Growth on stimulant medication; clarifying the confusion: A review

Western Clinical School, Nepean Campus, The University of Sydney, Australia.
Archives of Disease in Childhood (Impact Factor: 2.9). 09/2005; 90(8):801-6. DOI: 10.1136/adc.2004.056952
Source: PubMed


To get an overview of the studies of growth in height in children with attention deficit hyperactivity disorder (ADHD) treated with stimulant medication, to establish the consistencies and to try to resolve the discrepancies.
Twenty nine studies were reviewed following a Medline search: 22 related to children, six to late adolescents or adults, and one to children and adults.
Children: Eleven studies gave results consistent with height attenuation on stimulant medication: eight were longitudinal, one was cross-sectional, and two showed growth rebound on ceasing medication. Studies with negative findings were inadequately powered (n = 3), lacked controls or statistical analysis (n = 3), measured height velocity without reference to treatment duration (n = 2), or used inappropriate growth parameters (n = 1), controls (n = 1), or normative data (n = 1). Late adolescents/adults treated with stimulant medication in childhood: Two studies associated childhood gastrointestinal side effects with attenuated late adolescent or adult height; all six cross-sectional studies had negative findings. The methodologies varied widely but there was some consistency in the degree of attenuation shown in studies with positive findings. The most sensitive methods analysed the changes in z-scores (standard deviation scores) or calculated the height deficits from paired measurements taken before and after an initial period of treatment with stimulant medication. The height deficit amounted to approximately 1 cm/year during the first 1-3 years of treatment.
Further research is needed into the causal mechanisms, the rate of physical maturation, and the long term implications for final stature.

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    • "It has been reported that temporary discontinuation of treatment – the so called " drug holiday " – reverses therapy-related retardation in growth, and that children thus reach the age-specifi c expected growth curve (Ma et al. 1996; Poulton 2005). However, it is also known that the drug holiday might lead to problems for both the child and family by causing re-exacerbation of ADHD symptoms. "
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    ABSTRACT: Objectives: We aimed to explore whether the use of methylphenidate relates leptin, ghrelin, adiponectin, and brain-derived neurotrophic factor (BDNF). In addition, the relationship between methylphenidate-related weight loss in attention deficit hyperactivity disorder (ADHD) patients and these biomolecules were evaluated. Methods: Thirty ADHD patients receiving methylphenidate and 20 healthy controls were included. Leptin, ghrelin, adiponectin, and BDNF levels were measured at baseline and after two-month treatment in both groups. Results: At baseline, leptin, ghrelin, adiponectin, and BDNF levels were similar in the ADHD and control groups. The most common adverse events occurring in the ADHD group after a 2-month treatment period included loss of appetite (70%) and weight loss (66.7%). A significant difference was found in body weight, BMI, and CGI scores of the ADHD patients after the treatment. While post-treatment ghrelin and adiponectin levels were significantly higher in the ADHD group, BDNF level was significantly lower. Post-treatment decrease in leptin levels was not significant. Conclusions: Leptin and BDNF were not associated with poor appetite and/or weight loss due to methylphenidate treatment. However, ghrelin and adiponectin might be biomolecules that play a role in underlying neurobiological mechanisms of methylphenidate-related appetite or weight loss.
    International Journal of Psychiatry in Clinical Practice 07/2014; 18(4):1-34. DOI:10.3109/13651501.2014.940054 · 1.39 Impact Factor
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    • "metilfenidato) ha generando gran controversia. Varios autores sugieren que esta medicación podría causar retraso del crecimiento (Swanson et al., 2007; Charach, Figueroa, Chen, Ickowicz, y Schachar, 2006; Poulton, 2005), otros dicen que no hay tal relación (Pliszka, Matthews, Braslow y Watson, 2006; Spencer et al., 2006; Biederman et al., 2003; Sund y Zeiner, 2002), e investigaciones recientes apuntan que este tratamiento puede producir retraso mental o problemas cardiovasculares (Fung y Lee, 2009; Montañes, Gangoso y Martinez, 2009; Adler, 2008). Esta polémica ha provocado que algunas familias se muestren recelosas al tratamiento farmacológico de un trastorno que está causando serios problemas en diferentes ámbitos de la vida de los niños (académico, familiar, social...). "
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    ABSTRACT: The purpose of this study was to review the scientific literature on the influence of physical exercise in subjects with Attention Deficit Hyperactivity Disorder (ADHD) to propose how physical education may contribute to the treatment of this disorder. ADHD is causing diverse personal, family and academic problems. It is thought to have a multicomponent etiology, probably organic in origen with neurological, genetic, hormonal and environmental factors. Its main symptoms are inattention, hyperactivity, impulsivity, and very often, conduct disorders. Motor skills and personal relationships are often also affected. According to several sources, treatment should be pharmacological and also based in behavioral and psychoeducational intervention. The recent studies suggest that physical activity improves the core symptoms of ADHD and also that beneficts the executive function, inhibitory control, neurocognitive performance, behavior, motor skills, social, cognitive performance and academic performance of children with ADHD.
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    • "These results are consistent with previously reported evidence that psychostimulants are associated with loss of appetite and weight loss. One systematic review reported that children treated with psychostimulants showed a height deficit of approximately 1 cm/year during the first 1–3 years of treatment [39] and clinical guidelines recommend that patients receiving ADHD medication are monitored for weight, height, BMI and appetite every 6 months [40, 41]. High calorific snacks, late evening meals, dosing after meals, drug holidays, or switching to a different class or formulation of medication may be beneficial in some patients [41]. "
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    ABSTRACT: The aim of this study was to compare the efficacy and safety of the prodrug psychostimulant lisdexamfetamine dimesylate (LDX) and the non-stimulant noradrenergic compound atomoxetine (ATX) in children and adolescents with attention-deficit/hyperactivity disorder (ADHD) who had previously responded inadequately to methylphenidate (MPH). This 9-week, head-to-head, randomized, double-blind, active-controlled study (SPD489-317; NCT01106430) enrolled patients (aged 6-17 years) with at least moderately symptomatic ADHD and an inadequate response to previous MPH therapy. Patients were randomized (1:1) to an optimized daily dose of LDX (30, 50 or 70 mg) or ATX (patients <70 kg, 0.5-1.2 mg/kg with total daily dose not to exceed 1.4 mg/kg; patients ≥70 kg, 40, 80 or 100 mg). The primary efficacy outcome was time (days) to first clinical response. Clinical response was defined as a Clinical Global Impressions-Improvement (CGI-I) score of 1 (very much improved) or 2 (much improved). Secondary efficacy outcomes included the proportion of responders at each study visit and the change from baseline in ADHD Rating Scale (ADHD-RS-IV) and CGI-Severity scores. Tolerability and safety were assessed by monitoring treatment-emergent adverse events (TEAEs), height and weight, vital signs and electrocardiogram parameters. Endpoint was defined as the last post-baseline, on-treatment visit with a valid assessment. Of 267 patients randomized (LDX, n = 133; ATX, n = 134), 200 (74.9 %) completed the study. The median time to first clinical response [95 % confidence interval (CI)] was significantly shorter for patients receiving LDX [12.0 days (8.0-16.0)] than for those receiving ATX [21.0 days (15.0-23.0)] (p = 0.001). By week 9, 81.7 % (95 % CI 75.0-88.5) of patients receiving LDX had responded to treatment compared with 63.6 % (95 % CI 55.4-71.8) of those receiving ATX (p = 0.001). Also by week 9, the difference between LDX and ATX in least-squares mean change from baseline (95 % CI) was significant in favour of LDX for the ADHD-RS-IV total score [-6.5 (-9.3 to -3.6); p < 0.001; effect size 0.56], inattentiveness subscale score [-3.4 (-4.9 to -1.8); p < 0.001; effect size 0.53] and the hyperactivity/impulsivity subscale score [-3.2 (-4.6 to -1.7); p < 0.001; effect size 0.53]. TEAEs were reported by 71.9 and 70.9 % of patients receiving LDX and ATX, respectively. At endpoint, both treatments were associated with mean (standard deviation) increases in systolic blood pressure [LDX, +0.7 mmHg (9.08); ATX, +0.6 mmHg (7.96)], diastolic blood pressure [LDX, +0.1 mmHg (8.33); ATX, +1.3 mmHg (8.24)] and pulse rate [LDX, +3.6 bpm (10.49); ATX, +3.7 bpm (10.75)], and decreases in weight [LDX, -1.30 kg (1.806); ATX, -0.15 kg (1.434)]. LDX was associated with a faster and more robust treatment response than ATX in children and adolescents with at least moderately symptomatic ADHD who had previously responded inadequately to MPH. Both treatments displayed safety profiles consistent with findings from previous clinical trials.
    CNS Drugs 08/2013; 27(12). DOI:10.1007/s40263-013-0104-8 · 5.11 Impact Factor
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