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Jeffrey Baron - One of the best experts on this subject based on the ideXlab platform.
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Growth plate senescence and Catch up Growth
Endocrine development, 2011Co-Authors: Ola Nilsson, Jeffrey BaronAbstract:Longitudinal bone Growth is rapid in prenatal and early postnatal life, but then slows with age and eventually ceases. This Growth deceleration is caused primarily by a decrease in chondrocyte proliferation, and is associated with other structural, functional, and molecular changes collectively termed Growth plate senescence. Current evidence suggests that Growth plate senescence occurs because the progenitor chondrocytes in the resting zone have a limited replicative capacity which is gradually exhausted with increasing cell division. In addition, recent experimental findings from laboratory and clinical studies suggest that Growth plate senescence explains the phenomenon of Catch-up Growth. Growth-inhibiting conditions such as glucocorticoid excess and hypothyroidism delay the program of Growth plate senescence. Consequently, Growth plates are less senescent after these conditions resolve and therefore grow more rapidly than is normal for age, resulting in Catchup Growth.
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Catch up Growth after hypothyroidism is caused by delayed Growth plate senescence
Endocrinology, 2008Co-Authors: Rose Marino, Ola Nilsson, Anita Hegde, Kevin M Barnes, Lenneke Schrier, Joyce Emons, Jeffrey BaronAbstract:Catch-up Growth is defined as a linear Growth rate greater than expected for age after a period of Growth inhibition. We hypothesized that Catch-up Growth occurs because Growth-inhibiting conditions conserve the limited proliferative capacity of Growth plate chondrocytes, thus slowing the normal process of Growth plate senescence. When the Growth-inhibiting condition resolves, the Growth plates are less senescent and therefore grow more rapidly than normal for age. To test this hypothesis, we administered propylthiouracil to newborn rats for 8 wk to induce hypothyroidism and then stopped the propylthiouracil to allow Catch-up Growth. In untreated controls, the Growth plates underwent progressive, senescent changes in multiple functional and structural characteristics. We also identified genes that showed large changes in mRNA expression in Growth plate and used these changes as molecular markers of senescence. In treated animals, after stopping propylthiouracil, these functional, structural, and molecular senescent changes were delayed, compared with controls. This delayed senescence included a delayed decline in longitudinal Growth rate, resulting in Catch-up Growth. The findings demonstrate that Growth inhibition due to hypothyroidism slows the developmental program of Growth plate senescence, including the normal decline in the rate of longitudinal bone Growth, thus accounting for Catch-up Growth.
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impact of Growth plate senescence on Catch up Growth and epiphyseal fusion
Pediatric Nephrology, 2005Co-Authors: Ola Nilsson, Jeffrey BaronAbstract:In mammals, longitudinal bone Growth occurs rapidly in prenatal and early postnatal life, but then slows and eventually ceases. This deceleration, which reflects a decline in chondrocyte proliferation, was previously attributed to a hormonal or other systemic mechanism. However, new evidence suggests that it is due to a local mechanism within the Growth plate. In particular, recent findings suggest that Growth plate chondrocytes have a finite proliferative capacity that is gradually exhausted, causing Growth to slow and finally stop. This concept has provided insight into clinical phenomena including Catch-up Growth after transient Growth inhibition, Catch-down Growth after transient estrogen exposure, and epiphyseal fusion.
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Catch up Growth is associated with delayed senescence of the Growth plate in rabbits
Pediatric Research, 2001Co-Authors: Rachel I Gafni, Kevin M Barnes, Martina Weise, Daniel T Robrecht, Jodi L Meyers, Stacy Delevi, Jeffrey BaronAbstract:In mammals, release from Growth-inhibiting conditions results in Catch-up Growth. To explain this phenomenon, we proposed the following model:1) The normal senescent decline in Growth plate function depends not on age per se, but on the cumulative number of replications that Growth plate chondrocytes have undergone. 2) Conditions that suppress Growth plate chondrocyte proliferation therefore slow senescence. 3) After transient Growth inhibition, Growth plates are thus less senescent and hence show a greater Growth rate than expected for age, resulting in Catch-up Growth. To test this model, we administered dexamethasone to growing rabbits to suppress linear Growth. After stopping dexamethasone, Catch-up Growth occurred. In distal femoral Growth plates of untreated controls, we observed a senescent decline in the Growth rate and in the heights of the proliferative zone, hypertrophic zone, and total Growth plate. During the period of Catch-up Growth, in the animals previously treated with dexamethasone, the senescent decline in all these variables was delayed. Prior treatment with dexamethasone also delayed epiphyseal fusion. These findings support our model that linear Catch-up Growth is caused, at least in part, by a delay in Growth plate senescence.
Kenneth I Glassberg - One of the best experts on this subject based on the ideXlab platform.
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adolescent varicocelectomy does artery sparing influence recurrence rate and or Catch up Growth
Journal of Andrology, 2014Co-Authors: Angela M Fast, Shannon N Nees, Christopher M Deibert, Jason P Van Batavia, Kenneth I GlassbergAbstract:Summary The prevalence of varicocoeles is 15% in the general adolescent and adult male population and in 35–40% of men evaluated for infertility. While varicocelectomy can be performed using various methods and techniques, the laparoscopic approach allows for clear visualization of the testicular artery and lymphatics. Amongst urologists, particularly paediatric urologists, and andrologists there is much debate regarding the significance of testicular artery sparing when performing a varicocelectomy, with some believing that ligating the testicular artery impairs Catch-up Growth and future fertility. On the other hand, several studies have reported higher failure rates with artery preservation. To help resolve the debate regarding the significance of artery sparing, we sought to compare varicocoele recurrence rate and Catch-up Growth in patients who underwent artery sparing laparoscopic varicocelectomy compared with those who had the artery sacrificed. We identified 524 laparoscopic varicocelectomies in 425 patients from our adolescent varicocoele database. Only patients who had ultrasound determined testicular volume measurements pre-operatively and at least 6 months post-operatively were included. Post-operative persistence/recurrence of varicocoele, testicular atrophy and repeat varicocelectomy were noted. Catch-up Growth was compared between procedures in those with significant pre-operative asymmetry. Four hundred and forty primary laparoscopic varicocelectomies were performed in 355 patients (mean age: 15.5 years, range 9.3–20.6; mean follow-up: 32.9 months, range 6.0–128.9) who had both pre- and post-varicocelectomy scrotal Duplex Doppler ultrasound performed. The testicular artery was preserved in 54 varicocoeles (41 patients) and ligated in 384 varicocoeles (312 patients). We observed an increased rate of persistent/recurrent varicocoele in the artery-sparing vs. artery ligating patients (12.2% vs. 5.4%, p = 0.09). In addition, there was no difference in Catch-up Growth and no instance of testicular atrophy. As artery sparing varicocelectomy offered no advantage in regards to Catch-up Growth and was associated with a higher incidence of recurrent varicocoele, preservation of the artery does not appear to be routinely necessary in adolescent varicocelectomy.
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incidence significance and natural history of persistent retrograde venous flow after varicocelectomy in children and adolescents correlation with Catch up Growth
The Journal of Urology, 2013Co-Authors: Jason P Van Batavia, Angela M Fast, Shannon N Nees, Miguel A Mercado, Anthony Gaselberti, Kenneth I GlassbergAbstract:Purpose: Varying incidences and levels of persistent retrograde venous flow have been reported following adult and adolescent varicocelectomy but the significance remains unclear. We sought to determine the incidence and natural history of persistent flow and whether it had any effect on postoperative testicular Catch-up Growth.Materials and Methods: We retrospectively analyzed pre-varicocelectomy and post-varicocelectomy Doppler duplex ultrasound findings. Peak retrograde venous flow, maximum vein diameter, flow quality and varicocele grade were recorded at each visit. Catch-up Growth was defined as less than 15% testicular asymmetry at final visit.Results: Of 330 patients (median age 15.4 years) undergoing varicocelectomy (laparoscopic in 247, open in 83) 145 had residual retrograde venous flow after Valsalva maneuver with a mean peak of 13.3 cm per second. Of 290 patients with repeat Doppler duplex ultrasound (median followup 2.6 years) 124 had initial peak retrograde venous flow less than 20 cm per se...
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adolescent varicocele influence of tanner stage at presentation on the presence development worsening and or improvement of testicular hypotrophy without surgical intervention
The Journal of Urology, 2010Co-Authors: Jason P Van Batavia, Stephen A Poon, Solomon L Woldu, Peter M Raimondi, Benjamin A Spencer, Beverly J Insel, Kenneth I GlassbergAbstract:Purpose: Testicular asymmetry in adolescents with varicocele can worsen, remain unchanged or decrease on followup. We determined the incidence of testicular asymmetry at presentation by Tanner stage and the correlation between Tanner stage at presentation and subsequent changes in percent asymmetry (ability for Catch-up Growth or progressive asymmetry) without surgical intervention.Materials and Methods: We retrospectively studied the records of 115 boys with a mean age of 14.1 years (range 9.2 to 20.0) with grade 2 or 3 left varicocele who underwent testicular volume measurement at 2 visits at least that were a minimum of 6 months apart. Of the patients 92% and 8% underwent Doppler duplex ultrasound and orchidometry, respectively. Patients were divided into 2 groups, including those with less than 15% and those with 15% or greater asymmetry. Catch-up Growth was defined as less than 15% asymmetry at any subsequent visit.Results: At presentation 58%, 64%, 67%, 35% and 39% of Tanner 1 to 5 cases showed 15% ...
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adolescent varicocelectomy postoperative Catch up Growth is not secondary to lymphatic ligation
Journal of Pediatric Urology, 2009Co-Authors: Stephen A Poon, Kristin A Kozakowski, Joel G Decastro, Carl K Gjertson, Kenneth I GlassbergAbstract:Abstract Purpose The major indication for adolescent varicocelectomy is testicular asymmetry with the left testicle smaller than the right. Catch-up Growth following surgery is one of the parameters used to assess efficacy of surgery. However, it is not clear whether this represents true tissue Growth or increased interstitial fluid secondary to lymphatic obstruction. The purpose of this study was to compare Catch-up Growth in patients who underwent varicocelectomy with and without lymphatic preservation. Materials and methods We retrospectively analyzed the outcomes of 136 boys (mean age 15.1 years) who had 10% or greater preoperative testicular asymmetry and underwent varicocelectomy between 1997 and 2006. Surgery was either a laparoscopic nonlymphatic sparing or laparoscopic lymphatic sparing varicocelectomy. All patients had pre- and postoperative ultrasound volume measurements at least 6 months following surgery. The groups were compared for incidence of postoperative Catch-up Growth, achieving less than 10% testicular asymmetry. Results After a mean follow up of 24.7 months, Catch-up Growth was achieved in 62.8% of patients. There was no significant difference between the groups in regard to Catch-up Growth (51.7% vs 66.3%, P = 0.193). Conclusions Since no significant difference was found between the laparoscopic nonlymphatic sparing and laparoscopic lymphatic sparing varicocelectomies, we conclude that lymphatic obstruction is not the cause of Catch-up Growth.
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adolescent varicocelectomy is the potential for Catch up Growth related to age and or tanner stage
The Journal of Urology, 2009Co-Authors: Joel G Decastro, Stephen A Poon, Ahmad Shabsigh, Laurent Laor, Kenneth I GlassbergAbstract:Purpose: Adolescent varicocelectomy is associated with a 70% incidence of postoperative Catch-up Growth in boys with ipsilateral testicular hypotrophy. We determined whether preoperative patient age and Tanner stage were related to subsequent Catch-up Growth. In other words if patients are followed with a period of observation, will a window of opportunity be lost for achieving Catch-up Growth?Materials and Methods: We studied a total of 163 boys (mean age 15.1 years, range 10 to 24) with left or bilateral varicoceles who demonstrated 10% asymmetry or greater preoperatively, and had preoperative and postoperative testicular volume measurements available (using either ring orchidometer or ultrasound). Of these patients 59 also had preoperative Tanner stage recorded.Results: Of the patients with preoperative left hypotrophy 69% had achieved Catch-up Growth at last followup (mean followup 28 months). When treated as a continuous variable, or when divided into general prepubertal vs postpubertal groupings, ag...
Ola Nilsson - One of the best experts on this subject based on the ideXlab platform.
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Growth plate senescence and Catch up Growth
Endocrine development, 2011Co-Authors: Ola Nilsson, Jeffrey BaronAbstract:Longitudinal bone Growth is rapid in prenatal and early postnatal life, but then slows with age and eventually ceases. This Growth deceleration is caused primarily by a decrease in chondrocyte proliferation, and is associated with other structural, functional, and molecular changes collectively termed Growth plate senescence. Current evidence suggests that Growth plate senescence occurs because the progenitor chondrocytes in the resting zone have a limited replicative capacity which is gradually exhausted with increasing cell division. In addition, recent experimental findings from laboratory and clinical studies suggest that Growth plate senescence explains the phenomenon of Catch-up Growth. Growth-inhibiting conditions such as glucocorticoid excess and hypothyroidism delay the program of Growth plate senescence. Consequently, Growth plates are less senescent after these conditions resolve and therefore grow more rapidly than is normal for age, resulting in Catchup Growth.
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Catch up Growth after hypothyroidism is caused by delayed Growth plate senescence
Endocrinology, 2008Co-Authors: Rose Marino, Ola Nilsson, Anita Hegde, Kevin M Barnes, Lenneke Schrier, Joyce Emons, Jeffrey BaronAbstract:Catch-up Growth is defined as a linear Growth rate greater than expected for age after a period of Growth inhibition. We hypothesized that Catch-up Growth occurs because Growth-inhibiting conditions conserve the limited proliferative capacity of Growth plate chondrocytes, thus slowing the normal process of Growth plate senescence. When the Growth-inhibiting condition resolves, the Growth plates are less senescent and therefore grow more rapidly than normal for age. To test this hypothesis, we administered propylthiouracil to newborn rats for 8 wk to induce hypothyroidism and then stopped the propylthiouracil to allow Catch-up Growth. In untreated controls, the Growth plates underwent progressive, senescent changes in multiple functional and structural characteristics. We also identified genes that showed large changes in mRNA expression in Growth plate and used these changes as molecular markers of senescence. In treated animals, after stopping propylthiouracil, these functional, structural, and molecular senescent changes were delayed, compared with controls. This delayed senescence included a delayed decline in longitudinal Growth rate, resulting in Catch-up Growth. The findings demonstrate that Growth inhibition due to hypothyroidism slows the developmental program of Growth plate senescence, including the normal decline in the rate of longitudinal bone Growth, thus accounting for Catch-up Growth.
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impact of Growth plate senescence on Catch up Growth and epiphyseal fusion
Pediatric Nephrology, 2005Co-Authors: Ola Nilsson, Jeffrey BaronAbstract:In mammals, longitudinal bone Growth occurs rapidly in prenatal and early postnatal life, but then slows and eventually ceases. This deceleration, which reflects a decline in chondrocyte proliferation, was previously attributed to a hormonal or other systemic mechanism. However, new evidence suggests that it is due to a local mechanism within the Growth plate. In particular, recent findings suggest that Growth plate chondrocytes have a finite proliferative capacity that is gradually exhausted, causing Growth to slow and finally stop. This concept has provided insight into clinical phenomena including Catch-up Growth after transient Growth inhibition, Catch-down Growth after transient estrogen exposure, and epiphyseal fusion.
Umberto Simeoni - One of the best experts on this subject based on the ideXlab platform.
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54 effects of intrauterine Growth restriction and Catch up Growth on arterial blood pressure glucose tolerance and renal function in adult rats
Pediatric Research, 2005Co-Authors: Farid Boubred, Christophe Buffat, M Tsimaratos, C Oliver, J M Feuerstein, A Desobry, Martine Lelievrepegorier, Umberto SimeoniAbstract:Introduction: Low birth weight is associated with increased risk of arterial hypertension and metabolic diseases in adulthood. Rapid postnatal Catch-up Growth may constitute an additional risk factor. Aim: To investigate the effects of postnatal overfeeding (OF) after intrauterine Growth restriction (IUGR) in 12 month old, adult rats. Methods: 4 groups of animals were investigated: group I, controls: offspring of dams fed normal diet (NP, casein 22 %); group II: offspring of dams fed isocaloric low-protein diet (LP, casein 9 %); group III: postnatal OF (obtained by reduction of litter size); group IV: LP rats exposed to postnatal OF. Systolic blood pressure (SBP), glomerular number, renal function, fasting glycaemia and intraperitoneal glucose tolerance test were obtained Results: (mean +/- SEM). Offspring of dams fed LP diet had a 20 % birth weight and 38 % glomerular number reduction (p < 0.01). Catch-up Growth was associated with an elevated SBP from the age of 4 weeks (110 +/-3; 117 +/- 2; 116 +/- 3; 127 +/- 2 mmHg in groups NP, LP, OF, LP+OF rats respectively; p < 0.05). But the difference in SBP between LP and controls rats disappeared at the age of 12 months. Creatinine clearance decreased with age in LP+OF rats but reached statistical significance in males at 12 months (3.34 +/- 0.2; 4.26 +/-0.3; 4.61+/-1.6; 5.48 +/-1.6 ml/min/kg in LP+OF, LP, OF, controls respectively). Proteinuria was significantly higher in LP+OF rats than in controls at 4 months. At the age of 12 months, glucose tolerance was significantly altered in OF and LP+OF rats. Conclusion: Early Catch-up Growth in IUGR rats enhances alteration of SBP, glucose tolerance and renal function in adulthood. Early postnatal overfeeding may amplify single nephron hyperfiltration, and insulin-resistance associated with IUGR, resulting in cardiovascular and metabolic diseases at adulthood.
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36 effects of intrauterine Growth restriction iugr and postnatal Catch up Growth on arterial blood pressure bp glucose tolerance gt and renal function in adult rats
Pediatric Research, 2004Co-Authors: Farid Boubred, Christophe Buffat, M Pegorierlelievre, M Tsimaratos, C Oliver, Umberto SimeoniAbstract:36 Effects of Intrauterine Growth Restriction (Iugr) and Postnatal Catch-up Growth on Arterial Blood Pressure (Bp), Glucose Tolerance (Gt) and Renal Function in Adult Rats
Berit Kristrom - One of the best experts on this subject based on the ideXlab platform.
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gh dose reduction maintains normal prepubertal height velocity after initial Catch up Growth in short children
The Journal of Clinical Endocrinology and Metabolism, 2019Co-Authors: Ralph Decker, Kerstin Albertssonwikland, Berit Kristrom, Maria Halldin, Jan Gustafsson, Nilsosten Nilsson, Jovanna DahlgrenAbstract:Context GH responsiveness guides GH dosing during the Catch-up Growth (CUG) period; however, little is known regarding GH dosing during the prepubertal maintenance treatment period. Objective To evaluate whether SD score (SDS) channel parallel Growth with normal height velocity can be maintained after CUG by reducing the GH dose by 50% in children receiving doses individualized according to estimated GH responsiveness during the Catch-up period. Design and Settings Prepubertal children (n = 98; 72 boys) receiving GH during CUG (GH deficient, n = 33; non-GH deficient, n = 65), were randomized after 2 to 3 years to either a 50% reduced individualized dose (GHRID; n = 27; 20 boys) or unchanged individualized dose (GHUID; n = 38; 27 boys). Another 33 children (25 boys) continued a standard weight-based dose [43 µg/kg/d (GHFIX)]. Main Outcome Measures The primary endpoint was the proportion of children with ΔheightSDS within ±0.3 at 1 year after GH dose reduction compared with two control groups: GHUID and GHFIX. The hypothesis was that heightSDS could be maintained within ±0.3 with a reduced individualized GH dose. Results For the intention-to-treat population at 1 year, 85% of the GHRIDgroup maintained ΔheightSDS within ±0.3 vs 41% in the GHUIDgroup (P = 0.0055) and 48% in the GHFIXgroup (P = 0.0047). The ΔIGF-ISDS in the GHRID group was -0.75 ± 1.0 at 3 months (P = 0.003) and -0.72 ± 1.2 at 1 year compared with the GHUID group (0.15 ± 1.2; P = 0.005) and GHFIX group (0.05 ± 1.0; P = 0.02). Conclusions Channel parallel Growth (i.e., normal height velocity) and IGF-ISDS levels within ±2 were maintained after completed CUG using a 50% lower individualized dose than that used during the CUG period.
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Growth hormone gh dosing during Catch up Growth guided by individual responsiveness decreases Growth response variability in prepubertal children with gh deficiency or idiopathic short stature
The Journal of Clinical Endocrinology and Metabolism, 2009Co-Authors: Berit Kristrom, Maria Halldin, Jan Gustafsson, Nilsosten Nilsson, Jovanna Dahlgren, Stefan A Aronson, Sten A Ivarsson, Johan Svensson, T TuvemoAbstract:CONTEXT: Weight-based GH dosing results in a wide variation in Growth response in children with GH deficiency (GHD) or idiopathic short stature (ISS). OBJECTIVE: The hypothesis tested was whether individualized GH doses, based on variation in GH responsiveness estimated by a prediction model, reduced variability in Growth response around a set height target compared with a standardized weight-based dose. SETTING: A total of 153 short prepubertal children diagnosed with isolated GHD or ISS (n = 43) and at least 1 SD score (SDS) below midparental height SDS (MPH(SDS)) were included in this 2-yr multicenter study. INTERVENTION: The children were randomized to either a standard (43 microg/kg.d) or individualized (17-100 microg/kg.d) GH dose. MAIN OUTCOME MEASURE: We measured the deviation of height(SDS) from individual MPH(SDS) (diffMPH(SDS)). The primary endpoint was the difference in the range of diffMPH(SDS) between the two groups. RESULTS: The diffMPH(SDS) range was reduced by 32% in the individualized-dose group relative to the standard-dose group (P < 0.003), whereas the mean diffMPH(SDS) was equal: -0.42 +/- 0.46 and -0.48 +/- 0.67, respectively. Gain in height(SDS) 0-2 yr was equal for the GH-deficient and ISS groups: 1.31 +/- 0.47 and 1.36 +/- 0.47, respectively, when ISS was classified on the basis of maximum GH peak on the arginine-insulin tolerance test or 24-h profile. CONCLUSION: Individualized GH doses during Catch-up Growth significantly reduce the proportion of unexpectedly good and poor responders around a predefined individual Growth target and result in equal Growth responses in children with GHD and ISS.