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

Chronic pancreatitis (CP) is an inflammatory disorder that results in permanent impairment of the glandular anatomy of the pancreas with or without functional abnormalities. The pathogenesis of CP is usually unclear, except in the case of alcohol-induced disease. The most common symptoms of CP are abdominal pain, diarrhea, and weight loss often requiring recurring hospitalization. Over time, pancreatic endocrine and exocrine dysfunction may develop as the disease progresses, and a variety of complications can occur. Among the possible complications are nutrient malabsorption and diabetes mellitus. The treatment of CP is difficult and challenging for every physician. Relieving pain is the first step in treating CP. This symptom needs to be controlled, often with narcotics, which can cause dependence. Diarrhea usually indicates the presence of steatorrhea, which is often treated with a high-calorie, high-protein, and low-fat diet to minimize symptoms of the underlying disease and to promote weight retention or gain. Pancreatic replacement therapy is used to combat maldigestion and malabsorption. Patients with diabetes may need insulin therapy for glycemic control. The use of parenteral nutrition for bowel rest is a standard approach in patients with symptomatic CP. The use of jejunal enteral feeding recently has been evaluated for efficacy in CP patients. The role of pancreatic endotherapy in the management of CP is evolving. Several reports have suggested that endoscopic therapy aimed at decompressing the obstructed pancreatic duct can be associated with pain relief in some patients. Surgery should be considered in patients who fail medical therapy.
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PMID:Management of chronic pancreatitis. 1621 95

Cryptosporidiosis, caused by the protozoan parasite Cryptosporidium, causes self-limited diarrhea in immunocompetent hosts and severe life-threatening diarrhea in AIDS patients. Highly active antiretroviral therapy has been used to effectively treat cryptosporiosis in some but not all AIDS patients. Therefore, there is an urgent need for innovative drugs to treat this disease. Cryptosporidium infection results in intestinal pathophysiological changes such as glucose malabsorption, increased chloride ion (Cl(-)) secretion, and epithelial barrier disruption, leading to disease pathogenesis. In order to develop tools to combat this opportunistic pathogen, it is vital to understand mediators involved in disease pathogenesis. Substance P (SP), a neuropeptide and pain transmitter, is located in the gastrointestinal tract. SP can cause Cl(-) secretion in human gastrointestinal explants. However, its role in cryptosporidiosis has not been fully studied. Jejunal samples from macaques before and after Cryptosporidium parvum infection were assayed for SP and SP receptor mRNA and protein levels by reverse transcription-PCR and by immunohistochemistry and enzyme-linked immunosorbent assay, respectively. The role of SP in pathophysiological alterations, such as Cl(-) secretion and glucose malabsorption, was studied using tissues derived from macaques infected with C. parvum by the Ussing chamber technique. SP and SP receptor mRNA and protein expression levels were increased in jejunal samples following C. parvum infection and were accompanied by increased basal ion secretion and glucose malabsorption. In vitro treatment of samples obtained from infected macaques with the SP receptor antagonist aprepitant (Emend; Merck, Whitehouse Station, NJ) completely reversed the increase in basal ion secretion and corrected the glucose malabsorption. Our findings raise the possibility of using SP receptor antagonists for the treatment of symptoms associated with cryptosporidiosis.
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PMID:Substance P is responsible for physiological alterations such as increased chloride ion secretion and glucose malabsorption in cryptosporidiosis. 1715 91

Supplemental pancreatic enzyme preparations are provided to patients with conditions of pancreatic exocrine deficiency such as chronic pancreatitis and cystic fibrosis. These patients frequently experience steatorrhea, which occurs from inadequate fat absorption. The delivery of sufficient enzyme concentrations into the duodenal lumen simultaneously with meals can reduce nutrient malabsorption, improve the symptoms of steatorrhea, and in some cases alleviate the pain associated with chronic pancreatitis. Current clinical practices dictate administration of lipase 25,000-40,000 units/meal by using pH-sensitive pancrelipase microspheres, along with dosage increases, compliance checks, and differential diagnosis in cases of treatment failure. Despite the large number of specialty enzyme replacements available commercially, many patients remain dissatisfied with standard therapy, and future developments are needed to optimize treatment in these individuals.
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PMID:Pancreatic enzyme pharmacotherapy. 1754 72

Chronic pancreatitis (CP) is characterized by progressive and ultimately irreversible pancreatic injury. Alcohol abuse is the most common cause of CP in the Western world. As the pathophysiology of this disorder is better understood, it is probable that the treatment will be more successful. Therapeutic efforts for CP are focused on the treatment of maldigestion, pain, and diabetes. Dosage and timing of enteric-coated pancreatic enzymes are important issues in the treatment of malabsorption due to CP. Non-enteric-coated enzyme preparations along with acid suppression (histamine-2 blockers or proton-pump inhibitors) are of limited to modest effectiveness in treating pain caused by CP but are worth a trial in patients with less advanced disease. Extracorporeal shock wave lithotripsy (ESWL) of calcified stones is sometimes needed to achieve stone fragmentation before endoscopic removal. The role of ESWL alone in relieving calcified CP pain needs further study. Endoscopic therapy is aimed at decompressing the obstructed pancreatic duct and removal of pancreatic stone and is associated with pain relief in many patients. The role of endoscopic ultrasonography-guided celiac plexus block should be limited to treating those patients with CP whose pain has not responded to other modalities. Radiation therapy to the whole pancreas for CP pain relief is a revived treatment option that needs further study to confirm the safety and efficacy. Total pancreatectomy followed by autologous islet cell autotransplantation appears to be a potential therapeutic approach but should be considered as the last option in patients with refractory pain who have failed conventional medical, endoscopic, and surgical options.
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PMID:Current treatment options for chronic pancreatitis. 1789 74

Primary intestinal lymphangiectasis (PIL), also known as Waldmann's disease, is a rare protein-losing enteropathy characterized by abnormal enlargement of the lymphatic ducts in the bowel wall. The symptoms usually start in early infancy. We report a case of osteomalacia in a 63-year-old patient with delayed-onset of PIL, for which she was on dietary treatment. She presented with a 3-year history of mechanical pain in the back and pelvis. Mild ascites and edema with functional impairment of the lower limbs were noted. The neurological evaluation was normal. Blood tests showed hypocalcemia, hypophosphatemia, alkaline phosphatase elevation, and evidence of intestinal malabsorption. Radiographs of the pelvis disclosed a fracture, Looser's zones in the iliopubic rami and left femoral neck, and a washed-out appearance of the vertebras. Dual-energy X-ray absorptiometry showed bone loss with T-score values of -1.2SD at the lumbar spine and -2.5SD at the femoral necks. A diagnosis of osteomalacia related to vitamin D deficiency was given. Serum 25-OH-vitamin D was 18.2ng/ml (normal, 20-40ng/ml) and serum parathyroid hormone was 620pg/ml (normal, 15-65pg/ml), suggesting secondary hyperparathyroidism. Intramuscular vitamin D was given, together with oral calcium and an adequate diet. At follow-up 8 months later, small improvements were noted in the symptoms and absorptiometry findings.
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PMID:Osteomalacia in a patient with primary intestinal lymphangiectasis (Waldmann's disease). 1790 Sep 62

Nutrition is thought to influence disease status in patients with cystic fibrosis (CF). This cross-sectional study sought to evaluate nutrient intake and anthropometric data from 64 adult outpatients with cystic fibrosis. Nutrient intake from food and supplements was compared with the Dietary Reference Intakes for 16 nutrients and outcomes influenced by nutritional status. Attention was given to vitamin D and calcium given potential skeletal implications due to cystic fibrosis. Measurements included weight, height, body composition, pulmonary function, and serum metabolic parameters. Participants were interviewed about dietary intake, supplement use, pulmonary function, sunlight exposure, and pain. The participants' mean body mass index (+/-standard deviation) was 21.8+/-4.9 and pulmonary function tests were normal. Seventy-eight percent used pancreatic enzyme replacement for malabsorption. Vitamin D deficiency [25-hydroxyvitamin D (25OHD)<37.5 nmol/L] was common: 25 (39%) were deficient despite adequate vitamin D intake. Lipid profiles were normal in the majority, even though total and saturated fat consumption represented 33.0% and 16.8% of energy intake, respectively. Reported protein intake represented 16.9% of total energy intake (range 10%-25%). For several nutrients, including vitamin D and calcium, intake from food and supplements in many participants exceeded recommended Tolerable Upper Intake Levels. Among adults with cystic fibrosis, vitamin D deficiency was common despite reported adequate intake, and lipid profiles were normal despite a relatively high fat intake. Mean protein consumption was adequate, but the range of intake was concerning, as both inadequate or excessive intake may have deleterious skeletal effects. These findings call into question the applicability of established nutrient thresholds for patients with cystic fibrosis.
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PMID:Nutrient status of adults with cystic fibrosis. 1806 Aug 97

Prader-Willi syndrome (PWS) is a complex genetic disorder localized to chromosome 15 and is considered the most common genetic cause of the development of life-threatening obesity. Although some morbidities associated with PWS, including respiratory disturbance/hypoventilation, diabetes, and stroke, are commonly seen in obesity, others such as osteoporosis, growth hormone deficiency, and hypogonadism, and also altered pain threshold and inability to vomit, pose unique issues. Various bariatric procedures have been used to cause gastric stasis, decrease gastric volume, and induce malabsorption, with poor results in PWS patients in comparison with normal obese individuals.
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PMID:Critical analysis of bariatric procedures in Prader-Willi syndrome. 1816 38

Cryptosporidiosis, caused by the protozoan parasite Cryptosporidium parvum, causes self-limited diarrhea in normal hosts but can cause life-threatening diarrhea for immunosuppressed patients. There is an urgent need for new drugs to treat this chronic disease. Cryptosporidium parvum infection is associated with intestinal structural and pathophysiologic changes, including villi blunting and glucose malabsorption. Substance P (SP), a neuropeptide and pain transmitter, is associated with the gastrointestinal tract and is elevated in humans and macaques after experimental C. parvum challenge. To examine the relevance of SP in the pathogenesis of cryptosporidiosis, and to determine if SP receptor antagonism can be employed for treatment of cryptosporidiosis in immunosuppressed hosts, we used an immunosuppressed murine model (dexamethasone-immunosuppressed mice) that is frequently utilized for examining chemotherapeutic potential of drugs. Quantitative ELISA was used to measure intestinal SP levels in immunosuppressed mice with, and without, C. parvum infection. Intestinal physiological alterations, as studied by the Ussing chamber technique, plus weight change, fecal oocyst shedding, and villi measurements, were compared in infected mice with, and without, SP receptor antagonist (aprepitant) treatment. Immunosuppressed mice infected with C. parvum demonstrated increased SP levels as well as physiological alterations (glucose malabsorption), weight loss, fecal oocyst shedding, and structural alterations (increased intestinal villi blunting) compared to uninfected mice. Each of these defects was significantly inhibited by aprepitant treatment. These studies demonstrate the potential of SP receptor antagonism for treatment of pathogenesis of cryptosporidiosis in immunosuppressed hosts.
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PMID:Substance P receptor antagonism for treatment of cryptosporidiosis in immunosuppressed mice. 1857 2

This study evaluated serum nutrients in 23 patients who had previous Proplast/Teflon implants to their temporomandibular joints (TMJ) and continued to remain in chronic, severe, irresolvable pain despite subsequent surgical reconstruction. All of the patients were women, and their average age was 40.6 years (range, 28-55 years). Standard blood assays were performed for beta-carotene (vitamin A), folate, serum iron, ferritin, zinc, magnesium, and vitamins B1, B6, B12, and C. Each patient was deficient in at least one of these 10 elements, with an average of 3.3 elements. Some factors that may be responsible for the deficiency state include inadequate nutritional intake, malabsorption, utilization dysfunction, increased requirements, or drug interactions. In conclusion, the patient who has had multiple, complex TMJ operations with a history of TMJ Proplast/Teflon implants and poor treatment results may be suffering from an unrecognized malnutrition state, substantially adding to the patient's morbidity. Nutritional evaluations, dietary counseling, and appropriate medical management may improve the treatment outcomes for these patients.
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PMID:Serum nutrient deficiencies in the patient with complex temporomandibular joint problems. 1862 71

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


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