戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (１語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 in ratios (a screening parameter for primary aldosteronism).
2 ue for detecting biochemically overt primary aldosteronism.
3 ch to the diagnosis and subtyping of primary aldosteronism.
4 ms suggests low rates of testing for primary aldosteronism.
5 lopment of new treatment options for primary aldosteronism.
6 s for 4 days) to diagnose or exclude primary aldosteronism.
7 w-up of adrenalectomy for unilateral primary aldosteronism.
8  the recommended medical therapy for primary aldosteronism.
9 to correctly diagnose the subtype of primary aldosteronism.
10 Cav1.3 hyperactivity, in particular, primary aldosteronism.
11 including obstructive sleep apnea or primary aldosteronism.
12 Ca(2+) channel mutations in APAs and primary aldosteronism.
13 ratio is a useful screening tool for primary aldosteronism.
14 ten persists after adrenalectomy for primary aldosteronism.
15 extracellular fluid volume, e.g., in primary aldosteronism.
16 considered indicative of lateralized primary aldosteronism.
17 bserved even in subclinical forms of primary aldosteronism according to studies conducted primarily i
18 phenomenon is clinically relevant as primary aldosteronism affects nearly one in ten hypertensive adu
19                        Patients with primary aldosteronism also had higher adjusted risks for inciden
20  finding parallels an age-related autonomous aldosteronism and abnormal aldosterone physiology that p
21 w-up of adrenalectomy for unilateral primary aldosteronism and apply these criteria to an internation
22     These individuals had severe progressive aldosteronism and hyperplasia requiring bilateral adrena
23 has the potential to completely cure primary aldosteronism and hypertension when most of the APA is a
24 ackle GIRK4-related diseases such as primary aldosteronism and late-onset obesity.
25  immunostimulatory state that appears during aldosteronism and leads to a proinflammatory coronary va
26                            Classical primary aldosteronism and lesser degrees of aldosterone excess,
27                  Glucocorticoid-suppressible aldosteronism and Liddle's syndrome, each inherited as a
28 +) conductance in a Mendelian form of severe aldosteronism and massive bilateral adrenal hyperplasia.
29         Until the true prevalence of primary aldosteronism and monogenic forms of mineralocorticoid h
30 ously undescribed syndrome featuring primary aldosteronism and neuromuscular abnormalities.
31 understanding of the pathogenesis of primary aldosteronism and of its clinical phenotypes.
32 ls, as a confirmatory diagnostic for primary aldosteronism and to quantify the magnitude of renin-ind
33 s between resistant hypertension and primary aldosteronism and with obstructive sleep apnea.
34 h spans subclinical stages to florid primary aldosteronism, and from single-focal or multifocal to di
35 led insight in the genetic causes of primary aldosteronism, and mineralocorticoid receptor blockers h
36 that milder and subclinical forms of primary aldosteronism are highly prevalent, yet their contributi
37 ents who underwent adrenalectomy for primary aldosteronism at one tertiary medical center and was ext
38     No association was found between primary aldosteronism biomarkers and measures of arterial stiffn
39 d to assess whether early changes in primary aldosteronism biomarkers during young adulthood are asso
40 relative autonomy, characteristic of primary aldosteronism), but plasma aldosterone was only elevated
41 f patients diagnosed with unilateral primary aldosteronism by adrenal venous sampling who had undergo
42 ed subjects with hypertension due to primary aldosteronism by age 10.
43 an orthogonal treatment approach for primary aldosteronism by specifically targeting the interaction
44                                           In aldosteronism, Ca2+ and Mg2+ losses lead to a fall in [C
45                           Background Primary aldosteronism can arise from one or both adrenal glands.
46                                      Primary aldosteronism, characterized by overt renin-independent
47                                      Primary aldosteronism, characterized by renin-independent aldost
48                                      Primary aldosteronism comprises subtypes that need different the
49 locorticoid hypertension is probably primary aldosteronism; controlled posture studies to measure pla
50  tumors driving hormone excess, like primary aldosteronism, Cushing syndrome, and pheochromocytoma, c
51          The dichotomous paradigm of primary aldosteronism diagnosis and subtyping is being redefined
52 in a handful of conditions including primary aldosteronism, distal renal tubular acidosis, Liddle's d
53 ofrequency (RF) ablation in treating primary aldosteronism due to aldosterone-producing adenoma (APA)
54                                              Aldosteronism eventuates in a proinflammatory/fibrogenic
55                                           In aldosteronism, hypercalciuria and hypermagnesuria and ac
56 renin ratio, indicative of renin-independent aldosteronism (ie, subclinical primary aldosteronism), w
57 tricular dysfunction caused by chronic hyper-aldosteronism in vivo is completely prevented in cardiac
58 adrenocortical cell mass and the severity of aldosteronism in vivo, accounting for the milder phenoty
59 accompanies excretory Ca2+ losses induced by aldosteronism in which elevated parathyroid hormone leve
60    We present an interesting case of primary aldosteronism in which planar scintigraphy and SPECT wer
61 cal primary aldosteronism (renin-independent aldosteronism) in normotension.
62          Neurohormonal activation, including aldosteronism, in HF and RHT, has provided the pathophys
63 nal study using data from the Taiwan Primary Aldosteronism Investigation database.
64                                      Primary aldosteronism is a common cause of hypertension and is a
65                                      Primary aldosteronism is a common cause of treatment-resistant h
66                                      Primary aldosteronism is a nonsuppressible renin-independent ald
67                                      Primary aldosteronism is a potentially curable cause of hyperten
68 g2+ excretion and bone loss that accompanies aldosteronism is aggravated with furosemide and is atten
69                                        Thus, aldosteronism is associated with an activation of circul
70                                        Hyper-aldosteronism is associated with myocardial dysfunction
71 practice of MR antagonist therapy in primary aldosteronism is associated with significantly higher ri
72                                      Primary aldosteronism is common among patients with resistant hy
73                    The prevalence of primary aldosteronism is high and largely unrecognized.
74 hypertension after adrenalectomy for primary aldosteronism is independently associated with a lack of
75 biochemical phenotype of subclinical primary aldosteronism is negatively associated with cardiovascul
76                                      Primary aldosteronism is recognized as a severe form of renin-in
77                                      Primary aldosteronism is the most common curable cause of second
78                                      Primary aldosteronism is the most common single cause of hyperte
79                  Although unilateral primary aldosteronism is the most common surgically correctable
80                                              Aldosteronism may account for oxi/nitrosative stress, a
81           These results suggest that chronic aldosteronism may have a blood pressure-independent effe
82 rs of four kindreds with early onset primary aldosteronism of unknown cause.
83 r events was higher in patients with primary aldosteronism on MR antagonists than in patients with es
84 s are involved in the development of primary aldosteronism (PA) and hypercortisolism [Cushing's syndr
85 ve population the true prevalence of primary aldosteronism (PA) and its main subtypes, aldosterone-pr
86                                      Primary aldosteronism (PA) causes excess left ventricular (LV) h
87                                      Primary aldosteronism (PA) causes hypertension and is potentiall
88                                      Primary aldosteronism (PA) due to a unilateral aldosterone-produ
89 dosterone secretion in patients with primary aldosteronism (PA) impairs their cardiovascular system.
90                                      Primary aldosteronism (PA) is a common and underdiagnosed diseas
91                                      Primary aldosteronism (PA) is a common cause of secondary hypert
92                                      Primary aldosteronism (PA) is a common, but frequently overlooke
93                                      Primary aldosteronism (PA) is a common, potentially reversible,
94                                      Primary aldosteronism (PA) is common and associates with excess
95                                      Primary aldosteronism (PA) is one of the most common causes of s
96                                      Primary aldosteronism (PA) is the most common cause of secondary
97                                      Primary aldosteronism (PA) is the most common form of endocrine
98                                      Primary aldosteronism (PA) is the most frequent form of secondar
99 drenocortical hormone excess, due to primary aldosteronism (PA) or hypercortisolemia, causes hyperten
100 logical treatments on outcomes among primary aldosteronism (PA) patients.
101                                      Primary aldosteronism (PA) represents the most common cause of s
102                                      Primary aldosteronism (PA) results from renin-independent produc
103 pling (AVS) is crucial for subtyping primary aldosteronism (PA) to explore the possibility of curing
104                                      Primary aldosteronism (PA), an overt form of renin-independent a
105 st in aiding clinical diagnostics in primary aldosteronism (PA).
106 o localize aldosterone production in primary aldosteronism (PA).
107 alence and associated complications, primary aldosteronism remains largely under-recognized, with les
108 lly relevant spectrum of subclinical primary aldosteronism (renin-independent aldosteronism) in normo
109 he juxtaglomerular apparatus of the kidneys, aldosteronism resulting from adrenal cortical hyperplasi
110 of the hypertension of Kcnmb1(-/-) is due to aldosteronism, resulting from renal potassium retention
111 ction; whether this occurs also in secondary aldosteronism (SA) without hypertension is unknown.
112                        Screening for primary aldosteronism should nonetheless be done in every indivi
113                                 In rats with aldosteronism, spironolactone preserves skeletal strengt
114                                  The Primary Aldosteronism Surgical Outcome (PASO) study was an inter
115          These findings redefine the primary aldosteronism syndrome and implicate it in the pathogene
116  Review discusses how redefining the primary aldosteronism syndrome as a multidimensional spectrum wi
117                             Rates of primary aldosteronism testing (plasma aldosterone-renin) and the
118  a spectrum of subclinical renin-independent aldosteronism that increases risk for hypertension exist
119 gnized as a severe form of renin-independent aldosteronism that results in excessive mineralocorticoi
120 iddle syndrome and glucocorticoid-remediable aldosteronism, the abundance of plausible candidate gene
121 eyond this categorical definition of primary aldosteronism, there is a prevalent continuum of renin-i
122 compensatory diuresis that occurs in primary aldosteronism to correct and rebalance fluid homeostasis
123                    The importance of primary aldosteronism to public health derives from its high pre
124 dentified 602 eligible patients with primary aldosteronism treated with MR antagonists and 41 853 age
125 rdiovascular events in patients with primary aldosteronism treated with MR antagonists compared with
126  years or older, with a diagnosis of primary aldosteronism under the Endocrine Society's criteria, an
127 es (NOD) in patients with unilateral primary aldosteronism (uPA) remains underexplored.
128          We identified patients with primary aldosteronism using International Classification of Dise
129                                      Primary aldosteronism was confirmed by using the oral sodium-loa
130                  Biochemically overt primary aldosteronism was diagnosed when urinary aldosterone lev
131 -resistant hypertension, testing for primary aldosteronism was rare and was associated with higher ra
132                At 3-month follow-up, primary aldosteronism was resolved in 33 (92%) patients, with a
133 ndent aldosteronism (ie, subclinical primary aldosteronism), was associated with increased arterial s
134 ce estimates for biochemically overt primary aldosteronism were 11.3% (CI, 5.9% to 16.8%), 15.7% (CI,
135 ents whose hypertension and periodic primary aldosteronism were cured by adrenalectomy.
136  (1.6%) patients who were tested for primary aldosteronism were identified.
137 mutation is sufficient to cause mild primary aldosteronism, whereas loss of Ca(V)3.2 channel function
138 erproduction of aldosterone leads to primary aldosteronism, which is the most common form of secondar
139 ctional study assessed patients with primary aldosteronism who underwent simultaneous AVS at a single
140 dentifying patients with lateralized primary aldosteronism who would benefit from surgery.
141 al study of 677 participants without primary aldosteronism, who were studied on both high and restric
142 rtality was limited to patients with primary aldosteronism whose renin activity remained suppressed (
143 or the diagnosis and pathogenesis of primary aldosteronism with and without adrenal hyperplasia.
144  that Cav1.3 gain-of-function causes primary aldosteronism with seizures, neurologic abnormalities, a

 
Page Top