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)

Anorexia is associated with disorders of all systems. Anorexia represents a consistent clinical manifestation during acute and chronic pathophysiological processes (infection, inflammation, injury, toxins, immunological reactions, malignancy and necrosis). Anorexia during disease can be beneficial or deleterious depending on the timing and duration. Temporary anorexia during acute disease may be beneficial to an organism since a restriction in the intake of micro- and macro-nutrients will inhibit bacterial growth. Long-term anorexia during chronic disease, however, is deleterious to an organism and may be associated with cachexia, which can ultimately result in death. Various mechanisms participate in the anorexia observed during disease, including cytokine action. Anorexia induced by cytokines is proposed to involve modulation of hypothalamic-feeding associated sites, prostaglandin-dependent mechanisms, modifications of neurotransmitter systems, gastrointestinal, metabolic, and endocrine factors. In addition, the anorexia-cachexia syndrome is multifactorial and may involve chronic pain, depression or anxiety, hypogeusia and hyposmia, chronic nausea, early satiety, malfunction of the gastrointestinal system, metabolic alterations, cytokine action, production of other anorexigenic substances and/or iatrogenic causes (chemotherapy, radiotherapy). Cachexia may result not only from anorexia and a decreased caloric intake, but also from malabsorption and losses from the body (ulcers, hemorrhage, effusions), or a change in body metabolism. Research has focused on potential interventions to modify anorexia during disease and the anorexia-cachexia syndrome. Nutritional modifications and the use of specific steroids (such as megestrol acetate) are being tested in the clinical setting. Understanding the specific mechanisms responsible for anorexia during disease as well as their interactions is essential to develop interventions for the control of anorexia (during a critical time in a specific disease), and to devise less toxic immunotherapeutic regimens using cytokines.
 ...
PMID:Anorexia during acute and chronic disease. 905 54

Acute and chronic pancreatitis present challenging problems for the physician. In acute pancreatitis, initial efforts should be directed toward supporting the patient hemodynamically. Recognition and early treatment of complications such as shock, renal failure, respiratory failure, hypocalcemia, abscess, hemorrhage, or unremitting symptoms caused by an impacted stone in the common bile duct are necessary. The cause of the pancreatitis must be identified, possibly for acute therapy, but certainly to prevent recurrences and progression of disease. In chronic pancreatitis, insufficiencies of pancreatic function must be identified and consequent malabsorption and diabetes treated appropriately. The major challenge is the relief of chronic pain. It is hoped that this can be accomplished medically, but in carefully selected cases, specific types of surgery may be required.
 ...
PMID:Pancreatitis. Evaluation and treatment. 888 42

Pancreatic enzyme replacement therapy has proved useful in the treatment of malabsorption and persistent pain in patients with chronic pancreatitis. The formulation of pancreatic enzyme preparation varies considerably. Treatment of chronic pain is facilitated by the use of a high-protease enzyme preparation, preferably non-microsphere encoated. Treatment of steatorrhea is optimized by use of high-lipase-containing preparations.
 ...
PMID:Enzymatic therapy in patients with chronic pancreatitis. 1050 44

Nonmeckelian jejunoileal diverticula (JID) are rare, but potentially clinically significant lesions. Despite recent advances in modern diagnostic modalities, diagnosis of JID may be problematic. Upper gastrointestinal contrast series with small bowel follow-through examination and mainly enteroclysis are the 2 main diagnostic methods. In selected cases (mainly complicated JID), the physician could use other diagnostic methods, such as ultrasound, computed tomography, endoscopy, intraoperative endoscopy, laparoscopy, radiotagged erythrocyte bleeding scans, and selective mesenteric arteriography. JID may be clinically silent or symptomatic causing chronic pain or malabsorption or other acute complications, such as hemorrhage, inflammation, perforation, etc. Laparotomy remains the gold standard for definite diagnosis of asymptomatic and complicated diverticula. Treatment should be individualized. Surgery could be indicated, mainly in symptomatic diverticula. The extent of resection may be a problem, especially in patients with extensive disease involving large parts of the bowel. In these cases, clinical judgment is required from the part of surgeon to avoid short bowel syndrome.
 ...
PMID:Small intestinal nonmeckelian diverticulosis. 1914 69

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