Is biliary sludge a stone-in-waiting?

Sl, Werlin; Jp, Scott

doi:10.1016/s0022-3476(96)70061-6

Cited by 6 publications

(3 citation statements)

References 13 publications

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“…The natural history of biliary sludge in children with sickle cell disease finds that at a mean of 2.1 years of followup, about 65% of such patients do eventually develop gallstones, although not necessarily symptomatic ones. About 40% of patients originally with biliary sludge do not develop gallstones, despite the continued presence of sludge in most [133]. Most authors recommend yearly ultrasounds to access stone formation.…”

Section: Gastrointestinal/hepatobiliary Complicationsmentioning

confidence: 99%

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Beyond the Definitions of the Phenotypic Complications of Sickle Cell Disease: An Update on Management

Ballas

Kesen

Goldberg

et al. 2012

The Scientific World Journal

147

144

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The sickle hemoglobin is an abnormal hemoglobin due to point mutation (GAG → GTG) in exon 1 of the β globin gene resulting in the substitution of glutamic acid by valine at position 6 of the β globin polypeptide chain. Although the molecular lesion is a single-point mutation, the sickle gene is pleiotropic in nature causing multiple phenotypic expressions that constitute the various complications of sickle cell disease in general and sickle cell anemia in particular. The disease itself is chronic in nature but many of its complications are acute such as the recurrent acute painful crises (its hallmark), acute chest syndrome, and priapism. These complications vary considerably among patients, in the same patient with time, among countries and with age and sex. To date, there is no well-established consensus among providers on the management of the complications of sickle cell disease due in part to lack of evidence and in part to differences in the experience of providers. It is the aim of this paper to review available current approaches to manage the major complications of sickle cell disease. We hope that this will establish another preliminary forum among providers that may eventually lead the way to better outcomes.

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Section: Gastrointestinal/hepatobiliary Complicationsmentioning

confidence: 99%

“…Most authors recommend yearly ultrasounds to access stone formation. They reserve cholecystectomy only for patients with signs and symptoms of acute cholecystitis [133]. …”

Section: Gastrointestinal/hepatobiliary Complicationsmentioning

confidence: 99%

Beyond the Definitions of the Phenotypic Complications of Sickle Cell Disease: An Update on Management

Ballas

Kesen

Goldberg

et al. 2012

The Scientific World Journal

147

144

View full text Add to dashboard Cite

show abstract

“…In a previous study on 305 children with SCA, 50 (16.4%) of them had biliary sludge [8]. The question that is always asked is what is the significance of biliary sludge [31]? In a prospective study and follow-up of the 50 patients with biliary sludge, the majority of them (65.7%) developed gallstones [32].…”

Section: Biliary Sludgementioning

confidence: 99%

Hepatobiliary Manifestations of Sickle Cell Anemia

Issa

Al-Salem

2010

Gastroenterol Res

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Sickle cell anemia is one of the common hemoglobinopathies around the world. It results from a single change of one amino acid valine instead of glutamic acid in the hemoglobin beta change. This change leads to polymerization of the hemoglobin when the oxygen saturation is lowered, resulting in deformity of the red blood cells and microvascular occlusion. Sickle cell anemia can affect any part of the body and one of the main organs to be affected is the hepatobiliary system either directly from the sicklening process or indirectly as a result of chronic hemolysis and multiple blood transfusions. This manifests in several clinical conditions which poses diagnostic and therapeutic dilemmas to the treating physicians. These hepatobiliary manifestations will be outlined in this review.

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UGT1A1 promoter polymorphisms and the development of hyperbilirubinemia and gallbladder disease in children with sickle cell anemia

et al. 2008

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Genetic modifiers contribute to phenotypic variability in patients with sickle cell anemia (SCA). The influence of the bilirubin UDP-glucuronosyltransferase (UGT) 1A1 (TA) n TAA promoter polymorphism on bilirubin levels and gallbladder disease in SCA was examined using prospectively collected data from the Cooperative Study of Sickle Cell Disease. A total of 324 children with HbSS (median age 6.9 years) had UGT1A1 genotyping; 243 (75%) had common (TA) 6 or (TA) 7 alleles, whereas 81 (25.0%) had variant (TA) 5 or (TA) 8 alleles. The UGT1A1 genotype significantly influenced average bilirubin levels for the common alleles: 6/6 genotype 5 2.36 ± 1.13 mg/dL, 6/7 genotype 5 2.90 ± 1.54 mg/dL, and 7/7 genotype 5 4.24 ± 2.11 mg/dL (P < 0.0001). Thirty-nine percent of children with the 7/7 genotype had documented gallbladder disease, compared with 18.2% with the 6/7 genotype and only 9.9% with the wildtype 6/6 UGT1A1 genotype (P 5 0.001). To analyze the (TA) 5 and (TA) 8 variant alleles, three groups were generated, showing increasing bilirubin levels with increasing TA repeats and age. Group 3 (genotypes 6/8, 7/7, and 7/8) had a significantly greater rate of bilirubin change than Groups 1 (genotypes 5/6, 5/7, and 6/6) or 2 (genotype 6/7). These results validate previous smaller studies and confirm that the UGT1A1 promoter polymorphism exerts a powerful influence on bilirubin levels and the development of gallbladder disease in children with SCA. UGT1A1 genotyping should be considered as a screening tool for predicting children most likely to develop gallbladder disease at a young age. Am. J. Hematol. 83:800-803, 2008. V

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Is biliary sludge a stone-in-waiting?

Cited by 6 publications

References 13 publications

Beyond the Definitions of the Phenotypic Complications of Sickle Cell Disease: An Update on Management

Beyond the Definitions of the Phenotypic Complications of Sickle Cell Disease: An Update on Management

Hepatobiliary Manifestations of Sickle Cell Anemia

UGT1A1 promoter polymorphisms and the development of hyperbilirubinemia and gallbladder disease in children with sickle cell anemia

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