Comparison of different strategies in parathyroid scintigraphy imaging in the setting of multi-gland hyperparathyroidism [abstract]

Medical records of 140 patients, diagnosed with multigland primary, secondary or tertiary hyperparathyroidism were reviewed. Of those, 56 patients had complete preoperative parathyroid scintigraphy with subsequent surgical resection of abnormal glands. Parathyroid scintigraphy at our institution utilizes 99mTc sestamibi (MIBI) and 123I, and consists of early and delayed pinhole MIBI images of the neck, MIBI-123I subtraction imaging, and MIBI single photon computed tomography (SPECT). Four experienced nuclear medicine physician, without knowledge of clinical or laboratory results or final diagnosis, reviewed seven different imaging variations in separate sessions. The imaging variations were early MIBI only (EARLY), delayed MIBI only (DELAYED), comparison of early and delayed MIBI (E-D), subtraction (SUB), all planar (PLANAR), SPECT only (SPECT), and all images (ALL). The location of the abnormal parathyroid glands was recorded and compared with the embryologic designation of the abnormal glands assigned at the time of surgery

Comparison of different strategies in parathyroid scintigraphy imaging [abstract]

To retrospectively compare the various scintigraphic methods to discover the most accurate protocol for preoperative localization of single-gland disease, medical records of 710 patients, diagnosed with primary were reviewed. 293 patients had complete preoperative parathyroid scintigraphy with subsequent surgical resection of a single abnormal gland. Parathyroid scintigraphy at our institution utilizes 99mTc sestamibi (MIBI) and 123I, and consists of early and delayed pinhole MIBI images of the neck, including MIBI-123I subtraction imaging, as well as MIBI single photon emission computed tomography (SPECT) of the neck and chest. Four experienced nuclear medicine physicians, without knowledge of clinical or laboratory results or final diagnosis, reviewed seven different imaging variations in separate sessions. The imaging variations were early MIBI only (EARLY), delayed MIBI only (DELAYED), comparison of early and delayed MIBI (E-D), subtraction (SUB), all planar (PLANAR), SPECT only (SPECT), and all images (ALL)

Neurologic complications in percutaneous nephrolithotomy

Percutaneous nephrolithotomy (PCNL) has been the preferred procedure for the removal of large renal stones in Iran since 1990. Recently, we encountered a series of devastating neurologic complications during PCNL, including paraplegia and hemiplegia. There are several reports of neurologic complications following PCNL owing to paradoxical air emboli, but there are no reports of paraplegia following PCNL. Materials and Methods: We retrospectively reviewed the medical records of patients who had undergone PCNL in 13 different endourologic centers and retrieved data related to neurologic complications after PCNL, including coma, paraplegia, hemiplegia, and quadriplegia. Results: The total number of PCNL procedures in these 13 centers was 30,666. Among these procedures, 11 cases were complicated by neurologic events, and four of these cases experienced paraplegia. All events happened with the patient in the prone position with the use of general anesthesia and in the presence of air injection. There were no reports of neurologic complications in PCNL procedures performed with the patient under general anesthesia and in the prone position and with contrast injection. Conclusions: It can be assumed that using room air to opacify the collecting system played a major role in the occurrence of these complications. Likewise, the prone position and general anesthesia may predispose to these events in the presence of air injectio

Shortening of atrioventricular delay at increased atrial paced heart rates improves diastolic filling and functional class in patients with biventricular pacing

<p>Abstract</p> <p>Background</p> <p>Use of rate adaptive atrioventricular (AV) delay remains controversial in patients with biventricular (Biv) pacing. We hypothesized that a shortened AV delay would provide optimal diastolic filling by allowing separation of early and late diastolic filling at increased heart rate (HR) in these patients.</p> <p>Methods</p> <p>34 patients (75 ± 11 yrs, 24 M, LVEF 34 ± 12%) with Biv and atrial pacing had optimal AV delay determined at baseline HR by Doppler echocardiography. Atrial pacing rate was then increased in 10 bpm increments to a maximum of 90 bpm. At each atrial pacing HR, optimal AV delay was determined by changing AV delay until best E and A wave separation was seen on mitral inflow pulsed wave (PW) Doppler (defined as increased atrial duration from baseline or prior pacemaker setting with minimal atrial truncation). Left ventricular (LV) systolic ejection time and velocity time integral (VTI) at fixed and optimal AV delay was also tested in 13 patients. Rate adaptive AV delay was then programmed according to the optimal AV delay at the highest HR tested and patients were followed for 1 month to assess change in NYHA class and Quality of Life Score as assessed by Minnesota Living with Heart Failure Questionnaire.</p> <p>Results</p> <p>81 AV delays were evaluated at different atrial pacing rates. Optimal AV delay decreased as atrial paced HR increased (201 ms at 60 bpm, 187 ms at 70 bpm, 146 ms at 80 bpm and 123 ms at 90 bpm (ANOVA F-statistic = 15, p = 0.0010). Diastolic filling time (P < 0.001 vs. fixed AV delay), mitral inflow VTI (p < 0.05 vs fixed AV delay) and systolic ejection time (p < 0.02 vs. fixed AV delay) improved by 14%, 5% and 4% respectively at optimal versus fixed AV delay at the same HR. NYHA improved from 2.6 ± 0.7 at baseline to 1.7 ± 0.8 (p < 0.01) 1 month post optimization. Physical component of Quality of Life Score improved from 32 ± 17 at baseline to 25 ± 12 (p < 0.05) at follow up.</p> <p>Conclusions</p> <p>Increased heart rate by atrial pacing in patients with Biv pacing causes compromise in diastolic filling time which can be improved by AV delay shortening. Aggressive AV delay shortening was required at heart rates in physiologic range to achieve optimal diastolic filling and was associated with an increase in LV ejection time during optimization. Functional class improved at 1 month post optimization using aggressive AV delay shortening algorithm derived from echo-guidance at the time of Biv pacemaker optimization.</p

Supine Percutaneous Nephrolithotomy: CON

Advocates of supine percutaneous nephrolithotomy (PCNL) consider several theoretical advantages for this procedure. Despite the potential advantages of the supine PCNL, the majority of urologists have remained reluctant to perform this technique. This reluctance may be related to successful outcomes of prone PCNL and technical difficulties associated with supine PCNL. Feasibility of supine PCNL has been shown in different series and the current evidence, although limited and not fully organized, implies the application of this technique for patients with simple stones who are at high anesthesiological risk. However, there is no convincing evidence to support performing supine PCNL in morbidly obese patients and those with complex and multiple stones. Further randomized clinical trials of large sample size and high methodological quality are required to recommend extensive application of supine PCNL as an alternative to prone PCNL

Polymorphisms in hormone metabolism and growth factor genes and mammographic density in Norwegian postmenopausal hormone therapy users and non-users

Introduction: Mammographic density (MD) is one of the strongest known breast cancer risk factors. Estrogen and progestin therapy (EPT) has been associated with increases in MD. Dense breast tissue is characterized by increased stromal tissue and (to a lesser degree) increased numbers of breast epithelial cells. It is possible that genetic factors modify the association between EPT and MD, and that certain genetic variants are particularly important in determining MD in hormone users. We evaluated the association between MD and 340 tagging single nucleotide polymorphisms (SNPs) from about 30 candidate genes in hormone metabolism/growth factor pathways among women who participated in the Norwegian Breast Cancer Screening Program (NBCSP) in 2004. Methods: We assessed MD on 2,036 postmenopausal women aged 50 to 69 years using a computer-assisted method (Madena, University of Southern California) in a cross-sectional study. We used linear regression to determine the association between each SNP and MD, adjusting for potential confounders. The postmenopausal women were stratified into HT users (EPT and estrogen-only) and non-users (never HT). Results: For current EPT users, there was an association between a variant in the prolactin gene (PRL; rs10946545) and MD (dominant model, Bonferroni-adjusted P (Pb) = 0.0144). This association remained statistically significant among current users of norethisterone acetate (NETA)-based EPT, a regimen common in Nordic countries. Among current estrogen-only users (ET), there was an association between rs4670813 in the cytochrome P450 gene (CYP1B1) and MD (dominant model, Pb = 0.0396). In never HT users, rs769177 in the tumor necrosis factor (TNF) gene and rs1968752 in the region of the sulfotransferase gene (SULT1A1/SULT1A2), were significantly associated with MD (Pb = 0.0202; Pb = 0.0349). Conclusions: We found some evidence that variants in the PRL gene were associated with MD in current EPT and NETA users. In never HT users, variants in the TNF and SULT1A1/SULT1A2 genes were significantly associated with MD. These findings may suggest that several genes in the hormone metabolism and growth factor pathways are implicated in determining MD

Polymorphisms in hormone metabolism and growth factor genes and mammographic density in Norwegian postmenopausal hormone therapy users and non-users

Introduction Mammographic density (MD) is one of the strongest known breast cancer risk factors. Estrogen and progestin therapy (EPT) has been associated with increases in MD. Dense breast tissue is characterized by increased stromal tissue and (to a lesser degree) increased numbers of breast epithelial cells. It is possible that genetic factors modify the association between EPT and MD, and that certain genetic variants are particularly important in determining MD in hormone users. We evaluated the association between MD and 340 tagging single nucleotide polymorphisms (SNPs) from about 30 candidate genes in hormone metabolism/growth factor pathways among women who participated in the Norwegian Breast Cancer Screening Program (NBCSP) in 2004. Methods We assessed MD on 2,036 postmenopausal women aged 50 to 69 years using a computer-assisted method (Madena, University of Southern California) in a cross-sectional study. We used linear regression to determine the association between each SNP and MD, adjusting for potential confounders. The postmenopausal women were stratified into HT users (EPT and estrogen-only) and non-users (never HT). Results For current EPT users, there was an association between a variant in the prolactin gene (PRL; rs10946545) and MD (dominant model, Bonferroni-adjusted P (Pb) = 0.0144). This association remained statistically significant among current users of norethisterone acetate (NETA)-based EPT, a regimen common in Nordic countries. Among current estrogen-only users (ET), there was an association between rs4670813 in the cytochrome P450 gene (CYP1B1) and MD (dominant model, Pb = 0.0396). In never HT users, rs769177 in the tumor necrosis factor (TNF) gene and rs1968752 in the region of the sulfotransferase gene (SULT1A1/SULT1A2), were significantly associated with MD (Pb = 0.0202; Pb = 0.0349). Conclusions We found some evidence that variants in the PRL gene were associated with MD in current EPT and NETA users. In never HT users, variants in the TNF and SULT1A1/SULT1A2 genes were significantly associated with MD. These findings may suggest that several genes in the hormone metabolism and growth factor pathways are implicated in determining MD

Association between 9 IL6 tagging SNPs (with P-value less than 0.05) and MD after adjustment for age and BMI, based on an additive genetic model (N = 301).

a<p>based on map to Genome Build 37.3.</p>b<p>Number of women with wild-wild genotype.</p>c<p>Number of women with wild-variant genotype.</p>d<p>Number of women with variant-variant genotype.</p>e<p>Minor allele frequency.</p>f<p>Percent MD per variant allele based on additive model adjusted for age at mammogram (continuous) and BMI at mammogram (continuous).</p