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Russell Silver syndrome: a perspective on growth and the influence of growth hormone therapy.
IGF-I and IGF Binding Protein-3 Generation Tests and Response to Growth Hormone in Children with Silver-Russell Syndrome. The endocrine phenotype in silver-russell syndrome is defined by the underlying epigenetic alteration. GH treatment induces sustained catch-up growth in children with intrauterine growth retardation: 7-year results. Absence of catch-down growth in Russell-Silver syndrome after short-term growth hormone treatment.
Effect of long-term growth hormone treatment on final height of children with Russell-Silver syndrome.
While dealing with an elderly patient with repeated hypoglycaemic episodes, it is imperative to focus on the etiologies that are exclusive to this group like compromised renal function, polypharmacy or pharmacy error due to impaired cognition. Synthesis and secretion of insulin-like growth factor II by a leiomyosarcoma with associated hypoglycaemia. Non-islet cell tumour-induced hypoglycaemia: A review of the literature including two new cases. Hepatocellular carcinoma with persistent hypoglycaemia: Successful treatment with corticosteroid and frequent high carbohydrate intake. Epigenetics refers to chromatin modifications, which do not affect the DNA sequence itself, resulting in the regulation of gene expression.
Rare causes like coexisting hypoadrenalism or hypopituitarism, malignancy, and hypoglycaemia of islet or non islet cell origin are considered lower in the list once the common precipitating factors are ruled out. Epigenetic changes are crucial for development (allowing the differentiation of different cell types), as well as for X-chromosome inactivation and genomic imprinting. These epigenetic alterations contribute to the phenomenon of genomic imprinting wherein a certain cluster of genes undergo methylation resulting in differentially methylated regions (DMR's) also referred to as Imprinting control regions (ICR's).
These imprinted genes are responsible for the synchronized regulation of gene expression and hence play pivotal roles in fetal and placental growth.

Chest X-ray revealed some scattered pulmonary shadows for which a CT scan of chest was planned.
Paternally expressed genes enhance growth whereas maternally expressed genes restrain growth. During the hospital stay patient developed documented symptomatic and asymptomatic hypoglycaemia almost daily especially in morning hours including two episodes of severe hypoglycaemia for which endocrine opinion was taken.On reviewing the history, the patient was on metformin 500 mg and glimepride 1 mg, each twice a day after meals since 8 yrs. Imprinting errors in RSS involve mainly imprinting centers situated on chromosomes 7 and 11p15.
His blood glucose and other metabolic parameters were well controlled on this medication and he was very regular with regards to his diabetic diet and physical exercise. He did regular self blood glucose monitoring with a periodically calibrated glucometer and maintained a good record of his data.
Human chromosome 11p15 contains a cluster of imprinted genes that includes paternally expressed genes (IGF2 and KCNQ1OT1) and maternally expressed genes (such as CDKN1C and H19).
After birth, serum IGF-II is mainly produced in the liver where IGF2 imprinting is relaxed.
Patient also confirmed some of these relatively low values with laboratory plasma glucose values. Reduced IGF2 expression with ICR1 hypomethylation may therefore have its main effect on prenatal growth.
At this point of time the patient self adjusted his medications by gradually reducing the doses of Oral Hypoglycaemic Agent (OHA) or oral antidiabetic agents.
Due to persistent low blood glucose values despite of liberalized diet, he stopped all OHA after 3 months.
There was no history suggestive of any renal, hepatic disorder, alcohol consumption, diabetic retinopathy or any other underlying autoimmune disorder.
This could be either over-expression of a maternally expressed growth suppressor or under expression of a paternally expressed growth promoter.
The patient was not on angiotensin converting enzyme inhibitor (ACEI) or angiotensin receptor blocker (ARB) ACEI or ARBs, fluoroquinolones, sulphonamides.

The birth weight of affected infants is typically two or more SD below the mean, and postnatal growth two or more SD below the mean for length or height. However, RSS patients do not experience the catch up growth that is normally seen in SGA infants.
The growth in the first three years of life is slow, and from this point on it remains parallel to the curve but below the third percentile.
In the given clinical scenario, ectopic secretion of big IGF-2 from the tumor mass was suspected but big IGF-2 assay was not available. One possible mechanism evident from a previous study is that the IGFBP-3 increase in children with 11p15-RSS, in response to GH therapy, was more pronounced than the increase of IGF-I, indicating a disordered Co-regulation of the growth factor and its major binding protein. Growth hormone therapy is often considered for a child with RSS who has not acquired adequate catch-up growth at the age of 2 years.In particular, children with RSS have benefited from growth hormone supplementation even in the absence of growth hormone deficiency, [6] including significant growth acceleration and improved final height [7] and continued normal growth rate after the discontinuation of growth hormone therapy. Circulating levels of big IGF-2 are determined by size-exclusion acid chromatography or immunoblot analysis by polyacrylamide gel method. A greater increment in final height was observed in those patients with lower heights at start of treatment.
There was a significant improvement noted in the SDS score for height which clearly validates the use of rhGH therapy in children with RSS and other causes of short stature even in the absence of GHD. Assessment of RSS children for GHD should thus be advocated since it is a frequent accompaniment of RSS and based on potential evidence, it can be rectified with rHGH treatment. NICTH mainly occurs in patients with solid tumors of mesenchymal and epithelial origin, but rarely also in patients with tumors of haematopoietic and neuroendocrine origin [3] [Table 2]. In this case, the inadvertent and unexpected tight blood glucose control was a hint to underlying pathology.
NICTH should be considered in any cancer patient diabetic or nondiabetic without signs of vascular events or brain metastases especially in mesenchymal or malignant epithelial tumor.

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