23 research outputs found
Recurrent Disease in Patients With Sporadic Pheochromocytoma and Paraganglioma
Supplemental Appendix for manuscript 'Recurrent disease in patients with sporadic pheochromocytoma and paraganglioma
Sympathoinhibition by atorvastatin in hypertensive patients.
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89086.pdf (publisher's version ) (Open Access)BACKGROUND: Experimental animal data suggest that 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) might reduce enhanced sympathetic activity, a hallmark of hypertensive patients. This hypothesis was tested for the first time in patients with primary hypertension. METHODS AND RESULTS: Using a prospective, randomized, placebo-controlled, double-blind, cross-over design, a proof-of-principle trial was performed in 13 patients with mild to moderate primary hypertension, who were randomly assigned to a regimen of atorvastatin (80mg/day) for 3 weeks, followed by placebo for 3 weeks or to a regimen of placebo for 3 weeks, followed by atorvastatin (80mg/day) for 3 weeks. Microneurography was used at the end of each treatment period to measure sympathetic nervous system activity (muscle sympathetic nerve activity: MSNA). Heart rate variability (HRV) and plasma norepinephrine concentrations were also measured. Additionally, effects on blood pressure (BP) and heart rate (HR) were assessed by 24-h ambulatory BP measurement. Atorvastatin reduced postganglionic MSNA (atorvastatin 35.0+/-2.0 vs placebo: 39.2+/-1.5 bursts/min, P=0.008) and heart frequency corrected MSNA (atorvastatin: 58.5+/-2.0 vs placebo: 64.7+/-3.0 bursts/100 beats, P=0.02). Atorvastatin had no significant effect on plasma norepinephrine levels, HRV, BP or HR. CONCLUSIONS: In patients with mild to moderate hypertension, atorvastatin reduces postganglionic MSNA, which supports the hypothesis that HMG-CoA reductase plays a role in sympathetic nervous system activity
Π‘ΠΊΡΠΈΠ½ΡΠ½Π³ Π΅Π½Π΄ΠΎΠΊΡΠΈΠ½Π½ΠΎΡ Π³ΡΠΏΠ΅ΡΡΠ΅Π½Π·ΡΡ. ΠΠ°ΡΠΊΠΎΠ²Π° Π·Π°ΡΠ²Π° ΠΠ½Π΄ΠΎΠΊΡΠΈΠ½ΠΎΠ»ΠΎΠ³ΡΡΠ½ΠΎΠ³ΠΎ ΡΠΎΠ²Π°ΡΠΈΡΡΠ²Π°
Hypertension may be the initial clinical presentation for at least 15 endocrine disorders. An accurate diagnosis of endocrine hypertension provides clinicians with the opportunity to render a surgical cure or to achieve an optimal clinical response with specific pharmacologic therapy. It is challenging for the clinician to know when and how to perform case-detection testing for all the endocrine disorders in which hypertension may be the presenting symptom. Herein, we review the different forms of endocrine hypertension, with a focus on prevalence, clinical presentation, guidance on when to perform case detection testing, and currently available case-detection tests.Hypertension affects 28.6% of adults in United States. In most, hypertension is primary (essential or idiopathic), but a subgroup of approximately 15% has secondary hypertension. More than 50% of children who present with hypertension have a secondary cause. In young adults (< 40 years old), the prevalence of secondary hypertension is approximately 30%. The secondary causes of hypertension include renal causes (e.g., renal parenchymal disease) and endocrine causes. Hypertension may be the initial clinical presentation many endocrine disorders: pheochromocytoma and sympathetic paraganglioma, primary aldosteronism, hyperdeoxycorticosteronism (congenital adrenal hyperplasia β 11b-hydroxylase deficiency, 17a-hydroxylase deficiency, deoxycorticosterone-producing tumor, primary cortisol resistance), cushing syndrome, apparent mineralocorticoid excess / 11b-hydroxysteroid dehydrogenase deficiency, hyperparathyroidism, secondary hyperaldosteronism, renovascular hypertension, hypothyroidism, hyperthyroidism, obstructive sleep apnea and others.Clinical context is important. For example, case detection for endocrine hypertension may not be clinically important in an older patient with multiple life-limiting comorbidities. However, screening for endocrine hypertension may be key to enhancing and prolonging life in most patients with hypertension, especially younger patients.ΠΡΡΠ΅ΡΠΈΠ°Π»ΡΠ½Π°Ρ Π³ΠΈΠΏΠ΅ΡΡΠ΅Π½Π·ΠΈΡ ΠΌΠΎΠΆΠ΅Ρ Π±ΡΡΡ ΠΏΠ΅ΡΠ²ΠΎΠ½Π°ΡΠ°Π»ΡΠ½ΡΠΌ ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΈΠΌ ΠΏΡΠΎΡΠ²Π»Π΅Π½ΠΈΠ΅ΠΌ, ΠΏΠΎ ΠΌΠ΅Π½ΡΡΠ΅ΠΉ ΠΌΠ΅ΡΠ΅, 15 ΡΠ½Π΄ΠΎΠΊΡΠΈΠ½Π½ΡΡ
ΡΠ°ΡΡΡΡΠΎΠΉΡΡΠ². Π’ΠΎΡΠ½ΡΠΉ Π΄ΠΈΠ°Π³Π½ΠΎΠ· ΡΠ½Π΄ΠΎΠΊΡΠΈΠ½Π½ΠΎΠΉ Π³ΠΈΠΏΠ΅ΡΡΠ΅Π½Π·ΠΈΠΈ ΠΏΠΎΠ·Π²ΠΎΠ»ΡΠ΅Ρ ΠΊΠ»ΠΈΠ½ΠΈΡΠΈΡΡΠ°ΠΌ Π²ΡΠΏΠΎΠ»Π½ΠΈΡΡ Ρ
ΠΈΡΡΡΠ³ΠΈΡΠ΅ΡΠΊΠΎΠ΅ Π»Π΅ΡΠ΅Π½ΠΈΠ΅ ΠΈΠ»ΠΈ Π΄ΠΎΠ±ΠΈΡΡΡΡ ΠΎΠΏΡΠΈΠΌΠ°Π»ΡΠ½ΠΎΠ³ΠΎ ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ ΠΎΡΠ²Π΅ΡΠ° Π² Ρ
ΠΎΠ΄Π΅ ΡΠΏΠ΅ΡΠΈΡΠΈΡΠ΅ΡΠΊΠΎΠΉ ΡΠ°ΡΠΌΠ°ΠΊΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΎΠΉ ΡΠ΅ΡΠ°ΠΏΠΈΠΈ. ΠΠ»ΠΈΠ½ΠΈΡΠΈΡΡΡ Π²Π°ΠΆΠ½ΠΎ Π·Π½Π°ΡΡ, ΠΊΠΎΠ³Π΄Π° ΠΈ ΠΊΠ°ΠΊ ΡΠ»Π΅Π΄ΡΠ΅Ρ ΠΏΡΠΎΠ²ΠΎΠ΄ΠΈΡΡ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΠ΅ ΠΏΠΎ Π²ΡΡΠ²Π»Π΅Π½ΠΈΡ ΡΠ»ΡΡΠ°Π΅Π² Π²ΡΠ΅Ρ
ΡΠ½Π΄ΠΎΠΊΡΠΈΠ½Π½ΡΡ
Π½Π°ΡΡΡΠ΅Π½ΠΈΠΉ, ΠΏΡΠΈ ΠΊΠΎΡΠΎΡΡΡ
Π³ΠΈΠΏΠ΅ΡΡΠ΅Π½Π·ΠΈΡ ΠΌΠΎΠΆΠ΅Ρ ΡΠ²Π»ΡΡΡΡΡ ΡΠΈΠΌΠΏΡΠΎΠΌΠΎΠΌ. Π Π΄Π°Π½Π½ΠΎΠΉ ΡΡΠ°ΡΡΠ΅ ΡΠ°ΡΡΠΌΠΎΡΡΠ΅Π½Ρ ΡΠ°Π·Π»ΠΈΡΠ½ΡΠ΅ ΡΠΎΡΠΌΡ ΡΠ½Π΄ΠΎΠΊΡΠΈΠ½Π½ΠΎΠΉ Π³ΠΈΠΏΠ΅ΡΡΠ΅Π½Π·ΠΈΠΈ Ρ Π°ΠΊΡΠ΅Π½ΡΠΎΠΌ Π½Π° ΡΠ°ΡΠΏΡΠΎΡΡΡΠ°Π½Π΅Π½Π½ΠΎΡΡΡ ΠΈ ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΡΡ ΠΊΠ°ΡΡΠΈΠ½Ρ, Π° ΡΠ°ΠΊΠΆΠ΅ Π΄Π°Π½Ρ ΡΠ΅ΠΊΠΎΠΌΠ΅Π½Π΄Π°ΡΠΈΠΈ ΠΎΡΠ½ΠΎΡΠΈΡΠ΅Π»ΡΠ½ΠΎ ΡΠΎΠ³ΠΎ, ΠΊΠΎΠ³Π΄Π° ΡΠ»Π΅Π΄ΡΠ΅Ρ ΠΏΡΠΎΠ²ΠΎΠ΄ΠΈΡΡ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΡ Π΄Π»Ρ Π²ΡΡΠ²Π»Π΅Π½ΠΈΡ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡ, ΠΈ ΠΎΠΏΠΈΡΠ°Π½Ρ ΠΈΠΌΠ΅ΡΡΠΈΠ΅ΡΡ Π² Π½Π°ΡΡΠΎΡΡΠ΅Π΅ Π²ΡΠ΅ΠΌΡ Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΡΠ΅ΡΡΡ.ΠΡΡΠ΅ΡΠΈΠ°Π»ΡΠ½ΠΎΠΉ Π³ΠΈΠΏΠ΅ΡΡΠ΅Π½Π·ΠΈΠ΅ΠΉ ΡΡΡΠ°Π΄Π°Π΅Ρ 28,6% Π²Π·ΡΠΎΡΠ»ΠΎΠ³ΠΎ Π½Π°ΡΠ΅Π»Π΅Π½ΠΈΡ Π‘Π¨Π. Π Π±ΠΎΠ»ΡΡΠΈΠ½ΡΡΠ²Π΅ ΡΠ»ΡΡΠ°Π΅Π² ΠΎΠ½Π° ΡΠ²Π»ΡΠ΅ΡΡΡ ΠΏΠ΅ΡΠ²ΠΈΡΠ½ΠΎΠΉ (ΠΎΡΠ½ΠΎΠ²Π½ΠΎΠΉ ΠΈΠ»ΠΈ ΠΈΠ΄ΠΈΠΎΠΏΠ°ΡΠΈΡΠ΅ΡΠΊΠΎΠΉ), Π½ΠΎ ΠΏΡΠΈΠ±Π»ΠΈΠ·ΠΈΡΠ΅Π»ΡΠ½ΠΎ Ρ 15% ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² Π²ΡΡΠ²Π»ΡΠ΅ΡΡΡ Π²ΡΠΎΡΠΈΡΠ½Π°Ρ Π°ΡΡΠ΅ΡΠΈΠ°Π»ΡΠ½Π°Ρ Π³ΠΈΠΏΠ΅ΡΡΠ΅Π½Π·ΠΈΡ. ΠΠΎΠ»Π΅Π΅ 50% Π΄Π΅ΡΠ΅ΠΉ Ρ Π°ΡΡΠ΅ΡΠΈΠ°Π»ΡΠ½ΠΎΠΉ Π³ΠΈΠΏΠ΅ΡΡΠ΅Π½Π·ΠΈΠ΅ΠΉ ΠΈΠΌΠ΅ΡΡ Π²ΡΠΎΡΠΈΡΠ½ΡΡ ΠΏΡΠΈΡΠΈΠ½Ρ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡ. Π£ Π»ΡΠ΄Π΅ΠΉ ΠΌΠΎΠ»ΠΎΠΆΠ΅ 40 Π»Π΅Ρ ΡΠ°ΡΠΏΡΠΎΡΡΡΠ°Π½Π΅Π½Π½ΠΎΡΡΡ Π²ΡΠΎΡΠΈΡΠ½ΠΎΠΉ Π³ΠΈΠΏΠ΅ΡΡΠ΅Π½Π·ΠΈΠΈ ΡΠΎΡΡΠ°Π²Π»ΡΠ΅Ρ ΠΏΡΠΈΠΌΠ΅ΡΠ½ΠΎ 30%. ΠΡΠΎΡΠΈΡΠ½ΡΠ΅ ΠΏΡΠΈΡΠΈΠ½Ρ Π°ΡΡΠ΅ΡΠΈΠ°Π»ΡΠ½ΠΎΠΉ Π³ΠΈΠΏΠ΅ΡΡΠ΅Π½Π·ΠΈΠΈ Π²ΠΊΠ»ΡΡΠ°ΡΡ ΠΏΠΎΡΠ΅ΡΠ½ΡΠ΅ (Π½Π°ΠΏΡΠΈΠΌΠ΅Ρ, ΠΏΠ°ΡΠ΅Π½Ρ
ΠΈΠΌΠ°ΡΠΎΠ·Π½ΡΠ΅ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡ ΠΏΠΎΡΠ΅ΠΊ) ΠΈ ΡΠ½Π΄ΠΎΠΊΡΠΈΠ½Π½ΡΠ΅. ΠΠΈΠΏΠ΅ΡΡΠ΅Π½Π·ΠΈΡ ΠΌΠΎΠΆΠ΅Ρ Π±ΡΡΡ Π½Π°ΡΠ°Π»ΡΠ½ΡΠΌ ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΈΠΌ ΠΏΡΠΎΡΠ²Π»Π΅Π½ΠΈΠ΅ΠΌ ΠΌΠ½ΠΎΠ³ΠΈΡ
ΡΠ½Π΄ΠΎΠΊΡΠΈΠ½Π½ΡΡ
ΡΠ°ΡΡΡΡΠΎΠΉΡΡΠ²: ΡΠ΅ΠΎΡ
ΡΠΎΠΌΠΎΡΠΈΡΠΎΠΌΡ ΠΈ ΡΠΈΠΌΠΏΠ°ΡΠΈΡΠ΅ΡΠΊΠΎΠΉ ΠΏΠ°ΡΠ°Π³Π°Π½Π³Π»ΠΈΠΎΠΌΡ, ΠΏΠ΅ΡΠ²ΠΈΡΠ½ΠΎΠ³ΠΎ Π°Π»ΡΠ΄ΠΎΡΡΠ΅ΡΠΎΠ½ΠΈΠ·ΠΌΠ°, Π³ΠΈΠΏΠ΅ΡΠ΄Π΅Π·ΠΎΠΊΡΠΈΠΊΠΎΡΡΠΈΠΊΠΎΡΡΠ΅ΡΠΎΠ½ΠΈΠ·ΠΌΠ° (Π²ΡΠΎΠΆΠ΄Π΅Π½Π½Π°Ρ Π³ΠΈΠΏΠ΅ΡΠΏΠ»Π°Π·ΠΈΡ Π½Π°Π΄ΠΏΠΎΡΠ΅ΡΠ½ΠΈΠΊΠΎΠ² β 11Ξ²-Π³ΠΈΠ΄ΡΠΎΠΊΡΠΈΠ»Π°Π·Π½Π°Ρ Π½Π΅Π΄ΠΎΡΡΠ°ΡΠΎΡΠ½ΠΎΡΡΡ, 17Ξ±-Π³ΠΈΠ΄ΡΠΎΠΊΡΠΈΠ»Π°Π·Π½Π°Ρ Π½Π΅Π΄ΠΎΡΡΠ°ΡΠΎΡΠ½ΠΎΡΡΡ, Π΄Π΅Π·ΠΎΠΊΡΠΈΠΊΠΎΡΡΠΈΠΊΠΎΡΡΠ΅ΡΠΎΠ½-ΠΏΡΠΎΠ΄ΡΡΠΈΡΡΡΡΠ°Ρ ΠΎΠΏΡΡ
ΠΎΠ»Ρ, ΠΏΠ΅ΡΠ²ΠΈΡΠ½Π°Ρ ΡΠ΅Π·ΠΈΡΡΠ΅Π½ΡΠ½ΠΎΡΡΡ ΠΊΠΎΡΡΠΈΠ·ΠΎΠ»Π°), ΡΠΈΠ½Π΄ΡΠΎΠΌΠ° ΠΡΡΠΈΠ½Π³Π°, ΠΌΠ½ΠΈΠΌΠΎΠ³ΠΎ ΠΈΠ·Π±ΡΡΠΊΠ° ΠΌΠΈΠ½Π΅ΡΠ°Π»ΠΎΠΊΠΎΡΡΠΈΠΊΠΎΠΈΠ΄ΠΎΠ²/Π΄Π΅ΡΠΈΡΠΈΡΠ° 11Ξ²-Π³ΠΈΠ΄ΡΠΎΠΊΡΠΈΡΡΠ΅ΡΠΎΠΈΠ΄Π΄Π΅Π³ΠΈΠ΄ΡΠΎΠ³Π΅Π½Π°Π·Ρ, Π³ΠΈΠΏΠ΅ΡΠΏΠ°ΡΠ°ΡΠΈΡΠ΅ΠΎΠ·Π°, Π²ΡΠΎΡΠΈΡΠ½ΠΎΠ³ΠΎ Π³ΠΈΠΏΠ΅ΡΠ°Π»ΡΠ΄ΠΎΡΡΠ΅ΡΠΎΠ½ΠΈΠ·ΠΌΠ°, ΡΠ΅Π½ΠΎΠ²Π°ΡΠΊΡΠ»ΡΡΠ½ΠΎΠΉ Π³ΠΈΠΏΠ΅ΡΡΠ΅Π½Π·ΠΈΠΈ, Π³ΠΈΠΏΠΎΡΠΈΡΠ΅ΠΎΠ·Π°, Π³ΠΈΠΏΠ΅ΡΡΠΈΡΠ΅ΠΎΠ·Π°, ΠΎΠ±ΡΡΡΡΠΊΡΠΈΠ²Π½ΠΎΠ³ΠΎ Π°ΠΏΠ½ΠΎΡ ΡΠ½Π° ΠΈ Π΄Ρ.ΠΠΎΠ»ΡΡΠΎΠ΅ Π·Π½Π°ΡΠ΅Π½ΠΈΠ΅ ΠΈΠΌΠ΅Π΅Ρ ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΈΠΉ ΠΊΠΎΠ½ΡΠ΅ΠΊΡΡ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡ. ΠΠ°ΠΏΡΠΈΠΌΠ΅Ρ, Π²ΡΡΠ²Π»Π΅Π½ΠΈΠ΅ ΡΠ»ΡΡΠ°Π΅Π² ΡΠ½Π΄ΠΎΠΊΡΠΈΠ½Π½ΠΎΠΉ Π³ΠΈΠΏΠ΅ΡΡΠ΅Π½Π·ΠΈΠΈ ΠΌΠΎΠΆΠ΅Ρ Π½Π΅ ΠΈΠΌΠ΅ΡΡ ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ Π·Π½Π°ΡΠ΅Π½ΠΈΡ Ρ ΠΏΠΎΠΆΠΈΠ»ΠΎΠ³ΠΎ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠ° Ρ ΠΌΠ½ΠΎΠΆΠ΅ΡΡΠ²Π΅Π½Π½ΡΠΌΠΈ ΡΠΎΠΏΡΡΡΡΠ²ΡΡΡΠΈΠΌΠΈ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡΠΌΠΈ, ΠΊΠΎΡΠΎΡΡΠ΅ ΠΎΠ³ΡΠ°Π½ΠΈΡΠΈΠ²Π°ΡΡ ΠΊΠ°ΡΠ΅ΡΡΠ²ΠΎ ΠΆΠΈΠ·Π½ΠΈ. ΠΠ΄Π½Π°ΠΊΠΎ ΡΠΊΡΠΈΠ½ΠΈΠ½Π³ Π½Π° ΡΠ½Π΄ΠΎΠΊΡΠΈΠ½Π½ΡΡ Π³ΠΈΠΏΠ΅ΡΡΠ΅Π½Π·ΠΈΡ ΠΌΠΎΠΆΠ΅Ρ ΡΡΠ°ΡΡ ΠΊΠ»ΡΡΠΎΠΌ ΠΊ ΡΠ»ΡΡΡΠ΅Π½ΠΈΡ ΠΈ ΠΏΡΠΎΠ΄Π»Π΅Π½ΠΈΡ ΠΆΠΈΠ·Π½ΠΈ Π±ΠΎΠ»ΡΡΠΈΠ½ΡΡΠ²Π° ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² Ρ Π°ΡΡΠ΅ΡΠΈΠ°Π»ΡΠ½ΠΎΠΉ Π³ΠΈΠΏΠ΅ΡΡΠ΅Π½Π·ΠΈΠ΅ΠΉ, ΠΎΡΠΎΠ±Π΅Π½Π½ΠΎ ΠΌΠΎΠ»ΠΎΠ΄ΡΡ
.ΠΡΡΠ΅ΡΡΠ°Π»ΡΠ½Π° Π³ΡΠΏΠ΅ΡΡΠ΅Π½Π·ΡΡ ΠΌΠΎΠΆΠ΅ Π±ΡΡΠΈ ΠΏΠ΅ΡΠ²ΠΈΠ½Π½ΠΈΠΌ ΠΊΠ»ΡΠ½ΡΡΠ½ΠΈΠΌ ΠΏΡΠΎΡΠ²ΠΎΠΌ ΡΠΎΠ½Π°ΠΉΠΌΠ΅Π½ΡΠ΅ 15 Π΅Π½Π΄ΠΎΠΊΡΠΈΠ½Π½ΠΈΡ
ΡΠΎΠ·Π»Π°Π΄ΡΠ². Π’ΠΎΡΠ½ΠΈΠΉ Π΄ΡΠ°Π³Π½ΠΎΠ· Π΅Π½Π΄ΠΎΠΊΡΠΈΠ½Π½ΠΎΡ Π³ΡΠΏΠ΅ΡΡΠ΅Π½Π·ΡΡ Π΄ΠΎΠ·Π²ΠΎΠ»ΡΡ ΠΊΠ»ΡΠ½ΡΡΠΈΡΡΠ°ΠΌ Π·Π΄ΡΠΉΡΠ½ΠΈΡΠΈ Ρ
ΡΡΡΡΠ³ΡΡΠ½Π΅ Π»ΡΠΊΡΠ²Π°Π½Π½Ρ Π°Π±ΠΎ Π΄ΠΎΡΡΠ³ΡΠΈ ΠΎΠΏΡΠΈΠΌΠ°Π»ΡΠ½ΠΎΡ ΠΊΠ»ΡΠ½ΡΡΠ½ΠΎΡ Π²ΡΠ΄ΠΏΠΎΠ²ΡΠ΄Ρ ΠΏΡΠ΄ ΡΠ°Ρ ΡΠΏΠ΅ΡΠΈΡΡΡΠ½ΠΎΡ ΡΠ°ΡΠΌΠ°ΠΊΠΎΠ»ΠΎΠ³ΡΡΠ½ΠΎΡ ΡΠ΅ΡΠ°ΠΏΡΡ. ΠΠ»ΡΠ½ΡΡΠΈΡΡΡ Π²Π°ΠΆΠ»ΠΈΠ²ΠΎ Π·Π½Π°ΡΠΈ, ΠΊΠΎΠ»ΠΈ Ρ ΡΠΊ ΡΠ»ΡΠ΄ ΠΏΡΠΎΠ²ΠΎΠ΄ΠΈΡΠΈ Π΄ΠΎΡΠ»ΡΠ΄ΠΆΠ΅Π½Π½Ρ ΡΠΎΠ΄ΠΎ Π²ΠΈΡΠ²Π»Π΅Π½Π½Ρ Π²ΠΈΠΏΠ°Π΄ΠΊΡΠ² ΡΡΡΡ
Π΅Π½Π΄ΠΎΠΊΡΠΈΠ½Π½ΠΈΡ
ΠΏΠΎΡΡΡΠ΅Π½Ρ, ΠΏΡΠΈ ΡΠΊΠΈΡ
Π³ΡΠΏΠ΅ΡΡΠ΅Π½Π·ΡΡ ΠΌΠΎΠΆΠ΅ Π±ΡΡΠΈ ΡΠΈΠΌΠΏΡΠΎΠΌΠΎΠΌ. Π£ Π΄Π°Π½ΡΠΉ ΡΡΠ°ΡΡΡ ΡΠΎΠ·Π³Π»ΡΠ½ΡΡΡ ΡΡΠ·Π½Ρ ΡΠΎΡΠΌΠΈ Π΅Π½Π΄ΠΎΠΊΡΠΈΠ½Π½ΠΎΡ Π³ΡΠΏΠ΅ΡΡΠ΅Π½Π·ΡΡ Π· Π½Π°Π³ΠΎΠ»ΠΎΡΠΎΠΌ Π½Π° ΠΏΠΎΡΠΈΡΠ΅Π½ΡΡΡΡ Ρ ΠΊΠ»ΡΠ½ΡΡΠ½Ρ ΠΊΠ°ΡΡΠΈΠ½Ρ, Π° ΡΠ°ΠΊΠΎΠΆ ΠΏΡΠ΅Π΄ΡΡΠ°Π²Π»Π΅Π½Ρ ΡΠ΅ΠΊΠΎΠΌΠ΅Π½Π΄Π°ΡΡΡ ΡΠΎΠ΄ΠΎ ΡΠΎΠ³ΠΎ, ΠΊΠΎΠ»ΠΈ ΡΠ»ΡΠ΄ ΠΏΡΠΎΠ²ΠΎΠ΄ΠΈΡΠΈ Π΄ΠΎΡΠ»ΡΠ΄ΠΆΠ΅Π½Π½Ρ Π΄Π»Ρ Π²ΠΈΡΠ²Π»Π΅Π½Π½Ρ Π·Π°Ρ
Π²ΠΎΡΡΠ²Π°Π½Π½Ρ, Ρ ΠΎΠΏΠΈΡΠ°Π½Ρ Π½Π°ΡΠ²Π½Ρ Π΄ΡΠ°Π³Π½ΠΎΡΡΠΈΡΠ½Ρ ΡΠ΅ΡΡΠΈ.ΠΠ° Π°ΡΡΠ΅ΡΡΠ°Π»ΡΠ½Ρ Π³ΡΠΏΠ΅ΡΡΠ΅Π½Π·ΡΡ ΡΡΡΠ°ΠΆΠ΄Π°Ρ 28,6% Π΄ΠΎΡΠΎΡΠ»ΠΎΠ³ΠΎ Π½Π°ΡΠ΅Π»Π΅Π½Π½Ρ Π‘Π¨Π. Π£ Π±ΡΠ»ΡΡΠΎΡΡΡ Π²ΠΈΠΏΠ°Π΄ΠΊΡΠ² Π²ΠΎΠ½Π° Ρ ΠΏΠ΅ΡΠ²ΠΈΠ½Π½ΠΎΡ (ΠΎΡΠ½ΠΎΠ²Π½ΠΎΡ Π°Π±ΠΎ ΡΠ΄ΡΠΎΠΏΠ°ΡΠΈΡΠ½ΠΎΡ), Π°Π»Π΅ ΠΏΡΠΈΠ±Π»ΠΈΠ·Π½ΠΎ Ρ 15% ΠΏΠ°ΡΡΡΠ½ΡΡΠ² Π²ΠΈΡΠ²Π»ΡΡΡΡΡΡ Π²ΡΠΎΡΠΈΠ½Π½Π° Π°ΡΡΠ΅ΡΡΠ°Π»ΡΠ½Π° Π³ΡΠΏΠ΅ΡΡΠ΅Π½Π·ΡΡ. ΠΠΎΠ½Π°Π΄ 50% Π΄ΡΡΠ΅ΠΉ Π· Π°ΡΡΠ΅ΡΡΠ°Π»ΡΠ½ΠΎΡ Π³ΡΠΏΠ΅ΡΡΠ΅Π½Π·ΡΡΡ ΠΌΠ°ΡΡΡ Π²ΡΠΎΡΠΈΠ½Π½Ρ ΠΏΡΠΈΡΠΈΠ½Ρ Π·Π°Ρ
Π²ΠΎΡΡΠ²Π°Π½Π½Ρ. Π£ Π»ΡΠ΄Π΅ΠΉ, ΠΌΠΎΠ»ΠΎΠ΄ΡΠΈΡ
Π·Π° 40 ΡΠΎΠΊΡΠ², ΠΏΠΎΡΠΈΡΠ΅Π½ΡΡΡΡ Π²ΡΠΎΡΠΈΠ½Π½ΠΎΡ Π³ΡΠΏΠ΅ΡΡΠ΅Π½Π·ΡΡ ΡΡΠ°Π½ΠΎΠ²ΠΈΡΡ ΠΏΡΠΈΠ±Π»ΠΈΠ·Π½ΠΎ 30%. ΠΡΠΎΡΠΈΠ½Π½Ρ ΠΏΡΠΈΡΠΈΠ½ΠΈ Π°ΡΡΠ΅ΡΡΠ°Π»ΡΠ½ΠΎΡ Π³ΡΠΏΠ΅ΡΡΠ΅Π½Π·ΡΡ Π²ΠΊΠ»ΡΡΠ°ΡΡΡ Π½ΠΈΡΠΊΠΎΠ²Ρ (Π½Π°ΠΏΡΠΈΠΊΠ»Π°Π΄, ΠΏΠ°ΡΠ΅Π½Ρ
ΡΠΌΠ°ΡΠΎΠ·Π½Ρ Π·Π°Ρ
Π²ΠΎΡΡΠ²Π°Π½Π½Ρ Π½ΠΈΡΠΎΠΊ) ΡΠ° Π΅Π½Π΄ΠΎΠΊΡΠΈΠ½Π½Ρ. ΠΡΠΏΠ΅ΡΡΠ΅Π½Π·ΡΡ ΠΌΠΎΠΆΠ΅ Π±ΡΡΠΈ ΠΏΠΎΡΠ°ΡΠΊΠΎΠ²ΠΈΠΌ ΠΊΠ»ΡΠ½ΡΡΠ½ΠΈΠΌ ΠΏΡΠΎΡΠ²ΠΎΠΌ Π±Π°Π³Π°ΡΡΠΎΡ
Π΅Π½Π΄ΠΎΠΊΡΠΈΠ½Π½ΠΈΡ
ΡΠΎΠ·Π»Π°Π΄ΡΠ²: ΡΠ΅ΠΎΡ
ΡΠΎΠΌΠΎΡΠΈΡΠΎΠΌΠΈ Ρ ΡΠΈΠΌΠΏΠ°ΡΠΈΡΠ½ΠΎΡ ΠΏΠ°ΡΠ°Π³Π°Π½Π³Π»ΡΠΎΠΌΠΈ, ΠΏΠ΅ΡΠ²ΠΈΠ½Π½ΠΎΠ³ΠΎ Π°Π»ΡΠ΄ΠΎΡΡΠ΅ΡΠΎΠ½ΡΠ·ΠΌΡ, Π³ΡΠΏΠ΅ΡΠ΄Π΅Π·ΠΎΠΊΡΠΈΠΊΠΎΡΡΠΈΠΊΠΎΡΡΠ΅ΡΠΎΠ½ΡΠ·ΠΌΡ (Π²ΡΠΎΠ΄ΠΆΠ΅Π½Π° Π³ΡΠΏΠ΅ΡΠΏΠ»Π°Π·ΡΡ Π½Π°Π΄Π½ΠΈΡΠ½ΠΈΠΊΡΠ² β 11Ξ²-Π³ΡΠ΄ΡΠΎΠΊΡΠΈΠ»Π°Π·Π½Π° Π½Π΅Π΄ΠΎΡΡΠ°ΡΠ½ΡΡΡΡ, 17Ξ±-Π³ΡΠ΄ΡΠΎΠΊΡΠΈΠ»Π°Π·Π½Π° Π½Π΅Π΄ΠΎΡΡΠ°ΡΠ½ΡΡΡΡ, ΠΏΡΡ
Π»ΠΈΠ½Π°, ΡΠΎ ΠΏΡΠΎΠ΄ΡΠΊΡΡ Π΄Π΅Π·ΠΎΠΊΡΠΈΠΊΠΎΡΡΠΈΠΊΠΎΡΡΠ΅ΡΠΎΠ½, ΠΏΠ΅ΡΠ²ΠΈΠ½Π½Π° ΡΠ΅Π·ΠΈΡΡΠ΅Π½ΡΠ½ΡΡΡΡ ΠΊΠΎΡΡΠΈΠ·ΠΎΠ»Ρ), ΡΠΈΠ½Π΄ΡΠΎΠΌΡ ΠΡΡΠΈΠ½Π³Π°, ΡΡΠ²Π½ΠΎΠ³ΠΎ Π½Π°Π΄Π»ΠΈΡΠΊΡ ΠΌΡΠ½Π΅ΡΠ°Π»ΠΎΠΊΠΎΡΡΠΈΠΊΠΎΡΠ΄ΡΠ² / Π΄Π΅ΡΡΡΠΈΡΡ 11Ξ²-Π³ΡΠ΄ΡΠΎΠΊΡΠΈΡΡΠ΅ΡΠΎΡΠ΄Π΄Π΅Π³ΡΠ΄ΡΠΎΠ³Π΅Π½Π°Π·ΠΈ, Π³ΡΠΏΠ΅ΡΠΏΠ°ΡΠ°ΡΠΈΡΠ΅ΠΎΠ·Ρ, Π²ΡΠΎΡΠΈΠ½Π½ΠΎΠ³ΠΎ Π³ΡΠΏΠ΅ΡΠ°Π»ΡΠ΄ΠΎΡΡΠ΅ΡΠΎΠ½ΡΠ·ΠΌΡ, ΡΠ΅Π½ΠΎΠ²Π°ΡΠΊΡΠ»ΡΡΠ½ΠΎΡ Π³ΡΠΏΠ΅ΡΡΠ΅Π½Π·ΡΡ, Π³ΡΠΏΠΎΡΠΈΡΠ΅ΠΎΠ·Ρ, Π³ΡΠΏΠ΅ΡΡΠΈΡΠ΅ΠΎΠ·Ρ, ΠΎΠ±ΡΡΡΡΠΊΡΠΈΠ²Π½ΠΎΠ³ΠΎ Π°ΠΏΠ½ΠΎΠ΅ ΡΠ½Ρ ΡΠ° ΡΠ½.ΠΠ΅Π»ΠΈΠΊΠ΅ Π·Π½Π°ΡΠ΅Π½Π½Ρ ΠΌΠ°Ρ ΠΊΠ»ΡΠ½ΡΡΠ½ΠΈΠΉ ΠΊΠΎΠ½ΡΠ΅ΠΊΡΡ Π·Π°Ρ
Π²ΠΎΡΡΠ²Π°Π½Π½Ρ. ΠΠ°ΠΏΡΠΈΠΊΠ»Π°Π΄, Π²ΠΈΡΠ²Π»Π΅Π½Π½Ρ Π²ΠΈΠΏΠ°Π΄ΠΊΡΠ² Π΅Π½Π΄ΠΎΠΊΡΠΈΠ½Π½ΠΎΡ Π³ΡΠΏΠ΅ΡΡΠ΅Π½Π·ΡΡ ΠΌΠΎΠΆΠ΅ Π½Π΅ ΠΌΠ°ΡΠΈ ΠΊΠ»ΡΠ½ΡΡΠ½ΠΎΠ³ΠΎ Π·Π½Π°ΡΠ΅Π½Π½Ρ Π² Π»ΡΡΠ½ΡΠΎΠ³ΠΎ ΠΏΠ°ΡΡΡΠ½ΡΠ° Π· ΡΠΈΡΠ»Π΅Π½Π½ΠΈΠΌΠΈ ΡΡΠΏΡΡΠ½ΡΠΌΠΈ Π·Π°Ρ
Π²ΠΎΡΡΠ²Π°Π½Π½ΡΠΌΠΈ, ΡΠΊΡ ΠΎΠ±ΠΌΠ΅ΠΆΡΡΡΡ ΡΠΊΡΡΡΡ ΠΆΠΈΡΡΡ. ΠΠ΄Π½Π°ΠΊ ΡΠΊΡΠΈΠ½ΡΠ½Π³ Π½Π° Π΅Π½Π΄ΠΎΠΊΡΠΈΠ½Π½Ρ Π³ΡΠΏΠ΅ΡΡΠ΅Π½Π·ΡΡ ΠΌΠΎΠΆΠ΅ ΡΡΠ°ΡΠΈ ΠΊΠ»ΡΡΠ΅ΠΌ Π΄ΠΎ ΠΏΠΎΠ»ΡΠΏΡΠ΅Π½Π½Ρ Ρ ΠΏΡΠΎΠ΄ΠΎΠ²ΠΆΠ΅Π½Π½Ρ ΠΆΠΈΡΡΡ Π±ΡΠ»ΡΡΠΎΡΡΡ ΠΏΠ°ΡΡΡΠ½ΡΡΠ² ΡΠ· Π°ΡΡΠ΅ΡΡΠ°Π»ΡΠ½ΠΎΡ Π³ΡΠΏΠ΅ΡΡΠ΅Π½Π·ΡΡΡ, ΠΎΡΠΎΠ±Π»ΠΈΠ²ΠΎ ΠΌΠΎΠ»ΠΎΠ΄ΠΈΡ
Somatic SDHB mutation in an extraadrenal pheochromocytoma.
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52051.pdf (publisher's version ) (Open Access
Patient characteristics do not predict the individual response to antihypertensive medication: A cross-over trial
Background. International guidelines on hypertension management do not agree on whether
patient characteristics can be used for the first choice of treatment of uncomplicated essential
hypertension.
Objective. We wanted to identify predictive patient characteristics to the response of two different
classes of antihypertensive drugs in patients with newly diagnosed hypertension in primary care.
Methods. We conducted a prospective, open label, blinded endpoint cross-over trial in 120 patients
with a new diagnosis of hypertension from 10 family practices. Patients received 4 weeks of 12.5
mgr hydrochlorothiazide once daily and 4 weeks of 80 mgr valsartan once daily, each followed
by a 4-week washout. The sequence of drugs was randomized. Age, sex and menopausal state
were recorded at run in and 24 h ambulatory blood pressure, office blood pressure, plasma renin
concentration, NT-proBNP, potassium, estimated glomerular filtration rate, urinary albumin, body
mass index and waist circumference at each regimen change. The difference in systolic blood
pressure response between both study drugs, calculated from mean daytime ambulatory blood
pressures, was the main outcome measure.
Results. Ninety-eight patients (52% female; median age 53 years) were eligible for per-protocolanalysis.
None of the studied variables were predictive for the difference in systolic blood pressure
response. Individual systolic blood pressure responses ranged from an increase by 18 mmHg to a
decrease of 39 mmHg.
Conclusion. In a relevant group of primary care patients with newly diagnosed hypertension, we
were unable to detect predictors of treatment response. This study rather supports the United
States and European guidelines than the United Kingdom and Dutch guidelines on hypertension.This study was funded by the department of Primary and Community
Care, Radboud university medical center and by an unconditional grant of
Novartis to cover the material costs of the stud
Interaction in COPD experiment (ICE): A hazardous combination of cigarette smoking and bronchodilation in chronic obstructive pulmonary disease
Chronic obstructive pulmonary disease (COPD) is a highly prevalent disease, characterised by poorly reversible, obstructive airflow limitation. Alongside other comorbidities, COPD is associated with increased morbidity and mortality resulting from cardiovascular disease - mainly heart failure and ischemic heart disease. Both diseases share an important risk factor, namely, smoking. About 50% of COPD patients are active cigarette smokers. Bronchodilation is the cornerstone of pharmaceutical treatment for COPD symptoms, and half of all COPD patients use long-acting bronchodilating agents. Discussion about these agents is currently focusing on the association with overall mortality and morbidity in COPD patients, of cardiovascular origin in particular. Bronchodilation diminishes the hyperinflated state of the lung and facilitates the pulmonary deposition of cigarette smoke by deeper inhalation into the smaller airways. Smaller particles, as in smoke, tend to penetrate and depose more in these small airways. In addition, bronchodilation indeed increases carbon monoxide uptake in the lungs, an important gaseous compound of cigarette smoke. Since the number of cigarettes smoked is positively correlated to mortality from cardiac events, we therefore hypothesise that chronic bronchodilation increases cardiovascular disease and mortality in COPD patients who continue smoking by increasing pulmonary retention of pathogenic smoke constituents. Indeed, a recent meta-analysis is suggestive that long-acting anticholinergics might increase cardiovascular disease if patients exceed a certain number of cigarettes smoked. To demonstrate the fundamental mechanism of this pathogenic interaction we will perform a randomised placebo-controlled cross-over trial to investigate the effect of maximum bronchodilation on the retention of cigarette smoke constituents. In 40 moderate to severe COPD patients we measure the inhaled and exhaled amount of tar and nicotine, as well during maximum bronchodilation as during administration of placebo. The fraction of retention of tar and nicotine is subsequently calculated for both circumstances and analysed for association with bronchodilation. Further observational cohort studies or randomised clinical trials designed to monitor cardiovascular events may well evaluate the interaction. Since many patients are at risk for this possibly hazardous interaction, its relevance to our society and healthcare is potentially great. The implication will be that the urgency to quit smoking is intensified. Besides, chronic bronchodilation - specifically long-acting bronchodilators - needs to be discouraged in smoking COPD patients that refuse to quit
Bronchodilation and smoking interaction in COPD: A cohort pilot study to assess cardiovascular risk
Background: Smoking and bronchodilator treatment are both extensively studied as key elements in patients with chronic obstructive pulmonary disease. However, little is known about whether or not these elements interact in terms of developing cardiovascular diseases in patients with COPD. Objectives: To explore to what extent the risk of developing ischemic cardiovascular disease in COPD patients is mediated by smoking status, use of bronchodilators and - specifically - their interaction. Methods: We performed an observational pilot study on a relatively healthy Dutch COPD cohort from a primary care diagnostic center database with full information on spirometry tests, smoking status, bronchodilator use and other prescribed medication. We defined first ischemic cardiovascular events as primary outcome, measured by first prescription of antiplatelet drugs and/or nitrates. Unadjusted analyses by Kaplan-Meier were followed by adjusted Cox' proportional hazards. Results: 845 COPD patients, totaling 2,169 observation years, were included in the analyses. We observed an increased risk for nonfatal ischemic cardiovascular events by smoking (adjusted HR = 3.58, p = 0.001) and a protective effect of bronchodilators (adjusted HR = 0.43, p = 0.01). Although the protective effect of bronchodilators appears to be substantially minimized in patients that persist in smoking, we could not statistically confirm a hazardous interaction between bronchodilators and smoking (HR 2.50, p = 0.21). Conclusion: Our study reveals bronchodilators may protect from ischemic cardiovascular events in a relatively 'healthy' COPD population. We did not confirm a hazardous interaction between bronchodilators and smoking, although we observed current smokers benefit substantially less from the protective effect of bronchodilators
Plasma metanephrines in renal failure.
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49181.pdf (publisher's version ) (Closed access)BACKGROUND: Diagnosis of pheochromocytoma in renal failure poses a diagnostic dilemma due to lack of reliability of conventional urinary measurements of catecholamine excess. Measurements of the plasma metanephrines, normetanephrine and metanephrine (the O-methylated metabolites of norepinephrine and epinephrine), provide an alternative diagnostic test. The metanephrines may be measured as free metabolites or after a deconjugation step where measurements reflect mainly sulfate-conjugated metabolites. The influence of renal insufficiency states on these various measurements is unclear. METHODS: Plasma free and deconjugated metanephrines and catecholamines in 17 patients on dialysis with end-stage renal disease and 19 patients with renal insufficiency (creatinine clearance, 5-78 mL/min) were compared with levels in 89 hypertensives, 68 healthy normotensives, and 51 patients with von Hippel-Lindau syndrome. RESULTS: Patients with renal failure had up to two-fold higher plasma concentrations of catecholamines and free metanephrines, and more than 12-fold higher plasma concentrations of deconjugated metanephrines than comparison groups. Plasma free metanephrines and catecholamines were, respectively, within the 95% confidence intervals of reference groups in 75% and 42% of the dialysis patients, and in 74% and 68% of patients with renal insufficiency. In contrast, no dialysis patient and only half the renal insufficiency patients had plasma levels of deconjugated metanephrines within the reference intervals. Plasma levels of deconjugated metanephrines, but not free metanephrines, showed strong inverse relationships with creatinine clearance. CONCLUSION: Plasma concentrations of free metanephrines are relatively independent of renal function and are, therefore, more suitable for diagnosis of pheochromocytoma among patients with renal failure than measurements of deconjugated metanephrines