Original articleLaron's dwarfism: Studies on the nature of the defect*
References (31)
- et al.
An unusual variety of endocrine dwarfism: Subresponsiveness to growth hormone in a sexually mature dwarf
Lancet
(1968) - et al.
Pseudohypopituitary dwarfism with normal plasma growth hormone and low serum sulfation factor
J. Pediatr.
(1972) - et al.
Studies with human growth hormone (HGH): An attempt to correlate metabolic response during short-term administration with linear growth during prolonged therapy
Am. J. Med.
(1965) Rapid photoelectric method for the determination of glucose in blood and urine
J. Biol. Chem.
(1937)- et al.
Endocrine and metabolic adaptation to obesity and starvation
Am. J. Clin. Nutr.
(1968) - et al.
Implications of growth hormone release in sleep
Metabolism
(1970) - et al.
Genetic pituitary dwarfism with high serum concentration of growth hormone; a new inborn error of metabolism
Isr. J. Med. Sci.
(1966) - et al.
Pituitary dwarfism with high serum levels of growth hormone
Isr. J. Med. Sci.
(1968) - et al.
Genetic aspects of pituitary dwarfism due to absence or biological inactivity of growth hormone
Isr. J. Med. Sci.
(1968) - et al.
Administration of growth hormone to patients with familial dwarfism with high plasma immunoreactive growth hormone: Measurement of sulfation factor, metabolic and linear growth responses
J. Clin. Endocrinol. Metab.
(1971)
Defective sulfation factor generation: A possible etiological link in dwarfism
Trans. Assoc. Am. Physicians
Dwarfism with elevated levels of plasma growth hormone
N. Engl. J. Med.
Familial prenatal dwarfism with elevated serum immunoreactive growth hormone levels and endorgan unresponsiveness
Maandschr. Kindergeneeskd.
Primary plasma growth factor deficiency (sulfation factor and thymidine factor) presenting as hyposomatotrophic dwarfism
Radiographic atlas of skeletal development of the hand and wrist
Cited by (42)
Genetic causes of proportionate short stature
2018, Best Practice and Research: Clinical Endocrinology and MetabolismCitation Excerpt :Nomenclature has been confusing and evolved over time. The early descriptive name of “genetic pituitary dwarfism with high-serum GH” was changed to Laron dwarfism [54], Laron type dwarfism [55], and subsequently Laron syndrome (ls) [56], GH insensitivity, or GHR deficiency [57]. Because GH resistance can be primary or secondary, a consensus classification and nomenclature of GH insensitivity syndromes was published in 1993 [58].
Fifty seven years of follow-up of the Israeli cohort of Laron Syndrome patients-From discovery to treatment
2016, Growth Hormone and IGF ResearchCitation Excerpt :So the “IGF-I generation test” was born. The name Laron Dwarfism (later changed to Laron Syndrome (LS)) was coined by Elders et al. [9]. Definite evidence for GH resistance was found by liver biopsy in 2 LS patients, showing that I125hGH did not bind to the liver membranes of these patients, in contrast to membranes from controls (taken during renal transplants) [10].
Lessons from 50 years of study of laron syndrome
2015, Endocrine PracticeCitation Excerpt :In 1966 (1) and in 1968 (2), we described a disease characterized by severe growth retardation, obesity, and small genitalia, resembling congenital growth hormone (GH) deficiency (3) but with high serum GH levels and low to undetectable serum insulin-like growth factor 1 (IGF- 1). This disease was subsequently coined Laron dwarfism (4) and changed later to Laron syndrome (LS; Online Mendelian Inheritance in Man# 262500). The negative feedback between low IGF-1 and the hypothalamic growth hormone (growth hormone–releasing hormone) leads to an increased secretion of pituitary GH (5).
Molecular basis of Laron dwarfism
1991, Trends in Endocrinology and Metabolism
- *
Studies at the University of Arkansas Medical Center were supported in part by United States Public Health Service Grants, NS07638 and AM 12011; studies at Harbor General Hospital were supported by United States Public Health Service Grant AM 05638; clinical studies performed at Washington University School of Medicine were supported by United States Public Health Service Grant 2 R01 AM0156 from the National Institute of Arthritis and Metabolic Diseases.
- *
Recipient of a Career Program Award 5K3-HD-23-325.
- **
Recipient of a Clinical Research Center Research Grant RR 00036.
- ***
Recipient of United States Public Health Service Grant HD04270.
- ****
Recipient of Career Program Award 5K3-AM 18415.