Improved insulin sensitivity, preserved beta cell function and improved whole-body glucose metabolism after low-dose growth hormone replacement therapy in adults with severe growth hormone deficiency: a pilot study Diabetologia

The ageing process is accompanied by an increased prevalence of the signs and symptoms of physical fragility, including sarcopenia, a decrease in exercise tolerance, osteopenia, an increase in visceral adiposity and a worsening of quality of life. Adults with growth hormone deficiency (GHD) exhibit similar clinical signs, but it is possible to treat them with GH to ameliorate these signs and symptoms [1]. Yang et al (2019) noted that deletion on the short arm of chromosome 18 is a rare disorder characterized by intellectual disability, growth retardation, and craniofacial malformations (such as prominent ears, microcephaly, ptosis, and a round face). The phenotypic spectrum is wide, encompassing a range of abnormalities from minor congenital malformations to holoprosencephaly. These investigators presented the case of a 2-year-old girl with ptosis, a round face, broad neck with low posterior hairline, short stature, and panhypopituitarism. She Schober et al (1995) reported on a patient with 18p monosomy and GH deficiency due to pituitary hypoplasia, who showed an excellent response to GH-treatment.

A study on the efficacy of recombinant human growth hormone in patients with TS was initiated in 1983 in the United States, leading to the approval of this agent by the Food and Drug Administration in 1997 [20]. GH therapy in the United States is generally initiated at FDA-approved dose of 1.125 IU/kg per week (0.375 mg/kg per week) and adapted according to growth velocity and IGF-1 levels of girls with TS [21]. In Korea, the approved dose (1.0–1.4 IU/kg per week) is similar to but slightly higher than that in United states. Several studies have used doses of GH higher than those approved by the FDA, giving a relatively small gain in height with higher IGF-I levels compare to those with the approved dose [22]. Individual responses to GH are variable according to different protocols such as age at start of GH treatment, dosing regimens, consistency of treatment, management of puberty, and adjuvant therapy [11, 12, 23]. GH treatment started in toddler showed early normalization of short stature, however growth failure can be prevented if GH treatment is started before six years of age without interruption [12].

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In patients in whom insulin-induced hypoglycemia is contraindicated or unsafe or where appropriate testing arrangements are unavailable, the literature states that alternatives to ITT should be used. Informationnow states that intravenously administered arginine, either alone or in combination with GH-releasing hormone (GHRH), may be useful. When only intravenously administered arginine is used, cut-off values for a normal response are similar to those expected with ITT. When it is used in combination with GHRH, the response may be augmented and the cut-off level is somewhat higher (9 to 10 ng/ml). Available literature suggests tests that use of glucagon, propranolol, or levodopa has a lesser established diagnostic value in comparison to ITT.

One uncontrolled study has reported on final height in a small group of treated children with PWS. Presuming a treatment effect based on the change in standard deviation (SD) from the start of treatment to the completion of treatment, there was a change of 1.64 SD. Converting this SD improvement to cm in adult height, this corresponds to treated males being approximately 11 cm and treated females being approximately 9.8 cm taller than the presumptive height of untreated children.

Humatrope 72 IU Eli Lilly

Another method is to make frequent measurements of serum GH during the day and night, but this is no more effective than the standard method for detecting GHD. Formerly, the diagnosis of GHD in children was based on a peak serum GH concentration of 5 ng/ml or less in response to a provocative test, but a peak serum GH concentration of less than 10 ng/ml is now considered abnormal. However, because the available GH assays have not been standardized, the literature states that the cut-off value of less than 10 ng/ml is of limited usefulness, especially in borderline cases. When used in conjunction with these measures, however, the guidelines suggest a peak serum GH value of less than 10 ng/ml in response to stimulation is a reasonable definition of GHD, with values less than 5 ng/ml reflecting the most severe deficiency.

Both samples exhibited maximum absorbance at 280 nm with identical patterns, suggesting that the two samples were equivalent (Fig 5E). Using Fourier transform-infrared (FT-IR) spectroscopy, we scanned the samples over a range of 4000–400 (cm-1) and confirmed the same pattern between Genotropin and CGH942. Recombinant hGH was indirectly quantified using an hGH ELISA kit (Quantikine ELISA human growth hormone; R&D Systems, Minneapolis, MN, USA) following the manufacturer’s protocol. Assay readouts were measured spectrophotometrically at 450 nm using a microplate spectrophotometer (Model 680, Bio-Rad, Hercules, CA, USA).

There is some evidence that there is a greater risk of this in children than in adults. Literature suggests that girls who have Turner syndrome may have a greater risk of pancreatitis than other children taking growth hormone. In any child who develops lasting, severe abdominal pain, pancreatitis should be considered. Dosage of diabetes medicines may need to be adjusted during growth hormone treatment. Patients should be watched carefully if growth hormone is given along with glucocorticoid therapy and/or other drugs that are processed by the body in the same way. This study confirmed the efficacy and safety profiles of rhGH produced in transgenic pigs are equivalent to those of commercial somatropin.

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The recommended dose of GH therapy for children with PWS is 0.035 mg/kg/day. Nadir GH serum levels should be below 1 mg/L, preferably less than 0.4mg/L, in the two hours after 75‐g oral glucose load (oral glucose tolerance test [OGTT]). This criterion often is used for diagnosis of acromegaly and for follow‐up during treatment. If thyroxine is insufficient, then the literature indicates tests of GH secretion should be postponed until the thyroid deficiency is adequately replaced because GH secretion may be subnormal merely as a result of the hypothyroidism.

It is extremely rare for such a tumor to occur in childhood, but, when it does, the excessive GH can cause excessive growth, traditionally referred to as pituitary gigantism. Other drugs may affect Genotropin, including prescription and over-the-counter medicines, vitamins, and herbal products. Do not use if the medicine looks cloudy, has changed colors, or has particles in it.

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Although useful as a diagnostic procedure in children, the literature states that a test that uses clonidine is of dubious value for the diagnosis of GH deficiency in adults. In adults with a history of hypothalamic pituitary disease or cranial irradiation, generally only 1 provocative test of GH secretion is needed (NICE, 2003). Beneficial changes in body composition were observed at the end of the 6-month treatment period for the patients receiving GENOTROPIN as compared with the placebo patients. Lean body mass, total body water, and lean/fat ratio increased while total body fat mass and waist circumference decreased. These effects on body composition were maintained when treatment was continued beyond 6 months. Bone mineral density declined after 6 months of treatment but returned to baseline values after 12 months of treatment.

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