However, no single treatment has been shown to be universally efficacious and those that are of benefit are not without side-effects. Effective treatment regimens directed at both decreasing insulin resistance as well as the processes of necroinflammation leading to hepatic fibrosis have been investigated and include lifestyle intervention, surgical treatment, and pharmacotherapy. Lifestyle modification, weight loss, and physical activity represent the cornerstone of treatment.[3] Given the important role of insulin resistance in the pathophysiology of NASH, thiazolidinediones are used to improve insulin resistance. Thiazolidinediones

act as ligands for the peroxisomal proliferator-activated receptor-γ class of nuclear transcription factors leading to a decreased insulin resistance, decreased tumor necrosis factor α level, and high throughput screening compounds increased adiponectin level.

The results of several randomized, Ibrutinib in vitro controlled trials have found pioglitazone to improve insulin sensitivity, serum alanine aminotransferase levels, and histological features in NASH patients.[4] Ongoing large multicenter studies will provide additional information about long-term efficacy and safety of pioglitazone in patients with NASH. Many other medications have shown promising results in the investigations using animal models and in preliminary pilot studies. These include vitamin E, anti-oxidants, angiotensin receptor blockers, statins, fibrates, ezetimibe, and hepatoprotective agents. Because the sample sizes of these studies were relatively small and the durations were short, further validation is required. New therapeutic agents such as dipeptidylpeptidase-4 inhibitors and farnesoid X receptor agonists are around the corner. In NASH, hepatic iron overload is significantly related to liver injury, insulin resistance, and systemic inflammatory conditions. Iron reduction therapy (long-term phlebotomy with low-iron diet) has been shown MCE to reduce

hepatic oxidative stress and liver injury.[5] Multiple therapeutic approaches are also being actively tested. Finally, liver transplantation may be required in a small subgroup of patients with decompensated cirrhosis or HCC. “
“Poor feeding can be due many factors, including poor coordination of suck/swallow, gastrointestinal disease or social factors. Investigation is required where there is weight loss or inadequate weight gain, choking on feeds or recurrent aspiration pneumonia. This chapter presents a differential diagnosis of poor feeding in infancy. Delay in establishing feeds may indicate an underlying neurological condition. Children/adolescents with autistic spectrum disorders may have a very limited food repertoire, only eating a very few selected foods. Some children with Asperger’s report little appetite and no hunger and consequently may eat little. The chapter discusses the causes of poor feeding in the older child.