Laron syndrome | |
---|---|
Other names | genetic pituitary dwarfism (1966), Laron dwarfism (1973), Laron-type dwarfism (1984), growth hormone insensitivity (1994), hereditary somatomedin deficiency, growth hormone receptor deficiency (GHRD)(1999)[1] |
Growth hormone | |
Specialty | Endocrinology, Medical Genetics, Pediatrics |
Symptoms | Short stature, truncal obesity, facial dysmorphism[2] |
Usual onset | Present at birth |
Duration | Lifelong |
Causes | Autosomal recessive growth hormone receptor gene mutation (chromosome 5)[2] |
Risk factors | Hypoglycemia, seizures, reduced intellectual capacity, osteopenia[2] |
Differential diagnosis | STAT5b, IGF1 gene mutation, ALS deficiency, IGF-1 receptor mutation, familial short stature, malnutrition, hepatic disease, congenital growth delay, hypopituitarism[1] |
Treatment | IGF-1, Mecasermin[3] |
Frequency | 1–9 / 1,000,000 (approximately 250 known cases worldwide) [4][5] |
Laron syndrome (LS), also known as growth hormone insensitivity or growth hormone receptor deficiency (GHRD), is an autosomal recessive disorder characterized by a lack of insulin-like growth factor 1 (IGF-1; somatomedin-C) production in response to growth hormone (GH; hGH; somatotropin).[6] It is usually caused by inherited growth hormone receptor (GHR) mutations.[2][6]
Affected individuals classically present with short stature between −4 and −10 standard deviations below median height, obesity, craniofacial abnormalities, micropenis, low blood sugar, and low serum IGF-1 despite elevated basal serum GH.[7][5][8]
LS is a very rare condition with a total of 250 known individuals worldwide.[4][5] The genetic origins of these individuals have been traced back to Mediterranean, South Asian, and Semitic ancestors, with the latter group comprising the majority of cases.[5] Molecular genetic testing for growth hormone receptor gene mutations confirms the diagnosis of LS, but clinical evaluation may include laboratory analysis of basal GH, IGF-1 and IGFBP levels, GH stimulation testing, and/or GH trial therapy.
People with LS are unresponsive to growth hormone therapy; the disease is instead treated mainly with recombinant IGF-1, Mecasermin.[3]
Evidence has suggested that people with Laron syndrome have a reduced risk of developing cancer and diabetes mellitus type II, with a significantly reduced incidence and delayed age of onset of these diseases compared to their unaffected relatives.[9][10] The molecular mechanisms of increased longevity and protection from age-related disease among people with LS is an area of active investigation.[11]