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1.
Endocr Rev ; 37(1): 62-110, 2016 Feb.
Article in English | MEDLINE | ID: mdl-26720129

ABSTRACT

Growth failure is frequently encountered in children with chronic inflammatory conditions like juvenile idiopathic arthritis, inflammatory bowel disease, and cystic fibrosis. Delayed puberty and attenuated pubertal growth spurt are often seen during adolescence. The underlying inflammatory state mediated by proinflammatory cytokines, prolonged use of glucocorticoid, and suboptimal nutrition contribute to growth failure and pubertal abnormalities. These factors can impair growth by their effects on the GH-IGF axis and also directly at the level of the growth plate via alterations in chondrogenesis and local growth factor signaling. Recent studies on the impact of cytokines and glucocorticoid on the growth plate further advanced our understanding of growth failure in chronic disease and provided a biological rationale of growth promotion. Targeting cytokines using biological therapy may lead to improvement of growth in some of these children, but approximately one-third continue to grow slowly. There is increasing evidence that the use of relatively high-dose recombinant human GH may lead to partial catch-up growth in chronic inflammatory conditions, although long-term follow-up data are currently limited. In this review, we comprehensively review the growth abnormalities in children with juvenile idiopathic arthritis, inflammatory bowel disease, and cystic fibrosis, systemic abnormalities of the GH-IGF axis, and growth plate perturbations. We also systematically reviewed all the current published studies of recombinant human GH in these conditions and discussed the role of recombinant human IGF-1.


Subject(s)
Arthritis, Juvenile/therapy , Cystic Fibrosis/therapy , Evidence-Based Medicine , Growth Disorders/prevention & control , Inflammatory Bowel Diseases/therapy , Practice Guidelines as Topic , Puberty, Delayed/prevention & control , Adolescent , Animals , Arthritis, Juvenile/immunology , Arthritis, Juvenile/pathology , Arthritis, Juvenile/physiopathology , Child , Combined Modality Therapy , Cystic Fibrosis/immunology , Cystic Fibrosis/pathology , Cystic Fibrosis/physiopathology , Drug Therapy, Combination , Growth Disorders/etiology , Growth Disorders/immunology , Growth Disorders/pathology , Growth Plate/drug effects , Growth Plate/immunology , Growth Plate/metabolism , Growth Plate/pathology , Growth Substances/genetics , Growth Substances/metabolism , Growth Substances/therapeutic use , Human Growth Hormone/genetics , Human Growth Hormone/metabolism , Human Growth Hormone/therapeutic use , Humans , Inflammatory Bowel Diseases/immunology , Inflammatory Bowel Diseases/pathology , Inflammatory Bowel Diseases/physiopathology , Insulin-Like Growth Factor I/genetics , Insulin-Like Growth Factor I/metabolism , Insulin-Like Growth Factor I/therapeutic use , Puberty, Delayed/etiology , Puberty, Delayed/immunology , Puberty, Delayed/pathology , Recombinant Proteins/metabolism , Recombinant Proteins/therapeutic use
2.
Nat Rev Gastroenterol Hepatol ; 11(10): 601-10, 2014 Oct.
Article in English | MEDLINE | ID: mdl-24957008

ABSTRACT

Crohn's disease in childhood causes linear growth retardation, which has a substantial effect on management of this disease. By contrast, growth is rarely a problem in children presenting with ulcerative colitis. Depending on how growth failure is defined, approximately one-third of children with Crohn's disease have growth retardation at diagnosis. Although corticosteroids can suppress growth, decreased height at diagnosis demonstrates that this finding is a consequence of the disease and not merely an adverse effect of treatment. Both inflammation and undernutrition contribute to decreased height velocity. Increased cytokine production acts both on the hepatic expression of insulin-like growth factor 1 (IGF-1) and at chondrocytes of the growth plates of long bones. Growth hormone insensitivity caused by deranged immune function is a major mechanism in growth retardation. Resolution of inflammation is the cornerstone of treatment, but current studies on growth hormone and IGF-1 might yield therapies for those children whose inflammation is refractory to treatment.


Subject(s)
Adrenal Cortex Hormones/adverse effects , Androgens/therapeutic use , Crohn Disease/drug therapy , Growth Disorders/drug therapy , Immunosuppressive Agents/therapeutic use , Insulin-Like Growth Factor I/metabolism , Puberty, Delayed/drug therapy , Tumor Necrosis Factor-alpha/antagonists & inhibitors , Child , Crohn Disease/complications , Growth Disorders/etiology , Growth Disorders/immunology , Humans , Inflammation/complications , Inflammatory Bowel Diseases/complications , Inflammatory Bowel Diseases/drug therapy , Insulin-Like Growth Factor I/therapeutic use , Malnutrition/etiology , Puberty, Delayed/etiology , Puberty, Delayed/immunology
3.
Dermatol Clin ; 28(2): 357-9, xii, 2010 Apr.
Article in English | MEDLINE | ID: mdl-20447503

ABSTRACT

Puberty is the acquisition of secondary sexual characteristics, associated with a growth spurt, resulting in the attainment of reproductive function and final adult height. Delayed puberty is defined as the absence of any pubertal development at an age 2 standard deviations (SD) more than the mean, which corresponds to an age of approximately 14 years for boys and 13 years for girls. The degree to which growth and pubertal development are affected in chronic illness depends on the disease itself, as well as factors such as age of onset, duration and severity; the earlier the onset and the more severe the disease, the greater the effect on growth and pubertal development. Most children with severe types of epidermolysis bullosa have abnormal growth and pubertal delay. The possible pathophysiology is discussed.


Subject(s)
Epidermolysis Bullosa/complications , Epidermolysis Bullosa/immunology , Inflammation/complications , Puberty, Delayed/etiology , Puberty, Delayed/immunology , Adolescent , Adolescent Development , Female , Humans , Male
4.
Lik Sprava ; (3-4): 56-9, 2003.
Article in Russian | MEDLINE | ID: mdl-12889359

ABSTRACT

The paper submits data on the antigenic composition of HLA system in members of nuclear families of adolescent boys presenting with the delay in sexual maturation. Positive and negative associations of particular antigens with sexual underdevelopment are stated. Estimated in the families was the highest incidence rate of gaplotypes A 28-B 40, A 28-B 8, A 1-B 40, and A 3-B 40. The authors come out with a suggestion that it might be possible to use the identified antigens in prognostication of delayed puberty.


Subject(s)
HLA Antigens/genetics , Nuclear Family , Puberty, Delayed/genetics , Adolescent , Adult , Female , Gene Frequency , Haplotypes , Humans , Male , Middle Aged , Puberty, Delayed/immunology , Ukraine
5.
Tsitol Genet ; 34(1): 43-7, 2000.
Article in Russian | MEDLINE | ID: mdl-10808541

ABSTRACT

Frequency distribution of HLA antigens of A and B loci was examined in 138 adolescent boys aged 14-18 with delayed sexual development (DSD) of stages I-III, residing in the north-eastern region of Ukraine. Increase of A28- and B40-antigens and haplotypes A1-B40, A28-B40, A10-B40 determination frequencies was established. There were revealed positive and negative correlation between some of HLA antigens and DSD. Relative and attributive risks of DSD formation were calculated.


Subject(s)
HLA Antigens/genetics , Puberty, Delayed/genetics , Adolescent , Alleles , Chi-Square Distribution , Gene Frequency , Haplotypes , Humans , Male , Phenotype , Puberty, Delayed/immunology , Risk Factors , Ukraine
7.
Acta Endocrinol (Copenh) ; 119(3): 333-8, 1988 Nov.
Article in English | MEDLINE | ID: mdl-3188808

ABSTRACT

Insulin-like growth factor I levels were measured in a parallel fashion in 77 extracted sera using the INCSTAR RIA (radioimmunoassay) and in the EDTA plasma of the same subjects by the NICHOLS RIA. The subjects suffered from untreated hGH deficiency, short stature, delayed and precocious puberty and acromegaly. Significant differences (P less than 0.05) were found between the mean IGF-I levels of all groups using both RIA systems. However, using the INCSTAR RIA, 85% of IGF-I values in untreated hGH deficiency were below normal, and a rise in IGF-I detected in the sera of all 5 patients who were treated with hGH. Using NICHOLS RIA, 55% of basal IGF-I values were below normal and a hGH-stimulated rise in IGF-I was found in only two of the treated patients. The INCSTAR RIA seems more precise and reproducible than the NICHOLS RIA and enables better discrimination of hGH-deficient patients from age-matched controls.


Subject(s)
Insulin-Like Growth Factor I/blood , Radioimmunoassay/methods , Somatomedins/blood , Acromegaly/immunology , Adolescent , Adult , Child , Child, Preschool , Female , Growth Disorders/immunology , Growth Hormone/administration & dosage , Growth Hormone/deficiency , Humans , Male , Puberty, Delayed/immunology , Puberty, Precocious/immunology
8.
Obstet Gynecol ; 69(3 Pt 2): 503-5, 1987 Mar.
Article in English | MEDLINE | ID: mdl-3543775

ABSTRACT

The administration of pulsatile gonadotropin-releasing hormone (GnRH) has received increasing attention as a method of inducing ovulation or initiating puberty. Few side effects have been reported, although urticarial allergic reactions have been reported in the male. An 18-year-old female with hypogonadotropic hypogonadism and anosmia due to lack of endogenous GnRH was treated for 230 days using subcutaneous GnRH in an attempt to induce physiologic puberty. Just before anticipated menarche, therapy was discontinued because of the appearance of an urticarial reaction at the injection site as well as at previous injection sites. The presence of immunoglobulin G (IgG) antibodies against GnRH were subsequently identified in the patient's serum. These results further confirm the potential for antibody production to this small natural peptide in the female not previously exposed to GnRH. Some practical considerations for this form of therapy are highlighted.


Subject(s)
Amenorrhea/drug therapy , Drug Hypersensitivity/etiology , Pituitary Hormone-Releasing Hormones/adverse effects , Puberty, Delayed/drug therapy , Urticaria/chemically induced , Adolescent , Amenorrhea/immunology , Antibody Formation , Female , Humans , Immunoglobulin G/immunology , Puberty, Delayed/immunology , Urticaria/immunology
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