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PubMed1998

[Consensus 'diagnosis of short stature in children.' National Organization for Quality Assurance in Hospitals].

Each year about 2500 children in the Netherlands are referred to a specialist because of short stature. Aim of the consensus meeting: 'Diagnosis of short stature in childhood' by general practitioners, pediatricians and pediatric endocrinologists was to promote early diagnosis and treatment of aberrant growth but also to prevent unnecessary referral and interventions. For optimal treatment of growth disorders early diagnosis is of the utmost importance. Short stature is best detected by the use of standard deviation scores (SDS) instead of percentile lines. As cut-off point for referral SDS < -1.3 (< P10) was chosen in order to identify risk groups that need further evaluation. Based on international consensus a diagnostic classification of short stature is possible, distinguishing normal variants and (or) idiopathic short stature from primary and secondary growth disorders. Using target length, the growth curve in the SDS diagram, the actual age and puberty signs, the general practitioner can use a flow chart to determine whether there is a growth problem and whether this needs treatment in primary or secondary health care. Measuring skeletal age has no additional value. Attention should also be given to psychosocial problems as the cause or the effect of short stature.

Adolescent↗
PubMed1996

Hematologic disorders and growth factor support in HIV infection.

During the course of HIV disease a broad spectrum of hematologic disorders develop including abnormalities in blood cell generation, survival, and function Alterations in coagulation parameters may evolve associated with disruption of immunoglobulin or factor production. This article reviews the manifestations and pathophysiology of these abnormalities and discusses the role for growth factor support.

Blood Coagulation Disorders↗
PubMed1997

Urinary growth hormone excretion: results of a multicenter study in France.

Urinary growth hormone excretion (uGH), expressed as the average of three consecutive nocturnal measurements, was studied in 324 prepubertal and pubertal children without (n = 188) or with (n = 136) growth disorders. In prepubertal control children (n = 127), the mean uGH was 11.9 +/- 4.9 ng/l without any correlation with sex or age. During puberty, a significant increase of uGH was observed in both sexes (boys: prepubertal 12.3 +/- 4.84 vs. pubertal 16.2 +/- 4.7 ng/l; girls: prepubertal 11.6 +/- 4.99 vs. pubertal 18.3 +/- 8.5 ng/l). In children with growth disorders, the results observed in various categories show a highly significant decrease in organic hypopituitary patients (p < 10(-6)) and obese subjects (p < 10(-6)) when compared to normal prepubertal children. In contrast, a significant increase was observed in 5 Laron-type dwarfisms (p < 10(-6)). However, in 24 children with partial growth hormone deficiency assessed by blood measurements (two pharmacological tests between 5 and 10 ng/ml), the results were not significantly different from the controls (13.6 +/- 6.4 ng/l). In a group of 66 children with short stature and normal blood response to pharmacological tests, uGH concentrations were significantly higher than those of the control group (17.3 +/- 8.71 ng/l, p < 10(-6)). The data suggest that uGH measurements lead to findings comparable to blood measurements, avoiding the disturbance of pharmacological tests, in well-delimited categories of patients. In contrast, uGH measurements are not the best way to detect partial GH-deficient children, but may be used to screen partial peripheral GH resistance in children with nonendocrine short stature.

Adolescent↗
PubMed1983

[Stunted growth].

According to recent investigations more than half of all growth disorders are due to growth hormone (GH) deficiency. I. The cause of the classic hypothalamo-pituitary dwarfism is: 1. perinatally acquired lesions of the hypothalamus; 2. suprasellar tumours; 3. brain malformations; 4. hereditary disturbances of GH-synthesis. - II. Constitutional delay of growth and adolescent development is clinically characterised by harmonious delay of growth, skeletal development and sexual maturation. The typical aspect of the pituitary dwarf is missing. Whereas provocation tests for GH do not show reliable deviations, assessment of the spontaneous GH secretion during sleep usually demonstrates a significant GH-deficit. - III. Impairments of GH synthesis with production of a hormone which reacts in the RIA but exhibits reduced biological effectivity causes the same clinical picture as constitutional delay. The disorders I--III can successfully be treated by GH. - IV. Familial short stature is based on the summation of hereditary anlages of the parents. In principle, it is no endocrine disorder. However, the combination with disorders II and III occurs frequently ("Small/Delay" acc. to Tanner). - V. Intrauterine growth retardation is caused by maternal, placental or fetal factors. With most of the "small for dates" growth prognosis is good. However, if teratogenic agents, particularly alcohol is involved, and if the damage occurs in the first months of gestation, the prognosis is unfavorable. - VI. A great number of genetic disorders is connected with pre- and/or postnatal growth retardation, combined with typical malformations. Apart from few exceptions these syndromes are rare. Endocrine deviations are missing. - The therapeutic possibilities of GH and anabolics are thoroughly discussed.

Birth Injuries↗
PubMed2001

Diagnostic value of serum IGF-I and IGFBP-3 in growth hormone disorders in adults.

OBJECTIVE: To investigate the diagnostic value of serum insulin-like growth factor-I (IGF-I) and insulin-like growth factor-binding protein-3 (IGFBP-3) measurements in adult patients with acromegaly and GH deficiency (GHD). METHODS: Serum IGF-I and IGFBP-3 levels were measured in 39 active acromegalic patients, 34 adult patients with GHD and 150 healthy adults. Disease activity in patients with acromegaly was confirmed by nadir GH levels during an oral glucose tolerance test (OGTT). Among patients with acromegaly, 15 had not been treated previously and 24 had been treated but not cured. GHD in adults was diagnosed by an insulin tolerance test (ITT). Among patients with GHD, 15 were aged 20-40 years (9 men and 6 women) and 19 were aged over 40 years (9 men and 10 women). One hundred and fifty healthy subjects were recruited as a control group. To compare the individual serum IGF-I and IGFBP-3 levels of patients with the results of the gold standard, we calculated age- and sex-corrected standard deviation scores (SDS) for individual IGF-I and IGFBP-3 levels. The sensitivities of serum IGF-I and IGFBP-3 measurements for the disease diagnosis were analyzed using the mean +/- 2 SD of the values of healthy control subjects as a diagnostic cutoff, defining 95% specificity. RESULTS: The mean IGF-I and IGFBP-3 SDS levels were significantly higher in active acromegalic patients, both untreated and treated but not cured, than in the control subjects (p < 0.05). The sensitivities of serum IGF-I and IGFBP-3 measurements for the diagnosis of acromegaly were 97.4 and 81.8%, respectively. In untreated patients with acromegaly, the sensitivities of serum IGF-I and IGFBP-3 measurements for the diagnosis of disease were 100 and 100%, while these were 95.8 and 72.7% in treated patients with acromegaly. In adult patients with GHD, the mean IGF-I and IGFBP-3 SDS were significantly lower than those of the control subjects (IGF-I, -2.2 +/- 0.8 vs. 0.0 +/- 1.0 SDS, p < 0.0001); IGFBP-3, -1.7 +/- 1.2 vs. 0.0 +/- 1.0 SDS, p < 0.0001), but there was a considerable overlap between GHD in adults and the controls. In all patients with GHD, the sensitivities of serum IGF-I and IGFBP-3 measurements were 64.7 and 52.9%, respectively. In the group of women aged 20-40 years, the sensitivity of IGF-I measurement for the diagnosis of GHD was 100%, although the number of patients was only 6. CONCLUSION: Both serum IGF-I and IGFBP-3 measurements are comparable to an oral glucose tolerance test in patients with untreated acromegaly, but in acromegalic patients that have undergone surgery and/or radiotherapy, serum IGF-I is more valuable for determining disease activity than serum IGFBP-3. Serum IGF-I and IGFBP-3 measurements are not valuable for the diagnosis of GHD in adults, but in women aged 20-40 years serum IGF-I measurement appears to be useful in the diagnosis of GHD.

Acromegaly↗
PubMed2002

A variant microcephalic osteodysplastic slender-bone disorder with growth hormone deficiency and a pigmentary retinopathy.

We present the case of a 3-year-old boy with post-natal growth failure, microcephaly, developmental delay, facial dysmorphism, an evolving pigmentary retinopathy, pituitary hypoplasia, micropenis, and growth hormone (GH) deficiency. He has a microcephalic osteodysplastic slender-bone disorder with disharmonic delayed osseous maturation, most closely resembling patients with microcephalic osteodysplastic primordial dwarfism type II (MOPD II). Intrauterine growth retardation, a universal finding in the MOPD II, was absent in our patient.

Abnormalities, Multiple↗
PubMed1992

Serum and plasma epidermal growth factor in thyroid disorders.

Epidermal growth factor (EGF) is an important mitogen and its secretion in neonatal animals has been shown to be affected by thyroid hormone levels. EGF in blood of humans is found in both platelets (as reflected in its serum level) and in plasma; its origin in plasma remains unclear. Serum and plasma EGF were studied in a group of patients with thyroid disorders. Twenty hyperthyroid subjects (3M, 17F) aged 37.3 +/- 14.9 years and 10 hypothyroid patients (3M, 7F) aged 58.3 +/- 18.6 years were studied before and after euthyroidism was restored. Before treatment, serum EGF in the hyperthyroid patients was elevated compared to normal controls (501 +/- 376 vs 270 +/- 154 pmol/l, p less than 0.001). After treatment of hyperthyroidism, serum EGF returned to the normal levels (232 +/- 176 pmol/l). In contrast, serum EGF was not significantly different in the hypothyroid subjects either before or after treatment (151 +/- 194 and 237 +/- 153 pmol/l respectively). A significant correlation (r = 0.461, p less than 0.001) between serum EGF and serum-free thyroxine index (FTI) was found when all samples from both untreated and treated hyper- and hypothyroid patients were examined. Multiple regression analysis revealed that both serum FTI and platelet count independently affected the serum EGF levels. Similarly, plasma EGF was also elevated in untreated hyperthyroid patients with a median of 26.4 pmol/l (range less than 16.6-88.0), whereas all normal controls and hypothyroid subjects had unmeasurable levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

The neurocristopathies: reinterpretation based upon the mechanism of abnormal morphogenesis.

This review sets forth a broadened interpretation of the neurocristopathies based on the current understanding of the role of neural crest cells in normal development. Two general types of cristopathies are defined predicated on the abnormal mechanism involved in production of the defect or condition. Defects and disorders which constitute the originally defined neurocristopathies including pheochromocytoma, neurofibromatosis, and the multiple endocrine adenomatoses are best explained as dysplasias of neural crest derivatives. Affected individuals rarely exhibit true malformation of structure but do carry a lifetime risk for disordered growth of crest derived tissue. On the other hand, defects and disorders which derive from migrational abnormalities primarily of cranial neural crest cells such as frontonasal dysplasia, the DiGeorge sequence, and Waardenberg syndrome represent true malformations. The spectrum of involvement is usually definable at the time of diagnosis and disordered growth of crest derived tissue does not occur. The clinical implications of this distinction are discussed.

Cell Differentiation↗
PubMed2006

Matrix metalloproteinases: role in skeletal development and growth plate disorders.

Differentiation is the cellular process that regulates development of long bones and joint surface cartilage of synovial cavities. Growth plate cartilage development is commonly referred to as endochondral ossification which is the end stage of long bone development. Endochondral ossification proceeds as a continuum of chondrocyte proliferation cycles followed by non-proliferative phases coupled to extracellular matrix protein transformations that are regulated by proteins of the hedgehog family and by parathyroid-hormone-related peptide and its receptor, the parathyroid-hormone-related peptide receptor. A compelling body of evidence has now emerged implicating matrix metalloproteinases (MMPs) in the process of long bone lengthening and endochondral ossification. Among the MMPs, MMP-13 (collagenase-3), MMP-9 (92-kDa gelatinase; gelatinase B) and MMP-14 (MT1-MMP) are the most abundant proteinases that regulate cellular migration, alterations in the extracellular matrix and apoptosis in growth plate cartilage. Murine mutation or ablation models of growth plate development that target MMPs often result in skeletal abnormalities, indicating the critical role that MMPs play in these animal models and in skeletal maturation. Many of the MMPs that have been identified as regulating the spatial and temporal changes in rodent and rabbit endochondral ossification have also been identified by in situ hybridization and immunohistochemical analysis of human long bone development. Genetic manipulation to correct defective or dysfunctional MMP genes or MMP activity found in certain human chondrodysplasias may provide a novel strategy for treating medical disorders characterized by skeletal anomalies.

Animals↗
PubMed2006

Bystander effects are induced by CENU treatment and associated with altered protein secretory activity of treated tumor cells: a relay for chemotherapy?

In a previous study, it was reported that secondary untreated melanoma tumors implanted several weeks after and at distance from primary chloroethylnitrosourea (CENU)-treated tumors underwent differentiation and growth inhibition. To see whether the primary treated tumor released soluble factors that mediated the secondary tumor response, serum transfer experiments were performed in vivo. Administration of serum from CENU-treated tumor-bearing donors arrested tumor proliferation, decreased vessel formation and induced tumor metabolite alterations encompassing glutathione decrease and polyunsaturated fatty acid and phosphoethanolamine increase. These changes mimicked secondary tumor phenotype. To reproduce the model in vitro, cell culture supernatant transfer experiments were performed. CENU-treated cell cultures showed polyploidy and reactive oxygen species (ROS) production. Cell cultures challenged by a conditioned medium of CENU-treated cells underwent growth inhibition, cytoskeleton disorders, cytokinesis retardation, metabolite alterations, glutathione decrease and phosphoethanolamine increase, without ROS elicitation. Proteomics of CENU-treated cell conditioned media revealed altered protein secretion activity by CENU-treated cells. Among de novo secreted proteins, the most expressed were phosphatidylethanolamine-binding protein (PEBP), cardiovascular heat shock protein (cHsp), Rho-associated coiled-coil forming kinase 2 (ROCK) and actin fragments. These proteins testified of cytoskeleton disorders, growth inhibition and metabolite alterations. This article demonstrates the release by CENU-treated tumors of growth inhibitory differentiation-inducing soluble factors. These factors mediate remote bystander effects and attest persistent biological activity of residual tumors after chemotherapy.

Actins↗
PubMedDate not supplied

Central nervous system malformations in a perinatal/neonatal autopsy series.

Congenital malformations of the central nervous system (CNS) are among the most common anomalies, but data on the incidence of CNS malformations in autopsy populations are scant. We examined 4122 autopsies between the years 1958 and 1995. There were 363 cases (8.8%) with CNS malformations; 235 were neonates and 128 stillborns. The overall gender ratio was 1:1, although more male neonates and more female stillborns had malformations. The body weights ranged from 24 to 6440 g. Neural tube defects were the most common types of malformations (45.5%) and included anencephaly, meningoencephalocele, meningocele/meningomyelocele, craniospinal rachischisis, and spina bifida occulta. The incidences of other malformations were: congenital hydrocephalus (12.4%), neuronal/glial proliferation disorders such as micro- and macrocephaly (8.8%), neuronal migration disorders (8.8%), prosencephalon growth disorders such as holoprosencephaly and arhinencephaly (8.5%), abnormalities of the midline structures such as agenesis of corpus callosum (4.1%), developmental cysts (3.3%), cerebellar malformations (3%), and vascular malformations (2%). Miscellaneous malformations (3%) consisted of acephalia in four cases with twin reversed arterial perfusion (TRAP), two cases of hydranencephaly, and four cases of rare degenerative and metabolic encephalopathies.

Autopsy↗
PubMed1997

Abnormal expression of the p53 tumor suppressor gene in the conjunctiva of patients with pterygium.

PURPOSE: To determine whether pterygium is a disorder of abnormal growth by examining the expression of the p53 gene in the conjunctiva of patients with pterygium. METHODS: Immunostaining for abnormal expression of p53 was performed using mouse monoclonal antibody to human p53, pAb 240, on six eyes with primary pterygium and two eyes with recurrent pterygium. RESULTS: In three of the eight eyes with pterygium, specimens were positive for abnormal expression in the epithelium of the pterygium and in the superior bulbar conjunctiva. CONCLUSION: Abnormal p53 expression in the epithelium of primary and recurrent pterygium specimens suggests that pterygium is a growth disorder rather than a degeneration.

Antibodies, Monoclonal↗
PubMed1965

NEOPLASIA IN A CORAL?

Anomalous growths of the colonial, deep-water coral Madrepora kauaiensis are interpreted as neoplasia. Since tissue was not preserved, evidence is derived solely from skeletal examination and consists of unusually rapid growth and progressively disordered growth of skeletal structures.

Animals↗
PubMed2005

Mecasermin rinfabate: insulin-like growth factor-I/insulin-like growth factor binding protein-3, mecaserimin rinfibate, rhIGF-I/rhIGFBP-3.

Insmed is developing mecasermin rinfabate, a recombinant complex of insulin-like growth factor-I (rhIGF-I) and binding protein-3 (rhIGFBP-3) [insulin-like growth factor-I/insulin-like growth factor binding protein-3, rhIGF-I/rhIGFBP-3, SomatoKine], for a number of metabolic and endocrine indications. In the human body, IGF-I circulates in the blood bound to a binding protein-3 (IGFBP-3), which regulates the delivery of IGF-I to target tissues, and particular proteases clip them apart in response to stresses and release IGF-I as needed. IGF-I, a naturally occurring hormone, is necessary for normal growth and metabolism. For the treatment of IGF-I deficiency, it is desirable to administer IGF-I bound to IGFBP-3 to maintain the normal equilibrium of these proteins in the blood. Mecasermin rinfabate (rhIGF-I/rhIGFBP-3) mimics the effects of the natural protein complex in the bloodstream and would augment the natural supply of these linked compounds. The most advanced indication in development of mecasermin rinfabate is the treatment of severe growth disorders due to growth hormone insensitivity syndrome (GHIS), also called Laron syndrome. GHIS is a genetic condition in which patients do not produce adequate quantities of IGF because of a failure to respond to the growth hormone signal. This results in a slower growth rate and short stature. Mecasermin rinfabate also has potential as replacement therapy for IGF-I, which may become depleted in indications such as major surgery, organ damage/failure, traumatic injury, cachexia and severe burn trauma. It also has potential for the treatment of osteoporosis. Mecasermin rinfabate was developed by Celtrix using its proprietary recombinant protein production technology. Subsequently, Celtrix was acquired by Insmed Pharmaceuticals on 1 June 2000. Insmed and Avecia of the UK have signed an agreement for manufacturing mecasermin rinfabate and its components, rhIGF-1 and rhIGFBP-3. CGMP clinical production of mecasermin rinfabate and its components will be carried out in Avecia's Advanced Biologics Centre, Billingham, UK, which manufactures recombinant-based medicines and vaccines at the capacity of up to 1000L. In April 2004, Insmed announced that it acquired a lease to operate the manufacturing facility formerly operated by Baxter for the commercial production of SomatoKine in Boulder, CO, USA. With the two manufacturing facilities for SomatoKine, Insmed plans to meet the development and commercial demands for the product over the next several years. In its 2003 Form-10K, Insmed announced plans to conduct comparative studies with the previously used drug substance and the new substance produced by Avecia. The comparative data will be included in the regulatory filing for mecasermin rinfabate. Mecasermin rinfabate was originally licensed to Welfide for Japan. On 1 October 2001, Welfide Corporation merged with Mitsubishi-Tokyo Pharmaceuticals to form Mitsubishi Pharma Corporation. The new company is a subsidiary of Mitsubishi Chemical. In October 2004, Insmed announced that Tzamal Pharma has been granted exclusive distribution and marketing rights for mecasermin rinfabate in certain Middle Eastern territories including Israel. Tzamal Pharma also acquired exclusive rights to Insmed's named patient programme for the agent in these territories. Tzamal Pharma intends to begin the appropriate registration activities for mecasermin rinfabate in the treatment of children with growth hormone-insensitivity syndrome. This pivotal, 12-month, multicentre, open-label trial in 30 children with GHIS was initiated in June 2003 and was designed to evaluate the safety and efficacy of the agent in prepubescent children with GHIS. The 6-month endpoint data analysis showed that mecasermin rinfabate given as a once-daily injection was safe and well tolerated. The agent demonstrated a significant increase in height velocity in children with GHIS similar to that observed by Pfizer in their pivotal study with twice-daily injections of rhIGF-I. The full results from the pivotal trial are expected in 2005. In April 2003 Insmed initiated a named patient programme in Europe that will make available mecasermin rinfabate for the treatment of GHIS-Laron syndrome. The treatment of patients was initiated in Scandinavia, with authorisation pending in several other European countries. Mecasermin rinfabate will be made available to those GHIS patients who, in the opinion of their doctor, may benefit from IGF-I therapy. At precommercial scale quantities, the drug will be available on a limited basis.A phase II dose-ranging study in children with GHIS was completed at Saint Bartholomew's and the Royal London School of Medicine, London, UK. A single dose of mecasermin rinfabate delivered the same amount of IGF-1 as two daily injections of unbound IGF-1. No adverse events were reported. Insmed has acquired an exclusive licence to Pharmacia's regulatory filings concerning yeast-derived insulin-like growth factor 1 (IGF-1). These filings were used by Pharmacia to receive marketing approvals in several European countries and also in the IND application with the US FDA. Insmed believes that this licence will facilitate the development of mecasermin rinfabate for the treatment of children with GHIS. In January 2003, Insmed announced positive results from a double-blind, placebo-controlled, dose-ranging study of mecasermin rinfabate in adolescent patients with type 1 diabetes receiving insulin therapy. The study was conducted at the University of Cambridge, Cambridge, UK, under supervision of Prof. D. Dunger. The researchers from The Robarts Research Institute and the University of Western Ontario, Canada (leading investigator T.L. Delovitch, the Sheldon H. Weinstein scientist in Diabetes at the University of Western Ontario) have found that mecasermin rinfabate complex was significantly more effective than IGF-1 in reducing the severity of insulitis, beta cell destruction and delaying the onset of type 1 diabetes. The study was supported by grants from Canadian Institutes of Health and the Juvenile Diabetes Research Foundation. Insmed plans to initiate large-scale phase II clinical studies in this indication. At the BIO 2004 Annual International Convention (BIO-2004) in June 2004, Insmed announced that it has received a grant from the US National Institutes of Health (NIH)/Muscular Dystrophy Association (MDA) worth USD $6.5 million to investigate the efficacy of mecasermin rinfabate for the treatment of myotonic dystrophy. It has also been granted orphan drug status for the treatment of GHIS-Laron syndrome in the US and Europe. In December 2003, Insmed announced that mecasermin rinfabate was designated orphan drug status by the FDA for the treatment of extreme insulin resistance. This provides Insmed with 7 years of market exclusivity following approval of mecasermin rinfabate for this indication. Insmed has received orphan drug designation for mecasermin rinfabate in the treatment of extreme insulin resistance in Europe (October 2004). In November 2004, Insmed was granted the European patent EP1183042 entitled "Methods for Treating Diabetes". This patent corresponds with the US patent US 6,040,292 also entitled "Methods for Treating Diabetes". Both patents cover type 1 and type 2 diabetes mellitus and insulin resistant diabetes including type A insulin resistance (the least severe form of extreme insulin resistance syndromes). In January 2004, Insmed obtained a non-exclusive licence to the patents for use of IGF-I for the treatment of extreme or severe insulin-resistant diabetes from Fujisawa Pharmaceutical. Insmed will have worldwide rights in territories (excluding Japan) with existing valid patent claims including the US and Europe. Insmed holds 28 US issued or allowed patents for the composition, production, antibodies and methods of use of mecasermin rinfabate. These US patents expire at various times between the years 2010 and 2019. Insmed through their lawyers filed its defense and counterclaim to the alleged patent infringement brought by Tercica against Insmed in the London High Court of Justice. Insmed asserted that it did not infringe any valid patent claims as none of the claims of the patent were patentable because the subject matter was not new. Insmed also stated that the patent did not involve an inventive step, did not have capability of industrial application and had no clear description of the invention so that invention can be performed by the person skilled in the art. Insmed is seeking revocation of the patent on these grounds.

Drugs, Investigational↗
PubMed1990

Insulin-like growth factors and their binding proteins: review of functions and clinical applications.

Insulin-like Growth Factors I & II (IGFs I & II) circulate in a concentration 1000 times that of insulin. The effect of these growth factors appears to be regulated by their binding proteins. The clinical usefulness of the IGFs resides currently in the growth hormone disease states and their treatment, as well as tumour related hypoglycemia. The growth hormone dependent binding protein (mol. wt 53kD) appears to possess a role in growth disorders, whereas the growth hormone independent binding protein (mol. wt 28kD) has recently been found to exert a role in glucose homeostasis.

Acromegaly↗
PubMed2005

Production and growth related disorders and other metabolic diseases of poultry--a review.

In humans, metabolic complaints may be associated with a failure in one of the body hormone or enzyme systems, a storage disease related to lack of metabolism of secretory products because of the lack of production of a specific enzyme, or the breakdown or reduced activity of some metabolic function. Some of these disorders also occur in poultry, as do other important conditions such as those associated with increased metabolism, rapid growth or high egg production that result in the failure of a body system because of the increased work-load on an organ or system. These make up the largest group of poultry diseases classified as metabolic disorders and cause more economic loss than infectious agents. Poultry metabolic diseases occur primarily in two body systems: (1) cardiovascular ailments, which in broiler chickens and turkeys are responsible for a major portion of the flock mortality; (2) musculoskeletal disorders, which account for less mortality, but in broilers and turkeys slow down growth (thereby reducing profit), and cause lameness, which remains a major welfare concern. In addition, conditions such as osteoporosis and hypocalcaemia in table-egg chickens reduce egg production and can kill.

Animal Husbandry↗