forms of therapy, have been described One of these is glucocorticoid remediable hypertension, that evolves with suppressed plasma renin activity and normal or high serum aldosterone levels, that lead to an aldosterone/plasma renin activity ratio over 30. We report a 45 years old woman with a severe hypertension despite the use of antihypertensive medications. She had a plasma renin activity of less than 0.3 ng/ml/h, normal serum aldosterone levels (10 ng/ml) and thus a high aldosterone/plasma renin activity ratio. She had normal serum potassium and sodium levels. Due to the bad results of conventional antihypertensive medications, a treatment with dexamethasone was started that normalized blood pressure and allowed to discontinue other antihypertensive medications. This type of hypertensive must besought since non conventional treatments could be used for refractory hypertensive syndromes.
gps Mutations in Chilean patients harboring growth hormone-secreting pituitary tumors
(WALTER DE GRUYTER GMBH, 1999) Johnson, MC; Codner, E; Eggers, M; Mosso, L; Rodriguez, JA; Cassorla, F
Hypersecretion of GH is usually caused by a pituitary adenoma and about 40% of these tumors exhibit missense gsp mutations in Arg(201) or Gln(227) of the Gs(alpha) gene. We studied 20 pituitary tumors obtained from patients with GH hypersecretion, One tumor was resected from an 11 year-old boy with a 3 year history of accelerated growth, associated with increased concentrations of serum GH and IGF-I, which were not suppressed by glucose administration, The remaining 19 tumors were obtained from adult acromegalic patients, who had elevated baseline serum GH levels that did not show evidence of suppression after administration of glucose, The gsp mutations were studied by enzymatic digestion of the amplified PCR fragment of exon 8 (Arg(201)) and exon 9 (Gln(227)) with the enzymes NlaIII and NgoAIV, respectively. The tumors obtained from the boy and from nine of the 19 patients with acromegaly exhibited the gsp mutation R201H. None of the tumors had the Gln(227) mutation. The gsp positive patients tended to be older, had smaller tumors, and had preoperative basal serum GH levels which were significantly lower (21 +/- 6 vs 56 +/- 16 mu g/l, p < 0.05) than the gsp negative patients, In this study, we documented the presence of a gsp mutation in Arg(201) in a boy with gigantism and in approximately half of 19 Chilean adult patients with acromegaly, similar to other populations.
Mixed medullary and follicular carcinoma of the thyroid. Report of three cases
(1997) Trincado, P; Lopez, JM; Mosso, L; Ciani, S; Olea, E
Mixed medullary and follicular carcinoma of the thyroid shares secretory and immunohistochemical features of both follicular and parafollicular thyroidal cells. we report three women aged 34, 63 and 63 old with this type of tumor. Ifs diagnosis must be bore in mind in patients with thyroidal tumors and a histological appearance of a medullary or undifferentiated carcinoma. An early diagnosis of a mixed medullary and follicular carcinoma of the thyroid is important, considering its special treatment and negative prognosis.
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.
Serum 18-hydroxycortisol in primary aldosteronism, hypertension, and normotensives
(LIPPINCOTT WILLIAMS & WILKINS, 2001) Mosso, L; Gomez Sanchez, CE; Foecking, MF; Fardella, C
This study reports the determination of plasma 18-hydroxycortisol (18-OHF) using a new and easy enzyme-linked immunosorbent assay (ELISA) method in primary aldosteronism and compares the values found in essential hypertensives and normotensive controls. In primary aldosteronism, we evaluated usefulness of plasma 18-OHF determination and the dexamethasone suppression test in the diagnosis of glucocorticoid-remediable aldosteronism using the genetic test as the gold standard. We studied 31 primary aldosteronism patients, 101 essential hypertensives, and 102 healthy normotensive controls. The plasma 18-OHF was measured using a biotin-avidin enzyme-linked assay by a new and purified polyclonal antibody. The 18-OHF value in primary aldosteronism was 6.3 +/- 8.05 nmol/L; this value is significantly higher than the value found in essential hypertensives and normotensive controls (2.81 +/- 1.42 and 2.70 +/- 1.41 nmol/L, respectively; P <0.0005). In primary aldosteronism, 4 of 31 patients had 18-OHF levels that were 10 times higher than the normal upper limit (2.983 nmol/L). The dexamethasone suppression test in primary aldosteronism patients was positive (serum aldosterone <4 ng/dL) in 13 of 31 cases. A chimeric CYP11B1/CYP11B2 gene was demonstrated in 4 primary aldosteronism patients, corresponding to the same cases that had higher level of 18-OHF. In conclusion, plasma 18-OHF determination by this ELISA method is reliable for detecting glucocorticoid-remediable aldosteronism, and it does so better than the dexamethasone suppression test.
The A-6G mutation in the angiotensinogen gene is associated to high levels of aldosterone in essential hypertensives
(1999) Fardella, C; Zamorano, P; Gomez, L; Oestreicher, E; Pinto, M; Rojas, A; Montero, J; Soto, J; Mosso, L; Foradori, A
The treatment of papillary thyroid carcinoma of less than 10 mm diameter is a matter of controversy. The incidental finding of papillary microcarcinomas in autopsies is frequent and some authors postulate that these tumors are biologically inactive and should only be observed. We report a 21 years old woman with a papillary thyroid cancer of 6x5x5 mm and bilateral paratracheal metastases, that was subjected to a total thyroidectomy. She received 200 mCi of radioiodine. Two years after surgery, a new nodule of 9.6 mm diameter was detected by ultrasound, that was treated with a new dose of 200 mCi of radioiodine. One year later a suprasternal mass of 2 cm diameter and 3 enlarged lymph nodes were detected. She was subjected to a surgical lymph node dissection of the neck and the biopsy confirmed the presence of cancer. She received a new dose of 300 mCi of radioiodine. The mother of the patient had a 7 mm thyroid nodule that was also a papillary carcinoma.
The terminally ill patient
(2000) Bravo, M; Echeverria, C; Goic, A; Kottow, M; Lavados, M; Mosso, L; Perez, M; Quintana, C; Rojas, A; Rosselot, E; Serani, A; Taboada, P; Trejo, C; Soc Med Santiago; NCD Risk Factor Collaboration (NCD-RisC)
The classification of a patient as terminally ill is based on an expert diagnosis of a severe and irreversible disease and the absence of an effective available treatment, according to present medical knowledge. Terminal diseases must not be confused with severe ones, since the latter may be reversible with an adequate and timely treatment. The physician assumes a great responsibility at the moment of diagnosing a patient as terminally ill. The professional must assume his care until the moment of death. This care must be oriented to the alleviation of symptoms and to provide the best possible quality of life. Also, help must be provided to deal with personal, legal and religious issues that may concern the patient.

Browsing by Author "Mosso, L"

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