Effects Of Short Stature Research Articles

Assessment of Quality of Life in a Sample of Short Stature Iraqi Children with Growth Hormone Deficiency

Background: Short stature (SS) is defined as a height of 2.0 or more standard deviations (SD) below the population-specific mean height for age and gender. 2.5% of children have short stature, and it is one of the most frequent causes for children to see a growth specialist during their childhood. It is challenging to generalize about the effect of short stature on psycho-social adaption given the data currently available. Health-related quality of life (HrQoL) was generally shown to be lower in clinically identified short stature children than in population-based normal-sized reference groups. Aim: Examine the behavioral pattern and mental health of SS and its psychological influence on QoL of children/adolescence. In addition, compare the behavioral response and QoL between growth hormone deficiency GHD and control groups. Methods: It is a cross sectional study, included 80 participants (60 with GHD and 20 with normal height as control group) between 4 and 18 years old. The parents of the participants were given a parent-reported version of the written Quality of Life in Short Stature Youth QoLISSY questionnaire in Arabic in order to examine the association with the socio-demographic characteristics of the participants. Results: 51.25% female and 48.75% male included in this study, the mean age at assessment was 12.1 ± 2.7, and 11.8 ± 2.6 of the GHD and control group, respectively. There was significant difference in QoLISSY total score between GHD and control groups. The association between socio-demographic characteristics of the participants was significantly different. Conclusion: The QoL of Iraqi children with GHD showed lower scores in all domains of QoLISSY compared to normal children.

Does Stature Really Matter? The Effect of Short Stature on Adult Survivorship

Stature is a multifactorial growth process, influenced by genetics, health and nutrition. Short stature estimates from skeletal remains have traditionally been used as an indicator of a disruption in physiological growth processes within past populations, which may decrease adult survivorship. This project questions whether this non‐specific indicator of stress, affected the survivorship of individuals associated with the historic Arikara Native Americans of South Dakota (AD 1600–1832). Previous research suggests that short stature decreased survivorship among adult individuals from one archaeological site. In that study, the two sexes were pooled and survivorship was estimated relative to different time periods. In the current project, survivorship differences between the sexes were estimated, while time period was pooled. It is hypothesized that individuals with below average stature will exhibit a decrease in survivorship compared to their taller peers. One‐hundred and eighty‐four adult individuals, (79 females, 105 males), across four archaeological sites, were analyzed. Survivorship was estimated using Kaplan‐Meier estimates with log‐rank tests in SPSS version 22. Two analytical steps were taken. First, differences in survivorship between tall and short individuals were estimated per sex. Next, survivorship of tall females and tall males was compared and survivorship of short females and short males was compared. The results were not statistically significant. Therefore, short stature does not affect survivorship relative to sex. Broadly, these results suggest that the significance of short stature is context specific and cannot always be used as an indicator of decreased survivorship. It is recommended that researchers utilize multiple indicators of stress to infer survivorship and health in past populations. This project contributes to research focused on human growth, the disruption of physiological processes and their effects on adult survivorship.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

The effect of short stature, portal hypertension, and cholestasis on growth hormone resistance in children with liver disease.

Chronic liver disease is associated with GH resistance, which is characterized by high circulating GH and low insulin-like growth factor I (IGF-I) concentrations. Standard GH replacement has no effect on serum IGF-I in pediatric liver disease. The aims were to examine whether GH resistance can be overcome by supraphysiological GH and to determine whether GH resistance worsens with the progression of liver disease. Thirty children, divided into five groups whose liver disease was at clinically different stages, were studied. They were given 0.2 IU/kg x day GH for 4 days and then 0.4 IU/kg x day for the next 4 days. Serum IGF-I and binding proteins (IGFBPs) were measured by immunoassay. IGF-I was lower in all study groups than in normal controls. IGF-I, IGFBP-3, and acid-labile subunit rose in response to GH. The magnitude of the response reflected nutritional status and liver dysfunction; in particular, portal hypertension was associated with a poor IGF-I response. There was no change in IGFBP-2. GH resistance begins early in the natural history of childhood liver disease and develops with the progression of liver disease, particularly with portal hypertension. It may be partially overcome by supraphysiological GH administration, but the effect becomes smaller with worsening liver disease.

The Effect of Short Stature, Portal Hypertension, and Cholestasis on Growth Hormone Resistance in Children with Liver Disease

The Effect of Short Stature, Portal Hypertension, and Cholestasis on Growth Hormone Resistance in Children with Liver Disease

Height and mortality after myocardial infarction

A case-control analysis was conducted to determine the relationship between height and mortality among patients enrolled in the already completed Beta Blocker Heart Attack Trial (BHAT). In a basic model including height (continuous) and relevant covariates the relative risk (RR) per 4-inch reduction in height (approximately 1 standard deviation) was 1.18 (95% confidence interval, 0.92 to 1.51). When sex was considered, the effect of short stature on mortality was found to be restricted to male subjects. The male RR per 4-inch reduction in height was 1.26 (0.96 to 1.63) whereas for women it was 0.89 (0.49 to 1.59). In males not randomized to propranolol (untreated) the effect was further modified with a RR per 4-inch reduction in height of 1.41 (1.00 to 1.99). It is hypothesized that short stature could be a marker for factors operating as far back as childhood that predispose males to mortality from coronary heart disease in later life.

REGULATION OF THE GH-RECEPTOR (R) / BINDING PROTEIN (BP) BY GH PULSATILITY

GH secretion is pulsatile in man and in every mamalian species that has been so far studied. The magnitude of pulses, their frequency and their regularity vary. The R on it' part, undergoes cycles of internalization and recycling, which are in synchrony with the frequency of GH pulses. The present study correlated GH profiles with GH-R and GH-BP human and animal in the course of ontogenesis, effects of short stature, fasting, anorexia nervosa, obesity, diabetes, GH-therapy, acromegaly and cirrhosis. In short, slowly growing children GH-BP correlated negatively with mean GH-pulse amplitude and integrated concentration. GH pulsatility is high in newborns, fasting, anorexia nervosa, diabetes, acromegaly and cirrhosis. GH-BP is low in all these conditions. GH pulsatility is low, and GH-BP is high, in GH-therapy and obesity. Negative correlation of GH pulsatility with GH-BP exists across the mammalian class, with increasing pulsatility in rabbit < man < female rat < male rat < guinea pig, whereas GH-BP levels and liver membrane's GH-R decrease in the same order. Newborn rats have high GH pulsatility and low GH-R and GH-BP, whereas obese rats have low GH levels and high GH-receptors. It is concluded that the pattern of GH profiles is the major determinant of the GH-R / GH-BP, that the various physiological and pathological conditions regulate primarily the pattern of GH pulsatility, which, in turn, regulates the GH-R / GH-BP, and thereby exert the specific effects on target cells to promote or to suppress growth, or to express distinct metabolic actions.

Turner syndrome: A fresh look

Introduction of improved therapy for a disease often prompts a closer look and results in revision of previous concepts. The availability of biosynthetic human growth hormone (GH) has stimulated interest in a variety of growth disorders. There are two particularly important areas for clinical investigation: More complete information is needed as to which disorders respond to GH and what are the long-term beneficial and adverse effects. It is no less important to enhance our understanding of the psychological effects of short stature and its treatment. The ultimate goal of GH treatment is not to make the child taller, but to improve his or her well-being in the critical areas of family, school, and social life. It follows then that the efficacy of GH therapy cannot be evaluated by auxological measures alone. It is necessary to have a far better understanding than we now have of the impact of short stature on well-being in childhood and adult life. Biological parameters such as height do not affect the person in a direct way, but interact in a complex way to affect quality of life. It is particularly important to develop a better understanding of the effect of improving height in children with multiple anomalies or handicaps. Such children make up a large proportion of those followed in pediatric subspecialty clinics. The large-scale studies that are in progress should considerably enhance our knowledge of these important matters. The proceedings of the Turner symposium presented here are a valuable contribution toward a comprehensive understanding of one such syndrome comprised of multiple abnormalities. It represents a unique