**7. GH/IGF-1 and clinical parameters of children with cholestatic diseases before LT**

The patients included in the study had various etiologies of ESLD. Analysis of the structure of liver diseases showed that the largest group, about 60%, consisted of recipients with BA, a congenital malformation of the biliary tract (**Figure 11**).

*Growth Hormone and Insulin-like Growth Factor-1 in Children with Cholestatic Diseases… DOI: http://dx.doi.org/10.5772/intechopen.108301*

Plasma GH levels in the patients differed depending on the etiology of liver disease: 5.5 (4.8–13.7) ng/ml in Alagille syndrome, 4.9 (2.0–7.3) ng/ml in BA, 1.6 (1.2–2.3) ng/ml in others, 3.9 (1.3–4.8) ng/ml in Byler disease, 3.6 (1.5–5.2) ng/ml in BH, 3.9 (0.0–7.7) ng/ml in Caroli disease (**Figure 12**).

Comparative analysis of GH levels in children with different etiologies of liver disease using the Kruskal-Wallis test for several independent variables revealed no statistically significant differences in GH concentrations (*p* = 0.16). Pairwise comparison of GH concentrations in the groups with different diagnoses using the

**Figure 11.** *Structure of morbidity in the studied liver transplant recipients, BA, biliary atresia; BH, biliary hypoplasia.*

#### **Figure 12.**

*GH levels in the blood of children with various etiologies of liver disease, \* - p = 0.012 compared with the level in children with BA, BA, biliary atresia; BH, biliary hypoplasia.*

Mann-Whitney U test showed that the plasma GH level in children with ESLD resulting from BA was significantly higher than in patients grouped under "other" diseases (autoimmune and fulminant hepatitis, Von Gierke disease, portal vein developmental anomaly, Crigler-Najjar syndrome, Budd-Chiari syndrome, hepatoblastoma, alpha-1 antitrypsin deficiency, and previous liver transplant dysfunction), *p* = 0.012. No significant differences were found between the other groups.

Analysis of plasma IGF-1 concentrations depending on the etiology of liver disease showed that the hormone content in the blood of patients with Alagille syndrome was 12.6 (0.0–28.1) ng/ml, with BA 1.2 (0.0–20.0) ng/ml, others 42.3(3.3–72.3) ng/ml, Byler disease 25.1 (14.7–51.7) ng/ml, BH 1.1 (0.0–12.0) ng/ml, Caroli disease 3.6(0.0–8.7) ng/ml (**Figure 13**).

Multiple comparative analysis showed significant differences in IGF-1 levels in children with different etiologies of liver disease, *p* = 0.01 according to Kruskal-Wallis test. Pairwise comparison of IGF-1 levels in the groups with different diagnoses using the Mann-Whitney U test revealed that IGF-1 levels significantly differed in the group BA and "others" (*p* = 0.004), BA, and Byler disease groups (0.012). Differences were also found in the hormone level between the BH and "other" groups (p = 0.013).

It is possible that IGF-1 levels in the children depend on the etiology of liver disease; however, since the "other" group included various pathologies and each of them is small, further studies are needed for an unambiguous conclusion.

It is known that the nature of GH secretion differs in males and females and depends on age [62]. In our study, we could not identify a significant correlation between GH level and the age of patients before transplantation (r = −0.18, *p* = 0.10). This could be probably due to both impaired hormone secretion associated with the disease and by the age structure of the sample used in our work. In the control group,

#### **Figure 13.**

*The level of IGF-1 in the blood of children with various etiologies of liver disease, \* - p < 0.05 in comparison with the level in children with BA; BA, biliary atresia; BH, biliary hypoplasia.*

*Growth Hormone and Insulin-like Growth Factor-1 in Children with Cholestatic Diseases… DOI: http://dx.doi.org/10.5772/intechopen.108301*

there was also no significant correlation with age, which can be explained by the narrow age range of the sample and/or a small number of observations.

A comparative analysis of plasma GH levels in girls (4.7 (1.7–7.1) ng/ml) and boys (3.4 (1.6–7.2) ng/ml) with ESLD revealed no significant differences, *p* = 0.41. In the control group, we could not also identify significant differences in GH levels in healthy boys and girls.

Serum IGF-1 levels, like GH, change with age, while there are practically no sex differences in protein levels. In the studied children, no significant correlation was found between IGF-1 levels and age (r = −0.001, *p* = 0.96). In the control group, no significant differences were also found, which is obviously due to the narrow age range in the groups included in the study.

The IGF-1 content in girls and boys with ESLD was 3.9 (0.0–23.5) ng/ml and 11.1 (0.0–33.6) ng/ml, respectively, and did not differ significantly, *p* = 0.38. The result obtained showed that IGF-1 concentration in children with ESLD is not associated with the sex of the child. No significant differences were found in the control group either.

The absence of age and sex differences in GH and IGF-1 levels in the group of children aged 3 months to 5 years with ESLD can be explained by a number of reasons the absence of such differences at this early age, and impaired hormone secretion associated with the disease. Our data do not provide an unambiguous answer to this question due to the age composition of the study group. Of course, studies with a large number of observations and in more homogeneous age groups will be informative.
