Obesity

Author(s):  
Gary Butler ◽  
Jeremy Kirk

• Obesity is defined as: ‘An excess of body fat frequently resulting in a significant impairment of health and longevity’. • In most cases obesity is not due to an underlying endocrine disorder, although it may produce endocrine morbidity such as type 2 diabetes. • Although there are a number of different methods to assess overweight and obesity, the most common is body mass index (BMI): weight (kg)/height (m)2. • Classification is: • primary: exogenous or ‘simple’ obesity • secondary: ■ identified genetic syndromes, e.g. Prader–Willi, Bardet–Biedl, pseudohypoparathyroidism ■ monogenic disorders, e.g. leptin deficiency, leptin/melanocortin receptor defects ■ CNS disease, e.g. hypothalamic obesity ■ endocrine disorders, e.g. hypothyroidism, Cushing syndrome, growth hormone deficiency, precocious puberty ■ immobility, e.g. cerebral palsy ■ iatrogenic. • Generally, children with obesity which is: • primary often have a family history, tall stature, advanced bone age, and no dysmorphic features • secondary often have short stature, delayed bone age, dysmorphic features, and developmental delay. • Complications of obesity are multisystem: metabolic, cardiovascular, respiratory, gastrointestinal/hepatic, orthopaedic, neurological, dermatological, gynaecological, and psychological. • Therapy is aimed at modifiable factors restoring the balance between energy intake (e.g. dietary) and expenditure (e.g. exercise), and preferably a combination of both along with counselling and behaviour modification. There is currently only limited data on the benefits of pharmacotherapy and bariatric surgery.

Author(s):  
Fariba Naderi ◽  
Samira Rajabi Eslami ◽  
Sohrab Afshari Mirak ◽  
Mohammad Khak ◽  
Jalaladin Amiri ◽  
...  

AbstractGrowth hormone deficiency (GHD) is a major problem among children with short stature. In this study, the role of brain magnetic resonance imaging (MRI) in defining the underlying defects among short children with GHD is evaluated.In a cross-sectional study, data of 158 children were evaluated. Growth hormone (GH) levels were measured using stimulating tests and brain MRI with gadolinium contrast was applied, as well.Some 25.3% of patients had GHD with a mean age of 8.01±3.40 years. MRI results showed 35 as normal, four with pituitary hypoplasia, and one with microadenoma. The MRI results were significantly associated with GH levels and presence of other endocrine disorders. There was a significant association between prenatal disorders and patients’ bone age delay.In patients with severe GHD and patients with multiple pituitary hormone deficiencies, MRI is more likely to be abnormal, and bone age is much delayed in patients with history of prenatal disorders.


Author(s):  
Madeleine Willegger ◽  
Markus Schreiner ◽  
Alexander Kolb ◽  
Reinhard Windhager ◽  
Catharina Chiari

SummaryPainful orthopedic conditions associated with extreme tall stature and leg length discrepancy (LLD) include back pain and adopting bad posture. After failure of conservative treatment options, blocking of the growth plates (epiphysiodesis) around the knee emerged as gold standard in patients with tall stature and LLD in the growing skeleton. Surgical planning includes growth prediction and evaluation of bone age. Since growth prediction is associated with a certain potential error, adequate planning and timing of epiphysiodesis are the key for success of the treatment. LLD corrections up to 5 cm can be achieved, and predicted extreme tall stature can be limited. Percutaneous epiphysiodesis techniques are minimally invasive, safe and efficient methods with low complication rates. In general, a multidisciplinary approach should be pursued when treating children and adolescents with tall stature.


2013 ◽  
Vol 33 (1) ◽  
pp. 74-76
Author(s):  
S Basnet ◽  
A Eleena ◽  
AK Sharma

Many children are frequently brought to the paediatric clinic for evaluation of short stature. Evaluation for these children does not go beyond x-ray for bone age estimation and growth hormone analysis. Most of them are considered having constitutional or genetic cause for their short stature. However, shuttle dysmorphic features could be missed in many of them. Hence, many children might be having chromosomal anomaly as an underlying cause. We report a case of 40 months who had been evaluated several times in the past for pneumonia, otitis media and short stature is finally diagnosed to have Turner syndrome. DOI: http://dx.doi.org/10.3126/jnps.v33i1.8174 J Nepal Paediatr Soc. 2013;33(1):74-76


2016 ◽  
Author(s):  
Graham T McMahon ◽  
Robert G. Dluhy

The distribution of hormones throughout the human body results in presentations of endocrine disease that are diffuse and variable. Although some endocrine syndromes result in characteristic sets of symptoms and features, most patients experience a limited number of components of the syndrome and may note symptoms that are not typically syndromic. This review discusses presentations of endocrine diseases and the endocrine patient. Specific attention is given to endocrine testing, which can be achieved by measuring the hormone itself, stimulating or suppressing a hormone feedback loop, or measuring peripheral hormone receptor function. The chronic care relationship is explored as many patients with endocrine diseases require extended chronic care to achieve control of abnormal hormonal systems. The dependency on chronic care necessitates that endocrinologists develop particular expertise in managing illnesses over the long term. Tables list hormones and their associated syndromes, clusters of contrasting symptoms and signs of over- and underactivity of the thyroid and adrenal glands, approaches to endocrine testing and treatment, and variability in selected hormone concentrations over time. Figures show diagnostic criteria related to hypercalcemia, growth hormone deficiency, acromegaly, and adrenal incidentaloma. The chronic care model is also represented. This review contains 4 highly rendered figures, 4 tables, and 12 references.


1982 ◽  
Vol 99 (2) ◽  
pp. 166-173 ◽  
Author(s):  
M. Zachmann ◽  
D. Tassinari ◽  
W. Sorgo ◽  
G. U. Exner ◽  
B. Kempken ◽  
...  

Abstract. Twentythree boys with delayed adolescence (age 15.7 ± 2.0, bone age 12.4 ± 2.1 years) were studied. Their cortisol response to insulin was normal. After oral metyrapone (500 mg/m2 by mouth) one to three consecutive 12 h urine samples were collected for analysis of THS. Thirtyseven tests with 37 first, 21 second, and 11 third samples were carried out. The results could be divided into two main groups: 25 tests (group A) were subnormal in the first sample, 12 of them with a very weak (40 ± 8 μg/m2/12 h) and 13 with an insufficient (191 ± 16 μg/m2/12 h) THS response. Values in the second and third sample were higher, indicating a dealyed response. In 12 tests (group B), the results were normal (1016 ± 143 μg/m2/12 h) in the first and lower in the second and third samples. In three patients with repeated tests, there was improvement with increasing bone age. The THS-responses to metyrapone did not correlate with those of growth hormone, gonadotrophins, and TSH to stimuli. It is concluded that the THS-response to a single dose of metyrapone may be temporarily insufficient or delayed in delayed adolescence. We interpret this finding as showing transiently reduced or slow hypothalamic responsiveness.


2015 ◽  
Vol 10 (1) ◽  
pp. 38
Author(s):  
Carlos TORI TORI ◽  
Carlos ROE B.

We present a case of Klinefelter’s syndrome and short stature due to partial growth hormone deficiency. His height was below the third percentile for age and his bone age lagged behind four years. Cases like this are generally due to the presence of a an isochromosome Xq or to an isolated partial or total deficiency of growth hormone, or to partial or panhypopituitarism. We wish de emphasize the rare association between Klinefelter syndrome and growth hormone deficiency.


2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Fabiola romero ◽  
Sady Arzamendia ◽  
Dahiana Ferreira ◽  
Claudia Neves de Souza ◽  
Helen Lopez ◽  
...  

Abstract INTRODUCTION: Morsier Syndrome is a rare congenital malformation, characterized by hypoplasia / aplasia of the septum pellucidum and hypoplasia / aplasia of the optic nerves, in addition to pituitary and hypothalamic hormonal deficiencies. Klinefelter Syndrome is a sexual chromosomal genetic alteration, a frequent cause of male hypogonadism, The association of Morsier syndrome and Klinefelter is described below. CLINICAL CASE We report he case of a 12 year-old boy with psychomotor retardation and nystagumsho presented at 14 months of age with growth hormone deficiency (low weight and height,) and diabetes insipuidus with hypernatremia of of 159 mEq and low urinary density (less than 1,005). MRI showed an absence of septum pellucidum, thick right frontal cortical dysplasia with asymmetric appearance of the grooves, small optic chiasma, hypoplastic pitutary gland (3 mm height), compatible with Morsier syndrome. The physical examination draws attention to tall stature, and long lower limbs, facies with prominent forehead and hypertelorism, gynecomastia and small external genitalia for age. Hormonal evaluation revealed hypergonadotropic hypogonadism with a 47 XXY karyoteype suggeting Klinefelter syndrome. CONCLUSION: We report the first case of Morsier syndrome, associated to Klinefelter syndrome. Both syndromes may present with hypogonadism. However, the diagnosis of klinefelter syndrome was made based on the phenotypic characteristics of this patient including hyeprgonadotroic hypogonadism and abnormal karyotype analysis.


2021 ◽  
Vol 26 (4) ◽  
pp. 218-226
Author(s):  
Martin Oswald Savage ◽  
Helen Louise Storr

Determining the pathogenesis of pediatric growth disorders is often challenging. In many cases, no pathogenesis is identified, and a designation of idiopathic short stature is used. The investigation of short stature requires a combination of clinical, endocrinological, and genetic evaluation. The techniques used are described, with equal importance being given to each of the 3 approaches. Clinical skills are essential to elicit an accurate history, family pedigree, and symptoms of body system dysfunction. Endocrine assessment requires hormonal determination for the diagnosis of hormone deficiency and initiation of successful replacement therapy. Genetic analysis has added a new dimension to the investigation of short stature and now uses next-generation sequencing with a candidate gene approach to confirm probable recognizable monogenic disorders and exome sequencing for complex phenotypes of unknown origin. Using the 3 approaches of clinical, endocrine, and genetic probes with equal status in the hierarchy of investigational variables provides the clinician with the highest chance of identifying the correct causative pathogenetic mechanism in a child presenting with short stature of unknown origin.


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