Short Stature
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ayesha Javid, MBBS[2]
Synonyms and keywords:
Overview
Short stature is characterized as a condition in which the height of the person in the 3rd percentile is the average height of the age , sex, and population group. According to Ranke (1996), “Short stature is defined as a condition in which the height of an individual is two standard deviations (SD) below the corresponding mean height of a given age, sex and population group.” [1] [2]
Historical Perspective
- In 1967 by Pierre Maroteaux was the first man to ever mention dwarfism.
- He is largely credited for establishing the link between the genetic condition and prenatal micromelic for the patients with dwarfism.[3]
- In 1994, Dr. John Wasmoth and his team discovered the cause of achondroplasia while researching the topic of dwarfism.[4]
Classification
There are two types of short stature,
Proportionate short stature (PSS)
Proportionate short stature (PSS) is when the person is small, but limbs and trunk height are in proportions. [5]
Disproportionate short stature (DSS)
Whereas in disproportionate short stature (DSS), the normal proportion of limbs and trunk height is absent, and the individual shows a great difference in their sitting and standing height. [5]
Pathophysiology
- Short stature may be normal; therefore a detailed family history of growth patterns and direct measurement of the parents is an important part of evaluating if the short stature is due to the genetic causes and potentials of the child.[5]
- If the Short stature results from growth failure or premature closure of the epiphysial growth plates, it secondary to a pathologic condition or due to an inherited disorder. Therefore, pathophysiology depends on the underlying cause.[5]
Causes
Physiological causes of short stature
Familial short stature
- In familial short stature, individuals have low-normal height velocity throughout their life.[6]
- They have normal height velocity which distinguishes them from the pathologic causes of short stature.[6]
- Also, they can be distinguished from the individuals with constitutional growth delay, as their bone age is in accordance to their chronologic age. [6]
Constitutional delay of growth and puberty
- Constitutional delay of growth and puberty (CDGP) is also called constitutional short stature for pre-pubertal children, results in childhood short stature but leads to relatively normal height in adulthood.[7]
- Children are of normal size at birth. However, a severe and prolonged decrease in growth rate is observed starting at three to six months of age.[7]
- By three or four years of age, children with CDGP usually are growing at a low-normal rate. The growth curve that remains below the third percentile for height.[7]
- In addition children also have delayed pubertal maturation. This leads to a marked height discrepancy during the early teenage years compared with their peers but is followed by catch-up growth when they do enter puberty. The hallmark of CDGP is delayed skeletal age.[7]
Idiopathic short stature
- Idiopathic short stature (ISS) is a height below 2 standard deviation (SD) of the mean for age, in the absence of any endocrine, metabolic, or other causes.[8]
Small for gestational age infants with catch-up growth
- Most infants born small for gestational age (SGA) experience catch-up growth by two years of age. In this way, they are able to reach the normal range of their height.
- About 10 percent of SGA infants, particularly those born with more severe SGA, do not experience catch-up growth. This group of SGAinfants can be considered to have a pathologic pattern of growth. [9]
Pathologic causes of short stature
Systemic disorders with secondary effects on growth
Malnutrition
- Malnutrition can lead to short stature with a delayed pattern of growth. The hallmark is low weight-for-height.
- Malnutrition can be due to inadequate food supply, or it may be due to an underlying condition which affects food intake or absorption or increases energy requirement of the body. [10] [11]
Glucocorticoid therapy
- Glucocorticoids are used for the treatment of a variety of diseases in children, such as asthma, leading to growth failure in children. [11]
- Glucocorticoids can interfere with endogenous growth hormone secretion and action, bone formation, nitrogen retention, and collagen formation. [12]
- The growth effects of glucocorticoids are related to the type, dose, and duration of the exposure. If glucocorticoids are discontinued, children usually experience some catch-up growth. Growth impairment is more pronounced if it is given for a longer duration of action and when it is used daily as compared with an alternate-day regimen.[11]
Gastrointestinal disease
- Some chronic gastrointestinal diseases such as Inflammatory bowel disease and celiac disease results in short stature. Children tend to have a greater decrease in weight than the height (ie, they are underweight-for-height).
- The growth failure is caused by the inflammatory disease process, as well as decreased food intake, malabsorption, or glucocorticoids.
Rheumatologic disease
- Childhood rheumatologic diseases, especially systemic juvenile idiopathic arthritis, are frequently associated with growth retardation.[13]
- This can be partly due to the inflammatory process driven by the proinflammatory cytokines and also caused by the high-dose glucocorticoids often used for management.[14]
Chronic kidney disease
- Growth failure is seen in at least one-third of children with chronic kidney disease. [15]
- The primary causes of growth failure in children with chronic kidney disease are disturbances of growth hormone metabolism and its main mediator, insulin-like growth factor 1 (IGF-1). [15]
- Other factors may include metabolic acidosis, uremia, poor nutrition secondary to dietary restrictions, anorexia of chronic illness, anemia, calcium and phosphorus imbalance, renal osteodystrophy, or use of high-dose glucocorticoids. Affected patients are candidates for growth hormone therapy until renal transplantation, and some of these patients may also benefit from growth hormone therapy after transplantation. [15] [16]
Cancer
- Children with cancer have poor growth rate due to poor food intake, nausea, vomiting, and increased caloric utilization.[17] [18]
- Also, anorexia, nausea, and vomiting induced by chemotherapy and radiotherapy also can contribute to impaired growth.[17] [18]
Pulmonary disease
- In pulmonary diseases, such as cystic fibrosis, growth failure is caused by multiple mechanisms, including poor food intake, maldigestion or malabsorption, chronic and recurrent infection, and increased energy requirements.[19]
- In asthma, growth failure is usually due to the use of glucocorticoids for the treatment. [11]
Cardiac disease
- In severe congenital heart diseases, growth failure is common. Sometimes, it is the presenting feature of the heart disease.[20]
Immunologic disease
- Growth failure is associated with immunologic deficiencies such as common variable immunodeficiency or severe combined immunodeficiency syndrome, and infections such as HIV.[21]
Metabolic diseases
Metabolic disorders can lead to growth failure in children and adolescents.
- The most common metabolic disorder in children is type 1 diabetes mellitus. It causes short stature and attenuated growth because of the caloric deficit resulting from severe glucosuria. Also, type 1 diabetes causes a decrease in IGF-1 production or action, which has a negative correlation with adult height. Diabetes with very poor glycemic control leads to Mauriac syndrome, characterized by attenuated linear growth, and delayed puberty, hepatomegaly, and Cushingoid features.
- Vitamin D deficiency can lead to rickets in children characterized by abnormal epiphyseal development, bowing of the extremities, and diminished growth.
Genetic Causes
Several genetic disorders have prominent effects on growth.
- Turner's Syndrome [22]
- SHOX gene variant [23]
- Prader-Willi Syndrome [24]
- Noonan syndrome [25]
- Silver-Russell syndrome [5]
- Skeletal dysplasia/growth plate abnormalities [26]
Endocrine Causes
- Cushing syndrome: Cushing syndrome results in increased glucocorticoids and is characterized by the combination of weight gain and growth retardation, resulting in excessive weight-for-height. Glucocorticoids directly inhibits the development of epiphyseal cartilage in growing long bones resulting in growth retardation.[27]
- Hypothyroidism: Growth failure is an important feature of hypothyroidism. Due to hypothyroidism, the bone age is delayed. However, it is a treatable and reversible cause of short stature as once it is identified and treated, children achieve the normal growth potential.[28]
- Growth hormone deficiency: If growth hormone deficiency is congenital, then postnatal growth failure along with delayed bone age is seen. The patient has very low serum concentrations of growth hormone, IGF-1, and IGF-binding protein-3 (IGFBP-3. Additional findings are hypoglycemia, prolonged jaundice, and micropenis in boys, especially if gonadotropins are deficient as well. In children, whose height may still be within the normal range for age, has less severe growth failure. Acquired or secondary growth hormone deficiency occurs in case of intracranial tumor (eg, craniopharyngioma), cranial irradiation, and head trauma.[29]
Psychosocial short stature
It is a growth disorder that is observed between the ages of 2 and 15, caused by extreme emotional deprivation or stress which causes decrease in growth hormone (GH) and somatomedin secretion, resulting in very short stature. Patient's weight is inappropriate for the height with immature skeletal age. [30]
Differential Diagnosis
- Endocrine disorders: Growth hormone deficiency (GHD), insulin-like growth factor-1 (IGF-1), growth failure, constitutional growth delay, growth failure, stunted growth, structural brain abnormalities, or pituitary lesions, pituitary microadenomas, congenital hypothyroidism, idiopathic short stature, intrauterine growth deficiency, etc.[31]
- Genetic disorders: Down syndrome, Turner syndrome, 3M syndrome, Noonan syndrome, Prader-Willi syndrome, Aarskog syndrome, Silver-Russell syndrome, etc.
- Bone diseases: Dwarfism, Achondroplasia (short-limbed dwarfism), diastrophic dysplasia (short-limbed dwarfism), spondylo-epiphyseal dysplasia (short-trunk dwarfism), rickets, etc
- Chronic disorders: Cystic fibrosis, Crohn disease, juvenile idiopathic arthritis (JIA), anemia, chronic renal insufficiency, inflammatory bowel disorder, chronic malnutrition, etc
- Psychological distress [5]
Epidemiology and Demographics
In the United States, 2.5% of the population is short. [5] A study conducted on the school children age 4-16 years in the South Indian Population shows the overall prevalence of short stature was 2.86%.[32]
Gender
- Short stature is equally prevalent among both males and females, but studies show that boys were admitted more than the girls. This could be due to the reason that males are more likely to be brought to medical attention because of the prevalence of social expectations and pressures as compared to the females.
- On the other hand, in Rosario, Argentina, the higher prevalence was found in females (16.4%) than males (8.4%) (p<0.001).[21] The short stature in females was related to age, weight, and abdominal obesity.
Age
- Different ethnic groups have different average statures, which are essential to take into consideration while comparing mean parameters.
- Any individual who has not attained the union of epiphyseal plates, can get affected.
Race
- Short stature is more prevalent among Hispanic children as compared to the other populations.[33]
Risk Factors
- Common risk factors in the development of short stature are diet, environment, and genetics.[5]
Diagnosis
Diagnostic Criteria
- The diagnostic criteria of short stature is when the height is 2 or more standard deviations below the mean for age and gender within a population (below the 2.5th percentile).[34]
Symptoms
- Symptoms of the short stature depend on the underlying cause.
Physical Examination
- Short stature can be diagnosed by Anthropometric measurements including height vertex, body weight, trunk height, and limb length of an individual. These are assessed in relation to age, sex, and population.[34]
- In achondroplasia, enlarged head with frontal bossing, depressed nasal bridge, mid-face hypoplasia and skull.[34]
Laboratory Findings
The laboratory studies used to assess the major causes of short stature include,
- Measurement of serum levels of insulin-like growth factor-I (IGF-I), formerly named somatomedin C, and IGF binding protein-3 (IGFBP-3). Measurement of serum levels of growth hormone.[35]
- Karyotype for the genetic causes of the short stature.[36]
- Other tests include,
- CBC for hematologic diseases.[37]
- Serum total thyroxine (total T4) and thyrotropin (TSH) levels to test for hypothyroidism.[38]
- Antiendomysial immunoglobulin A (IgA) and immunoglobulin G (IgG), transglutaminase IgG, and antigliadin IgG titers for gluten enteropathy. Erythrocyte sedimentation rate for inflammatory bowel disease.[39]
- Serum transferrin and pre-albumin concentrations for malnutrition.[40]
- Sweat chloride test for cystic fibrosis. [41] [42]
Electrocardiogram
- In Noonan syndrome, which is one of the genetic cause of short stature, electrocardiogram (ECG) shows left axis deviation, abnormal R/S ratio over the left precordium, and an abnormal Q wave. [43]
- In Turner's Syndrome, ECG findings include ectopic supraventricular and ventricular activity. [34]
X-ray
- Xray anteroposterior view of left hand and wrist is done to assess the bone age in children with short stature.
- Xray findings of longstanding untreated hypothyroidism include epiphyseal dysgenesis. The spine shows platyspondyly and thoraco-lumbar kyphosis.[44]
Ultrasound
- Ultrasound helps in evaluation of thyroid pathologies, such as thyroid dysgenesis, ectopic thyroid gland, goiter or thyroid mass. [44]
CT scan
There are no CT scan findings associated with [disease name].
OR
[Location] CT scan may be helpful in the diagnosis of [disease name]. Findings on CT scan suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
OR
There are no CT scan findings associated with [disease name]. However, a CT scan may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].
MRI
- MRI is the modality of choice for the evaluation of pituitary-hypothalamic axis (PHA) in order to identify Congenital hypopituitarism or brain tumor, which can cause isolated growth hormone deficiency (IGHD) or multiple pituitary hormone deficiencies (MPHDs) leading to growth retardation.[45]
- In achondroplasia, MRI brain reveals small base of the skull, narrowed foramen magnum, syringomyelia, myelomalacia, hydrocephalus, and lumbar spinal stenosis.[44]
Other Diagnostic Studies
- [Disease name] may also be diagnosed using [diagnostic study name].
- Findings on [diagnostic study name] include [finding 1], [finding 2], and [finding 3].
Treatment
Medical Therapy
- The primary management of short stature should be to treat the underlying cause.[5]
- If the short stature is caused due to a hormonal deficiency it should be managed with hormonal treatment.[5]
- These include treating growth hormone deficiencies and constitutional growth delays with gonadotropin-releasing hormone analogues (GnRHa), aromatase inhibitors, recombinant human insulin-like growth factor- 1 (RhIGF-1), low-dose androgen therapy, recombinant human growth hormone (rhGH) etc. [46]
- In addition to treating the underlying cause, patients should be provided with psychosocial counselling and support in order to help them cope with psychosocial distress as a result of their short stature.[5]
Surgery
- Bone lengthening surgery is being performed not only for the treatment of dwarfism and/or skeletal deformities caused by congenital abnormalities, tumors and infections.[47] [48]
- The surgery is performed using Ilizarov method with circular external fixation. This is called cosmetic leg lengthening or symmetrical extended limb lengthening. [49] [50]
Prevention
- There are no primary preventive measures available for short stature.
References
- ↑ "StatPearls". 2020. PMID 32310491 Check
|pmid=value (help). - ↑ "StatPearls". 2020. PMID 31855368 PMID: 31855368 Check
|pmid=value (help). - ↑ Pauli RM (2019). "Achondroplasia: a comprehensive clinical review". Orphanet J Rare Dis. 14 (1): 1. doi:10.1186/s13023-018-0972-6. PMC 6318916. PMID 30606190 PMID: 30606190 Check
|pmid=value (help). - ↑ Shiang R, Thompson LM, Zhu YZ, Church DM, Fielder TJ, Bocian M; et al. (1994). "Mutations in the transmembrane domain of FGFR3 cause the most common genetic form of dwarfism, achondroplasia". Cell. 78 (2): 335–42. doi:10.1016/0092-8674(94)90302-6. PMID 7913883 PMID: 7913883 Check
|pmid=value (help). - ↑ 5.00 5.01 5.02 5.03 5.04 5.05 5.06 5.07 5.08 5.09 5.10 "StatPearls". 2020. PMID 32310491 PMID: 32310491 Check
|pmid=value (help). - ↑ 6.0 6.1 6.2 "StatPearls". 2020. PMID 32644549 PMID: 32644549 Check
|pmid=value (help). - ↑ 7.0 7.1 7.2 7.3 Soliman AT, De Sanctis V (2012). "An approach to constitutional delay of growth and puberty". Indian J Endocrinol Metab. 16 (5): 698–705. doi:10.4103/2230-8210.100650. PMC 3475892. PMID 23087852 PMID: 23087852 Check
|pmid=value (help). - ↑ 8.0 8.1 Vlaski J, Katanić D, Privrodski JJ, Kavecan I, Vorguicn I, Obrenović M (2013). "[Idiopathic short stature]". Srp Arh Celok Lek. 141 (3–4): 256–61. doi:10.2298/sarh1304256v. PMID 23745354 PMID: 23745354 Check
|pmid=value (help). - ↑ 9.0 9.1 Fewtrell MS, Morley R, Abbott RA, Singhal A, Stephenson T, MacFadyen UM; et al. (2001). "Catch-up growth in small-for-gestational-age term infants: a randomized trial". Am J Clin Nutr. 74 (4): 516–23. doi:10.1093/ajcn/74.4.516. PMID 11566651 PMID: 11566651 Check
|pmid=value (help). - ↑ Checkley W, Epstein LD, Gilman RH, Cabrera L, Black RE (2003). "Effects of acute diarrhea on linear growth in Peruvian children". Am J Epidemiol. 157 (2): 166–75. doi:10.1093/aje/kwf179. PMID 12522024 PMID: 12522024 Check
|pmid=value (help). - ↑ 11.0 11.1 11.2 11.3 Waqar Rabbani M, Imran Khan W, Bilal Afzal A, Rabbani W (2013). "Causes of short stature identified in children presenting at a tertiary care hospital in Multan Pakistan". Pak J Med Sci. 29 (1): 53–7. doi:10.12669/pjms.291.2688. PMC 3809182. PMID 24353507 PMID: 24353507 Check
|pmid=value (help). - ↑ Allen DB (1996). "Growth suppression by glucocorticoid therapy". Endocrinol Metab Clin North Am. 25 (3): 699–717. doi:10.1016/s0889-8529(05)70348-0. PMID 8879994 PMID 8879994 Check
|pmid=value (help). - ↑ de Zegher F, Reynaert N, De Somer L, Wouters C, Roelants M (2018). "Growth Failure in Children with Systemic Juvenile Idiopathic Arthritis and Prolonged Inflammation despite Treatment with Biologicals: Late Normalization of Height by Combined Hormonal Therapies". Horm Res Paediatr. 90 (5): 337–343. doi:10.1159/000489778. PMID 29940586 PMID 29940586 Check
|pmid=value (help). - ↑ Bechtold S, Roth J (2009). "Natural history of growth and body composition in juvenile idiopathic arthritis". Horm Res. 72 Suppl 1: 13–9. doi:10.1159/000229758. PMID 19940490 PMID 19940490 Check
|pmid=value (help). - ↑ 15.0 15.1 15.2 Oliveira JC, Siviero-Miachon AA, Spinola-Castro AM, Belangero VM, Guerra-Junior G (2008). "[Short stature in chronic kidney disease: physiopathology and treatment with growth hormone]". Arq Bras Endocrinol Metabol. 52 (5): 783–91. doi:10.1590/s0004-27302008000500010. PMID 18797585 PMID: 18797585 Check
|pmid=value (help). - ↑ Mahan JD, Warady BA, Consensus Committee (2006). "Assessment and treatment of short stature in pediatric patients with chronic kidney disease: a consensus statement". Pediatr Nephrol. 21 (7): 917–30. doi:10.1007/s00467-006-0020-y. PMID 16773402 PMID: 16773402 Check
|pmid=value (help). - ↑ 17.0 17.1 Nandagopal R, Laverdière C, Mulrooney D, Hudson MM, Meacham L (2008). "Endocrine late effects of childhood cancer therapy: a report from the Children's Oncology Group". Horm Res. 69 (2): 65–74. doi:10.1159/000111809. PMID 18059086 PMID 18059086 Check
|pmid=value (help). - ↑ 18.0 18.1 Clayton PE, Shalet SM, Morris-Jones PH, Price DA (1988). "Growth in children treated for acute lymphoblastic leukaemia". Lancet. 1 (8583): 460–2. doi:10.1016/s0140-6736(88)91246-9. PMID 2893877 PMID 2893877 Check
|pmid=value (help). - ↑ Karlberg J, Kjellmer I, Kristiansson B (1991). "Linear growth in children with cystic fibrosis. I. Birth to 8 years of age". Acta Paediatr Scand. 80 (5): 508–14. doi:10.1111/j.1651-2227.1991.tb11894.x. PMID 1872173 PMID 1872173 Check
|pmid=value (help). - ↑ 20.0 20.1 Thommessen M, Heiberg A, Kase BF (1992). "Feeding problems in children with congenital heart disease: the impact on energy intake and growth outcome". Eur J Clin Nutr. 46 (7): 457–64. PMID 1623850 PMID 1623850 Check
|pmid=value (help). - ↑ "StatPearls". 2020. PMID 29763203 PMID: 29763203 Check
|pmid=value (help). - ↑ Seo GH, Kang E, Cho JH, Lee BH, Choi JH, Kim GH; et al. (2015). "Turner syndrome presented with tall stature due to overdosage of the SHOX gene". Ann Pediatr Endocrinol Metab. 20 (2): 110–3. doi:10.6065/apem.2015.20.2.110. PMC 4504991. PMID 26191517 PMID: 26191517 Check
|pmid=value (help). - ↑ Rappold G, Blum WF, Shavrikova EP, Crowe BJ, Roeth R, Quigley CA; et al. (2007). "Genotypes and phenotypes in children with short stature: clinical indicators of SHOX haploinsufficiency". J Med Genet. 44 (5): 306–13. doi:10.1136/jmg.2006.046581. PMC 2597980. PMID 17182655.
- ↑ Monzavi R, Fefferman RA, Pitukcheewanont P (2005). "Prader-Willi syndrome and mosaic Turner's syndrome". J Pediatr Endocrinol Metab. 18 (7): 711–7. doi:10.1515/jpem.2005.18.7.711. PMID 16128248 PMID: 16128248 Check
|pmid=value (help). - ↑ "StatPearls". 2020. PMID 30335302 PMID: 30335302 Check
|pmid=value (help). - ↑ Feingold KR, Anawalt B, Boyce A, Chrousos G, de Herder WW, Dungan K; et al. (2000). "Endotext". PMID 25905353 PMID: 25905353 Check
|pmid=value (help). - ↑ Lodish MB, Gourgari E, Sinaii N, Hill S, Libuit L, Mastroyannis S; et al. (2014). "Skeletal maturation in children with Cushing syndrome is not consistently delayed: the role of corticotropin, obesity, and steroid hormones, and the effect of surgical cure". J Pediatr. 164 (4): 801–6. doi:10.1016/j.jpeds.2013.11.065. PMC 3963265. PMID 24412141 PMID: 24412141 Check
|pmid=value (help). - ↑ Virmani A, Menon PS, Karmarkar MG, Kochupillai N, Seth V, Ghai OP; et al. (1987). "Evaluation of thyroid function in children with undiagnosed short stature in north India". Ann Trop Paediatr. 7 (3): 205–9. doi:10.1080/02724936.1987.11748508. PMID 2445271 PMID: 2445271 Check
|pmid=value (help). - ↑ Collett-Solberg PF, Ambler G, Backeljauw PF, Bidlingmaier M, Biller BMK, Boguszewski MCS; et al. (2019). "Diagnosis, Genetics, and Therapy of Short Stature in Children: A Growth Hormone Research Society International Perspective". Horm Res Paediatr. 92 (1): 1–14. doi:10.1159/000502231. PMC 6979443 Check
|pmc=value (help). PMID 31514194 PMID: 31514194 Check|pmid=value (help). - ↑ Blizzard RM, Bulatovic A (1992). "Psychosocial short stature: a syndrome with many variables". Baillieres Clin Endocrinol Metab. 6 (3): 687–712. doi:10.1016/s0950-351x(05)80119-3. PMID 1524559 PMID: 1524559 Check
|pmid=value (help). - ↑ Derrick KM, Gomes WA, Gensure RC (2018). "Incidence and Outcomes of Pituitary Microadenomas in Children with Short Stature/Growth Hormone Deficiency". Horm Res Paediatr. 90 (3): 151–160. doi:10.1159/000489456. PMID 30261514 PMID: 30261514 Check
|pmid=value (help). - ↑ Velayutham K, Selvan SSA, Jeyabalaji RV, Balaji S (2017). "Prevalence and Etiological Profile of Short Stature among School Children in a South Indian Population". Indian J Endocrinol Metab. 21 (6): 820–822. doi:10.4103/ijem.IJEM_149_17. PMC 5729667. PMID 29285442 PMID: 29285442 Check
|pmid=value (help). - ↑ Grimberg A, Feemster KA, Pati S, Ramos M, Grundmeier R, Cucchiara AJ; et al. (2011). "Medically underserved girls receive less evaluation for short stature". Pediatrics. 127 (4): 696–702. doi:10.1542/peds.2010-1563. PMC 3065076. PMID 21422085 PMID: 21422085 Check
|pmid=value (help). - ↑ 34.0 34.1 34.2 34.3 Musilová J, Kölbel F, Král J, Simper D, Michalová K (1993). "[Cardiovascular changes in Turner's syndrome]". Vnitr Lek. 39 (2): 198–202. PMID 8506669 PMID: 8506669 Check
|pmid=value (help). - ↑ Laron Z (2001). "Insulin-like growth factor 1 (IGF-1): a growth hormone". Mol Pathol. 54 (5): 311–6. doi:10.1136/mp.54.5.311. PMC 1187088. PMID 11577173 PMID: 11577173 Check
|pmid=value (help). - ↑ Ye CJ, Stilgenbauer L, Moy A, Liu G, Heng HH (2019). "What Is Karyotype Coding and Why Is Genomic Topology Important for Cancer and Evolution?". Front Genet. 10: 1082. doi:10.3389/fgene.2019.01082. PMC 6838208 Check
|pmc=value (help). PMID 31737054 PMID: 31737054 Check|pmid=value (help). - ↑ Bi H, Wang G, Li Z, Zhou L, Zhang M, Ye J; et al. (2020). "Erratum: Long Noncoding RNA (lncRNA) Maternally Expressed Gene 3 (MEG3) Participates in Chronic Obstructive Pulmonary Disease through Regulating Human Pulmonary Microvascular Endothelial Cell Apoptosis". Med Sci Monit. 26: e927410. doi:10.12659/MSM.927410. PMC 7518006 Check
|pmc=value (help). PMID 32955036 Check|pmid=value (help). - ↑ Soh SB, Aw TC (2019). "Laboratory Testing in Thyroid Conditions - Pitfalls and Clinical Utility". Ann Lab Med. 39 (1): 3–14. doi:10.3343/alm.2019.39.1.3. PMC 6143469. PMID 30215224 PMID: 30215224 Check
|pmid=value (help). - ↑ Vermeire S, Van Assche G, Rutgeerts P (2006). "Laboratory markers in IBD: useful, magic, or unnecessary toys?". Gut. 55 (3): 426–31. doi:10.1136/gut.2005.069476. PMC 1856093. PMID 16474109 PMID: 16474109 Check
|pmid=value (help). - ↑ Bharadwaj S, Ginoya S, Tandon P, Gohel TD, Guirguis J, Vallabh H; et al. (2016). "Malnutrition: laboratory markers vs nutritional assessment". Gastroenterol Rep (Oxf). 4 (4): 272–280. doi:10.1093/gastro/gow013. PMC 5193064. PMID 27174435 PMID: 27174435 Check
|pmid=value (help). - ↑ Mishra A, Greaves R, Massie J (2005). "The relevance of sweat testing for the diagnosis of cystic fibrosis in the genomic era". Clin Biochem Rev. 26 (4): 135–53. PMC 1320177. PMID 16648884 PMID: 16648884 Check
|pmid=value (help). - ↑ Landon C, Rosenfeld RG (1987). "Short stature and pubertal delay in cystic fibrosis". Pediatrician. 14 (4): 253–60. PMID 3331206 PMID: 3331206 Check
|pmid=value (help). - ↑ Raaijmakers R, Noordam C, Noonan JA, Croonen EA, van der Burgt CJ, Draaisma JM (2008). "Are ECG abnormalities in Noonan syndrome characteristic for the syndrome?". Eur J Pediatr. 167 (12): 1363–7. doi:10.1007/s00431-008-0670-9. PMID 18270737 PMID: 18270737 Check
|pmid=value (help). - ↑ 44.0 44.1 44.2 Kao SC, Waziri MH, Smith WL, Sato Y, Yuh WT, Franken EA (1989). "MR imaging of the craniovertebral junction, cranium, and brain in children with achondroplasia". AJR Am J Roentgenol. 153 (3): 565–9. doi:10.2214/ajr.153.3.565. PMID 2763957 PMID: 2763957 Check
|pmid=value (help). - ↑ Chaudhary V, Bano S (2012). "Imaging in short stature". Indian J Endocrinol Metab. 16 (5): 692–7. doi:10.4103/2230-8210.100641. PMC 3475891. PMID 23087851 PMID: 23087851 Check
|pmid=value (help). - ↑ Lanes R, González Briceño LG (2017). "Alternatives in the Treatment of Short Stature". Adv Pediatr. 64 (1): 111–131. doi:10.1016/j.yapd.2017.03.004. PMID 28688585 PMID: 28688585 Check
|pmid=value (help). - ↑ Cattaneo R, Villa A, Catagni M, Tentori L (1988). "Limb lengthening in achondroplasia by Ilizarov's method". Int Orthop. 12 (3): 173–9. doi:10.1007/BF00547160. PMID 3182120 PMID: 3182120 Check
|pmid=value (help). - ↑ Ottaviani G, Randelli P, Catagni MA (2005). "Segmental cement extraction system (SEG-CES) and the Ilizarov method in limb salvage procedure after total knee cemented prosthesis removal in a former osteosarcoma patient". Knee Surg Sports Traumatol Arthrosc. 13 (7): 557–63. doi:10.1007/s00167-004-0575-8. PMID 15660273 PMID: 15660273 Check
|pmid=value (help). - ↑ Stathis SL, O'Callaghan MJ, Williams GM, Najman JM, Andersen MJ, Bor W (1999). "Behavioural and cognitive associations of short stature at 5 years". J Paediatr Child Health. 35 (6): 562–7. doi:10.1046/j.1440-1754.1999.00427.x. PMID 10634984 PMID: 10634984 Check
|pmid=value (help). - ↑ Kranzler JH, Rosenbloom AL, Proctor B, Diamond FB, Watson M (2000). "Is short stature a handicap? A comparison of the psychosocial functioning of referred and nonreferred children with normal short stature and children with normal stature". J Pediatr. 136 (1): 96–102. doi:10.1016/s0022-3476(00)90057-x. PMID 10636982 PMID: 10636982 Check
|pmid=value (help).