Worlds lit on preg and PA. Can some one make a new file in our folders: PA in pregnancy and upload this. Thanks

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Begin forwarded message:Date: May 26, 2011 11:15:01 PM CDTTo: lowerbp2@...Subject: PubMed Search Results This message contains search results from the National Center for Biotechnology Information (NCBI) at the U.S. National Library of Medicine (NLM). Do not reply directly to this messageSender's message: Pregnancy Sent on: Fri May 27 00:10:13 2011 54 selected items pubmed ResultsItems 1 -54 of 54 1. Eur J Endocrinol. 2011 Mar;164(3):405-12.A case of primary aldosteronism in pregnancy: do LH and GNRH receptors have a potential role in regulating aldosterone secretion?Albiger NM, Sartorato P, Mariniello B, Iacobone M, Finco I, Fassina A, Mantero F.SourceDivision of Endocrinology, Department of Medical and Surgical Sciences, University of Padua, Via Ospedale 105, 35128 Padua, Italy. nora.albiger@...AbstractOBJECTIVE: The mechanisms inducing steroidogenesis in primary aldosteronism (PA) remain poorly defined. It was recently demonstrated that some G-protein-coupled receptors are abnormally expressed in aldosterone-producing adenomas (APA). We evaluated the potential role of LH and GNRH receptors (LHR (or LHCGR) and GNRHR) in regulating aldosterone secretion in a patient with APA arising during pregnancy (index case) and in a subset of other patients with PA.PATIENTS AND METHODS: GNRH test was performed in the index case, 11 other PA, and 5 controls. GNRHR and LHR expressions were examined in 23 APA and 6 normal tissues.RESULTS: Aldosterone response increased significantly (114%) in the index case after GNRH test was performed preoperatively, while it was blunted after adrenalectomy. Aldosterone also increased after human chorionic gonadotropin and triptorelin stimulation. A partial aldosterone response to GNRH was observed in other 7/11 PA, while a significant response was observed in two patients. Controls did not respond to GNRH test. GNRHR was overexpressed and LHR expression was moderate in the APA tissue from the index case. Moreover, LHR was found in normal adrenals and overexpressed in 6/22 APA. GNRHR was overexpressed in 6/22 APA, 2 of them with a 95- and 109-fold higher expression than normal. A correlation between the clinical and molecular findings was observed in five out of seven patients.CONCLUSION: We describe a case of PA diagnosed during pregnancy, which appeared to correlate with aberrant LHR and GNRHR expression. Our findings suggest that a subset of patients with PA has aberrant LHR and GNRHR expression, which could modulate aldosterone secretion.PMID: 21330483 [PubMed - indexed for MEDLINE]Related citations 2. Clin Endocrinol (Oxf). 2011 Feb;74(2):278-9. doi: 10.1111/j.1365-2265.2010.03901.x.Progesterone increase counteracts aldosterone action in a pregnant woman with primary aldosteronism.Ronconi V, Turchi F, Zennaro MC, Boscaro M, Giacchetti G.PMID: 21054479 [PubMed - indexed for MEDLINE]Related citations 3. J Korean Med Sci. 2009 Dec;24(6):1220-3. Epub 2009 Nov 9.Symptomatic hypocalcemia in primary hyperaldosteronism: a case report.Pai SG, Shivashankara KN, Pandit V, Sheshadri S.SourceDepartment of Medicine, Kasturba Medical College, Manipal, Karnataka, India. sachingpai@...AbstractThe metabolic alterations caused by hyperaldosteronism are being increasingly recognized and have generated considerable interest among the medical fraternity. Hyperaldosteronism is suspected to have a pivotal role in the patho-physiology of congestive cardiac failure where it has been studied extensively. But its effects on calcium metabolism, parathyroid metabolism and renal handling of calcium are less well described. Recent experimental models have shed light into the roles played by previously unknown mechanisms in causing these metabolic alterations. We hereby report a case of primary hyperaldosteronism due to adrenal adenoma (Conn's syndrome) who presented with a myriad of clinical features including symptomatic hypocalcemia, significant weight loss along with uncontrolled hypertension for a prolonged period before eventually detected to have primary hyperaldosteronism. Surgical removal of the causative tumor resulted in prompt disappearance of all the symptoms and signs and regain of lost weight.PMCID: PMC2775880 Free PMC Article PMID: 19949688 [PubMed - indexed for MEDLINE]Related citations 4. Can J Surg. 2009 Oct;52(5):E188-90.Laparoscopic treatment of primary hyperaldosteronism in a pregnant patient.Nursal TZ, Caliskan K, Ertorer E, Parlakgumus A, Moray G.SourceDepartment of General Surgery, Adana Teaching and Research Center, Ankara, Turkey. tznursal@...PMCID: PMC2769106 Free PMC Article PMID: 19865553 [PubMed - indexed for MEDLINE]Related citations 5. Aust N Z J Obstet Gynaecol. 2009 Oct;49(5):558.Primary aldosteronism and pregnancy: a case report.Lu W, Zheng F, Li H, Ruan L.SourceEndocrine and Metabolism Department, Sir Run Run Shaw Hospital, College of Medicine, Zhejiang University, Hangzhou, China.PMID: 19780745 [PubMed - indexed for MEDLINE]Related citations 6. Am J Med Sci. 2009 Dec;338(6):500-4.Bartter's syndrome in pregnancy: review of potassium homeostasis in gestation.Luqman A, Kazmi A, Wall BM.SourceUniversity of Tennessee Health Science Center, Memphis, Tennessee, USA.AbstractA 26-year-old G3P2 Hispanic female presented with acute urinary retention and profound hypokalemia (serum potassium 1.6 mEq/L) during her 13th week of pregnancy. Placement of an indwelling bladder catheter resulted in immediate urine output of 1700 mL. Potassium was administered aggressively and urinary retention resolved. She reported the use of herbal products containing licorice and corn silk tea (zea maize extract). She was taking no medication other than prenatal vitamins and had no known prior medical problems. Despite discontinuance of the herbal supplement and tea and aggressive oral potassium replacement, severe asymptomatic hypokalemia persisted. Twenty-four-hour urine studies and blood chemistry determinations, subsequently, were consistent with Bartter's syndrome. At the time of hospital discharge, she was receiving 480 mEq of oral potassium daily. Potassium-sparing diuretics were not prescribed, because successful pregnancy outcomes have been reported in patients with Bartter's syndrome and Gitelman syndrome without normalization of potassium levels. Hypokalemia (2.5-3.0 mEq/L) persisted throughout an otherwise uncomplicated pregnancy with delivery of a healthy child at 35 weeks of gestation.PMID: 19770791 [PubMed - indexed for MEDLINE]Related citations 7. Intern Med J. 2009 Feb;39(2):135-6.Familial hyperaldosteronism type 1 in pregnancy.Hamilton E, O'Callaghan C, O'Brien RM, Stowasser M, Gordon R, Zajac J, Grossmann M.PMID: 19356193 [PubMed - indexed for MEDLINE]Related citations 8. Endocr Pathol. 2009 Spring;20(1):66-72.Primary aldosteronism with aldosterone-producing adenoma consisting of pure zona glomerulosa-type cells in a pregnant woman.Shigematsu K, Nishida N, Sakai H, Igawa T, Suzuki S, Kawai K, Takahara O.SourceDepartment of Pathology, Japanese Red-Cross Nagasaki Atomic Bomb Hospital, Nagasaki, 852-8511, Japan. shigek@...AbstractAldosterone-producing adenoma (APA) consisting of pure zona glomerulosa (ZG)-type cells is extremely rare, and primary aldosteronism complicated by pregnancy is also rare. We report a case of APA discovered in a 32-year-old pregnant woman who visited our hospital for hypertension and hypokalemia at 26 weeks gestation. Elevated plasma aldosterone concentration and hypokalemia were observed, and an magnetic resonance imaging scan demonstrated a right adrenal mass. A laparoscopic adrenalectomy was performed because of refractory hypokalemia. Pathologically, the adrenal mass was diagnosed as APA, and in addition to the cytological features, in situ hybridization and real-time polymerase chain reaction proved that all the component cells were ZG-type cells. The cells also showed estrogen receptor beta immunoreactivity and melanocortin 2 receptor mRNA expression, suggesting that estrogen and/or ACTH might be related to the proliferation of APA cells during pregnancy. Our case is the first report of APA consisting of ZG-type cells discovered during pregnancy.PMID: 19199080 [PubMed - indexed for MEDLINE]Related citations 9. Ther Adv Cardiovasc Dis. 2009 Apr;3(2):123-32. Epub 2009 Jan 26.Hyperaldosteronism in pregnancy.Escher G.SourceUniversity Hospital of Berne, Division of Nephrology and Hypertension, Berne, Switzerland. genevieve.escher@...AbstractAldosterone is a key regulator of electrolyte and water homeostasis and plays a central role in blood pressure regulation. Hormonal changes during pregnancy, among them increased progesterone and aldosterone production, lead to the required plasma volume expansion of the maternal body as an accommodation mechanism for fetus growth. This review discusses the regulation of aldosterone production by aldosterone synthase (CYP11B2); the impact on aldosterone secretion due to the presence of a chimeric gene originating from a crossover between CYP11B1 and CYP11B2 in glucocorticoid remediable aldosteronism (GRA) - the inherited form of hypertension; enhanced aldosterone production in aldosterone-producing adenoma (APA); and idiopathic hyperaldosteronism (IHA). Features of hyperaldosteronism are also found in patients with apparent mineralocorticoid excess (AME), in which glucocorticoids exacerbate activation of the mineralocorticoid receptor (MR) because of a defect in the 11beta-hydroxysteroid dehydrogenase type 2 enzyme. Regulation of aldosterone production and tissue-specific activation of the mineralocorticoid receptor are prerequisites for optimal control of body fluids and blood pressure during pregnancy and contribute largely to the wellbeing of the mother-to-be.PMID: 19171690 [PubMed - indexed for MEDLINE]Related citations 10. J Obstet Gynaecol. 2007 Oct;27(7):730-1.Conn's syndrome in pregnancy successfully treated with amiloride.Al-Ali NA, El-Sandabesee D, Steel SA, Roland JM.Sourceborough and Stamford Foundation Hospitals NHS Trust, UK.PMID: 17999306 [PubMed - indexed for MEDLINE]Related citations 11. Vnitr Lek. 2006 Oct;52(10):906-8.[Primary aldosteronism in gravidity]. [Article in Slovak]Kreze A Jr, Pura M, Dobáková M, Földesová N.SourceII. Interní oddĕlení FN Bulovka, Praba. krezejr@...AbstractEndocrinology and obstetrics have one thing in common--diagnosis and treatment endocrine diseases in gravidity. These are modified by physiological changes in gravidity, often missing data and tests in normal condition and the influence of diagnosis and treatment on the pregnant female and fetus have also to be taken into consideration. If diagnosis of primary aldosteronism is suspected, suprimed plasmatic renin activity is determinant indicator (disregarding arterial hypertension, hypokaliaemia, hyperkaliuresis and proteinuria) as well as ultrasound diagnostics or adrenal gland diagnostics means magnetic resonance imaging. Aldosteron produced adenomas may by treated by adrenalectomy in the second trimester, late diagnosed adenoma and hyperplastic forms are treated by the administration of the respective medicaments.PMID: 17063801 [PubMed - indexed for MEDLINE]Related citations 12. Endocr J. 2006 Aug;53(4):461-6. Epub 2006 Jul 5.Laparoscopic adrenalectomy on a patient with primary aldosteronism during pregnancy.Kosaka K, Onoda N, Ishikawa T, Iwanaga N, Yamamasu S, Tahara H, Inaba M, Ishimura E, Ogawa Y, Hirakawa K.SourceDepartment of Surgical Oncology, Osaka City University Graduate School of Medicine, Osaka, Japan.AbstractA pregnant 26-year-old woman was referred for evaluation and management of progressive hypertension and hypokalemia at 14 weeks of gestation. Her plasma aldosterone level was markedly elevated and magnetic resonance imaging showed a right adrenal tumor. Primary aldosteronism due to an aldosterone producing-adenoma was diagnosed. Because of progressive severe hypertension, a laparoscopic adrenalectomy was performed at 17 weeks of gestation. The procedure was completed without complication, and plasma aldosterone and potassium levels rapidly improved post-operatively. However, her hypertension persisted and the growth retardation of the fetus was found. Regrettably, intrauterine fetal death was confirmed at 26 weeks of gestation. Histological examination of the placenta revealed that the placental artery had very thick walls which had apparently caused a critical failure in fetal blood flow. The optimal timing of laparoscopic surgery during pregnancy and perioperative management were subsequently discussed. Free Article PMID: 16820705 [PubMed - indexed for MEDLINE]Related citations 13. Trends Endocrinol Metab. 2005 Apr;16(3):92-7.Monogenic low renin hypertension.New MI, Geller DS, Fallo F, RC.SourceDepartment of Pediatrics, Mount Sinai School of Medicine, 1 Gustave Levy Place, Box 1198, New York, NY 10029, USA. maria.new@...AbstractMonogenic forms of low renin hypertension can now be identified in a large and heterogeneous family of hypertensive patients with highly specific etiologies and similar clinical manifestations. These include the following well-characterized disorders: apparent mineralocorticoid excess, Liddle's Syndrome, steroid 11beta-hydroxylase (11beta-OHD) and steroid 17-hydroxylase (17-OHD) deficiencies, glucocorticoid-remediable hyperaldosteronism (familial hyperaldosteronism type I), familial hyperaldosteronism type II, hypertension exacerbated by pregnancy and primary hyperaldosteronism (Conn's syndrome). The successful elucidation of specific DNA mutations in most of these conditions has emphasized the role of molecular genetics in hypertension, a field in which diagnosis can now be made on proven genetic evidence. The current knowledge of these genetic markers enables practitioners to make precise diagnoses, and to initiate specific therapy, in patients with these relatively uncommon but interesting and often treatable forms of hypertension.PMID: 15808805 [PubMed - indexed for MEDLINE]Related citations 14. Rev Med Chil. 2002 Dec;130(12):1399-405.[Primary aldosteronism and pregnancy: report of 2 cases]. [Article in Spanish]Germain AM, Kottman C, Valdés G.SourceDepartamentos de Nefrología y Obstetricia/Ginecología, Facultad de Medicina, Pontificia Universidad Católica, Santiago.AbstractBased on two patients, we discuss the difficulties in diagnosing and managing primary aldosteronism in pregnancy, which derive from changes of the renin-angiotensin-aldosterone axis, from the uncertainty regarding blood pressure control along gestation and postpartum, and from the contraindication to the use of spironolactone. The first case is a 27 years old woman with a long standing refractory hypertension, a hemorrhagic stroke with left brachial hemiplegia and crural hemiparesia, two miscarriages, one stillbirth and one offspring with intrauterine growth retardation. Due to hypokalemia, a plasma aldosterone/renin activity ratio of 91, and a negative genetic screening for glucocorticoid remediable aldosteronism (GRA), a primary hyperaldosteronism with normal adrenals in CT scan was diagnosed, and good blood pressure control was attained with spironolactone. After two and a half years of normotension, a fifth pregnancy, managed with methyldopa evolved with satisfactory blood pressures, plasma potassium, fetal growth, uterine and umbilical arterial resistance indexes, and maternal endothelial function. At 37 1/2 weeks of pregnancy the patient delivered a healthy newborn weighing 2,960 g. Blood pressure rose during the 48 hours of postpartum in the absence of proteinuria and required i.v. hydralazine. The second patient is a 37 years old woman, with known refractory hypertension for 7 years, hypokalemia, plasma aldosterone/renin activity ratio greater than 40, normal adrenals in the CAT scan, and a negative genetic screening for GRA. She had normotensive pregnancies 5 and 3 years prior to the detection of hypertension, with hypertensive crisis in both postpartum periods, retrospectively considered as expressions of primary hyperaldosteronism.PMID: 12611241 [PubMed - indexed for MEDLINE]Related citations 15. J Clin Endocrinol Metab. 2002 Jul;87(7):3187-91.Glucocorticoid remediable aldosteronism: low morbidity and mortality in a four-generation italian pedigree.Mulatero P, di Cella SM, TA, Milan A, Mengozzi G, Chiandussi L, Gomez- CE, Veglio F.SourceDepartment of Medicine and Experimental Oncology, Hypertension Unit, San Vito Hospital, University of Turin, Strada San Vito 34, 10133 Turin, Italy. paolo.mulatero@...AbstractGlucocorticoid remediable hyperaldosteronism (GRA) is a monogenic form of inherited hypertension caused by a chimeric gene originating from an unequal cross-over between the 11 beta-hydroxylase (CYP11B1) and aldosterone synthase (CYP11B2) genes. GRA is characterized by high plasma levels of aldosterone (regulated by ACTH) with suppressed plasma renin activity and the production of two rare steroids, 18hydroxycortisol and 18oxocortisol. Affected patients usually show severe hypertension and an elevated frequency of stroke at a young age. Affected women have a high risk of developing preeclampsia during pregnancy. Here, we describe a 5-generation pedigree from Sardinia in which the presence of the chimeric gene is demonstrated in 4 generations. This family displays a mild phenotype with average blood pressure levels of 131/86 mm Hg for GRA+ patients. The occurrence of stroke is very low, and preeclampsia was not observed in 29 pregnancies from 8 GRA+ mothers. We investigated whether the cross-over site (between the CYP11B1 and CYP11B2 genes) or biochemical characteristics could explain this phenotype. The cross-over site was located at the end of intron 3, in the same region as described in other families. We found a significant correlation between blood pressure and 18hydroxycortisol, 18oxocortisol, and plasma aldosterone levels, but not with kallikrein. However, none of the biochemical or genetic parameters investigated could explain the mild phenotype of the family. Free Article PMID: 12107222 [PubMed - indexed for MEDLINE]Related citations 16. Am J Perinatol. 2002 Jan;19(1):31-6.Diagnosis and management of primary aldosteronism in pregnancy: case report and review of the literature.Okawa T, Asano K, Hashimoto T, Fujimori K, Yanagida K, Sato A.SourceDepartment of Obstetrics and Gynecology, Fukushima Medical University, School of Medicine, Fukushima, Japan.AbstractPrimary aldosteronism rarely complicates pregnancy. We present a woman with primary aldosteronism in pregnancy associated with severe preeclampsia. A 33-year-old Japanese woman with hypertension was referred to our hospital at 25 weeks of gestation. Her blood pressure was 180/100 mmHg, and laboratory tests identified a low serum potassium level and moderate proteinuria on urinalysis. The fetus was diagnosed with growth restriction. Plasma renin activity (PRA) value was 2.2 ng/mL/h and plasma aldosterone concentration (PAC) was elevated (260 pg/mL). The patient was treated medically. At 27 weeks of gestation, we noted persistent late fetal heart rate decelerations associated with uterine contractions. Therefore, elective caesarean section was performed and she was delivered of a 698-g female. After delivery, PRA declined and PAC remained elevated. Abdominal computerized tomography scan and I131-iodochoresterol scan revealed a tumor in the left adrenal gland. Laparoscopic adrenalectomy was performed and confirmed the clinical diagnosis.PMID: 11857094 [PubMed - indexed for MEDLINE]Related citations 17. Chin Med J (Engl). 1999 Jun;112(6):574-5.Primary aldosteronism in pregnancy: review of cases.Wang W, Long W, Li G, Yang H.SourceDepartment of Gynaecology and Obstetrics, Zhabei District Central Hospital, Shanghai 200070, China.PMID: 11601343 [PubMed - indexed for MEDLINE]Related citations 18. J Nippon Med Sch. 2000 Aug;67(4):275-9.Primary aldosteronism in pregnancy.Matsumoto J, Miyake H, Isozaki T, Koshino T, Araki T.SourceIshikawa Hospital, Urawa City, Saitama.AbstractAldosteronism is a rare complication of pregnancy. We report a case of a 26-year-old woman who became pregnant soon after a diagnosis of primary aldosteronism due to left adrenal adenoma was made. Only oral potassium supplementation was required in addition to routine prenatal care until 36 weeks' gestation. Subsequently, antihypertensive medication was needed to control elevated blood pressure. A healthy male infant was delivered by cesarean section because of abruptio placentae. The postoperative course was uneventful. Left adrenalectomy was conducted eight months after delivery under laparoscopic visualization. In this case report, we discuss management of aldosteronism in pregnancy and review the literature. Free Article PMID: 10938597 [PubMed - indexed for MEDLINE]Related citations 19. J Laparoendosc Adv Surg Tech A. 2000 Jun;10(3):169-71.Laparoscopic adrenalectomy for primary hyperaldosteronism during pregnancy.Shalhav AL, Landman J, Afane J, Levi R, Clayman RV.SourceDepartment of Surgery (Urology), Washington University School of Medicine, St. Louis, Missouri 63110, USA.AbstractLaparoscopic adrenalectomy was performed early in the second trimester of pregnancy in a woman with an aldosteronoma causing hypertension (254/154 mm Hg). The patient was later delivered of a healthy baby. With suitable precautions and timing, major laparoscopic surgery can be performed safely during pregnancy.PMID: 10883996 [PubMed - indexed for MEDLINE]Related citations 20. Am J Obstet Gynecol. 2000 Mar;182(3):745-6.Primary aldosteronism as a cause of severe postpartum hypertension in two women.Nezu M, Miura Y, Noshiro T, Inoue M.SourceDepartment of Internal Medicine, Yamanashi Prefecture Central Hospital, Kofu, Yamanashi, Japan.AbstractTwo women who first had the clinical features of primary aldosteronism in the postpartum period are described. Their gestations were virtually uneventful. After delivery, however, progressively severe hypertension (Joint National Committee VI, stage 3) with hypokalemia developed. Pregnancy may conceal the clinical symptoms of primary aldosteronism that causes unexpected severe hypertension in the postpartum period.PMID: 10739546 [PubMed - indexed for MEDLINE]Related citations 21. Hypertension. 2000 Feb;35(2):668-72.Glucocorticoid-remediable aldosteronism and pregnancy.Wyckoff JA, Seely EW, Hurwitz S, BF, Lifton RP, Dluhy RG.SourceEndocrine Hypertension Division, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.AbstractGlucocorticoid-remediable aldosteronism (GRA) is a hereditary form of primary hyperaldosteronism that presents with hypokalemia and hypertension from childhood onward. GRA is characterized by the ectopic production of aldosterone in the cortisol-producing zona fasciculata under the regulation of adrenocorticotrophic hormone. Despite the early age of onset, no previous reports of pregnancy and GRA exist. Therefore, we set out to describe the maternal and fetal outcomes of pregnancy in women with GRA. Data regarding the blood pressure and pregnancy outcomes were collected in a retrospective chart review of prenatal and hospital records of 35 pregnancies in 16 women with genetically proven GRA. A total of 6% of pregnancies in women with GRA (GRA+) were complicated by preeclampsia. The published rates of preeclampsia in general obstetric populations vary from 2.5% to 10%. Despite the lack of an apparent increase in the rate of preeclampsia, GRA+ women with chronic hypertension had a high rate (39%) of pregnancy-aggravated hypertension. Starting with a higher baseline blood pressure, maternal blood pressure plotted over the time course of pregnancy followed a quadratic curve similar to that previously described in normal pregnancy. Mean gestational age at delivery was 39.1 weeks. Mean birth weight, excluding the 3 sets of twins, was 3219 g. However, infants of GRA+ mothers with pregnancy-aggravated hypertension tended to have lower birth weights than those that did not (3019 g versus 3385 g, respectively; P=0.08). The primary cesarean section rate was 32%, which is approximately double that seen in other general or hypertensive obstetric populations. In summary, GRA+ women did not seem to have an increased risk of preeclampsia. However, GRA+ women with chronic hypertension seem to be at an increased risk for an exacerbation of their hypertension during pregnancy. Free Article PMID: 10679515 [PubMed - indexed for MEDLINE]Related citations 22. Wien Klin Wochenschr. 1999 Oct 29;111(20):855-7.Primary aldosteronism caused by aldosterone-producing adenoma in pregnancy--complicated by EPH gestosis.Kreze A Jr, Kothaj P, Dobáková M, Rohon S.SourceInternal Clinic, F. D. Roosevelt's Hospital, Banska Bystrica, Slovak Republic.AbstractPregnancy in conjunction with primary aldosteronism is an unusual occurrence. We report a 28-year-old woman who presented with mild hypertension and hypokalemia as manifestations of primary aldosteronism caused by an aldosterone-producing adenoma in the left adrenal gland during pregnancy. Although the diagnosis was straightforward, the patient refused to undergo the proposed operation during the second trimester of her pregnancy. She was not admitted to hospital until she developed EPH gestosis in the 27th week of gestation, which had an unfavourable outcome for the infant who died nine days after delivery. The patient underwent a laparoscopic adrenalectomy which resulted in normalization of blood pressure and blood potassium levels. In cases of aldosterone-producing adenoma, surgery in the second trimester is the most appropriate option to avoid a poor obstetric outcome.PMID: 10586491 [PubMed - indexed for MEDLINE]Related citations 23. Intern Med. 1999 Jan;38(1):36-9.Primary aldosteronism with aldosterone-producing adrenal adenoma in a pregnant woman.Fujiyama S, Mori Y, Matsubara H, Okada S, Maruyama K, Masaki H, Yonemoto T, Nagata T, Umeda Y, Matsuda T, Iwasaka T, Inada M.SourceSecond Department of Internal Medicine, Kansai Medical University, Osaka.AbstractA 30-year-old pregnant woman complained of muscle weakness at 29 weeks' gestation. She was hypertensive with severe hypokalemia. Lower plasma renin activity and higher aldosterone level than the normal values in pregnancy suggested primary aldosteronism. A cesarean delivery was performed at 31 weeks' gestation because of pulmonary congestion. The neonatal course was uncomplicated. The laparoscopic adrenalectomy for a 2.0-cm right adrenal adenoma resulted in normalizing of her blood pressure and serum potassium level. Although primary aldosteronism is rare, especially during pregnancy, it should be always considered as one of etiologies of hypertension in pregnancy. Free Article PMID: 10052740 [PubMed - indexed for MEDLINE]Related citations 24. Semin Perinatol. 1998 Dec;22(6):471-84.Endocrine causes of hypertension in pregnancy--when to start looking for zebras.Keely E.SourceDepartment of Medicine, University of Ottawa, Ontario, Canada.AbstractHypertension is a common medical disorder in pregnancy that may predate or first appear in pregnancy. Endocrine disorders rarely are the cause of the elevated blood pressure. However, it is essential to have a high index of suspicion because they carry much higher fetal and maternal morbidity and mortality risks. Endocrine disorders presenting as hypertension are primarily the result of autonomous production of renin, aldosterone, cortisol, or catecholamines. This report discusses the physiological changes in pregnancy, presentation, investigation, and management of these disorders.PMID: 9880117 [PubMed - indexed for MEDLINE]Related citations 25. South Med J. 1997 Feb;90(2):243-5.Pregnancy complicated by primary aldosteronism.Webb JC, Bayliss P.SourceDepartment of Obstetrics and Gynecology, Beaumont Army Medical Center, El Paso, Tex., USA.AbstractPregnancy is rarely complicated by aldosteronism. We report the case of a 32-year-old woman who became pregnant soon after primary aldosteronism was diagnosed. Only antihypertensive medication and oral potassium supplementation were required in addition to routine prenatal care. A healthy female infant was delivered at term. In this case, no adrenal adenoma was identified. We discuss management of aldosteronism in pregnancy and review the literature.PMID: 9042183 [PubMed - indexed for MEDLINE]Related citations 26. Ir J Med Sci. 1995 Oct-Dec;164(4):279-80.Primary aldosteronism in pregnancy--should it be treated surgically?Aboud E, De Swiet M, Gordon H.SourceNorthwick Park Hospital, Harrow, Middlesex.AbstractWe report a case of primary aldosteronism in pregnancy that was treated surgically by removal of the adenoma in the 2nd trimester. Only a few cases have been reported in the English literature due to the rarity of the condition. Primary aldosteronism follows a variable course in pregnancy. In the majority of cases the hypertension and hypokalaemia are made worse, necessitating antihypertensive medication to control the blood pressure. Some of the drugs required for treatment are known to affect the fetus. In a minority of cases the hypertension improves with pregnancy. This is thought to be due to the high levels of progesterone which is an aldosterone antagonist. Primary aldosteronism invariably gets worse in the post partum period, irrespective of the antenatal course of the disease. Surgery seems to be the treatment of choice for this condition, provided the adenoma is localised. It has the advantage of offering an immediate solution, avoids fetal complications of medical treatment and possible deterioration in the post partum period.PMID: 8522430 [PubMed - indexed for MEDLINE]Related citations 27. Obstet Gynecol. 1995 Oct;86(4 Pt 2):644-5.Diagnosis and surgical treatment of primary aldosteronism in pregnancy: a case report.Baron F, Sprauve ME, Huddleston JF, Fisher AJ.SourceDepartment of Gynecology and Obstetrics, Emory University School of Medicine, Atlanta, Georgia, USA.AbstractBACKGROUND: Aldosterone-producing adrenal adenomas are rare, especially during pregnancy. We report a patient who presented in the early second trimester, was diagnosed with primary aldosteronism, and was treated successfully by adrenalectomy.CASE: A 17-year-old black nulliparous woman was found to have a blood pressure (BP) of 150/82 mmHg when she registered for prenatal care at 14 weeks' gestation. Initial laboratory assessment revealed a markedly diminished serum potassium level of 2.1 mmol/L. Further laboratory evaluation detected decreased random plasma renin activity and an elevated aldosterone level. Magnetic resonance imaging revealed a 2-cm right adrenal lesion. She was diagnosed with an adrenal adenoma and successfully underwent an adrenalectomy at 17 weeks' gestation. Postoperatively, her BP and serum potassium level normalized. She spontaneously delivered a normal male infant at term.CONCLUSION: Although primary hyperaldosteronism is a rare clinical entity, it must be considered when hypertension and hypokalemia are present concurrently. Antepartum medical management can be difficult, often resulting in poor obstetric outcome. Surgery in the second trimester is an effective option.PMID: 7675397 [PubMed - indexed for MEDLINE]Related citations 28. Am J Obstet Gynecol. 1995 May;172(5):1655-6.Spironolactone therapy during human pregnancy.Groves TD, Corenblum B.Comment inAm J Obstet Gynecol. 1996 Jan;174(1 Pt 1):297. PMID: 7755100 [PubMed - indexed for MEDLINE]Related citations 29. Obstet Gynecol. 1991 Sep;78(3 Pt 2):489-91.Idiopathic aldosteronism in pregnancy.Neerhof MG, Shlossman PA, Poll DS, Ludomirsky A, Weiner S.SourceDepartment of Obstetrics and Gynecology, Pennsylvania Hospital, Philadelphia.AbstractThis is the first reported case of the idiopathic type of primary aldosteronism in pregnancy. The severely hypertensive patient was unresponsive to treatment with high doses of four antihypertensive agents administered concurrently. A drastic improvement in blood pressure was noted within 24 hours of beginning enalapril maleate, although subsequent deterioration in fetal status led to delivery at 26 weeks' gestation. Alternatives to standard medical therapy may be necessary for this rare but potentially life-threatening disease during pregnancy.PMID: 1870802 [PubMed - indexed for MEDLINE]Related citations 30. Presse Med. 1990 Nov 24;19(39):1810.[Conn's adenoma in pregnancy]. [Article in French]Schlienger JL, Duval J, Langer B, Jaeck D, Schlaeder G.PMID: 2148006 [PubMed - indexed for MEDLINE]Related citations 31. Gynakol Rundsch. 1990;30(1):16-21.[Primary aldosteronism in pregnancy]. [Article in German]Casper F, Seufert R, Riedmiller H, Bauer H.SourceFrauenklinik, Universität Mainz, BRD.AbstractPrimary hyperaldosteronism (Conn's syndrome) rarely occurs during pregnancy. The concurrence of hypertension combined with hypokalemia and revealing subjective symptoms such as paresthesia, muscular weakness and lassitude can suggest this infrequent diagnosis. The diagnosis is confirmed on the one hand by chemical tests demonstrating an aldosterone level far above normal and clearly suppressed renin activity, and on the other hand through ultrasound for a morphological diagnosis. We consider causal surgical treatment with adrenalectomy as the therapy of choice during early pregnancy.PMID: 2347511 [PubMed - indexed for MEDLINE]Related citations 32. Geburtshilfe Frauenheilkd. 1989 Sep;49(9):830-1.[Primary hyperaldosteronism (Conn syndrome) and pregnancy]. [Article in German]Spitzer D, Haidbauer R, Staudach A, Höfle S, Bolzano K, Frick J.SourceLandesfrauenklinik Salzburg, 1. Medizin LKA Salzburg.AbstractBecause of the atypical symptomatology, which can mimic an EPH-gestosis, the physiological elevation of serum aldosterone in the third trimester and restricted diagnostic possibilities, the diagnosis of primary hyperaldosteronism during pregnancy is difficult. A case of an adrenal adenoma during pregnancy is reported.PMID: 2806856 [PubMed - indexed for MEDLINE]Related citations 33. Am J Obstet Gynecol. 1984 Dec 1;150(7):892-3.Primary aldosteronism in pregnancy.Colton R, GO, Fishman LM.PMID: 6391175 [PubMed - indexed for MEDLINE]Related citations 34. Am J Obstet Gynecol. 1984 Nov 15;150(6):786-7.Primary hyperaldosteronism during pregnancy.Merrill RH, Dombroski RA, MacKenna JM.PMID: 6496601 [PubMed - indexed for MEDLINE]Related citations 35. Jpn Heart J. 1983 Nov;24(6):995-1006.Elevation of plasma renin activity during pregnancy and rupture of a dissecting aortic aneurysm in a patient with primary aldosteronism.Shimizu A, Aoi W, Akahoshi M, Utsunomiya T, Doi Y, Suzuki S, Kuramochi M, Hashiba K.AbstractThis is a case report of a 37-year-old Japanese woman with primary aldosteronism who was found to have high plasma renin activity during toxemia of pregnancy and who died of a dissecting aneurysm of the aorta about 2 years later. The autopsy findings showed cystic medial necrosis in the aorta and a right adrenocortical adenoma. The dissecting aneurysm in this case is probably related to hypertension and cystic medial necrosis. A definite diagnosis of primary aldosteronism cannot be made during toxemia of pregnancy, and it is necessary to do serial determinations of plasma renin activity and plasma aldosterone concentration after delivery to confirm the diagnosis.PMID: 6368896 [PubMed - indexed for MEDLINE]Related citations 36. South Med J. 1983 Apr;76(4):514-6.Aldosteronism in pregnancy: association with virilization of female offspring.Elterman JJ, Hagen GA.AbstractWe have described a case of maternal primary aldosteronism in which there is virilization of the female offspring. The most common causes of virilization are considered unlikely on the basis of clinical and laboratory data. The report illustrates the exacerbation of aldosteronism that occurs postpartum and emphasizes a conservative approach to intravenous potassium therapy during delivery.PMID: 6836370 [PubMed - indexed for MEDLINE]Related citations 37. Aust N Z J Med. 1982 Oct;12(5):537-9.Primary hyperaldosteronism in pregnancy.Hammond TG, Buchanan JD, Scoggins BA, Thatcher R, Whitworth JA.AbstractWe report a case of primary hyperaldosteronism in a 37-year-old woman presenting early in pregnancy with hypertension and hypokalaemia. Plasma renin concentration was suppressed and unaffected by sodium restriction or upright posture at 16 and 35 weeks gestation, or seven days post-partum. Recumbent plasma aldosterone was elevated, and normal postural response lost both at 35 weeks gestation and seven days post-partum. Vaginal delivery, following induction at 38 weeks, was uncomplicated. Two months postpartum C.T. scan and adrenal venous catheterisation studies indicated a left sided adenoma and left adrenalectomy was performed. Within seven days the patient was normotensive with normal serum potassium and urinary aldosterone on no treatment.PMID: 6960878 [PubMed - indexed for MEDLINE]Related citations 38. Am J Obstet Gynecol. 1982 Sep 1;144(1):28-34.Urinary free 18-hydroxycorticosterone, plasma aldosterone, and urinary aldosterone metabolites in normal pregnancy.Bauknecht H, Vecsei P, Endres H, Hettenbach A.AbstractThe final steps in aldosterone biosynthesis are unclear. Undecided is whether 18-hydroxycorticosterone is a precursor of aldosterone or an end product. 18-Hydroxycorticosterone is secreted in close relationship to aldosterone. To get adequate information on the status of aldosterone in pregnancy, determination of more than one parameter of aldosterone seems to be necessary. Urinary excretion of free 18-hydroxycorticosterone, tetrahydroaldosterone, aldosterone-18-glucuronide, free aldosterone, and the plasma concentration of aldosterone were measured by radioimmunoassay in 16 primigravid women in the last trimester of normal pregnancy and in 13 healthy nonpregnant women. All steroids measured were significantly increased in pregnancy. The ratios of aldosterone-18-glucuronide to tetrahydroaldosterone in the two groups were not significantly different, so that significant changes in renal or hepatic aldosterone metabolism could not be demonstrated in pregnancy. When pregnant women with ankle edema (n = 7) were compared to pregnant women without edema (n = 9), no differences in steroid patterns could be found. The increased excretion of 18-hydroxycorticosterone in pregnancy confirms the state of hyperaldosteronism in normal pregnancy which is associated with an increase in biologically active, free aldosterone. Dissociation in the excretion of the two aldosterone metabolites and free aldosterone was found in three pregnant women, in whom excretion of aldosterone-18-glucuronide was increased but excretion of tetrahydroaldosterone and free aldosterone was in the normal nonpregnant range.PMID: 7114109 [PubMed - indexed for MEDLINE]Related citations 39. Clin Exp Hypertens A. 1982;4(9-10):1685-93.Aldosterone-producing-adenoma (A-P-A): effect of pregnancy.Gordon RD, Tunny TJ.AbstractSerial measurements of plasma renin activity, plasma progesterone and urinary aldosterone were made before, during and after pregnancy in a patient from whom an A-P-A was later removed with cure of hypertension and hypokalemia. Despite 16-fold increases in urinary aldosterone during pregnancy, plasma renin activity levels became unsuppressed, and hypertension and hypokalemia were reversed. Increases in plasma progesterone or other steroids, competitively inhibiting the effects of aldosterone on its receptor, may explain remission of A-P-A and reversal of renin suppression during pregnancy. In a second patient, the features of primary aldosteronism appeared immediately after a pregnancy, and removal of an A-P-A cured hypertension and hypokalemia. A-P-A is more common in females and may appear following pregnancy. Urinary aldosterone was 6-fold higher after pregnancy than before. Thus, sex steroids may not only protect from hyperaldosteronism but may also stimulate growth of A-P-A's.PMID: 6754149 [PubMed - indexed for MEDLINE]Related citations 40. J Clin Endocrinol Metab. 1981 Aug;53(2):331-7.Overproduction of sodium-retaining steroids by the zona glomerulosa is adrenocorticotropin-dependent and mediates hypertension in dexamethasone-suppressible aldosteronism.Gill JR Jr, Bartter FC.AbstractDexamethasone suppressed urinary aldosterone to less than 1.5 micrograms/day in 1-2 days and lowered blood pressure in a woman and in her 2 1/2-yr-old daughter, both of whom have hypertension and hyporeninemia and are members of a kindred with dexamethasone-suppressible aldosteronism. ACTH given for 7 days produced a sustained increase in aldosterone production and a rise in blood pressure in both patients. The abnormal suppression with dexamethasone and further stimulation with ACTH indicate that the aldosteronism is ACTH-dependent in this disorder. The cause of the ACTH-dependence of aldosterone production in this disorder is unknown but may represent continued stimulation rather than the usual (secondary) inhibition by ACTH of 11-hydroxylation and 18-hydroxylation in zone glomerulosa cells. Blood pressure was normal during treatment with spironolactone and during pregnancy, when the action of aldosterone and other similar steroids was presumably blocked by an increased production of progesterone; this suggests that the hypertension is dependent upon sodium-retaining steroids such as aldosterone. Aminoglutethimide given during treatment with ACTH decreased urinary aldosterone and blood pressure and increased PRA, with minimal effects on plasma cortisol or urinary 17-hydroxycorticosteroids. These results provide additional evidence that aldosterone, acting alone or in conjunction with other steroids synthesized by the zona glomerulosa, mediates the hypertension and hyporeninemia of dexamethasone-suppressible aldosteronism.PMID: 6265487 [PubMed - indexed for MEDLINE]Related citations 41. Jpn Heart J. 1978 Nov;19(6):946-53.Primary aldosteronism aggravated during peripartum period.Aoi W, Doi Y, Tasaki S, Mitsuoka T, Suzuki S, Hashiba K.AbstractTwo cases are reported of a 30-year-old and of a 28-year-old Japanese women with primary aldosteronism in whom metabolic and blood pressure abnormalities were aggravated during peripartum period. The characteristic findings in 2 present cases are as follows; 1) lower blood pressure during pregnancy, 2) elevated blood pressure during peripartum period, and 3) after parturition, serum potassium decreased, and the blood pressure elevated. The reason why the hypertension and hypokalemia associated with primary aldosteronism were ameliorated during pregnancy was thought to be due to the increased secretion of progesterone. Furthermore, the rapid recurrence of symptoms, increase in blood pressure, and hypokalemia in the post-partum period could be related to elevated prolactin and decreased progesterone levels.PMID: 750675 [PubMed - indexed for MEDLINE]Related citations 42. Cesk Gynekol. 1978 Jun;43(5):380-1.[Primary aldosteronism (Conn's syndrome) in pregnancy]. [Article in Czech]Hájek Z, Horký K, Pokorný A.PMID: 667999 [PubMed - indexed for MEDLINE]Related citations 43. Med Klin. 1974 Dec 13;69(50):2043-50.[Oral contraceptives and arterial hypertension]. [Article in German]Losse H, Risse E, Wessels F.AbstractThere have been numerous accounts of women on ovulation inhibitors developing hypertension or reactifying or intensifying previous hypertension. Concerning frequency of significant hypertension in pill users, there are reports varying from .66% (or even 0%) to 19%. The time interval between start of medication and manifestation of hypertension also varies according to different sources from 7 days to 5 years, with the critical point usually around 6-8 weeks. Degree of hypertension after ovulation inhibitors ranges from mildly significant increases in systolic and/or diastolic blood pressure to malignant hypertension with irreversible kidney insufficiency. Early observable symptoms of hypertension include migrainelike headaches and rapid weight gain (sodium and water retention). After discontinuation of the medication, normal blood pressure is attained either within a few days or after 6-8 months. If normalization of blood pressure does not occur spontaneously there may be other causes (e.g., secondary vascular disorders). Concerning pathogenesis of ovulation-inhibitor-related hypertension, changes (increases) in the renin-angiotensin-aldosterone system are assumed to play a major role (almost all women on the pill exhibit elevated renin-angiotensin-aldosterone activity). Sodium retention may also be determinative. Many clinical and laboratory studies have demonstrated that it is the estrogen content of ovulation inhibitors that is responsible for the increased plasma renin activity. The study recommends: 1) women who wish oral contraceptive therapy should give careful family and personal histories and be tested for blood pressure before and during treatment (monthly, then after 6 months twice yearly); 2) careful supervision is indicated for women with high blood pressure or other cardiovascular disorders in their history, present or former kidney disorders, arterial hypertension, pregnancy toxemias, adipositas, or diabetes mellitus; 3) abnormal weight gain may be an early symptom; 4) if any rise in blood pressure is observed, ovulation inhibitor medication should be discontinued immediately; and 5) ovulation inhibitor-induced hypertension should be considered in differential diagnosis in young women with arterial hypertension.PMID: 4374645 [PubMed - indexed for MEDLINE]Related citations 44. Vopr Okhr Materin Det. 1971 Jul;16(7):81-3.[Pregnancy following surgical treatment of primary aldosteronism]. [Article in Russian]Barkhatova TP, Gerasimenko PP.PMID: 5133769 [PubMed - indexed for MEDLINE]Related citations 45. J Obstet Gynaecol Br Commonw. 1970 Oct;77(10):928-31.The effects of progesterone on the responses of the cardiovascular system to intravenous infusions of aldosterone.Lloyd IJ, Burstyn PG, Horrobin DF, Kahuho SK, Mulimba O, Webala GS.PMID: 5473326 [PubMed - indexed for MEDLINE]Related citations 46. J Clin Endocrinol Metab. 1967 Nov;27(11):1628-32.Pregnancy and primary aldosteronism.Biglieri EG, Slaton PE Jr.PMID: 6075591 [PubMed - indexed for MEDLINE]Related citations 47. J Clin Endocrinol Metab. 1967 Mar;27(3):385-8.Plasma renin activity and aldosterone secretion in a pregnant woman with primary aldosteronism.Gordon RD, Fishman LM, Liddle GW.PMID: 5337160 [PubMed - indexed for MEDLINE]Related citations 48. Geburtshilfe Frauenheilkd. 1966 Feb;26(2):141-54.[Activity of renin/angiotensin system and secretion of aldosterone during pregnancy]. [Article in German]Gross F.PMID: 4293051 [PubMed - indexed for MEDLINE]Related citations 49. Br Med J. 1965 Nov 20;2(5472):1215-9.Plasma renin concentration in human hypertension . II. Renin in relation to aetiology.Brown JJ, Davies DL, Lever AF, on JI.PMCID: PMC1846624 Free PMC Article PMID: 5849134 [PubMed - indexed for MEDLINE]Related citations 50. Proc R Soc Med. 1965 Aug;58:575-6.CONN'S SYNDROME WITH ASSOCIATED PREGNANCY.BOUCHER BJ, MASON AS.PMCID: PMC1898830 Free PMC Article PMID: 14341826 [PubMed - indexed for MEDLINE]Related citations 51. Proc R Soc Med. 1965 Mar;58:175-6.BILATERAL ALDOSTERONAMATA.GARDNER F.PMCID: PMC1898107 Free PMC Article PMID: 14269766 [PubMed - indexed for MEDLINE]Related citations 52. Obstet Gynecol. 1964 Feb;23:200-8.PRIMARY ALDOSTERONISM IN PREGNANCY.CRANE MG, ANDES JP, HARRIS JJ, SLATE WG.PMID: 14117325 [PubMed - indexed for MEDLINE]Related citations 53. Ginekol Pol. 1964 Jan-Feb;35:141-8.[ALDOSTERONE AND ITS ROLE IN OBSTETRICS]. [Article in Polish]KUCZYNSKA SICINSKA J.PMID: 14126147 [PubMed - indexed for MEDLINE]Related citations 54. Geburtshilfe Frauenheilkd. 1962 Oct;22:893-7.[On aldosteronism in pregnancy]. [Article in German]STARK G.PMID: 13983447 [PubMed - indexed for MEDLINE]Related citations