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Indian Pediatr 2016;53:
543 |
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Clippings
Theme: Pediatric Gastroenterology & Hepatology
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Vyom Aggarwal
Email:
[email protected]
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Role of Serum autotaxin in causation of pruritis in
cholestatic liver disease (J Pediatr Gastroenterol Nutr.
2016;62:530-5).
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Pruritus is a common symptom of cholestatic liver disorders but not all
cholestatic conditions (with similar bilirubin levels) are associated
with intense itching, indicating role of some extraneous factor
influencing its causation and severity. This study evaluated autotaxin
(ATX), a lysophospholipase, as a potential cause for pruritus in
pediatric cholestatic diseases. The study group of 45 children comprised
of 14 with pruritic liver disease, 9 with non pruritic cholestasis and
22 healthy controls. Serum ATX activity was significantly increased in
pruritic children with cholestatic syndromes in comparison to
nonpruritic cholestatic diseases and healthy controls. Authors concluded
that the serum ATX activity is associated with itch intensity in
children with cholestatic diseases, and that the ATX inhibitors may be
useful antipruritic agents in pediatric cholestatic disorders.
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Probiotics for reducing the risk of
necrotizing enterocolitis and sepsis in preterms (Lancet.
2016;387: 649-60)
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In this multicentric, randomized controlled phase-3 study, 1315 preterm
infants (gestational age 23-30 wk) were randomly assigned to receive
probiotic (B. breve BBG-001) mixed in dilute elemental infant
formula or dilute infant formula alone, within 48 hours of birth.
Sixty-one infants (9%) in the probiotic group had necrotizing
enterocolitis compared with 66 (10%) in the control group (adjusted RR
0·93; 95% CI 0·68, 1·27). Seventy-three (11%) infants in the probiotic
group had sepsis compared with 77 (12%) in the control group (adjusted
RR 0·97; 95% CI 0·73, 1·29); 54 (8%) deaths occurred before discharge in
the probiotic group compared with 56 (9%) in the placebo group (RR 0·93;
95% CI 0·67, 1·30). This well-controlled study with large sample size
suggests that there is evidence of no benefit of routine use of this
probiotic (B. breve BBG-00) for prevention of necrotizing
enterocolitis and sepsis in very preterm infants.
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Can we do away with duodenal biopsy for
diagnosing celiac disease? (Arch Dis Child. 2016;
101:172-6)
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Celiac disease is now defined as a genetically predisposed autoimmune
systemic condition characterized by the presence of a variable
combination of gluten-dependent enteropathy, other clinical
manifestations, and specific antibodies such as serum anti-transglutaminase
IgA (anti tTG-IgA) and anti-endomysium IgA (AEA). Until very recently,
biopsy demonstration of villous atrophy was considered essential for
diagnosing celiac disease. In 2012, the European Society of
Paediatric Gastroenterology, Hepatology and Nutrition (ESPGHAN) proposed
a new algorithm that allows diagnosis of celiac disease without a
duodenal biopsy in selected, highly symptomatic cases with high titers
of serum anti tTG-IgA antibodies, positivity for AEA and for human
leucocyte antigen (HLA) DQ2 or DQ8. In this prospective study, children
diagnosed with celiac disease without a duodenal biopsy (group 1; n=51),
following these guidelines, and children diagnosed with a duodenal
biopsy, matched for sex, age and year of diagnosis (group 2; n=92),
were enrolled over a 3-year period. All patients were put on a
gluten-free diet (GFD), and were followed up for clinical conditions and
laboratory testing at 6 months every year since diagnosis (median follow
up: 1.9 years). At the end of follow-up, the two groups were
statistically comparable in terms of clinical and nutritional status,
anti-transglutaminase IgA antibody titers, quality of life, adherence to
a GFD, and number of supplementary medical consultations. It appears
that diagnosis of celiac disease without a duodenal biopsy has no
negative consequences, at least during a medium-term follow-up.
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Ursodeoxycholic acid for treatment of indirect
hyperbilirubinemia in infants (J Pediatr Gastroenterol
Nutr. 2016 62:97-100)
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Hyperbilirubinemia is a common problem in neonatal period and
phototherapy is a proven effective modality of its therapy. The authors
investigated the role of oral ursodeoxycholic acid as an adjunct to
phototherapy in neonatal hyperbilirubinemia. Eighty neonates were
randomized to receive either oral ursodeoxycholic acid (10 mg/kg/d in 2
divided doses; n=40) in addition to phototherapy or only
phototherapy (n=40). Total serum bilirubin levels were estimated
every 12 hours, till it was below 10 mg/dL). The two groups were then
compared with regard to bilirubin levels at different time points and
duration of phototherapy using the generalized estimating equation (GEE)
test. The mean (SD) of total bilirubin in the intervention group was 12
( 1.6), 10 9 ( 1.1), and 9.8 ( 0.2) mg/dL 12, 24, and 48 hours after the
beginning of phototherapy, respectively. On the contrary, these measures
were 14.4 (1.3), 12.5 (1.4), and 10.1 (1.1) mg/dL in the control group,
respectively (P < 0.05). The mean (SD) time required for
phototherapy to decrease the bilirubin level to <10 mg/dL was 15.5 (6)
and 44.6 (13.3) hours in the case and the control group, respectively (P
= 0.001). Authors concluded that ursodeoxycholic acid has an additive
effect with phototherapy in neonates with indirect hyperbilirubinemia.
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