CYCLIC CUSHING'S DISEASE IN A WOMAN OF 32 YEARS WITH SEVERE HYPERCORTISOLISM
AACE ePoster Library. PAZ-IBARRA J. 05/13/15; 97781; 839
Jose PAZ-IBARRA
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Abstract
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Objective: To report a case of cyclic hypercortisolism in Cushing's disease (CD).
Methods: Clinical and paraclinical characteristics of a patient with CD are presented.
Results or Case Presentation: Female, 32 years, with history of infertility, PCOS and DM treated with metformin and insulin; 22 d before admission, has altered behavior, doing activities that then no further recalls, palpitations, flushing. The day of admission to the ER presents psychomotor agitation, sensory disorder, and severe hypokalemia and hyperglicemia so is hospitalized. At examination: alert, cushingoid, weight: 60kg BMI: 23 PA: 120/60mmHg, FC: 92x', FR 16x'; skin: moderate hirsutism, multiple bruises and no stretch marks. small bearings in supraclavicular fossa, small dorsal hump, edema ++ / +++ lower limbs. Analyses: Glicemia 459mg%, Na:149, K:1.99, F >50ug/dl, ACTH: 386pg/ml, TSH: 1.54 uU/ml, T4Libre: 0.54ng/dl; Peptide C: 0.27ng/ml, E2: 29pg/ml, Pg: 0.80ng/ml, LH: 0.10mIU/ml, PRL: 7.25ng/mL, Androstenedione >10ng/ml, DHEAS: 265ug/ml, free Testo: 3.20pg/ml. Basal UFC1: 919.35ug/d, basal UFC2: 1592.5ug/d, UFC post Dexa8: 132 ug/d. Serum F post Dexa8 >50ug/dl. EV infusion of Dexa 7mg (Basal F: 90.30ug/dl, F 4pm: 13.5ug/dl, F 24h post: 98.10ug/dl; MRI: nodule 8mm on the right side of the pituitary; TEM TAP (-). Suspecting ectopic CS, IPSS which was not performed for non-medical reasons stated being subjected to internal jugular vein catheterization. Central ACTH 120pg/ml and peripheral ACTH 60pg/ml, ratio ACTH Central/Peripheral: 2.0. Start Ketoconazole 600 mg/d PO; awaiting surgical intervention controls of ACTH are taken: 44.60pg/ml, androstenedione:2.07, DHEAS: 32.60, F:18.6ug/dl.
Discussion: CD is the most common cause of spontaneous CS with 60 to 70%, is the result of ACTH hypersecretion by a pituitary adenoma. CS is a cyclical pattern of hypercortisolism, wherein the biochemical production of cortisol fluctuate rhythmically. Clinical suspicion of CS, we demonstrate the presence of hypercortisolism, breaking the circadian cycle and the failure to exogenous corticosteroid withdrawal. In our patient, we show increased levels of UFC and serum F, UFC suppression > 90% post Dexa8, early suppression of serum F post IV infusion Dexa7mg and IJV catheterization (S:81%) with an ratio central/eripheral> 1.6 that guides us CD.
Conclusion: We report a case with typical clinical and paraclinical Cushing's disease associated with a fluctuating severe hypercortisolism.
Methods: Clinical and paraclinical characteristics of a patient with CD are presented.
Results or Case Presentation: Female, 32 years, with history of infertility, PCOS and DM treated with metformin and insulin; 22 d before admission, has altered behavior, doing activities that then no further recalls, palpitations, flushing. The day of admission to the ER presents psychomotor agitation, sensory disorder, and severe hypokalemia and hyperglicemia so is hospitalized. At examination: alert, cushingoid, weight: 60kg BMI: 23 PA: 120/60mmHg, FC: 92x', FR 16x'; skin: moderate hirsutism, multiple bruises and no stretch marks. small bearings in supraclavicular fossa, small dorsal hump, edema ++ / +++ lower limbs. Analyses: Glicemia 459mg%, Na:149, K:1.99, F >50ug/dl, ACTH: 386pg/ml, TSH: 1.54 uU/ml, T4Libre: 0.54ng/dl; Peptide C: 0.27ng/ml, E2: 29pg/ml, Pg: 0.80ng/ml, LH: 0.10mIU/ml, PRL: 7.25ng/mL, Androstenedione >10ng/ml, DHEAS: 265ug/ml, free Testo: 3.20pg/ml. Basal UFC1: 919.35ug/d, basal UFC2: 1592.5ug/d, UFC post Dexa8: 132 ug/d. Serum F post Dexa8 >50ug/dl. EV infusion of Dexa 7mg (Basal F: 90.30ug/dl, F 4pm: 13.5ug/dl, F 24h post: 98.10ug/dl; MRI: nodule 8mm on the right side of the pituitary; TEM TAP (-). Suspecting ectopic CS, IPSS which was not performed for non-medical reasons stated being subjected to internal jugular vein catheterization. Central ACTH 120pg/ml and peripheral ACTH 60pg/ml, ratio ACTH Central/Peripheral: 2.0. Start Ketoconazole 600 mg/d PO; awaiting surgical intervention controls of ACTH are taken: 44.60pg/ml, androstenedione:2.07, DHEAS: 32.60, F:18.6ug/dl.
Discussion: CD is the most common cause of spontaneous CS with 60 to 70%, is the result of ACTH hypersecretion by a pituitary adenoma. CS is a cyclical pattern of hypercortisolism, wherein the biochemical production of cortisol fluctuate rhythmically. Clinical suspicion of CS, we demonstrate the presence of hypercortisolism, breaking the circadian cycle and the failure to exogenous corticosteroid withdrawal. In our patient, we show increased levels of UFC and serum F, UFC suppression > 90% post Dexa8, early suppression of serum F post IV infusion Dexa7mg and IJV catheterization (S:81%) with an ratio central/eripheral> 1.6 that guides us CD.
Conclusion: We report a case with typical clinical and paraclinical Cushing's disease associated with a fluctuating severe hypercortisolism.
Objective: To report a case of cyclic hypercortisolism in Cushing's disease (CD).
Methods: Clinical and paraclinical characteristics of a patient with CD are presented.
Results or Case Presentation: Female, 32 years, with history of infertility, PCOS and DM treated with metformin and insulin; 22 d before admission, has altered behavior, doing activities that then no further recalls, palpitations, flushing. The day of admission to the ER presents psychomotor agitation, sensory disorder, and severe hypokalemia and hyperglicemia so is hospitalized. At examination: alert, cushingoid, weight: 60kg BMI: 23 PA: 120/60mmHg, FC: 92x', FR 16x'; skin: moderate hirsutism, multiple bruises and no stretch marks. small bearings in supraclavicular fossa, small dorsal hump, edema ++ / +++ lower limbs. Analyses: Glicemia 459mg%, Na:149, K:1.99, F >50ug/dl, ACTH: 386pg/ml, TSH: 1.54 uU/ml, T4Libre: 0.54ng/dl; Peptide C: 0.27ng/ml, E2: 29pg/ml, Pg: 0.80ng/ml, LH: 0.10mIU/ml, PRL: 7.25ng/mL, Androstenedione >10ng/ml, DHEAS: 265ug/ml, free Testo: 3.20pg/ml. Basal UFC1: 919.35ug/d, basal UFC2: 1592.5ug/d, UFC post Dexa8: 132 ug/d. Serum F post Dexa8 >50ug/dl. EV infusion of Dexa 7mg (Basal F: 90.30ug/dl, F 4pm: 13.5ug/dl, F 24h post: 98.10ug/dl; MRI: nodule 8mm on the right side of the pituitary; TEM TAP (-). Suspecting ectopic CS, IPSS which was not performed for non-medical reasons stated being subjected to internal jugular vein catheterization. Central ACTH 120pg/ml and peripheral ACTH 60pg/ml, ratio ACTH Central/Peripheral: 2.0. Start Ketoconazole 600 mg/d PO; awaiting surgical intervention controls of ACTH are taken: 44.60pg/ml, androstenedione:2.07, DHEAS: 32.60, F:18.6ug/dl.
Discussion: CD is the most common cause of spontaneous CS with 60 to 70%, is the result of ACTH hypersecretion by a pituitary adenoma. CS is a cyclical pattern of hypercortisolism, wherein the biochemical production of cortisol fluctuate rhythmically. Clinical suspicion of CS, we demonstrate the presence of hypercortisolism, breaking the circadian cycle and the failure to exogenous corticosteroid withdrawal. In our patient, we show increased levels of UFC and serum F, UFC suppression > 90% post Dexa8, early suppression of serum F post IV infusion Dexa7mg and IJV catheterization (S:81%) with an ratio central/eripheral> 1.6 that guides us CD.
Conclusion: We report a case with typical clinical and paraclinical Cushing's disease associated with a fluctuating severe hypercortisolism.
Methods: Clinical and paraclinical characteristics of a patient with CD are presented.
Results or Case Presentation: Female, 32 years, with history of infertility, PCOS and DM treated with metformin and insulin; 22 d before admission, has altered behavior, doing activities that then no further recalls, palpitations, flushing. The day of admission to the ER presents psychomotor agitation, sensory disorder, and severe hypokalemia and hyperglicemia so is hospitalized. At examination: alert, cushingoid, weight: 60kg BMI: 23 PA: 120/60mmHg, FC: 92x', FR 16x'; skin: moderate hirsutism, multiple bruises and no stretch marks. small bearings in supraclavicular fossa, small dorsal hump, edema ++ / +++ lower limbs. Analyses: Glicemia 459mg%, Na:149, K:1.99, F >50ug/dl, ACTH: 386pg/ml, TSH: 1.54 uU/ml, T4Libre: 0.54ng/dl; Peptide C: 0.27ng/ml, E2: 29pg/ml, Pg: 0.80ng/ml, LH: 0.10mIU/ml, PRL: 7.25ng/mL, Androstenedione >10ng/ml, DHEAS: 265ug/ml, free Testo: 3.20pg/ml. Basal UFC1: 919.35ug/d, basal UFC2: 1592.5ug/d, UFC post Dexa8: 132 ug/d. Serum F post Dexa8 >50ug/dl. EV infusion of Dexa 7mg (Basal F: 90.30ug/dl, F 4pm: 13.5ug/dl, F 24h post: 98.10ug/dl; MRI: nodule 8mm on the right side of the pituitary; TEM TAP (-). Suspecting ectopic CS, IPSS which was not performed for non-medical reasons stated being subjected to internal jugular vein catheterization. Central ACTH 120pg/ml and peripheral ACTH 60pg/ml, ratio ACTH Central/Peripheral: 2.0. Start Ketoconazole 600 mg/d PO; awaiting surgical intervention controls of ACTH are taken: 44.60pg/ml, androstenedione:2.07, DHEAS: 32.60, F:18.6ug/dl.
Discussion: CD is the most common cause of spontaneous CS with 60 to 70%, is the result of ACTH hypersecretion by a pituitary adenoma. CS is a cyclical pattern of hypercortisolism, wherein the biochemical production of cortisol fluctuate rhythmically. Clinical suspicion of CS, we demonstrate the presence of hypercortisolism, breaking the circadian cycle and the failure to exogenous corticosteroid withdrawal. In our patient, we show increased levels of UFC and serum F, UFC suppression > 90% post Dexa8, early suppression of serum F post IV infusion Dexa7mg and IJV catheterization (S:81%) with an ratio central/eripheral> 1.6 that guides us CD.
Conclusion: We report a case with typical clinical and paraclinical Cushing's disease associated with a fluctuating severe hypercortisolism.
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