Primary aldosteronism can alter peripheral levels of transforming growth factor beta and tumor necrosis factor alpha.

UNLABELLED: Primary aldosteronism (PA) is the most common secondary cause of hypertension that has recently been implicated in alterations of the immune system and progression of cardiovascular disease. OBJECTIVE: To study the cytokines transforming growth factor beta1 (TGF-beta1), tumor necrosis factor alpha (TNF-alpha), and interleukin 10 (IL-10) in patients with PA and essential hypertensives (EH) and evaluate its association with the renin-angiotensin-aldosterone system. PATIENTS AND METHODS: We studied 26 PA and 52 EH patients as controls, adjusted by their blood pressure, body mass index, age, and gender. In both groups, PA and EH, we measured serum aldosterone (SA), plasma renin activity (PRA), and cytokines TGF- beta1, TNF-alpha, and IL-10. In addition, 17 PA patients were treated for 6 months with spironolactone, a mineralocorticoid receptor (MR) antagonist. RESULTS: PA patients had lower levels of TGF-beta1 (17.6+/-4.1 vs 34.5+/-20.5 pg/ml, p<0.001) and TNF-alpha (17.0+/-4.4 vs 35.6+/-21.7 pg/ml, p<0.001) and similar IL-10 levels (99.7+/-18.7 vs 89.4+/-49.5 pg/ml, p: ns), as compared with EH controls. TGF-beta1 and TNF-alpha levels showed a remarkable correlation with SA/PRA ratio in the total group (PA+EH). The treatment of PA patients with spironolactone increased the TGF-beta1 levels (18.3+/-5.9 to 28.4+/-6.3 pg/ml, p<0.001), while TNF-alpha, and IL-10 remained unchanged. CONCLUSION: Our results showed that PA patients have lower TGF-beta1 and TNF-alpha cytokine serum levels than EH. TGF-beta1 levels were restored with spironolactone, showing a MR-dependent regulation. In this way, the chronic aldosterone excess modifies the TGF-beta1 levels, which could produce an imbalance in the immune system homeostasis that may promote an early proinflammatory cardiovascular phenotype.

Case report: Successful IVF programme after conservatively treated endometrial cancer.

Some cases of successful pregnancy after conservative endometrial cancer management have been reported. This paper presents such a case, an infertile patient with conservatively treated endometrial cancer (stage 1a grade 1) who conceived and carried a successful pregnancy after IVF treatment. The conservative treatment consisted of hysteroscopic biopsies and oral megestrol acetate 600 mg daily for 3 months. At the end of the treatment the endometrial cancer remitted to simple endometrial hyperplasia. IVF was performed immediately and 32 days after embryo transfer an intrauterine single gestational sac with fetal pole and heartbeat was detected by transvaginal ultrasound. The woman received routine obstetric care and a caesarean section was performed at 38 weeks of gestation. The histological evaluation after delivery showed no evidence of recurrent disease. Twenty-six months after the delivery, the woman is healthy and free of the disease. It is concluded that conservative treatment of stage 1a and grade 1 endometrial adenocarcinoma is an available option in young women who wish to preserve their fertility.

[Mechanical characteristics of the human bladder wall and application of the results in a finite elements model to study the pelvic floor]. / Studio delle caratteristiche meccaniche della vescica umana e applicazione in un modello agli elementi finiti per lo studio del pavimento pelvico.

AIM: There is no radiological method capable of providing a real-time, dynamic 3D illustration of the pelvic organs and supporting structures during stress, physiological regressions and pathological alterations. This paper describes the determination of the mechanical characteristics of the human bladder, the application of the results in a numerical 3D finite elements model of the pelvis and the processing of the model in the presence or absence of urethro-pelvic and pubo-vescical ligaments supporting the pelvis. METHODS: A 3D numerical finite element model of the human pelvis has been realised starting from CT image and Mimics (Materialise), Rhinoceros (Robert Mc Neel and Associates), Patran (MSC) e Marc (MSC) programs. The mechanical characteristic of human bladder specimen have been studied in vitro drawn up from human bladder removed for neoplasia. Results have been introduced in a numeric model. After the definition of bond and load applied, we made the simulation and numerical structural analysis with and without some ligaments that link pelvic fascia and urethra at the pubis. RESULTS: The study of mechanical data of bladder reports structural differences between lateral wall, trigone wall and anterior wall in correlation to the topographical disposition of fibres of detrusor and its thickness. Dynamics investigation performed in the absence of cervical urethra ligaments of suspension and pelvic fascia showed that the anatomical deflections of pelvic fascia modified the distributions of loads toward centripetal deviation, stressing even more the perineal area and the sphincter tract. CONCLUSIONS: The study shows that trigone is the area with the greatest stiffness in comparison with other areas of the bladder and that it has the greatest strength to tensile loads. This study has shown that pelvic fascia, urethropelvic and pubovescical ligaments are cardinal supports that cannot be neglected in a dynamic numerical analysis. Dynamic simulation of the model in the absence of the ligaments confirms the role of surgical techniques used for their reconstruction following their section during radical surgery.

Elevación del cortisol urinario en hipertensos esenciales hiporreninémicos / Free urinary cortisol is elevated in patients with low-renin essential hypertension

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 microg/gr and 30.9 +/- 8.8 microg/gr, respectively. The upper limit was set at 48.5 microg/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 x 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.

Genetic study of patients with dexamethasone-suppressible aldosteronism without the chimeric CYP11B1/CYP11B2 gene.

Glucocorticoid-remediable aldosteronism is an inherited disorder caused by a chimeric gene duplication between the CYP11B1 (11beta-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.

Serum 18-hydroxycortisol in primary aldosteronism, hypertension, and normotensives.

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.

[Reversible myocardial ischemia in hypothyroidism: Case report]. / Isquemia miocárdica reversible en el hipotiroidismo: comunicación de un caso.

A silent, reversible myocardial ischemia with normal coronary angiography and reversible with thyroid hormone substitution, has been recently described in hypothyroid patients. We report a 49 years old male with an abnormal exercise electrocardiogram detected in a preventive medical examination. He had laboratory evidence of hypothyroidism and a history of two years of asthenia and progressive coarsening of the voice. The Thallium myocardial perfusion study, showed an alteration of coronary flow during exercise in the septum and lower wall of the left ventricle. Thyroid hormone substitution was started and three months later, a coronary angiography was normal. After six months a repeated Thallium perfusion study and exercise electrocardiogram were informed as normal.

[Bone turnover in lactating adolescent: evaluation at the end of pregnancy, during and after the weaning period]. / Recambio óseo en nodrizas adolescentes: evaluación al término de la gestación, lactancia y postdestete.

BACKGROUND: There is paucity of information about bone metabolism during pregnancy or breast feeding in teenagers. AIM: To study bone turnover at the end of pregnancy and during breast feeding in teenagers and correlate it with environmental, hormonal or nutritional variables. SUBJECTS AND METHODS: Thirty teenagers during their breast feeding period after a first pregnancy and 30 nulliparous girls matched for age, age of menarche and body mass index were assessed three weeks after delivery (period 1), at six months of breast feeding (period 2) and one year after the lactating period (period 3). Calcium intake and plasma calcium, phosphorus, alkaline phosphatases, parathormone, estradiol and prolactin were measured. Calcium, creatinine and hydroxyproline were also measured in a morning urine sample. RESULTS: Lactating and control girls were aged 16.3 +/- 0.8 and 16.1 +/- 0.7 years old respectively. Calcium intake in lactating and control girls was 798 +/- 421 and 640 +/- 346 g/day respectively in period 1, 612 +/- 352 and 592 +/- 309 mg/day in period 2 and 495 +/- 180 and 456 +/- 157 g/day in period 3. During periods 1 and 2, lactating girls had higher alkaline phosphatases (161 +/- 37 compared to 119 +/- 28 U/l and 149 +/- 37 compared to 106 +/- 23 U/l), parathormone (4.3 +/- 2.6 compared to 2.8 +/- 0.8 ng/dl and 3.6 +/- 1.6 compared to 3.0 +/- 0.9 ng/dl) and urinary hydroxyproline (95 +/- 16 compared to 63 +/- 15 mg/g creatinine and 84 +/- 19 compared to 59 +/- 15 mg/g creatinine). No differences were observed in period 3. No correlation between bone turnover variables, body mass index or hormonal parameters, was observed. CONCLUSIONS: In teenagers, there is an increase in bone turnover at the end of pregnancy, that persists during the lactating period. These changes are not related to nutritional or hormonal variables.

Primary hyperaldosteronism in essential hypertensives: prevalence, biochemical profile, and molecular biology.

There is evidence that primary aldosteronism (PA) may be common in patients with essential hypertension (EH) when determinations of serum aldosterone (SA), plasma renin activity (PRA), and the SA/PRA ratio are used as screening. An inherited form of primary hyperaldosteronism is the glucocorticoid-remediable aldosteronism (GRA) caused by an unequal crossing over between the CYP11B1 and CYP11B2 genes that results in a chimeric gene, which has aldosterone synthase activity regulated by ACTH. The aim of this study was to evaluate the prevalence of PA and the GRA in 305 EH patients and 205 normotensive controls. We measured SA (1-16 ng/dL) and PRA (1-2.5 ng/mL x h) and calculated the SA/PRA ratio in all patients. A SA/PRA ratio level greater than 25 was defined as being elevated. PA was diagnosed in the presence of high SA levels (>16 ng/dL), low PRA levels (<0.5 ng/mL x h), and very high SA/PRA ratio (>50). Probable PA was diagnosed when the SA/PRA ratio was more than 25 but the other criteria were not present. A Fludrocortisone test was done to confirm the diagnosis. GRA was differentiated from other forms of PA by: the aldosterone suppression test with dexamethasone, the high levels of 18-hydroxycortisol, and the genetic detection of the chimeric gene. In EH patients, 29 of 305 (9.5%) had PA, 13 of 29 met all the criteria for PA, and 16 of 29 were initially diagnosed as having a probable PA and confirmed by the fludrocortisone test. Plasma potassium was normal in all patients. The dexamethasone suppression test was positive for GRA in 10 of 29 and 18-hydroxycortisol levels were high in 2 of 29 patients who had also a chimeric gene. In normotensive subjects, 3 of 205 (1.46%) had PA, and 1 of 205 had a GRA. In summary, we found a high frequency of normokalemic PA in EH patients. A high proportion of PA suppressed SA with dexamethasone, but only a few had a chimeric gene or high levels of 18-hydroxycortisol. These results emphasize the need to further investigate EH patients.

[Excess of mineralocorticoids in essential hypertension: clinical-diagnostic approach]. / Exceso de mineralocorticoides en hipertensos esenciales: enfoque clínico-diagnóstico.

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 at 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/b 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.

A(-6)G variant of angiotensinogen gene and aldosterone levels in hypertensives.

Recently, a novel mutation in the promoter region of the angiotensinogen gene that involves the presence of an adenine instead of a guanine 6 bp upstream from the transcription initiation site (A(-6)G) has been shown to induce an increase in gene transcription. The aim of this study was to determine the prevalence of the A(-6)G mutation in essential hypertensive patients and to correlate it with aldosterone and renin activity levels. We studied 191 hypertensives. We measured levels of aldosterone (plasma and urinary) and plasma renin activity. We determined the variants A and G using a mutagenically separated polymerase chain reaction technique. In 191 hypertensives, the A variant was detected in 266 of 382 (69.6%) and the G variant in 116 of 382 alleles (30.4%). Plasma aldosterone was significantly higher in patients homozygous for AA than in those homozygous for GG (369+/-208 versus 246+/-142 pmol/L). Urinary aldosterone was significantly higher in homozygous AA than in AG or GG patients (62.4+/-39.4 versus 50.8+/-25.2 and 37.4+/-22.3 nmol/d, respectively). When the patients were grouped according to the presence or absence of the A allele, the aldosterone levels and the plasma aldosterone/plasma renin activity ratio were significantly higher in patients with the A allele. The presence of the A variant was associated with higher levels of aldosterone. These results suggest that the presence of the A variant could determine the appearance of arterial hypertension through higher transcription activity of the angiotensinogen gene and concomitant aldosterone production.

[Hyperthyroxinemia and clinical euthyroidism. Report of one case]. / Hipertiroxinemia con eutiroidismo clínico: análisis a propósito de un caso.

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 micrograms/dl (N 6.1-12.5), a free thyroxin of 2.9 ng/dl (N 0.8-1.4), a TSH of 3.4 microIU/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 micrograms/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.

[Hypertension and mineralocorticoids. Usefulness of renin and aldosterone measurements]. / Hipertensión arterial y mineralocorticoides: utilidad de las mediciones de renina y aldosterona.

Recently, some genetic forms of hypertension have been well characterized. These forms can be globally called mineralocorticoid hypertension and are due to different alterations of the renin-angiotensin-aldosterone system (SRAA). Among these, classic primary hyperaldosteronism and its glucocorticoid remediable variety, in which hypertension is secondary to aldosterone production, must be considered. There are also conditions in which mineralocorticoid activity does not depend on aldosterone production. These conditions generate a hyporeninemic hyperaldosteronism, observed in Liddle syndrome, apparent mineralocorticoid hypertension, 11- and 17-hydroxylase deficiency, among others. The detection of these forms of hypertension is only feasible if the renin-angiotensin-aldosterone system is assessed, measuring renin and aldosterone levels. This article reviews these forms of hypertension, their clinical workup and their relevance in the usual hypertensive patients.

Gps mutations in Chilean patients harboring growth hormone-secreting pituitary tumors.

Hypersecretion of GH is usually caused by a pituitary adenoma and about 40% of these tumors exhibit missense gsp mutations in Arg201 or Gln227 of the Gs, 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 (Arg201) and exon 9 (Gln227) 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 Gln227 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 microg/l, p<0.05) than the gsp negative patients. In this study, we documented the presence of a gsp mutation in Arg201 in a boy with gigantism and in approximately half of 19 Chilean adult patients with acromegaly, similar to other populations.

[High prevalence of undiagnosed primary hyperaldosteronism among patients with essential hypertension]. / Alta prevalencia de hiperaldosteronismo primario no diagnosticado en hipertensos catalogados como esenciales.

BACKGROUND: Classically, primary hyperaldosteronism was diagnosed in no more than 1% of patients with hypertension, when hypokalemia was used as the screening test. However, numerous patients with primary hyperaldosteronism do not have hypokalemia and the disease remains undiagnosed. AIM: To assess the prevalence of normokalemic primary hyperaldosteronism among patients classified as having essential hypertension. PATIENTS AND METHODS: One hundred hypertensive patients with a blood pressure over 145/95 were studied. Plasma aldosterone and plasma renin activity were measured in all. A primary hyperaldosteronism was diagnosed when high aldosterone levels (over 16 ng/dl) and low plasma renin activity (below 0.5 ng/ml/h) coexisted in two blood tests or the aldosterone/plasma renin activity ratio was over 50. A probable primary hyperaldosteronism was diagnosed when the ratio was between 25 and 50 and these patients were subjected to a Fludrocortisone test to confirm the diagnosis. A dexametasone suppression test was done to discard glucocorticoid remediable aldosteronism. An adrenal TAC scan was done to all patients with primary hyperaldosteronism. RESULTS: A diagnosis of primary hyperaldosteronism was reached in ten patients. Seven had elevated aldosterone and low plasma renin activity. In three the diagnosis was confirmed with the fludrocortisone test. All ten patients had normal serum potassium levels. Dexametasone suppression test was positive in three patients, that normalized their blood pressure levels. Adrenal TAC scans showed an adenoma in one patient and hyperplasia in another. CONCLUSIONS: Primary hyperaldosteronism is more frequent than previously thought, it is overlooked when hypokalemia is used as the screening test and it can only be diagnosed measuring plasma aldosterone and renin activity.

[Renal angiolipoma associated with bilateral double ureter. A clinical case]. / Angiomiolipoma renale in doppio distretto bilaterale. Caso clinico.

Renal angiomyolipoma is a rare renal tumor usually associated with tuberous sclerosis, a syndrome characterized by adenoma sebaceum, mental insufficiency and epilepsy. The authors present a rare case of renal angio-myolipoma associated with bilateral double ureter, in a young male patient not affected by tuberous sclerosis. Histologically, the angiomyolipoma is defined by the presence of smooth muscular cells, new formed vessels and fat. Clinical diagnosis requires the utilization of various imaging techniques, like intravenous pyelogram, ultrasonic scan, CT scan, and FNA (Fine Needle Aspiration). In the histopathologic diagnosis of angiomyolipoma the use of immunohistochemical techniques with different antibodies has been helpful, for the necessity to differentiate angiomyolipoma from other epithelial tumors, as renal cell carcinoma and sarcomatous neoplasms. As for as treatment is concerned, the indication for surgery is still maintained by two factors not affected by these diagnostic improvements: tumor size and presence of symptoms. Tumor size is an important predictive growth factor of the tumor. In the absence of symptoms a close follow-up with ultrasonographic scan may be indicated, keeping in mind the possible presence of a synchronous renal cell carcinoma. Hemorrhage can be a fatal complication of renal angiomyolipoma, requiring emergency surgery or embolization.

[Functioning and non-functioning parathyroid cysts: entities with different origin and clinical characteristics in 2 cases]. / Quistes paratiroideos funcionantes y no funcionantes: entidades con origen y clínica diferente en dos casos.

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.

[Hypertension treatable with glucocorticoids: report of a case]. / Hipertensión arterial tratable con glucocorticoides: communicación de un caso.

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 hypertension must be sought since non conventional treatments could be used for refractory hypertensive syndromes.