Progression In Adulthood Research Articles

Different glaucoma progression rates by age groups in young myopic glaucoma patients

We aimed to investigate the age-related glaucoma progression rates in myopic normal tension glaucoma (NTG). In this long-term retrospective cohort (7.2 ± 3.5 years), we grouped patients based on their age at initial presentation: group A (age < 30 years, 60 eyes), group B (30 ≤ age < 40, 66 eyes), and group C (40 ≤ age < 50 years, 63 eyes). We used a linear mixed-effects model to estimate retinal nerve fiber layer (RNFL) defect width enlargement rates. Group A showed a significantly faster rate of RNFL defect progression (3.01 ± 1.74°/year) than those of groups B and C (2.05 ± 1.55°/year and 2.06 ± 1.29°/year, P = 0.004 and 0.002). The difference was more marked when calculated for the first 10 years of follow-up in group A, B, and C (3.95 ± 2.70°/year, 2.39 ± 1.64°/year, and 1.98 ± 1.31°/year), and between the periods of age < 30 years, 30 ≤ age < 40 years, and 40 ≤ age < 50 years within group A. This is the first evidence of rapid glaucoma progression in the young adulthood and stabilization in older age in myopic NTG. Clinicians should consider the potentially aggressive course of glaucoma, especially in younger patients with myopic NTG, in contrast to the general slow progression in adulthood.

Factors influencing myopia stabilisation in young myopic adult Singaporeans

PurposeTo evaluate factors influencing stabilisation of myopia in the Singapore Cohort of Risk factors for Myopia.MethodsWe evaluated the longitudinal natural history of 424 myopic participants from 1999 to 2022. The...

Characterization of Vps13b-mutant mice reveals neuroanatomical and behavioral phenotypes with females less affected

The vacuolar protein sorting-associated protein 13B (VPS13B) is a large and highly conserved protein. Disruption of VPS13B causes the autosomal recessive Cohen syndrome, a rare disorder characterized by microcephaly and intellectual disability among other features, including developmental delay, hypotonia, and friendly-personality. However, the underlying mechanisms by which VPS13B disruption leads to brain dysfunction still remain unexplained.To gain insights into the neuropathogenesis of Cohen syndrome, we systematically characterized brain changes in Vps13b-mutant mice and compared murine findings to 235 previously published and 17 new patients diagnosed with VPS13B-related Cohen syndrome.We showed that Vps13b is differentially expressed across brain regions with the highest expression in the cerebellum, the hippocampus and the cortex with postnatal peak. Half of the Vps13b−/− mice die during the first week of life. The remaining mice have a normal lifespan and display the core phenotypes of the human disease, including microcephaly, growth delay, hypotonia, altered memory, and enhanced sociability. Systematic 2D and 3D brain histo-morphological analyses reveal specific structural changes in the brain starting after birth. The dentate gyrus is the brain region with the most prominent reduction in size, while the motor cortex is specifically thinner in layer VI. The fornix, the fasciculus retroflexus, and the cingulate cortex remain unaffected. Interestingly, these neuroanatomical changes implicate an increase of neuronal death during infantile stages with no progression in adulthood suggesting that VPS13B promotes neuronal survival early in life. Importantly, whilst both sexes were affected, some neuroanatomical and behavioral phenotypes were less pronounced or even absent in females. We evaluate sex differences in Cohen patients and conclude that females are less affected both in mice and patients.Our findings provide new insights about the neurobiology of VPS13B and highlight previously unreported brain phenotypes while defining Cohen syndrome as a likely new entity of non-progressive infantile neurodegeneration.

Shared Molecular Mechanisms among Alzheimer's Disease, Neurovascular Unit Dysfunction and Vascular Risk Factors: A Narrative Review.

Alzheimer’s disease (AD) is the most common type of dementia, affecting 24 million individuals. Clinical and epidemiological studies have found several links between vascular risk factors (VRF), neurovascular unit dysfunction (NVUd), blood-brain barrier breakdown (BBBb) and AD onset and progression in adulthood, suggesting a pathogenetic continuum between AD and vascular dementia. Shared pathways between AD, VRF, and NVUd/BBB have also been found at the molecular level, underlining the strength of this association. The present paper reviewed the literature describing commonly shared molecular pathways between adult-onset AD, VRF, and NVUd/BBBb. Current evidence suggests that VRF and NVUd/BBBb are involved in AD neurovascular and neurodegenerative pathology and share several molecular pathways. This is strongly supportive of the hypothesis that the presence of VRF can at least facilitate AD onset and progression through several mechanisms, including NVUd/BBBb. Moreover, vascular disease and several comorbidities may have a cumulative effect on VRF and worsen the clinical manifestations of AD. Early detection and correction of VRF and vascular disease by improving NVUd/BBBd could be a potential target to reduce the overall incidence and delay cognitive impairment in AD.

Subclinical Atherosclerosis Progression in Obese Children with Relevant Cardiometabolic Risk Factors Can Be Assessed through Carotid Intima Media Thickness

Given the growing obesity rates among children, a more complete evaluation of their potential cardiometabolic risk is needed. Carotid intima-media thickness (CIMT), a marker of endothelial distress and a predictor of atherosclerotic progression in adulthood, may complete the day-to-day evaluation of children at risk. Multiple risk factors act as additional precipitant causes of atherosclerosis. We analyzed 60 patients aged 6–17 years old by measuring their CIMT using the Aixplorer MACH 30 echography machine automatic measurement software. All subjects were clinically and anamnestically assessed to identify risk factors. CIMT values are significantly higher in older children and boys. Over 20 kg weight gain during pregnancy and other at-risk disorders (p = 0.047), family history of cardiovascular risk (p = 0.049), hypertension (p = 0.012), and smoking (p = 0.015) are linked to increased CIMT. Our study also supports international data on artificial postnatal nutrition, high/low birth weight, and sedentary lifestyle being linked to increased CIMT. Significant correlations were detected between CIMT and the entire lipid panel. Weight excess and abdominal adiposity in children is clearly linked to increased CIMT. Moreover, waist circumference and TG/HDL-c are significant predictors of CIMT. Although each parameter of the lipid panel is correlated to CIMT, fasting glucose is not.

Progression of a supra-valvular aortic stenosis in adulthood during 13 years

Supra-valvular aortic stenosis is a congenital condition that rarely progresses in adulthood [1]. Here, we presented a rare case of supra-valvular aortic stenosis progression in adulthood. A 27-yea...

Sporadic late-onset nemaline myopathy with monoclonal gammopathy of undetermined significance: Report of four patients

Sporadic late-onset nemaline myopathy (SLONM) is a rare, acquired muscle disease presenting with subacute progression in adulthood. It can be accompanied by a monoclonal gammopathy of undetermined significance (MGUS). We describe clinical and histopathological findings of four SLONM patients with MGUS. In all patients, nemaline rod, inter-myofibrillary network disruption, atrophic changes, peripheral basophilic discoloration, vacuole without rim, and cytoplasmic body without inflammation were seen. Three out of four patients were treated with prednisolone in combination with IVIG monthly and had an appropriate response to the treatment. The optimal first-line treatment remains unclear in SLONM-MGUS, although corticosteroids plus IVIg is associated with favorable clinical response. These treatment modalities might be used as an optional treatment before autologous stem cell transplantation; however, further studies with a higher number of patients are required.

Clinical Course of Extracranial Arteriovenous Malformations.

Despite many advances in the knowledge of vascular malformations, extracranial arteriovenous malformations (AVMs) remain an enigma and are usually misdiagnosed and mismanaged due to their associated rare morbidity. This study aimed to describe the clinical course and emphasize the progressive nature of AVMs through a retrospective study of 446 patients. Patients with cutaneous and soft-tissue AVMs presenting to our Vascular Anomalies Center between March 2011 and March 2017 were reviewed. Medical records were examined for disease course, age at first presentation at our institution, distributions and locations of lesions, clinical staging, progression, and previous treatments. Progression was defined as advancement to a higher Schobinger stage from a lower stage. A total of 446 patients (mean age, 25.6 ± 14.0 years) were enrolled in this study, including 232 (52.0%) males (gender ratio, 1.08:1). Arteriovenous malformations lesions in 76.7% (342/446) of the patients were located in the head and neck. Children with Stage I AVMs had a 41.9% risk of progression before adolescence and an 80.0% risk of progression before adulthood. Nearly all patients (96.2%) showed progression in adulthood. Diffuse lesions were more likely to progress than localized lesions (P < 0.05) in childhood and adolescence. Lesions in the head and neck regions were less likely to progress than those in other regions in childhood (P = 0.005). A total of 216 (48.4%) patients had undergone previous treatments. Among these patients, bleomycin showed an unintentional positive effect in the treatment of AVMs. Extracranial AVMs have a continuously progressive nature. A full understanding regarding the progressive course of AVMs can lead patients and physicians to attach importance to early diagnosis and management. Meanwhile exploring innovative treatments should be focused in the future to prevent potential destructive progression.

Effect of genetic background on the cardiac phenotype in a mouse model of Emery-Dreifuss muscular dystrophy

A-type lamins gene (LMNA) mutations cause an autosomal dominant inherited form of Emery-Dreifuss muscular dystrophy (EDMD). EDMD is characterized by slowly progressive muscle weakness and wasting and dilated cardiomyopathy, often leading to heart failure-related disability. EDMD is highly penetrant with poor prognosis and there is currently no specific therapy available. Clinical variability ranges from early onset with severe presentation in childhood to late onset with slow progression in adulthood. Genetic background is a well-known factor that significantly affects phenotype in several mouse models of human diseases. This phenotypic variability is attributed, at least in part, to genetic modifiers that regulate the disease process. To characterize the phenotype of A-type lamins mutation on different genetic background, we created and phenotyped C57BL/6JRj-LmnaH222P/H222P mice (C57Lmnap.H222P) and compared them with the 129S2/SvPasCrl-LmnaH222P/H222P mice (129Lmnap.H222P). These mouse strains were compared with their respective control strains at multiple time points between 3 and 10 months of age. Both contractile and electrical cardiac muscle functions, as well as survival were characterized. We found that 129Lmnap.H222P mice showed significantly reduced body weight and reduced cardiac function earlier than in the C57Lmnap.H222P mice. We also revealed that only 129Lmnap.H222P mice developed heart arrhythmias. The 129Lmnap.H222P model with an earlier onset and more pronounced cardiac phenotype may be more useful for evaluating therapies that target cardiac muscle function, and heart arrhythmias.

324 An Initial Description of Adult Men With Progression Of Chordee To A Fibrotic Disorder Of The Tunica Albuginea

Congenital curvature from chordee without hypospadias involves excessive tunical elasticity, whereas Peyronie's disease (PD) involves acquired tunica albuginea fibrosis. We describe a subpopulation of men with congenital curvature from chordee who experienced curvature progression in adulthood. Retrospective review of all patients (>18 years of age) with chordee without hypospadias presenting to our center from 1/2015-7/2016 for evaluation of worsening curvature. Ten patients were evaluated (mean age 34.0 years, SD 13.7), most commonly presenting with worsening deformity causing cosmetic distress as well as compromised ability to engage in intercourse, and/or partner discomfort. Patients described a mean subjective curvature of 51.5° (SD 21.1°), pain (30%), hinge effect (10%), shortening (20%), and poor erection quality (10%). There were no reported traumatic events preceding worsening curvature. Reduced shaft elasticity was identified in 70% with palpable areas of fibrosis including septal cord or tunical thickening. Stretched penile length was 11.9 cm (SD 1.9). Via in-office artificial erection, 60% had a maximum rigidity score of 8-9/10 with 55.5° mean curvature (SD 17.9°, range 30.0-90.0°). Ventral curvature was present in 70%, 40% had narrowing, and there was no noted hinge, calcification or corporal fibrosis. Seven patients elected to undergo tunica albuginea plication (TAP). All 7 patients noted satisfaction with the result, were functionally straight (<15° residual curvature), and had no change in erectile function. Pain resolved following TAP in the two patients that initially presented with pain. The median decrease in stretched penile length at initial postoperative visit was 0.75 cm (range 1.0-2.0 cm), however, no patients reported significant penile shortening. Traction therapy was recommended to restore preoperative penile length. One patient with erectile dysfunction (57 years old) underwent placement of a 3 piece inflatable penile prosthesis and manual modeling, with straight, satisfactory erections postoperatively.

Actions of Estrogenic Endocrine Disrupting Chemicals on Human Prostate Stem/Progenitor Cells and Prostate Carcinogenesis

Substantial evidences from epidemiological and animal-based studies indicate that early exposure to endocrine disrupting chemicals (EDCs) during the developmental stage results in a variety of disorders including cancer. Previous studies have demonstrated that early estrogen exposure results in life-long reprogramming of the prostate gland that leads to an increased incidence of prostatic lesions with aging. We have recently documented that bisphenol A (BPA), one of the most studied EDCs with estrogenic activity has similar effects in increasing prostate carcinogenic potential, supporting the connection between EDCs exposure and prostate cancer risk. It is well accepted that stem cells play a crucial role in development and cancer. Accumulating evidence suggest that stem cells are regulated by extrinsic factors and may be the potential target of hormonal carcinogenesis. Estrogenic EDCs which interfere with normal hormonal signaling may perturb prostate stem cell fate by directly reprogramming stem cells or breaking down the stem cell niche. Transformation of stem cells into cancer stem cells may underlie cancer initiation accounting for cancer recurrence, which becomes a critical therapeutic target of cancer management. We therefore propose that estrogenic EDCs may influence the development and progression of prostate cancer through reprogramming and transforming the prostate stem and early stage progenitor cells. In this review, we summarize our current studies and have updated recent advances highlighting estrogenic EDCs on prostate carcinogenesis by possible targeting prostate stem/progenitor cells. Using novel stem cell assays we have demonstrated that human prostate stem/progenitor cells express estrogen receptors (ER) and are directly modulated by estrogenic EDCs. Moreover, employing anin vivohumanized chimeric prostate model, we further demonstrated that estrogenic EDCs initiate and promote prostatic carcinogenesis in an androgen-supported environment. These findings support our hypothesis that prostate stem/progenitor cells may be the direct targets of estrogenic EDCs as a consequence of developmental exposure which carry permanent reprogrammed epigenetic and oncogenic events and subsequently deposit into cancer initiation and progression in adulthood.

Reply from Author: Missing the Forest for the Trees

We thank Dr Ong Siew Chey for his sincere comments. He opines that professional behaviour is a refl ection of an innate character trait, that behaviour is shaped early and is diffi cult to modify later, and that there are 3 ways of making doctors conform to professional norms. We would like to reframe the issue as this traditional view oversimplifi es and limits the appreciation of the complex problem of professionalism. Firstly, the pessimistic notion that ethical/moral behaviours are hard to change with increasing seniority is fortunately refuted by evidence. Advances in moral reasoning increase with age throughout a person’s lifespan, and this progression in adulthood is correlated with education. 1 Secondly, even though character traits do infl uence professional behaviour, these traits are but one of several factors infl uencing professionalism when we take a systems perspective. 2,3 Organisational culture is another component of the system infl uencing professional behaviours. 3 In psychology, the phenomenon of “moral elevation” describes how others are motivated to behave ethically when they see others doing likewise. 4 Regardless of a person’s traits, an institutional culture of ethical behaviour is another system component that can promote professional behaviour in both senior and junior doctors.

G.P.284: Dysferlinopathy caused by protein misfolding: The novel murine animal model Dysf-MMex38

Limb-girdle muscular dystrophy 2B (LGMD2B) is caused by mutations in the dysferlin gene (DYSF). There are no mutational hotspots. Approximately one third of all mutations are missense mutations causing misfolding and protein aggregation, premature degradation and amyloid formation. There is no therapy. We could show that by treating patients’ primary myotubes with short dysferlin-specific peptides the endogenous produced missense mutant dysferlin can be relocated to the sarcolemma. There, it regains its proper function as a membrane repair protein. The human missense mutation DYSF p.L1341P causes all characteristics of a protein misfolding disease in dysferlinopathy. We therefore generated the first knock-in mouse model carrying the analogous murine missense mutation in exon 38 (Dysf p.L1360P, NP_001071162.1) named MMex38 (B6;129P2-Dysftm1.1Mdcb). Natural disease course was investigated at 8, 13 and 21 weeks of age (n = 36). We performed body composition, analyzed treadmill performance and voluntary running as well as protein analysis and histology of proximal and distal muscles. Evaluation of ER stress and membrane resealing assays complete the assessment. The targeted mutation leads to a dystrophic phenotype in 13 week old mice with a continuous disease progression in adulthood. Total body weight of 21 week old MMex38 was increased compared to WT controls without changes in the percentage of fat, free body fluid and lean tissue. Three weeks of treadmill exercise exposed significant endurance impairment in 19 to 21 week old MMex38 compared to controls. Histology revealed a distinct dystrophic pattern in 13 week old MMex38 and number of necrotic and regenerating fibres increased highly significant with age. In the immunofluorescence no dysferlin was detected at the sarcolemma. The successful generation of an animal model for protein misfolding in dysferlinopathy allows the investigation of pharmacokinetics and -dynamics of dysferlin-derived peptides in vivo.

Progressive adult antimetropia

Antimetropia, a sub‐classification of anisometropia, is a rare refractive condition in which one eye is myopic and the fellow eye is hyperopic. This case report describes the ocular characteristics and atypical refractive progression in an adult male with a moderate degree of non‐amblyopic antimetropia over a 20‐year period. The potential mechanisms underlying unilateral axial elongation, anisometropia and myopia progression in adulthood are discussed.

Main findings from the prospective Cardiovascular Risk in Young Finns Study

To provide a comprehensive overview on the main findings from the Cardiovascular Risk in Young Finns Study. This prospective multicenter study initiated in 1980 (N = 3596, baseline age 3-18 years) has followed up study participants over 30 years to investigate childhood risk factors for cardiometabolic outcomes in adulthood. Childhood BMI, socioeconomic status, parental risk factor status, as well as genetic polymorphisms are independent predictors of adult obesity, hypertension, and dyslipidemia. Results from the Young Finns Study and other follow-up studies have shown that conventional childhood risk factors, such as dyslipidemia, obesity, elevated blood pressure and smoking, are predictive of subclinical atherosclerosis in young adults. Recent findings suggest that childhood lifestyle (diet, physical activity) is associated with subclinical atherosclerosis and its progression in adulthood. Concerning the timing of risk factor measurements, they seem to be predictive of adult atherosclerosis from the age of 9 onwards. From a clinical point of view, a recent observation suggesting that the adverse cardiometabolic effects of childhood overweight/obesity are reversed among those who become nonobese adults, provides optimism during the days of obesity epidemic. Current data suggest that childhood risk factors are associated with higher risk of subclinical atherosclerosis in adulthood. Future studies among aging cohorts followed since childhood will provide data on their influence on clinical cardiovascular outcomes.

The embodiment of adverse childhood experiences and cancer development: potential biological mechanisms and pathways across the life course.

To explore current evidence of the physiological embedding of stress to discuss whether adverse childhood experiences (ACE) causing chronic or acute stress responses may alter fundamental biological functions. A non-systematic review of the literature was carried out using keyword searches in Pubmed and the web of science from May to October 2011. In reference to the literature identified, we examine the potential biological pathways potentially linking exposure to ACE and cancer development and progression in adulthood. These mechanisms, in interaction with social position, and mediated by subsequent environmental exposures, may ultimately lead to the development of cancer. The experience of acute or chronic stressors during sensitive periods of childhood development which can induce several known biological responses, are likely to have an impact on subsequent biological and behavioural functions depending on the timing of initial exposures, and subsequently mediated by later exposures. For this reason, childhood exposure to adversity is a likely source of both acute and chronic stressors, and can be examined as an important initial exposure on a pathway towards adult ill health. Such pathways justify a life course approach to understanding cancer aetiology, which may have its origins early in life.

A Novel Movement Disorder in Related Male Labrador Retrievers Characterized by Extreme Generalized Muscular Stiffness

To describe the clinical phenotype of a new motor disorder in Labrador Retrievers. Case series study. Seven young male Labrador Retrievers presented for evaluation of stiff gait. All affected dogs had generalized muscular stiffness, persistent at rest and resulting in restricted joint movements. They showed a forward flexed posture, festinating gait, and bradykinesia. Signs developed between 2 and 16 months of age and tended to stabilize in adulthood. Needle electromyogram in the conscious state showed continuous motor unit activity in resting epaxial and proximal limb muscles. This activity was abolished by general anesthesia. Muscle and nerve histopathology was normal. In 2 dogs necropsied, astrocytosis was evident throughout the spinal cord gray matter, reticular formation and caudate nuclei. Decreased neuronal counts were selectively found in the spinal cord Rexed's lamina VII, but not in VIII and IX. Pedigree analysis showed that the affected dogs were from 5 related litters. This new hypertonicity syndrome in Labrador Retrievers is unique because of the selective distribution of the histological lesions, the lack of progression in adulthood, and its exclusive occurrence in male dogs. Pedigree analysis suggests an X-linked hereditary disease, although other modes of inheritance cannot be ruled out with certainty. We hypothesize that altered output from basal nuclei and reticular formation together with motor neuron disinhibition caused by a decreased number of spinal cord interneurons leads to the muscular stiffness.

Extracranial Arteriovenous Malformations: Natural Progression and Recurrence after Treatment

Arteriovenous malformation is a dynamic vascular anomaly; it expands with age and after treatment. This study analyzed the pattern of arteriovenous malformation progression and frequency of recurrence after therapy. Patients with cutaneous and soft-tissue arteriovenous malformation were reviewed. Progression was defined as advancement to a higher Schobinger stage (I through IV) before treatment. Recurrence was defined as expansion following embolization or resection. The effect of sex, location, size, adolescence, pregnancy, and stage on progression or recurrence was analyzed. The study included 272 patients. Children with stage I arteriovenous malformation had a 43.8 percent risk of progression before adolescence and an 82.6 percent risk before adulthood; the remaining children had progression in adulthood. Progression was more common during adolescence (56.0 percent; 95 percent confidence interval, 46.5 to 65.2) compared with childhood (38.8 percent; 95 percent confidence interval, 32.4 to 45.4) (p = 0.002). The average age at progression was 12.7 +/- 11.1 years. Diffuse arteriovenous malformations were more likely to progress compared with localized lesions (p < 0.001). Sex (p = 0.46), location (p = 0.36), and pregnancy (p = 0.20) did not influence expansion. Resection (with or without embolization) had a lower recurrence rate (81 percent) and longer time to recurrence (42.7 percent >1 year), compared with embolization alone (98 percent and 14.4 percent >1 year, respectively) (p < 0.001). Recurrence was less likely when lower staged lesions were treated (p < 0.001) and did not correlate with sex (p = 0.10), location (p = 0.60), size (p = 0.07), or age (p = 0.21). Arteriovenous malformation is likely to progress before adulthood, particularly during adolescence, and usually reexpands following treatment. Resection (with or without embolization) for lower staged or localized arteriovenous malformation offers the best chance for long-term control.

IDIOPATHIC SCOLIOSIS

Idiopathic scoliosis (IS) most commonly develops during adolescence, but may present at any age from infancy through adulthood. Patients with IS are evaluated clinically and radiographically to determine whether the deformity is, in fact, idiopathic, to elucidate any symptoms related to the scoliosis, and to characterize the deformity itself. In patients who have not yet reached skeletal maturity, the treatment of IS is often prophylactic, with the aim of preventing the curve from reaching a magnitude that would make continued progression in adulthood likely. Adult patients with IS are most frequently treated because of symptoms, usually back or leg pain. IS is typically treated with anterior or posterior spinal fusion; treatment of very young patients is complicated by the need to allow growth to continue while controlling the scoliosis.

Why do we treat adolescent idiopathic scoliosis? What we want to obtain and to avoid for our patients. SOSORT 2005 Consensus paper

BackgroundMedicine is a scientific art: once science is not clear, choices are made according to individual and collective beliefs that should be better understood. This is particularly true in a field like adolescent idiopathic scoliosis, where currently does not exist definitive scientific evidence on the efficacy either of conservative or of surgical treatments.Aim of the studyTo verify the philosophical choices on the final outcome of a group of people believing and engaged in a conservative treatment of idiopathic scoliosis.MethodsWe performed a multifaceted study that included a bibliometric analysis, a questionnaire, and a careful Consensus reaching procedure between experts in the conservative treatment of scoliosis (SOSORT members).ResultsThe Consensus reaching procedure has shown to be useful: answers changed in a statistically significant way, and 9 new outcome criteria were included. The most important final outcomes were considered Aesthetics (100%), Quality of life and Disability (more than 90%), while more than 80% of preferences went to Back Pain, Psychological well-being, Progression in adulthood, Breathing function, Scoliosis Cobb degrees (radiographic lateral flexion), Needs of further treatments in adulthood.DiscussionIn the literature prevail outcome criteria driven by the contingent treatment needs or the possibility to have measurement systems (even if it seems that usual clinical and radiographic methods are given much more importance than more complex Disability or Quality of Life instruments). SOSORT members give importance to a wide range of outcome criteria, in which clinical and radiographic issues have the lowest importance.ConclusionWe treat our patients for what they need for their future (Breathing function, Needs of further treatments in adulthood, Progression in adulthood), and their present too (Aesthetics, Disability, Quality of life). Technical matters, such as rib hump or radiographic lateral alignment and rotation, but not lateral flexion, are secondary outcomes and only instrumental to previously reported primary outcomes. We advocate a multidimensional, comprehensive evaluation of scoliosis patients, to gather all necessary data for a complete therapeutic approach, that goes beyond x-rays to reach the person and the family.