Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hepatic osteodystrophy consists of three types: osteomalacia, osteoporosis, and periosteal reaction with new bone formation. Secondary hyperparathyroidism is very rare, if it occurs at all. The cause of osteomalacia appears to be vitamin D deficiency due to a lack of vitamin D substrate. In the presence of adequate substrates, 25-OHD and dihydroxy vitamin D metabolites are formed. The vitamin D deficiency results in osteomalacia and malabsorption of calcium and phosphorus. The osteomalacia can be treated successfully with vitamin D supplements. In some patients calcium, phosphorus, and magnesium supplements may be required. The aetiology and treatment of the osteoporosis and the periosteal reactions remain obscure.
 ...
PMID:Hepatic osteodystrophy. 70 74

It is well known that insulin resistance affects osteodystrophy, and there is an important relationship between insulin resistance and hepato-biliary disease. It is also well known that hepato-biliary and pancreatic disease is associated with osteodystrophy. In the present review, we describe the mechanism of diabetes and osteodystrophy due to hepato-biliary and pancreatic disease. Hepatic osteodystrophy is associated with malabsorption, abnormalities of vitamin D metabolism, inflammatory cytokines, receptor activator of NF-kappaB ligand, and insulin-like growth factor-1. In particular, tumor necrosis factor-alpha and malabsorption are important factors for viral and alcoholic hepatitis, respectively. Malabsorption due to steatorrhea is important for cholestatic disease and chronic pancreatitis. A greater focus on non-alcoholic steatohepatitis (NASH) and further investigations to clarify the relationship between osteodystrophy and NASH are needed.
 ...
PMID:[Hepato-biliary and pancreatic disease and osteodystrophy]. 1972 Nov 98

Improved survival of orthotopic liver transplantation (OLT) has shifted the focus of patient care to quality of life, including prevention and treatment of pre- and post-transplant complications. End-stage liver failure affects bone length and strength, causing growth failure and hepatic osteodystrophy. Growth failure affects 60% of children assessed for OLT. Optimization of nutrition may prevent further stunting of growth before OLT but is rarely successful. Catch-up growth is observed following steroid withdrawal usually from 18 months post OLT. Whether growth hormone treatment would benefit the 20% of children who fail to regain normal height needs to be tested in randomized controlled trials. Hepatic osteodystrophy in children comprises vitamin D deficiency rickets, low bone mass and fractures caused by malnutrition and malabsorption. Vitamin D deficiency should be treated aggressively with cholecalciferol (D2) or ergocalciferol (D3). The active vitamin D metabolites alphacalcidol or calcitriol are used to increase calcium absorption from the gut but do nothing to replace vitamin D stores. Children before and after OLT have an increased prevalence of fractures of 10-13% and 12-38%, respectively. Most fractures are vertebral, and are related to low spine BMD. They often occur asymptomatically but may also cause chronic pain and later scoliosis. The main risk groups are infants with cholestatic liver disease, and adolescents with later OLT and greater BMI. Fracture prediction in these children is limited. OLT also bears the risk of avascular bone necrosis (4%), and development of scoliosis (13-38%). This paper reviews the literature and presents preventative and therapeutic strategies to improve bone length and strength.
 ...
PMID:Growth and bone health in chronic liver disease and following liver transplantation in children. 2052 40

With improved survival of orthotopic liver transplantation (OLT) in children, prevention and treatment of pre- and posttransplant complications have become a major focus of care. End-stage liver failure can cause endocrine complications such as growth failure and hepatic osteodystrophy, and, like other chronic illnesses, also pubertal delay, relative adrenal insufficiency, and the sick euthyroid syndrome. Drug-induced diabetes mellitus post-OLT affects approximately 10% of children. Growth failure is found in 60% of children assessed for OLT. Despite optimisation of nutrition, rarely can further stunting of growth before OLT be prevented. Catch-up growth is usually observed after steroid weaning from 18 months post-OLT. Whether growth hormone treatment would benefit the 20% of children who fail to catch up in height requires testing in randomised controlled trials. Hepatic osteodystrophy in children comprises vitamin D deficiency rickets, low bone mass, and fractures caused by malnutrition and malabsorption. Vitamin D deficiency requires aggressive treatment with ergocalciferol (D2) or cholecalciferol (D3). The active vitamin D metabolites alphacalcidol or calcitriol increase gut calcium absorption but do not replace vitamin D stores. Prevalence of fractures is increased both before OLT (10%-28% of children) and after OLT (12%-38%). Most fractures are vertebral, are associated with low spine bone mineral density, and frequently occur asymptomatically, but they may also cause chronic pain. Fracture prediction in these children is limited. OLT in children is also associated with a greater risk of developing avascular bone necrosis (4%) and scoliosis (13%-38%). This article reviews the literature on endocrine and skeletal complications of liver disease and presents preventive screening recommendations and therapeutic strategies.
 ...
PMID:Endocrine and bone metabolic complications in chronic liver disease and after liver transplantation in children. 2206 32