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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gastrointestinal (GI) problems at high altitude are commonplace. The manifestations differ considerably in short-term visitors, long-term residents and native highlanders. Ethnic food habits and social norms also play a role in causing GI dysfuntion. Symptoms like nausea and vomiting are common manifestations of acute mountain sickness and are seen in 81.4% short-term visitors like mountaineers. Anorexia is almost universal and has a mutifactorial causation including effect of hormones like leptin and cholecystokinin and also due to hypoxia itself. Dyspepsia and flatulence are other common symptoms. Diarrhoea, often related to poor hygiene and sanitation is also frequently seen especially among the short-term visitors. Peptic ulceration and upper gastro-intestinal haemorrhage are reported to be common in native highlanders in the' Peruvian Andes (9.6/10000 population per year) and also from Ladakh in India. A hig h incidence o f gastriccarcinoma is also reported, especially from Bolivia (138.2 cases per 10000 population per year). Megacolon and sigmoid volvulus are common lower GI disorders at high altitude. The latter accounted for 79% of all intestinal obstructions at a Bolivian hospital. Thrombosis of the portosystemic vascultature and splenic hematomas has been reported from India. Malnutrition is multifactorial and mainly due to hypoxia. Fat malabsorption is probably significant only at altitudes > 5000m. Neonatal hyperbilirubinemia was found to be four times more common in babies born at high altitude in Colorado than at sea level. Gall stones disease is common in Peruvian highlands. A high seroprevalence of antibodies to H pylori (95%) has been found in Ladakh but its correlation to the prevalence of upper gastro-intestinal disease has not been proven.
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PMID:Gastrointestinal problems at high altitude. 1754 91

The pancreas is a retroperitoneal organ that releases water, bicarbonate and digestive enzymes by the main pancreatic duct (MPD) into the duodenum. Chronic pancreatitis (CP) is typically caused, in adults, by chronic alcohol abuse and, less frequently hypertriglyceridemia, primary hyperparathyroidism or cystic fibrosis. Exocrine dysfunction results in malabsorption of fat and subsequent steatorrhea. Damage to pancreatic endocrine function is a late finding in CP and results in hyperglycaemia or overt diabetes mellitus. Care of patients with CP principally involves management of pain. A significant change in the pain pattern or the sudden onset of persistent symptoms suggests the need to rule out other potential etiologies, including peptic ulcer disease, biliary obstruction, pseudocysts, pancreatic carcinoma, and pancreatic duct stricture or stones, then is important to establish a secure diagnosis. Management of pain should then proceed in a judicious stepwise approach avoiding opioids dependence. Patients should be advised to stop alcohol intake. Fat malabsorption and other complications may also arise. Management of steatorrhea should begin with small meals and restriction in fat intake. Pancreatic enzyme supplements can relieve symptoms and reduce malabsorption in patients who do not respond to dietary restriction. Enzymes at high doses should be used with meals. Treatment with acid suppression to reduce inactivation of the enzymes from gastric acid are recommended. Supplementation with medium chain triglycerides and fat soluble vitamin replacement may be required. Management of other complications (such as pseudocysts, bile duct or duodenal obstruction, pancreatic ascites, splenic vein thrombosis and pseudoaneurysms) often requires aggressive approach with the patient kept on total parenteral nutrition to minimize pancreatic stimulation.
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PMID:[Nutritional repercussions and management of chronic pancreatitis]. 1871 12

Recent data report that the incidence of peptic ulcer is decreasing in the general population; conversely, the rates of gastric and duodenal ulcer hospitalization and mortality remain very high in older patients. Two major factors that might explain this epidemiological feature in the elderly population are the high prevalence of Helicobacter pylori infection and the increasing prescriptions of gastroduodenal damaging drugs, including NSAIDs and/or aspirin (acetylsalicylic acid). The main goals for treating peptic ulcer disease in old age are to reduce recurrence of the disease and to prevent complications, especially bleeding and perforation. The available treatments for peptic ulcer are essentially based on gastric acid suppression with antisecretory drugs and the eradication of H. pylori infection. The aim of this article is to report the available data on clinical efficacy and tolerability of peptic ulcer treatments in elderly patients and provide recommendations for their optimal use in this special population. Proton pump inhibitor (PPI)-based triple therapies for 7 days are highly effective for the cure of H. pylori-positive peptic ulcers as well as for reducing ulcer recurrence. Antisecretory drugs are also the treatment of choice for NSAID- or aspirin-related peptic ulcers and are useful as preventive therapy in chronic users of NSAIDs and low-dose aspirin as antiplatelet therapy. Antisecretory PPI therapy has a favourable tolerability profile in geriatric patients; however, monitoring is suggested in older patients with frequent pulmonary infections, gastrointestinal malabsorption, unexplained chronic diarrhoea, osteoporosis or those taking concomitant cytochrome P450 2C19-metabolized medications. The overall approach to the geriatric patient should include a comprehensive geriatric assessment that ensures multidimensional evaluation of the patient in order to better define the clinical risk of adverse outcomes in the older patient with peptic ulcer and its complications.
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PMID:Optimal management of peptic ulcer disease in the elderly. 2058 49

We report a 74-year-old man with Wernicke's encephalopathy (WE) whose only prior illness was peptic ulcer disease. Upper gastrointestinal endoscopy demonstrated gastric ulcer scars accompanied by marked deformity, without pathologic evidence of malignancy. WE due to peptic ulcer disease in previous reports was substantially associated with thiamine deficiency due to recurrent vomiting or surgical procedures. In our case, however, there was no history of vomiting or gastrointestinal surgery. Besides, we thoroughly ruled out other known clinical settings related to WE. There is the possibility that peptic ulcer disease itself provoked thiamine deficiency due to malabsorption.
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PMID:Wernicke's Encephalopathy in a Patient with Peptic Ulcer Disease. 2176 41

The parathyroid glands are the main regulator of plasma calcium and have a direct influence on the digestive tract. Parathyroid disturbances often result in unknown long-standing symptoms. The main manifestation of hypoparathyroidism is steatorrhea due to a deficit in exocrine pancreas secretion. The association with celiac sprue may contribute to malabsorption. Hyperparathyroidism causes smooth-muscle atony, with upper and lower gastrointestinal symptoms such as nausea, heartburn and constipation. Hyperparathyroidism and peptic ulcer were strongly linked before the advent of proton pump inhibitors. Nowadays, this association remains likely only in the particular context of multiple endocrine neoplasia type 1/Zollinger-Ellison syndrome. In contrast to chronic pancreatitis, acute pancreatitis due to primary hyperparathyroidism is one of the most studied topics. The causative effect of high calcium level is confirmed and the distinction from secondary hyperparathyroidism is mandatory. The digestive manifestations of parathyroid malfunction are often overlooked and serum calcium level must be included in the routine workup for abdominal symptoms.
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PMID:Digestive manifestations of parathyroid disorders. 2203 19

H. pylori is a gram-negative pathogen, etiologically associated with atrophic and non-atrophic gastritis, peptic ulcer, primary gastric B-cell lymphoma and gastric carcinoma. Several observations demonstrated a correlation between H. pylori and malabsorption of essential nutrients; epidemiological studies have shown an association between H. pylori infection and iron deficiency anemia, while the absorption of some vitamins such as vitamin B12, vitamin A, vitamin C, folic acid and Vitamin E may be affected by the infection. The main mechanism related to malabsorption of this components is the modified intragastric pH (hypo- achlorhydria) due to H. pylori infection. Moreover H. pylori is also able to determine a modification of gastrointestinal hormones by reducing plasma levels of ghrelin and increasing those of leptin and gastrin, thus affecting appetite and promoting the occurrence of dyspeptic symptoms. On the other hand, H. pylori eradication has been shown to improve serum level of iron and vitamin B12, has some effects on Vitamin A and Vitamin E absorption and has a late effects on ghrelin levels. As a consequence of those effects, H. pylori is also associated with childhood malnutrition in developing countries either for the occurrence of malabsorption or for an increased susceptibility to enteric infections caused by hypochlorhydria.
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PMID:Nutritional aspects of Helicobacter pylori infection. 2210 25

Osteoporosis has finally been recognized as an important disorder in men. Men have osteoporotic fractures about 10 years later in life than women. Owing to increasing life expectancy, more fractures are predicted. Important risk factors for men include advancing age, smoking or chronic obstructive pulmonary disease, glucocorticoid therapy, and androgen deprivation therapy for prostate cancer. Other groups at risk for osteoporosis include those with alcohol abuse, men on enzyme-inducing antiseizure drugs, and those with malabsorption or history of surgery for peptic ulcer disease. History and physical examination will likely reveal secondary causes of osteoporosis. Some, but not all organizations, recommend screening for osteoporosis in men older than age 70. In the USA, The Department of Veterans Affairs recommends case finding rather than screening. Evaluation starts with bone mineral density testing by dual energy X-ray absorptiometry of the spine, hip, and in some cases forearm. A few laboratory tests can be helpful, including measurement of 25-hydroxyvitamin D. Most studies of osteoporosis therapy in men are small; but alendronate, risedronate, zoledronic acid, and teriparatide are FDA-approved to increase bone density in men with osteoporosis. A new potent antiresorptive agent, denosumab, increased bone density dramatically in men on androgen deprivation therapy and is approved for this indication in Europe. Recognition, diagnosis, and treatment of osteoporosis in men should lead to fewer fractures and probably fewer deaths.
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PMID:Osteoporosis in men: insights for the clinician. 2287 Apr 78

Helicobacter pylori (HP) is a gram-negative flagellated pathogen acid-resistant bacterium; it belongs to the order Campylobacterales that is wide spread all over the world, infecting more than 50% of the world population. HP infection is etiologically associated with non-atrophic and atrophic gastritis, peptic ulcer and with 3 to 6-fold increased relative risk for developing gastric adenocarcinoma and mucosa-associated lymphoid tissue (MA LT) lymphoma. For this reason HP is recognized by the World Health Organization as a Class I human carcinogen. In the last years a lot of studies clarified the role of this pathogen in nutrition and metabolism; particularly, it has been shown that it is able to induce malabsorption of several nutrients like iron, cobalamin, vitamin C and vitamin E, with strong consequences on nutritional status. Interesting, this bacterium is able to produce different biological effects on hormones like ghrelin and leptin controlling both appetite and growth, mostly depending on the time of acquisition of the infection and of its treatment. In this review, the authors focused their attention on nutritional effects of HP infection and particularly on the role that diet, food, plants and specific nutrients can play in its treatment, considering that HP eradication rates, with standard triple-therapy, have fallen to a low level in the last years.
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PMID:Helicobacter pylori and nutrition: a bidirectional communication. 3075 76

Primary biliary cholangitis is a slowly progressive immune-mediated cholestatic disease that causes a destruction of the intrahepatic bile ducts and may lead to cirrhosis of the liver, end-stage liver disease, and the need for liver transplantation. The disease is among the most common reasons why adults require liver transplantation. The primary signs of the disease include the presence of antimitochondrial and antinuclear antibodies, elevated alkaline phosphatase, hyperbilirubinemia, hypercholesterolemia, and histologic features, such as intense inflammation with a florid duct lesion and hepatic fibrosis. The patient's quality of life is impacted by fatigue, pruritus, malabsorption syndrome, sicca syndrome, osteoporosis, and challenges coping with chronic illness. Advanced practice registered nurses need to understand the pathophysiology, clinical presentation, diagnostic approaches, disease and symptom management, and priority nursing assessment and care in patients with this rare disease to differentiate it from primary sclerosing cholangitis, autoimmune hepatitis, obstructed bile duct lesions, drug-induced cholestasis, cholestasis in pregnancy, cholangiocarcinoma, hepatic malignancy, and peptic ulcer disease.
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PMID:A Clinical Review of Primary Biliary Cholangitis. 3225 Dec 26

Helicobacter pylori infection is a severe global health problem that is closely associated with acid-related diseases and gastric malignancies. Eradicating H. pylori is strongly recommended for lowering peptic ulcer recurrence and preventing gastric cancer. The current approved H. pylori eradication regimen combines a proton pump inhibitor (PPI) with two antibiotics. Unfortunately, this regimen failed to meet expectations mostly due to antibiotic resistance and insufficient gastric acid suppression. Vonoprazan, a novel potassium-competitive acid blocker, showed promising results as a PPI replacement. Vonoprazan inhibits gastric acid secretion by acting as a reversible competitive inhibitor against potassium ions and forming disulfide bonds with the cysteine molecule of H+/K+-ATPase. Vonoprazan has superior pharmacological characteristics over PPI, such as no requirement for acid activation, stability in acidic conditions, shorter optimum acid suppression period, and resistance to cytochrome P (CYP)2C19 polymorphism. Several comparative randomized controlled trials and meta-analyses revealed the superiority of vonoprazan in eradicating H. pylori, notably the resistant strains. The adverse effect caused by vonoprazan is long-term acid suppression that may induce elevated gastrin serum, hypochlorhydria, and malabsorption. All vonoprazan studies have only been conducted in Japan. Further studies outside Japan are necessary for universally conclusive results.
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PMID:The Potential Benefits of Vonoprazan as Helicobacter pylori Infection Therapy. 3299 41


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