Effect of Prednisolone, Physical Activity, Fat Intake, Choleretic Agents on the Serum Bilirubin Level in a Case of Constitutional Hepatic Dysfunction (Gilbert's Disease)

1957 ◽  
Vol 32 (2) ◽  
pp. 325-331 ◽  
Author(s):  
F. Gilbert McMahon
2005 ◽  
Vol 72 (1) ◽  
pp. 83-84
Author(s):  
Pankaj Garg ◽  
Rajeev Krishak

2021 ◽  
Vol 17 (2) ◽  
pp. 199-203
Author(s):  
Tehreem Afzal ◽  
Naveed Butt ◽  
Shahzad Munir ◽  
Nazish Zia

Objective: To compare the mean change in the bilirubin levels with addition of probiotics to standard treatment for the management of neonatal jaundice. Methodology: The randomized controlled trial was undertaken at the Neonatal Intensive Care Unit of the Paediatrics Department, Federal Government Polyclinic (Post Graduate Medical Institute), Islamabad from 1st April to 30th September 2019.  Neonates with hyperbilirubinemia requiring phototherapy were randomly divided into two groups, each having 30 patients. Group A received probiotics along with phototherapy while group B received phototherapy alone. Primary outcome was serum total bilirubin, which was calculated on 0, 1 and 3 days of treatment. Duration of phototherapy and patient's outcome was also recorded. Data was analyzed statistically using SPSS v. 23. Results: The mean serum bilirubin level after 24 hours was 14.27 ± 4.35 mg/dl in combination group while 16.43 ± 4.36 mg/dl in phototherapy group (p > 0.05). After 48 hours, the mean serum bilirubin level was 12.37 ± 3.33 mg/dl in combination group while 14.09 ± 3.60 mg/dl in phototherapy group (p > 0.05). After 72 hours, the mean serum bilirubin level was 11.09 ± 2.87 mg/dl in combination group while 11.72 ± 2.96 mg/dl in phototherapy group (p > 0.05). The mean time required of blue light phototherapy was 43.47 ± 20.71 hours in combination group while 61.53 ±28.27 hours in phototherapy group (p < 0.05). All neonates were discharged. Conclusion: Addition of probiotics to standard treatment decreased the time required for the phototherapy in neonatal jaundice. However no statistically significant difference was seen in the bilirubin levels between the two groups.


1970 ◽  
Vol 4 (2) ◽  
pp. 71-76
Author(s):  
Nilufa Akhter ◽  
Noorzahan Begum ◽  
Waqar Ahmed Khan

Background: G6PD deficiency is one of the common inherited enzymatic disorder associated with high incidence of severe neonatal hyperbilirubinemia. Objectives: To observe G6PD status in male, term neonates with jaundice and its correlation with serum level of bilirubin. Methods: This cross sectional study was conducted on 90 male, term neonates with jaundice, age ranged from 3 to 12 days (Group B) in the Department of Physiology, Bangabandhu Sheikh Mujib Medical University (BSMMU) between July 2007 to June 2008. On the basis of total serum bilirubin (TSB) level, study group was further divided into B1(TSB <15mg/dl), B2(TSB 15-20mg/dl) and B3 (TSB>20mg/dl). For comparison age and sex matched 30 apparently healthy neonates (Group A) were also included in the study. Erythrocyte G6PD level was measured by Spectrophotometric method by using kit of Randox. Serum bilirubin level was measured by standard laboratory technique. For statistical analysis ANOVA, independent sample "t" test and Pearson's correlation coefficient test were performed as applicable by using SPSS windows version-12. Results: In this study, erythrocyte G6PD levels were significantly lower in moderate (p<0.01) and severe (p<0.001) hyperbilirubinemic group in comparison to that of control group . However, this enzyme level was lower in mild group compared to that of control but the difference was statistically non significant. Again, this enzyme levels were significantly lower in moderate (p<0.05) and severe (p<0.01) group than that of mild group and also between severe and moderate hyperbilirubinemic group (p<0.05). In this study, G6PD enzyme deficient were found in 1(3.33%) and 6(20%) subjects of group B2 and B3 respectively. Though, percentage of the subjects with enzyme deficiency were higher in severe group ( B3 ) compared to that of moderate group( B2 ) but the difference was statistically not significant. However, no enzyme deficient patient were found in control group (A) and mild hyperbilirubinemic group (B1). Serum bilirubin level showed significant (p<0.05) positive (r=+.429) correlation with erythrocyte G6PD level in control group (A). On the other hand, this level was negatively correlated with G6PD enzyme in groups B1 (r= -.127), B2 (r=-.120) and B3 ( r= -.671) but significant negative correlation in group B3 (p<0.01). Conclusion: The results of the study revealed that severity of hyperbilirubinemia depends on degree of G6PD deficiency. Therefore, early detection of this enzymopathy and close surveillance of the affected neonates may be important in reducing the complications of severe hyperbilirubinemia. Key words: Glucose-6-PD, Hyperbilirubinemia, Neonates DOI: 10.3329/jbsp.v4i2.4176 J Bangladesh Soc Physiol. 2009 Dec;4(2): 71-76  


Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 1682-1682 ◽  
Author(s):  
Adekunle D. Adekile ◽  
Ferdane Kutlar ◽  
Kathleen McKie ◽  
Anthony Addington ◽  
Dedrey Elam ◽  
...  

Abstract The chronic hemolysis of sickle cell anemia (SCA) produces hyperbilirubinemia but serum bilirubin level varies considerably and the modulating factors have not been fully elucidated. One identified genetic factor is the uridine diphosphate glucuronosyl transferase 1A (UGT1A) gene promoter polymorphism in which homozygosity for the (AT)7 allele has been associated with increased bilirubin levels in children with SCA. The same association has been reported in apparently healthy individuals, in β-thalassemia, G6PD deficiency, neonatal jaundice and hereditary spherocytosis. In the present study, in addition to UGT1A promoter genotype, serum bilirubin level was related to other genetic modifiers - βS-globin gene haplotype, Hb F, co-inherited α-thal trait, age and gender. The patients were randomly selected from the sickle cell clinic, Medical College of Georgia. UGT1A promoter genotypes were determined using automated sequencing and spreadex gel electrophoresis. Other investigations were with standard techniques. There were 67 SCA patients (41 males, 26 females), aged 2 to 44 years (mean of 20.6±10.7). Ten (14.9%) patients were homozygous for the (AT)6 UGT1A allele, 22 (32.8%) were homozygous for the (AT)7, while 35 (52.2%) were heterozygous for the two. Serum bilirubin was significantly higher in the homozygous (AT)7 group (3.7±1.5, 5.6±2.4 and 3.8±2.3 mg/dl respectively). It was also significantly higher in males than females (4.9±2.7 vs 3.7±1.7 mg/dl) and highest in patients aged >10 years. Co-inherited α-thal trait did not significantly affect the levels. There was a significant negative linear correlation (r = −0.304, p=0.016) of serum bilirubin with Hb F. Hb F was also significantly higher among females than males and when the different age groups were compared, it was highest in those <10 years old. Apart from UGT1A (AT)7 homozygosity, Hb F significantly influences serum bilirubin level in steady-state SCA. This is probably mediated via its hemolysis-sparing effect. Our (AT)7 homozygotes, including both children and adults, had significantly higher mean serum bilirubin level as previously reported by others. Indeed, when only the adults were analyzed, there was a distinct trimodal distribution among the 6/6, 6/7 and 7/7 UGT1A genotypes with serum bilirubin levels of 3.9 ± 0.9, 4.9 ± 2.2 and 5.8 ± 2.5 mg/dl respectively. Among children (<10 years), this trimodal distribution is lost, which supports the premise that a high Hb F is probably more important in modulating serum bilirubin levels in this age group. Serum Bilirubin and Other Parameters Grouped According to UGT1A1 Genotype UGT1A1 Genotype Age (yrs) Hb (g/dl) Retics (%) Hb F (%) Bilirubin (mg/dl) 6/6 (n=10) 18.1±8.7 7.9±1.2 11.3±4.7 8.4±6.4 3.7±1.5 6/7 (n=35) 17.9±10.9 8.7±1.3 11.4±4.2 10.9±8.6 3.8±2.3 7/7 (n=22) 26.1±9.3 8.3±2.1 10.9±4.8 6.6±5.4 5.6±2.4


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