Abstract
Background
Brain ischemia may affect hypothalamic-pituitary axis function, which may influence the outcomes of patients with internal carotid artery (ICA) stenosis/occlusion. The objective of this study was to determine the influence of successful carotid revascularization on pituitary function in patients with severe ICA stenosis/occlusion.
Methods
This study was conducted from April 2009 to December 2014. Patients receiving successful endovascular interventions for severe ICA stenosis/occlusion were enrolled. The patients were divided into 2 groups: group 1 with abnormal ipsilateral cerebral perfusion, and group 2 without. Endocrine profiles were measured before and > 1 year after the procedure. Computed tomography perfusion studies were used to assess brain perfusion.
Results
Thirty-seven patients received successful interventions. Three patients were excluded due to re-stenosis before 1 year. There were 23 and 11 patients in group 1 and 2, with mean ages of 68 and 69 years, respectively. In the female patients, follicular stimulating hormone (FSH) and luteinizing hormone (LH) increased significantly (p = 0.043) after the interventions with a stable estradiol level in group 1. In contrast, FSH, LH and estradiol showed a decreasing trend in group 2. In the male patients, FSH and LH increased significantly (p < 0.01) after the interventions with a stable testosterone level in group 1, while testosterone showed a decreasing trend in group 2. Thyroid stimulating hormone increased significantly in the women in both groups, and in the men in group 1.
Conclusions
Successful revascularization for severe ICA stenosis/occlusion may improve their pituitary function, especially FSH and LH levels.
Keywords: Brain perfusion, Carotid stenosis, Carotid stenting, Pituitary function
INTRODUCTION
Brain tissue is highly sensitive to ischemia, and different regions of the brain have varying thresholds for ischemic damage.1,2 Abnormal activation of the hypothalamic-pituitary-adrenal axis is a hallmark response to acute brain ischemia.3 Abnormal pituitary hormone secretion has been observed in patients after acute ischemic stroke.4,5 Endocrine changes following brain ischemia may even predict clinical outcomes.6 Inflammation following ischemic insult is considered to be the underlying mechanism, however results of anti-inflammation therapy are inconsistent.7 Significant carotid stenosis increases the risk of stroke.8 Moreover, hypo-perfusion caused by high-grade internal carotid artery (ICA) stenosis can lead to cognitive impairment and decline.9 In patients with severe ICA stenosis, carotid artery stenting (CAS) not only reduces the risk of embolic stroke, but may also improve brain ischemia and neurocognitive function.10-12 Moreover, CAS has been shown to provide reliable long-term results and consistent reductions in systolic and diastolic blood pressure in patients with carotid stenosis.13,14 We conducted the present study to evaluate the correlation of baseline cerebral perfusion status with endocrine changes, especially the hypothalamic-pituitary axis, following successful revascularization in patients with severe ICA disease.
METHODS
Patients
All patients were 18 years of age or older. From April 2009 to December 2014, endovascular interventions were attempted in 207 consecutive patients with severe ICA stenosis or occlusion. The indication was > 50% diameter stenosis in symptomatic patients, and > 80% in asymptomatic patients.11 We excluded patients who had had an ischemic stroke within the past 2 weeks, and those with vascular disease precluding catheter-based techniques, intracranial aneurysm or arteriovenous malformation, history of bleeding disorder, any surgery planned within the next 30 days, life expectancy < 1 year, educational level below elementary school, aphasia, right-sided hemiparesis, marked depression, or moderate and severe dementia. We also excluded patients receiving repeated revascularizations, those with significant bilateral carotid disease, previous head and neck radiotherapy, or endocrine disorders. Brain computed tomography (CT) perfusion studies with Diamox (acetazolamide) stress were performed before and 3 months after the carotid intervention. Endocrine profiles before and > 1 year after the procedure were collected in 41 patients, including adrenocorticotropic hormone (ACTH), follicular stimulating hormone (FSH), growth hormone (GH), luteinizing hormone (LH), prolactin, thyroid stimulating hormone (TSH), cortisol, dehydroepiandrosterone sulfate (DHEAS), estradiol, free thyroxine (fT4), and testosterone.
Interventional procedure and clinical follow-up
Aspirin 100 mg and clopidogrel 75 mg/day were started 7 days before the procedure. Heparin was administered during the intervention to maintain an activated clotting time between 200 and 250 seconds. The definition of ICA occlusion and details of the procedure have been described previously. Blood samples were obtained before the intervention. Procedure success was defined as a final residual diameter stenosis < 20% with thrombolysis in cerebral infarction grade 3 flow after the procedure, without neurological complications. All patients were sent to the intensive care unit for overnight monitoring, where systolic blood pressure was carefully maintained between 100 to 140 mmHg. Aspirin and clopidogrel were continued for ≥ 3 months after the intervention if not contraindicated. Neurological sequelae, intracranial hemorrhage, and death were recorded. Follow-up ultrasound examinations were scheduled at 3 months after the intervention. Follow-up hormone profiles were checked ≥ 1 year after the index procedure to obtain chronic stable endocrine parameters, avoiding other confounding clinical variables.15 The review of the clinical information and radiologic records of the patients and endocrine profile checkups were approved by the Institutional Review Board at National Taiwan University Hospital. Informed consent was obtained from all subjects, and all methods were carried out in accordance with the relevant guidelines and regulations.
CT perfusion analysis
Multi-detector CT perfusion was performed to evaluate cerebral blood volume (CBV), cerebral blood flow (CBF), time to peak (TTP) and mean transit time (MTT). The topographic pattern was categorized into absence of asymmetry, watershed zone hypoperfusion, and vascular territory hypoperfusion. A grading system for qualitative assessments of perfusion in the regions of interest was proposed as follows: 0, complete perfusion; 1, hypoperfusion with preserved cerebral vascular reactivity (a lower peak, delayed TTP, increased MTT, decreased CBF, and normal or elevated CBV); and 2, hypoperfusion without adequate cerebral vascular reactivity (the same as 1 but with a decrease in CBV).16
Statistical analysis
Continuous data were presented as median (interquartile range), and discrete data were given as counts and percentages. Fisher’s exact test was used to compare groups of categorical data, and the Wilcoxon-Mann Whitney test was used to compare groups of continuous unpaired data. Paired continuous data were compared using the Wilcoxon signed-rank test. A two-sided p value of < 0.05 was considered to be statistically significant. Stata/SE version 14.0 for Windows (StataCorp LP, College Station, Texas) was used for statistical analyses.
RESULTS
Patient characteristics
Four patients were excluded because of unsuccessful revascularization, and another 3 patients were excluded due to re-occlusion detected within 1 year by follow-up duplex. Therefore, a total of 34 patients (24 men, mean age 68 years) were included in the analysis. Twenty patients (59%) had prior ipsilateral ischemic events, with 14 patients (41%) having their last event within 6 months [i.e., NASCET (North American Symptomatic Carotid Endarterectomy Trial) symptomatic]. Impaired ipsilateral cerebral perfusion as detected in baseline CT perfusion studies was found in 23 patients, including 10 with ICA occlusion and 13 with ICA stenosis.
Grouping for analysis
The patients were divided into 2 groups for analysis based on the pre-procedural CT perfusion results: group 1 (n = 23) consisted of those with abnormal ipsilateral cerebral perfusion; and group 2 (n = 11) consisted of those without perfusion abnormality. Table 1 summarizes their baseline demographics and clinical characteristics. Figure 1 shows examples of normal and abnormal cerebral perfusion CT images.
Table 1. Basic characteristics.
| Group 1 (n = 23) | Group 2 (n = 11) | p value | |
| Gender (female:male) | 5:18 | 5:6 | 0.232 |
| Age (year) | 68 (65-79) | 69 (62-77) | 1 |
| Diabetes mellitus | 7 (30%) | 2 (18%) | 0.682 |
| Hypertension | 17 (74%) | 6 (55%) | 0.434 |
| Hyperlipidemia | 14 (61%) | 5 (45%) | 0.475 |
| Smoking | 11 (48%) | 4 (36%) | 0.715 |
| Coronary artery disease | 15 (65%) | 8 (73%) | 1 |
| Peripheral arterial disease | 3 (13%) | 1 (9%) | 1 |
| Prior myocardial infarction | 2 (9%) | 0 | 1 |
| CKD stage 4 or 5 | 1 (4%) | 2 (18%) | 0.239 |
| Symptomatic ICAS | 11 (48%) | 3 (27%) | 0.295 |
| ICAO | 10 (43%) | 0 (0%) | 0.013 |
| Prior CVA | 16 (70%) | 4 (36%) | 0.135 |
Fisher’s exact test was used to obtain p-values except for the variate of age in which Wilcoxon-Mann Whitney test was used.
Age and follow up interval were presented as median (interquartile range). Other data was presented as number (percentage).
CKD, chronic kidney disease; CVA, cerebrovascular accident; ICAO, internal carotid artery occlusion; ICAS, internal carotid artery stenosis.
Figure 1.
Examples of cerebral perfusion CT. A patient with right ICAS and normal cerebral perfusion with balanced CBF (A), CBV (B), and MTT (C). The other patient with right ICAS and abnormal cerebral perfusion with decreased ipsilateral CBF (D), prolonged ipsilateral MTT (E) and balanced CBV (F). CBF, cerebral blood flow; CBV, cerebral blood volume; ICAS, internal carotid artery stenosis; MTT, mean transit time.
Endocrine changes
Baseline hormone profiles are summarized in Table 2. Table 3 and 4 show the hormone levels before and years after the intervention in group 1 and 2. There were no significant differences in any baseline hormone level including GH, prolactin, DHEAS, ACTH, cortisol, TSH, fT4, FSH, LH, estradiol and testosterone before the intervention between group 1 and group 2. A borderline increase in GH was observed in the women in group 1 and 2, but a decrease was noted in the men in group 2. FSH and LH were significantly increased years after the intervention in the women (FSH: 67.7 vs. 78.7 mIU/ml, p = 0.043; LH: 24.7 vs. 28 mIU/ml, p = 0.043) with a stable estradiol level in group 1. In contrast, FSH, LH and estradiol had a decreasing trend in group 2. FSH and LH significantly increased years after the intervention in the men (FSH: 8.1 vs. 12.2 mIU/ml, p < 0.01; LH: 5.3 vs. 7.7, p < 0.01) with a stable testosterone level in group 1, while testosterone had a decreasing trend in group 2. TSH significantly increased in the women in both groups (2.16 vs. 3.21 μIU/ml in group 1, p = 0.043; 1.55 vs. 3.12 μIU/ml in group 2, p = 0.043) and in the men in group 1 (1.31 vs. 2.33 μIU/ml, p < 0.01). Serum fT4 remained stable in both groups. The changes in other hormones before and after the intervention are shown in Table 3 and 4.
Table 2. Hormone survey before intervention.
| Group 1 (n = 23) | Group 2 (n = 11) | p value of two groups before intervention | |
| GH (ng/mL) | |||
| Female | 0.05 (0.04-0.06) | 0.07 (0.04-0.11) | 0.6752 |
| Male | 0.5 (0.12-1.48) | 0.73 (0.09-2.03) | 0.9468 |
| Prolactin (ng/ml) | |||
| Female | 5.6 (4.6-13.5) | 15.8 (11.8-18.1) | 0.2506 |
| Male | 9.5 (6.6-13.4) | 11.2 (6.5-16) | 0.8939 |
| DHEAS (μg/dL) | |||
| Female | 61.6 (32.6-74.6) | 82.3 (75.1-86.3) | 0.1745 |
| Male | 145.6 (92.9-263.1) | 188.6 (169.4-231) | 0.6407 |
| ACTH (pg/ml) | |||
| Female | 19.3 (2.5-23.2)0 | 32 (14-90.2) | 0.1745 |
| Male | 33.6 (15.2-47.8) | 18.1 (15.4-24.7) | 0.4237 |
| Cortisol (μg/dL) | |||
| Female | 8.1 (6.6-11.5) | 13.7 (11.8-19.9) | 0.0758 |
| Male | 13.4 (11.4-17.4) | 12.5 (10.8-16.6) | 0.6407 |
| TSH (μIU/ml) | |||
| Female | 2.16 (1.41-3.48) | 1.55 (1.43-2.06) | 0.4647 |
| Male | 1.31 (0.78-2.59) | 1.92 (1.55-2.15) | 0.4237 |
| fT4 (ng/dL) | |||
| Female | 1.27 (1.16-1.28) | 1.51 (1.21-1.52) | 0.1732 |
| Male | 1.27 (1.13-1.38) | 1.24 (1.14-1.58) | 0.8939 |
| FSH (mIU/ml) | |||
| Female | 67.7 (51.2-75.8) | 69.6 (24.5-76.8) | 0.9168 |
| Male | 8.1 (4.4-13.5) | 10.6 (7.9-12) | 0.3013 |
| LH (mIU/ml) | |||
| Female | 24.7 (24.2-26.9) | 36.2 (14.5-37) | 0.6015 |
| Male | 5.3 (3.5-7.9) | 6.2 (3.9-7.9) | 0.5708 |
| Estrodiol (pg/ml) | |||
| Female | 24.9 (11.5-36.2) | 16.3 (8.3-21.1) | 0.4647 |
| Male | 29 (21.9-37.1) | 29.4 (26.9-32.1) | 1 |
| Testosterone (ng/dL) | |||
| Female | 15.6 (8.1-18) | 14.1 (13.6-16.9) | 0.754 |
| Male | 370.6 (102-456.6) | 561.8 (442.6-688.7) | 0.0196 |
1. Hormone levels are presented by median (interquartile range). 2. p values are calculated with Wilcoxon-Mann Whitney test.
ACTH, adrenocorticotropic hormone; DHEAS, dehydroepiandrosterone sulfate; FSH, follicular stimulating hormone; fT4, free thyroxine; GH, growth hormone; LH, luteinizing hormone; TSH, thyroid stimulating hormone.
Table 3. Hormone survey in group 1 patients (n = 23).
| Before intervention | After intervention | p value | |
| GH (ng/mL) | |||
| Female | 0.05 (0.04-0.06) | 0.65 (0.28-0.77) | 0.0431 |
| Male | 0.5 (0.12-1.48) | 0.14 (0.08-0.38) | 0.0245 |
| Prolactin (ng/ml) | |||
| Female | 5.6 (4.6-13.5) | 9.9 (6.4-10.8) | 0.5002 |
| Male | 9.5 (6.6-13.4) | 10.7 (9.1-13.2) | 0.3061 |
| DHEAS (μg/dL) | |||
| Female | 61.6 (32.6-74.6) | 54.1 (40.3-82.4) | 0.8927 |
| Male | 145.6 (92.9-263.1) | 121 (69.6-281.2) | 0.2145 |
| ACTH (pg/ml) | |||
| Female | 19.3 (2.5-23.2) | 18.8 (17.3-26.4) | 0.5002 |
| Male | 33.6 (15.2-47.8) | 26.2 (21.3-40.2) | 0.9826 |
| Cortisol (μg/dL) | |||
| Female | 8.1 (6.6-11.5) | 16.8 (14.9-16.9) | 0.0431 |
| Male | 13.4 (11.4-17.4) | 16.4 (13.6-21) | 0.1024 |
| TSH (μIU/ml) | |||
| Female | 2.16 (1.41-3.48) | 3.21 (2.71-5.9) | 0.0431 |
| Male | 1.31 (0.78-2.59) | 2.33 (1.38-3.11) | 0.0016 |
| fT4 (ng/dL) | |||
| Female | 1.27 (1.16-1.28) | 1.26 (1.18-1.35) | 0.4922 |
| Male | 1.27 (1.13-1.38) | 1.23 (1.14-1.43) | 0.9653 |
| FSH (mIU/ml) | |||
| Female | 67.7 (51.2-75.8) | 78.7 (72.6-95.3) | 0.0431 |
| Male | 8.1 (4.4-13.5) | 12.2 (7.1-26.7) | 0.0003 |
| LH (mIU/ml) | |||
| Female | 24.7 (24.2-26.9) | 28 (26.8-39.7) | 0.0431 |
| Male | 5.3 (3.5-7.9)0 | 7.7 (4.5-15.5) | 0.0014 |
| Estrodiol (pg/ml) | |||
| Female | 24.9 (11.5-36.2) | 27.8 (12-32.4) | 0.4164 |
| Male | 29 (21.9-37.1) | 28.5 (24.2-34.4) | 0.3958 |
| Testosterone (ng/dL) | |||
| Female | 15.6 (8.1-18) | 20.4 (17.6-21.5) | 0.0568 |
| Male | 370.6 (102-456.6) | 372.3 (31.7-445.2) | 0.5862 |
1. Hormone levels are presented by median (interquartile range). 2. p values are calculated with Wilcoxon-Mann Whitney test.
ACTH, adrenocorticotropic hormone; DHEAS, dehydroepiandrosterone sulfate; FSH, follicular stimulating hormone; fT4, free thyroxin; GH, growth hormone; LH, luteinizing hormone; TSH, thyroid stimulating hormone.
Table 4. Hormone survey in group 2 patients (n = 11).
| Before intervention | After intervention | p value | |
| GH (ng/mL) | |||
| Female | 0.07 (0.04-0.11) | 0.81 (0.52-1.22) | 0.0431 |
| Male | 0.73 (0.09-2.03) | 0.24 (0.07-0.63) | 0.1730 |
| Prolactin (ng/ml) | |||
| Female | 15.8 (11.8-18.1) | 12 (8-14.4) | 0.3452 |
| Male | 11.2 (6.5-16) | 8.5 (8.1-10.6) | 0.9165 |
| DHEAS (μg/dL) | |||
| Female | 82.3 (75.1-86.3) | 70.7 (70.4-73.1) | 0.138 |
| Male | 188.6 (169.4-231) | 130.4 (63.2-196.5) | 0.3454 |
| ACTH (pg/ml) | |||
| Female | 32 (14-90.2) | 8.8 (8.6-21.1) | 0.0431 |
| Male | 18.1 (15.4-24.7) | 20.9 (19.3-24.9) | 0.9165 |
| Cortisol (μg/dL) | |||
| Female | 13.7 (11.8-19.9) | 13.3 (11.2-24.3) | 0.8927 |
| Male | 12.5 (10.8-16.6) | 17.5 (14.5-21.5) | 0.2489 |
| TSH (μIU/ml) | |||
| Female | 1.55 (1.43-2.06) | 3.12 (2.35-4.85) | 0.0431 |
| Male | 1.92 (1.55-2.15) | 2.21 (1.49-3.67) | 0.3454 |
| fT4 (ng/dL) | |||
| Female | 1.51 (1.21-1.52) | 1.37 (1.35-1.45) | 0.6858 |
| Male | 1.24 (1.14-1.58) | 1.34 (1.11-1.48) | 0.9165 |
| FSH (mIU/ml) | |||
| Female | 69.6 (24.5-76.8) | 60.8 (54.6-67.2) | 0.5002 |
| Male | 10.6 (7.9-12) | 18.7 (10.4-74.7) | 0.0747 |
| LH (mIU/ml) | |||
| Female | 36.2 (14.5-37) | 25.5 (23.8-43.3) | 0.3452 |
| Male | 6.2 (3.9-7.9) | 12.7 (6-53.6) | 0.0464 |
| Estrodiol (pg/ml) | |||
| Female | 16.3 (8.3-21.1) | 5 (5-7.1)0 | 0.0568 |
| Male | 29.4 (26.9-32.1) | 27.8 (24.9-35.7) | 0.7525 |
| Testosterone (ng/dL) | |||
| Female | 14.1 (13.6-16.9) | 15.7 (8.5-25) | 0.6858 |
| Male | 561.8 (442.6-688.7) | 447.9 (359-574.3) | 0.0747 |
1. Hormone levels are presented by median (interquartile range). 2. p values are calculated with Wilcoxon-Mann Whitney test.
ACTH, adrenocorticotropic hormone; DHEAS, dehydroepiandrosterone sulfate; FSH, follicular stimulating hormone; fT4, free thyroxin; GH, growth hormone; LH, luteinizing hormone; TSH, thyroid stimulating hormone.
DISCUSSION
The brain is a highly vascular organ and vulnerable to ischemic insults. The anterior pituitary gland receives arterial supply from the superior hypophyseal artery, a branch of the ICA, while the posterior pituitary gland receives blood supply from the ICA and posterior communicating artery. Hypothalamic-pituitary axis dysfunction is a hallmark of acute brain ischemia, found in 82% of patients with mild to moderate stroke,17 and it has been correlated with the extent of brain damage, neurologic deficits, and clinical outcomes.6,18-20 If irreversible cellular damage is the underlying mechanism, pituitary dysfunction should be permanent after stroke. On the other hand, if insufficient perfusion to the pituitary gland is the underlying mechanism, these changes following acute and chronic ischemia may be reversible, and treatment to correct ischemia may reverse endocrine dysfunction and improve clinical outcomes. In the present study, FSH, LH, and TSH levels increased significantly after successful carotid revascularization in the patients with baseline abnormal cerebral perfusion, and the estradiol level in women and testosterone level in men remained stable years after the intervention. In contrast, FSH and LH in both males and females, estradiol in females, and testosterone in males had a decreasing trend in the patients without baseline perfusion defects. To the best of our knowledge, this is the first study in the literature to report such observations.
GH deficiency and central hypogonadism have been reported in 40% of patients following acute stroke.15 These pituitary dysfunctions have been reported in both the acute phase and long-term phase.4,21 In the current cohort, the mean age was 68 years and all of the female patients were post-menopausal, and gonadotropin levels are expected to decline over time.22 In our present study, however, pituitary gonadotropin levels including FSH and LH increased significantly in group 1 after revascularization. This unique finding of a significant increase in LH and FSH in group 1 may be explained by restored and improved pituitary perfusion.
The impact of pituitary reperfusion on gonadal hormones may be more complex, as pelvic reproductive organs are involved. Gonadal hormone levels should decrease with age (group 2, Table 4), however the testosterone level of the male patients with impaired brain perfusion was significantly lower at baseline (Table 2). Moreover, the aging decline in group 1 was actually slow or corrected following the intervention (Table 3). This phenomenon was also found in estradiol levels in the female patients. This "reversal" of an aging decline in gonadal hormones in group 1 patients may be explained by the increase in LH and subsequent increase in testosterone production both in the men and women. This would further lead to increases in estradiol level in postmenopausal woman. Therefore, the restoration of brain perfusion may improve pituitary/gonadal axis function.
Another interesting finding is the change in TSH levels. In a geriatric population, TSH will increase as part of the aging process. Thyroid gland function tends to decline, and an average 13% increase in TSH over a 13-year period has been reported, especially in women.19,22 We also observed this increase in TSH in the female patients in both groups, while the corresponding fT4 levels remained unchanged. There was also a significant increase in TSH level in the men after revascularization in group 1 (77% vs. 15%), but not in group 2. An increasing TSH level in the elderly has been associated with a lower mortality rate, while mortality has been positively correlated with serum thyroxin level.20 The beneficial effect of carotid revascularization on life span also warrants further investigations.
GH levels increased in the women in both groups after the intervention, however it decreased in the men in both groups, but only significantly in group 1. Adults secrete less GH as they get older, but more with higher sex hormone levels.22,23 In addition, elderly women have higher GH secretion than elderly men.24 The inferred stimulatory action of testosterone on pulsatile GH release in humans is likely to be mediated via estrogen rather than androgen receptors.23 In our cohort, the women had a significant increase in group 1, which could be the result of better pituitary perfusion and higher estrogen level after the intervention. The decrease in GH in the men in both groups could be the result of aging, male gender, and lower estrogen level after the intervention. However, in the present study, the timing of blood sampling was random, making the interpretation of changes in GH difficult. Moreover, other confounding factors such as body mass index, abdominal visceral adiposity, and blood sugar, were not controlled in this study. ACTH decreased in the women in group 2, and cortisol increased in the women of group 1, however neither showed significant changes in the other patients. Due to the fact that blood samples were obtained just before the interventions, it was impossible to control the diurnal timing or to apply provocation tests. Therefore, the changes in GH, ACTH and cortisol are very difficult to interpret. The mental and physical stress related to the interventions, the timing of obtaining the blood samples, and the fasting prior to the procedures would all affect the hormone assay results. Further research taking these factors into consideration is mandatory to clarify the relationship between brain perfusion and pituitary function regarding the GH and adrenal axis.
Carotid stenting and endarterectomy both prevent stroke in patients with severe ICA stenosis.25,26 Moreover, successful stenting corrects cerebral ischemia and may improve neurocognitive function in ICA stenosis/occlusion patients with objective perfusion impairment.12 The improvement in perfusion may also reverse pituitary dysfunction, and further augment the improvement in neurocognitive function. Future studies are warranted to evaluate the correlation between neuro-endocrine changes and neurocognitive function after carotid revascularization.
Limitations
The number of patients is relatively small, and a larger cohort with longer follow-up is required to validate the current findings. Other pituitary hormones such as oxytocin, anti-diuretic hormone, and insulin-like growth factor 1 were not checked, so the conclusion on pituitary function may be incomplete. Random blood sampling timing made the interpretation of changes in GH, ACTH and cortisol difficult. Even though the patency of carotid stent was proved by carotid duplex, no corresponding follow-up at the time of blood sampling was done. This limited the understanding of brain perfusion status in patients with baseline abnormal cerebral perfusion. A consistent protocol, even with provocation tests, is necessary in the future studies.
CONCLUSIONS
Successful revascularization for severe carotid stenosis/occlusion improved pituitary function, most notably in FSH, LH, and TSH, in the patients with objective baseline abnormal cerebral perfusion.
Acknowledgments
This submitted work is supported by grant from National Taiwan University Hospital (NTUH. 105-N3198) and Liver Disease Prevention & Treatment Research Foundation. We thank the staff of the Eighth Core Lab, Department of Medical Research, National Taiwan University Hospital for technical support during the study.
DECLARATION OF INTERESTS
All the authors declare no conflict of interest.
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