Growth hormone treatment of growth hormone-deficient adults results in a marked increase in Lp(a) and HDL cholesterol concentrations.

Edén, Staffan; Wiklund, O.; Oscarsson, Jan; Rosén, Thord; Bengtsson, Bengt‐Åke

doi:10.1161/01.atv.13.2.296

Cited by 211 publications

(141 citation statements)

References 47 publications

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“…Increase of plasma triglycerides or VLDL-triglyceride concentration and lowering of plasma HDL-cholesterol concentration are commonly found in insulin-resistant individuals with obesity or type 2 diabetes (37). As observed in several studies, Lp(a) increased during GH substitution (38,39) but no difference between the GH-deficient group and the control group could be found at the end of the study, questioning the clinical importance.…”

Section: Discussionmentioning

confidence: 69%

A dose titration model for recombinant GH substitution aiming at normal plasma concentrations of IGF-I in hypopituitary adults

Ekman

Lindström²,

Nyström³

et al. 2002

European Journal of Endocrinology

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Objective: To evaluate a dose titration model for recombinant human GH substitution in adult patients with GH deficiency, aiming at normal plasma levels of IGF-I. Design and methods: Eighteen patients participated and a start dose of 0.17 mg GH/day was used except by two men who started with 0.33 mg/day. To demonstrate a clear GH effect the patients were first titrated, with steps of 0.17 mg GH/day every 6 -8 weeks, to IGF-I levels in the upper range of age-adjusted reference values. The GH dose was then reduced 1 dose step and kept for a further 6 months. For comparison we investigated 17 healthy control subjects. Results: Plasma IGF-I was increased after 2 weeks on the start dose and did not increase further for up to 8 weeks. Women had significantly lower GH sensitivity than men measured as net increment of IGF-I on the start dose of GH. GH sensitivity was not changed by age. The plasma IGF-I levels increased from 76:3^47:0 (S.D.) to 237^97 mg=l at the end of the study ðP , 0:001Þ; and similar IGF-I levels were obtained in both sexes. The maintenance median GH dose was 0.33 mg/day in males and 0.83 mg/day in females ðP ¼ 0:017Þ: The GH dose correlated negatively with age in both sexes. Body weight, very low density triglycerides, lipoprotein(a) (Lp(a)), and fasting insulin increased, whereas insulin sensitivity index (QUICKI) decreased significantly. In comparison with the controls, the patients had lower fasting blood glucose, fasting insulin and Lp(a) levels at baseline, but these differences disappeared after GH substitution. The two groups had equal insulin sensitivity (QUICKI), but 2 h oral glucose tolerance test values of blood glucose and insulin were significantly higher in the patients at the end of the study. Conclusions: In conclusion our data suggest that the starting dose of GH substitution and the dose titration steps should be individualised according to GH sensitivity (gender) and the IGF-I level aimed for (age). The reduced insulin sensitivity induced by GH substitution could be viewed as a normalisation if compared with control subjects.

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Section: Discussionmentioning

confidence: 69%

A dose titration model for recombinant GH substitution aiming at normal plasma concentrations of IGF-I in hypopituitary adults

Ekman

Lindström²,

Nyström³

et al. 2002

European Journal of Endocrinology

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“…Moreover, increased total cholesterol, LDL-C, apo-B levels, triglycerides and lipoprotein(a) levels, and a normal or decreased HDL-C, were found in GH deficient patients. [61][62][63] Also, increased peripheral insulin resistance and impaired glucose tolerance were observed in these subjects. 64 Accordingly, GH deficiency might be involved in the development of the components of the metabolic syndrome.…”

Section: Discussionmentioning

confidence: 85%

Metabolic syndrome in childhood cancer survivors.

Subramani

Scott

Sneha

et al. 2017

JCO

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145 Background: Reavan in 1988 noted that several risk factors for cardiovascular diseases commonly cluster together, and he recognised them as a disease, named syndrome X, currently known as metabolic syndrome. Metabolic syndrome is a group of disorders related to insulin resistance, characterized clinically by central obesity, hyperglycemia, dyslipidemia and hypertension. There is a growing body of evidence indicating that pediatric cancer survivors are at a greater risk of developing metabolic syndrome. We studied the prevalence of metabolic syndrome in children with cancer who completed their treatment and on follow up. Methods: All relevant past medical data (of the disease, treatment and all events) were collected from the medical records. Tanner staging was perfomred, height was measured using a Harpenden stadiometer. Weight/WAIST circumference were measured. The body mass index (BMI) was calculated as weight (kg)/(height (m)²). BMI ≥90thcentile as per CDC chart was taken as abnormal. Blood pressure was measured on the right arm of the patient. Presence of family history of diabetes, cardiovascular diseases and hypercholesterolemia were taken. Fasting Blood sugar, insulin, HbA1C, lipid profile were done. We used IDF(International diabetes federation) criteria to assess the metabolic syndrome among cancer survivors. This study was approved by our university ethics comittee. Results: Seventy five children who fulfilled the inclusion criteria were included in this study. Out of which 48 were males and 27 were females. Among these, majority of children are treated for acute lymphoblastic leukemia. 8.25% of total population satisfied the criteria of metabolic syndrome. Age, gender, diagnosis, modality of treatment were not to be of statistical significance, however majority of children with metabolic syndrome are in adolescent group. Conclusions: With the better care committed to children with cancer even in developing country, the survival rates are greatly improving and so metabolic syndrome is becoming the major target for intervention in the follow up of cancer survivors. As metabolic syndrome cannot treated by a single drug therapy, it is necessary to have cancer survivors follow up screening.

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“…In a double-blind placebo-controlled study on 22 patients with hypopituitarism, Weaver et al (18) found no significant increase in Lp(a) after 6 months of GH treatment, but in a subgroup of eight patients who received GH for a total of 12 months a modest but significant rise in Lp(a) was observed. In a double-blind, cross-over study of GH treatment in GHD adults, Eden et al (19) reported a marked almost twofold increase in Lp(a) after only 6 weeks of treatment, which was sustained after 26 weeks. However, in a double-blind placebo-controlled trial on 18 patients with severe GHD no significant effect of GH replacement was observed after 2 months of treatment (20).…”

Section: Introductionmentioning

confidence: 99%

The effect of recombinant human GH replacement therapy on lipoprotein(a) and other lipid parameters in adults with acquired GH deficiency: results of a double-blind and placebo-controlled trial

Nolte

Rädisch

Armstrong

et al. 1997

European Journal of Endocrinology

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The effect of GH substitution on serum lipids and lipoproteins, and in particular lipoprotein(a) (Lp(a)), was investigated in 32 adults with postoperative (acquired) GH deficiency as part of a double-blind, placebo-controlled trial. Seventeen men and fifteen women, aged 18-59 years (mean 42 years) from two centres (Hannover and Göttingen) were randomly assigned to two groups. Group P (placebo) received placebo for the first 12 months and recombinant human GH (rhGH) for the following 12 months (open phase). Group V (verum) was treated with rhGH for two consecutive periods of 12 months each. The target dose of rhGH was 2 U/m 2 per day, given subcutaneously daily at bedtime. Serum concentrations of Lp(a), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C) and triglycerides were determined at 0, 12 and 24 months. In group V, Lp(a) increased significantly in the first as well as in the second year of treatment (P=0.02, 12 months versus baseline; P=0.016, 24 months versus 12 months). In contrast, Lp(a) levels remained unchanged in group P during the first 12 months (P=0.826 versus baseline), but increased significantly (P=0.002) during the second year, when all patients were administered GH. The increase in Lp(a) after 12 months of rhGH replacement therapy in all 32 patients was significant for Lp(a) baseline concentrations both above and below 20 mg/dl and was independent of the apolipoprotein(a) isoforms. Total and LDL-C decreased significantly after 1 year and triglycerides after 2 years in group V. A significant reduction was also observed in the TC/HDL-C and the LDL-C/HDL-C ratios. Our study shows an unfavorable effect of rhGH replacement therapy on Lp(a) levels, which is, however, counteracted by a favorable effect of rhGH on TC, LDL-C and the TC/LDL-C and LDL-C/HDL-C ratios.

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Growth hormone treatment of growth hormone-deficient adults results in a marked increase in Lp(a) and HDL cholesterol concentrations.

Cited by 211 publications

References 47 publications

A dose titration model for recombinant GH substitution aiming at normal plasma concentrations of IGF-I in hypopituitary adults

A dose titration model for recombinant GH substitution aiming at normal plasma concentrations of IGF-I in hypopituitary adults

Metabolic syndrome in childhood cancer survivors.

The effect of recombinant human GH replacement therapy on lipoprotein(a) and other lipid parameters in adults with acquired GH deficiency: results of a double-blind and placebo-controlled trial

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