Deceleration Of Linear Growth Research Articles

Bringing nutritional ketosis to the table as an option for healing the pediatric brain.

Our core premise is that personalized variations of a ketogenic diet are likely to benefit pediatric patients with neuropsychiatric symptoms across multiple domains. Although pediatric epilepsy is currently a well-accepted indication for a strict ketogenic diet, there is a dearth of knowledge and therefore clinical guidelines upon which to recommend nutritional ketosis for pervasive pediatric conditions such as autism spectrum disorder and ADHD, even when comorbid epilepsy is present. However, there are published cohort studies and current clinical trials implementing medical ketogenic therapies for cognitive impairment, psychiatric comorbidities, motor disability, and even neuroinflammation. As holistic practitioners, it is imperative that we consider the health of a child in its entirety - and additionally offer the ketogenic diet as a therapeutic option when it may be synergistic in treating extra-neurologic diseases such as obesity. While there are uniquely pediatric potential adverse side effects such as linear growth deceleration and micronutrient deficiencies, previous trials in epilepsy and our center's experience have already proven the ketogenic diet to be a low-risk intervention when optimized with appropriate patient monitoring and support.

Growth hormone treatment improves final height and nutritional status of children with chronic kidney disease and growth deceleration.

Growth retardation is a common complication of chronic kidney disease (CKD) in children. Treatment with recombinant human growth hormone (rhGH) has been used to help short children with CKD to attain a height more in keeping with their age group, but the scientific evidence regarding the effect of rhGH on final height is scarce. Final heights of children with CKD receiving rhGH treatment (cases) were compared with final heights of a matched cohort of children with CKD that did not receive rhGH therapy (controls). Sixty-eight rhGH-treated cases (44 boys) were compared with 92 untreated controls (60 boys). Mean duration of rhGH therapy was 4.2±0.9years; rhGH dose was 0.3±0.07mg/kg/week. Height SDS at baseline was lower in rhGH-treated patients than in controls (-2.00±1.02 versus -0.96±1.11, p<0.001). Baseline height SDS was significantly lower than target height SDS in both groups. Height SDS significantly improved from baseline to final height attainment in rhGH-treated patients, while it slightly decreased in controls (mean SDS variation 0.69±1.05 in rhGH-treated cases versus -0.15±1.2 in controls). Final height SDS was -1.25±1.06 in rhGH-treated cases and -1.06±1.17 in controls (p=0.29). Target adjusted final height SDS was -0.91±1.03 in rhGH-treated cases and -0.61±1.17 in controls (p=0.1). Long-term rhGH therapy is able to reduce the linear growth deceleration of children with CKD, and ultimately to improve their final height, reducing the difference with target height.

Exploration of non‐nutritional factors associated with stunting in 24 month old children of rural Bangladesh

Nutrition interventions in the critical first 2 years of life have had only modest effects on stunting, a length for age Z‐score (LAZ) &lt; ‐ 2, suggesting that non‐nutritional factors contribute to compromised growth. We are assessing gut permeability and environmental exposures at 24 mo of age as potential causes of linear growth deceleration in 180 children of rural Bangladesh, where over half of children are stunted. Data on health, maternal and infant diet, and growth were characterized from the intrauterine period to 24 mo of age in children in the context of a community‐based, randomized trial to assess maternal antenatal micronutrient supplements on birth outcomes. Mean (±SD) LAZ (% stunted) was −1.47±1.2 (29%) at birth (n=178), −1.37±1.19 (22%) at 6 mo (n=169), −1.86±1.12 (42%) at 12 mo (n=162), and −1.97±1.11 (46%) (n=121) at 24 mo, revealing increasingly compromised linear growth after 6 mo, consistent with timing of complementary feeding and enhanced exposure to pathogenic stimuli. Gut permeability assessed by the lactulose:mannitol test; chronic pathogenic exposure assessed by elevated immunoglobulins, cytokines, and acute phase markers; and aflatoxin exposure at 24 mo will be presented. Associations of these factors with LAZ and individual growth trajectories will be explored. Support: Gates Foundation Grant 614, Grand Challenges Exploration

Progressive pituitary hyperplasia over the course of 2 years demonstrated on magnetic resonance imaging in a patient with long standing, profound primary hypothyroidism

Pituitary hyperplasia secondary to primary hypothyroidism and subsequent regression following thyroid replacement has been well described. We report a 12 year-old male who was retrospectively found to have progressive pituitary hyperplasia over the course of 2 years prior to his diagnosis of primary hypothyroidism, as documented on annual brain magnetic resonance imaging (MRI) for Arnold Chiari Type 1 malformation. He presented to Endocrinology with a 2-year history of fatigue, worsening daily headaches and linear growth deceleration. The diagnosis of primary hypothyroidism as the cause for his pituitary hyperplasia was made. He was started on levothyroxine with subsequent regression of pituitary hyperplasia demonstrated on repeat brain MRI six months later. This case is the first that demonstrates progressive pituitary hyperplasia from early in the course to diagnosis of hypothyroidism. It also illustrates that pituitary hyperplasia noted on routine brain MRI can be a presenting sign of primary hypothyroidism that should prompt endocrinologic evaluation.

Autoimmune Neuromuscular Disorders in Childhood

Opinion statementAutoimmune neuromuscular disorders in childhood include Guillain-Barré syndrome and its variants, chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), juvenile myasthenia gravis (JMG), and juvenile dermatomyositis (JDM), along with other disorders rarely seen in childhood. In general, these diseases have not been studied as extensively as they have been in adults. Thus, treatment protocols for these diseases in pediatrics are often based on adult practice, but despite the similarities in disease processes, the most widely used treatments have different effects in children. For example, some of the side effects of chronic steroid use, including linear growth deceleration, bone demineralization, and chronic weight issues, are more consequential in children than in adults. Although steroids remain a cornerstone of therapy in JDM and are useful in many cases of CIDP and JMG, other immunomodulatory therapies with similar efficacy may be used more frequently in some children to avoid these long-term sequelae. Steroids are less expensive than most other therapies, but chronic steroid therapy in childhood may lead to significant and costly medical complications. Another example is plasma exchange. This treatment modality presents challenges in pediatrics, as younger children require central venous access for this therapy. However, in older children and adolescents, plasma exchange is often feasible via peripheral venous access, making this treatment more accessible than might be expected in this age group. Intravenous immunoglobulin also is beneficial in several of these disorders, but its high cost may present barriers to its use in the future. Newer steroid-sparing immunomodulatory agents, such as azathioprine, tacrolimus, mycophenolate mofetil, and rituximab, have not been studied extensively in children. They show promising results from case reports and retrospective cohort studies, but there is a need for comparative studies looking at their relative efficacy, tolerability, and long-term adverse effects (including secondary malignancy) in children.

The short child.

1. Maria G. Vogiatzi, MD* 2. Kenneth C. Copeland, MD† 1. 2. *Instructor of Pediatrics, New York Hospital-Cornell Medical College, New York, NY. 3. 4. †Professor of Pediatrics, Baylor College of Medicine, Houston, TX. 1. Determination of height velocity is the most critical factor in evaluating the growth of a child. 2. A decreased height velocity after the third year of life indicates pathology unless proven otherwise. 3. Constitutional delay of growth and adolescence (CDGA) and familial short stature (FSS), the two most common entities associated with short stature, are characterized by deceleration of linear growth during the first 2 or 3 years of life. 4. Weight-for-height ratio may help distinguish “systemic” disorders (including gastrointestinal, renal, cardiopulmonary, and immunologic) from endocrinopathies. 5. Dysmorphic features are variable but important clues supportive of a diagnosis of genetic disorders. 6. Children who have congenital growth hormone (GH) deficiency often present in the newborn period with hypoglycemia in combination with prolonged hyperbilirubinemia. Growth represents a sentinel for the general health of a child. However, the distinction between normal and abnormal growth may be difficult to make at times. The purpose of this review is to highlight differences between growth patterns associated with normal variations and those associated with pathologic conditions. A method of categorizing growth patterns is used that is based principally on analyses of height velocity, weight for height, and abnormal physical features. Determination of height velocity is the single most critical factor in evaluating the growth of a child, and the simplest way to determine whether a height velocity is normal for age is to observe whether a height is “crossing” percentiles on the linear growth curve. Weight-for-height ratio may be helpful in distinguishing “systemic” disorders (including gastrointestinal, renal, cardiopulmonary, and immunologic) from endocrinopathies. The short child who has one of the “systemic” disorders typically is short and thin; the child who has an endocrinopathy usually is short and well-nourished or frankly obese. Dysmorphic features, disproportionate shortening, a history of intrauterine growth retardation (IUGR), and mental retardation are variable but important clues …

Growth pattern in the Apert syndrome.

In this paper, we demonstrate that a discernible and unique growth pattern characterizes the Apert syndrome. The keys to understanding Apert newborn measurement values are brain size and cranial configuration. Both true megalencephaly and coronal synostosis are present at birth. Thus, the head is unusually heavy and the cranium is disproportionately high. Mean newborn length and weight are above the normal 50th centile. Of our newborn patients, 16% exceeded 4,000 g in weight. Preterm infants were appropriate or slightly large for gestational age. A biphasic linear growth pattern was found. In childhood, deceleration of linear growth occurs so that most values fall between the 5th and 50th centiles. From adolescence to adulthood, deceleration becomes more pronounced. This 2-step linear growth deceleration results in large measure from rhizomelic shortness of the lower limbs. Puberty takes place within the normal time frame. Although a disproportionate amount of the megalencephaly accounts for the dramatic increase in head height, the widely patent midline calvarial defect, allowing the brain to expand anteriorly into the metopic area, and some increase in the head breadth permit the mean head circumference at birth to normalize slightly above the 50th centile. During the growth period, the head circumference was studied in surgically unoperated Apert patients from the 1960s and earlier. The natural history of the growing cranium consists of gradual deceleration in head circumference from slightly above the 50th centile at birth to within or at -2 SD later on.

The treatment of difficult atopic dermatitis in childhood with oral beclomethasone dipropionate.

Beclomethasone dipropionate (BDP) is a synthetic glucocorticoid with great topical potency. It has previously been demonstrated to be an effective treatment for childhood atopic dermatitis (AD) when given orally. We have monitored linear growth and adrenal function in a group of children treated with oral BDP for severe AD. Stable control of disease was achieved in 10/14 patients (mean dose: 1000 micrograms/day, range 800-1800). At this maintenance dose, there was evidence of deceleration of linear growth in 7/10 patients. There was no significant difference between pre-treatment 8 a.m. plasma cortisol levels and those on the maintenance dose. However, there was a reduction in 24-hour urinary cortisol excretion during maintenance treatment, although this did not reach statistical significance. We regard oral BDP as a useful treatment in widespread childhood atopic AD that has not responded adequately to topical therapy. However, it is mandatory that growth be monitored carefully during its use.

Physical growth and development in patients with Rett syndrome.

Linear growth and sexual development was assessed in 21 girls who fulfilled the clinical criteria of Rett syndrome. Ten (48%) showed growth retardation with length or height below the 5th centile and an additional 8 (38%) had shifted their linear growth downward sometime during the first years of life. All the girls had age-appropriate sexual development with menarche in 6 at a mean age of 11 2/12 years. Early deceleration of linear growth, growth retardation and normal sexual development appear to be useful markers in the clinical definition of Rett syndrome.

The effects of prostaglandin A1 and prostaglandin B1 on the differentiation of cartilage in the chick embryo

In organ cultures of chick embryonic limb rudiments the mean length of explants treated with 25 microgram/ml prostaglandin B1 (PGB1) was significantly smaller than that of paired controls (P < 0.001) after 4, 6 and 8 days in vitro. The deceleration of linear growth was constant during 8 days in vitro. Growth inhibition was confirmed by a statistically significant decrease in explant dry weight after 8 days of culture. However, PGB1 caused no observable alteration in the histological structure of the explants. The possible role of PGB1 in the physiological control of cartilage growth is postulated. Explants similarly treated with prostaglandin A1 (PGA1) at concentrations of 15 microgram/ml for 8 days or 20 microgram/ml for 4 and 8 days exhibited "comma" and "inverted commas" phenomena, caused by the intermingling of chondroblasts from the epiphyseal and flattened-cell zones, which thus ceased to be distinct entities. Adenylate cyclase in the plasma membrane may be involved in this disturbance of cartilage differentiation.