Bilateral adrenalectomy for severe hypertension in congenital adrenal hyperplasia due to 11β-hydroxylase deficiency: Long term follow-up

Kacem, M.; Moussa, A.; Khochtali, I.; Nabouli, R.; Morel, Yves; Zakhama, A.

doi:10.1016/j.ando.2008.12.005

Cited by 23 publications

(11 citation statements)

References 26 publications

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“…There was rapid resolution of hypertension 15 days post operatively. The 11-deoxycortisol levels were high later on during follow-up with normal blood pressure and no clear focus of adrenal rest tissue [206]. Another case similarly reports persistent elevation in 11-deoxycortisol and DOC after bilateral adrenalectomy with normalization of blood pressure within 1 year postoperatively [96].…”

Section: Adrenalectomymentioning

confidence: 88%

“…To date, five case reports of 11βOHD are known where bilateral adrenalectomy has been described as a successful surgical management option in patients with poorly controlled hypertension, end-organ damage secondary to hypertension, hypokalemia and extreme features of hyperandrogenism requiring high doses of glucocorticoid replacement [40,96,205,206]. The long-term follow-up after bilateral adrenalectomy has been reported in one case that was followed until 72 months.…”

Section: Adrenalectomymentioning

confidence: 97%

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Clinical perspectives in congenital adrenal hyperplasia due to 11β-hydroxylase deficiency

2016

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Congenital adrenal hyperplasia due to 11 beta-hydroxylase deficiency is a rare autosomal recessive genetic disorder. It is caused by reduced or absent activity of 11β-hydroxylase (CYP11B1) enzyme and the resultant defects in adrenal steroidogenesis. The most common clinical features of 11 beta-hydroxylase deficiency are ambiguous genitalia, accelerated skeletal maturation and resultant short stature, peripheral precocious puberty and hyporeninemic hypokalemic hypertension. The biochemical diagnosis is based on raised serum 11-deoxycortisol and 11-deoxycorticosterone levels together with increased adrenal androgens. More than 100 mutations in CYP11B1 gene have been reported to date. The level of in-vivo activity of CYP11B1 relates to the degree of severity of 11 beta-hydroxylase deficiency. Clinical management of 11 beta-hydroxylase deficiency can pose a challenge to maintain adequate glucocorticoid dosing to suppress adrenal androgen excess while avoiding glucocorticoid-induced side effects. The long-term outcomes of clinical and surgical management are not well studied. This review article aims to collate the current available data about 11 beta-hydroxylase deficiency and its management.

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Section: Adrenalectomymentioning

confidence: 88%

Section: Adrenalectomymentioning

confidence: 97%

Clinical perspectives in congenital adrenal hyperplasia due to 11β-hydroxylase deficiency

2016

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“…Debido a la severidad y cronicidad de la HTA, era pertinente evaluar la existencia de otras complicaciones. Se realizaron los exámenes necesarios y no se encontraron hallazgos en órgano blanco como retinopatía hipertensiva, falla renal y/o ataque isquémico transitorio descritos en otras series (11,14).…”

Section: Discussionunclassified

Manejo con cinco antihipertensivos en paciente con pubertad precoz. Reporte de caso

Ruiz-Rivera

Mendoza-Rojas

2018

iatreia

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“…Juga ada peningkatan nodul-nodul pada korteks. Kacem et al (2009) menyatakan sel hiperplasia yang berdifusi dan nodul-nodul pada zona fasciculata pada kedua adrenal pada dua pasien hipertensi. Sel-sel memiliki sitoplasma berwarna hijau gelap yang mengandung pigmen lipofuscin.…”

Section: Pendahuluanunclassified

“…Perubahan seluler yang ditemukan pada zona glomerulosa, zona fasikulata dan zona retikularis dan medulla, diberi skor (-) bila tidak ditemukan perubahan seluler, skor (+) bila perubahan seluler yaitu hiperplasia, cytoplasmic vacuolization, hipertropi, nodul-nodul, kongesti, hemoragi, cysts dan atropi. Ini sesuai dengan Boulkroun et al (2010) dan Kacem et al (2009), melaporkan bahwa abnormalitas jaringan yang ditemui pada hipertensi adalah hiperplasia, hipertropi, cysts, nekrosis sel, cytoplasm vacuolization, dan nodul-nodul.…”

Section: Evaluasi Histopatologiunclassified

Perubahan Patologi Seluler Kelenjar Adrenal Tikus Hipertensi dengan Terapi Sel Punca Mesenkimal Sumsum Tulang (CELLULER STUDY OF ADRENAL GLAND IN HYPERTENSIVE RATS WITH IMPACT OF BONE MARROW MESENCHYMAL STEM CELLS THERAPY)

Rumlaklak¹,

Sulistiawati²,

Sajuthi³

et al. 2018

JVet

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The purpose of this study was to investigate changes in cellular pathology of adrenal gland as impact of bone marrow mesenchymal stem cells (BMMSC) therapy in hypertensive rats. The research used ten male wistar rats with age ± 10-12 weeks with body weight ± 200-250 grams which is devided into two different groups ie BMMSc(-) hyprtention and BMMSc(+) hypertension. Rats are conditioned with hypertention using Hasbinoto et al method. Right nephrectomy and left carotid communic artery ligation are performed on all rats. Rats are injected with deoxycorticosterone acetate (DOCA), then 0.12 % of âaminopropionitrile fumarate (BAPN) is added into drinking water. 1% NaCl solution was administered as drinking water during the study. Rats were evaluated for particular indicator ie blood pressure then were euthanized for adrenal organs collections. The data that obtained then analysed using qualitative descriptive. The result of the study indicate hypertention therapy using BMMSC can repair cell damaged of the adrenal gland such as hyperplasia, nodules, cysts and cytoplasm vacuolization.

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Bilateral adrenalectomy for severe hypertension in congenital adrenal hyperplasia due to 11β-hydroxylase deficiency: Long term follow-up

Cited by 23 publications

References 26 publications

Clinical perspectives in congenital adrenal hyperplasia due to 11β-hydroxylase deficiency

Clinical perspectives in congenital adrenal hyperplasia due to 11β-hydroxylase deficiency

Manejo con cinco antihipertensivos en paciente con pubertad precoz. Reporte de caso

Perubahan Patologi Seluler Kelenjar Adrenal Tikus Hipertensi dengan Terapi Sel Punca Mesenkimal Sumsum Tulang (CELLULER STUDY OF ADRENAL GLAND IN HYPERTENSIVE RATS WITH IMPACT OF BONE MARROW MESENCHYMAL STEM CELLS THERAPY)

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