Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The failure of standard oral pancreatic enzyme replacement therapy to correct malabsorption in patients with advanced pancreatic insufficiency is likely due to acid-peptic inactivation of ingested enzymes. Theoretically, the use of cimetidine, an H2-receptor antagonist, in conjunction with oral enzymes, would permit greater transgastric passage of ingested enzymes with resulting improvement in intraluminal lipolysis. To test this hypothesis, we studied the effects of orally administered cimetidine in two groups of patients by utilizing a previously validated double-marker perfusion technique. Cimetidine, in varying doses, had no effect on postprandial exocrine pancreatic function in 16 duodenal ulcer patients without pancreatic disease. In six patients with pancreatic insufficiency, cimetidine produced a pronounced decrease in the output of gastric acid and secretory volume, resulting in reduction of postprandial acidity and intragastric volume. These actions of cimetidine should retard or prevent inactivation of ingested enzymes and also increase their intragastric concentration, with resulting enhancement of luminal duodenal enzyme activity. Supplemental cimetidine may thus be useful in the medical management of patients who fail to respond to routine pancreatic extract therapy alone.
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PMID:Rationale for the use of cimetidine in pancreatic insufficiency. 34 Aug 5

Fat malabsorption in patients with chronic alcoholic pancreatitis and cystic fibrosis may lead to vitamin and essential fatty acid deficiency in addition to steatorrhea. In clinical practice it can be difficult to achieve complete correction of malabsorption and elimination of steatorrhea. The earliest treatment methods used the oral administration of porcine pancreatic enzyme preparations. These conventional enzymes, however, were unstable in the acidic intragastric environment. Subsequently, medications to neutralize or reduce gastric acidity (H2-blockers, antacids, or bicarbonate) were added to improve the stability of the conventional enzymes. Enteric-coated enzyme preparations were then developed that would release only in an alkaline milieu, protecting the enzymes from acid denaturation. The newest and potentially most exciting modalities for the treatment of fat malabsorption are acid-stable lipases, obtained either from a fungal source or through the expression of cloned genes for the enzymes utilizing recombinant DNA techniques. The advantages and disadvantages of the various medications for the therapy of fat malabsorption in pancreatic insufficiency are reviewed.
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PMID:Enzyme therapy for malabsorption in exocrine pancreatic insufficiency. 266 33

Pancreatic enzyme therapy may be beneficial to all patients with chronic pancreatitis, even those in whom the condition is very mild. The goal of enzyme therapy should be to restore normal gastrointestinal physiology as completely as possible. Monitoring of body weight is recommended as the main measure of treatment efficacy. Most pancreatic enzyme preparations presently employed are porcine in origin and must meet certain standards of quality for human consumption. The amount of active lipase in the duodenum determines the quantity of enzymes to be given. An appropriate diet is also important for relieving symptoms of pancreatic insufficiency and improving nutritional status. Although administration of large amounts of proteases has provided pain relief in some patients, the rationale for using enzymes to relieve pain in chronic pancreatitis has not been generally accepted. Gastric acid plays a role in malabsorption, since administered enzymes may be destroyed by gastric acid. Also, acidic conditions in the duodenum decrease the efficacy of pancreatic enzymes administered with meals. Histamine-H2-receptor antagonists may decrease gastric acidity but there are certain drawbacks to long-term use of these agents. The use of enteric-coated microspheres overcomes many of the problems associated with enzyme destruction. Patients with chronic pancreatitis display considerable individual variation in their treatment requirements. Therapy must be tailored to meet the need for adequate disease control as well as for social and emotional acceptability by the patient. The attending physician and the patient share the responsibility for maintaining appropriate therapy.
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PMID:Theory and practice in the individualization of oral pancreatic enzyme administration for chronic pancreatitis. 270 51

Bacterial contamination of the small bowel in the elderly can occur without any anatomical defect, but the importance and pathogenesis of this phenomenon are debatable. We describe two such patients, both with profound vitamin B12 deficiency. Clinical recovery took place without specific treatment of the bacterial overgrowth. In one patient with pernicious anemia, malabsorption of xylose and fat was corrected after vitamin B12 therapy. In the other gastric acidity was normal, but unsuspected mesenteric ischemia led to gangrene of the bowel. In old age there may be more than one explanation for vitamin B12 deficiency and for bacterial overgrowth. Vitamin B12 deficiency within the intestinal cells may be one common factor leading to malabsorption.
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PMID:Small bowel contamination and vitamin B12 deficiency in the elderly. 376 May 23

Giardia lamblia infection may be asymptomatic or may produce diarrhea with or without malabsorption. Many drugs were used for treatment of giardiasis, but none proved to be ideal since all have potential troublesome side effects as they are absorbed from the intestine. In this study, a locally acting drug aminosidine-sulphate (gabbroral) has been tried in treatment of experimental giardiasis in a rat model under different conditions of gastric acidity which is one of the main local factors affecting the pathogenicity of the organism. The best results were obtained in the group with hyperacidity which was induced by indomethacin (indocid) with significant improvement in the pathological picture and parasitic count. While in experimental animals with normal acidity there was only partial eradication of the parasite. However, in the group with hypoacidity induced by cimetidine (cimetex), the drug showed no beneficial effects since most organisms invaded the deeper layers of the intestine escaping the local action of the drug.
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PMID:Aminosidine sulphate in experimental giardiasis. 760 72

Colonization of the gut by intestinal bacteria begins at birth and progresses rapidly in the immediate postnatal period. Host defense mechanisms that mediate enteric colonization include gastric acidity and intestinal motility. The small bowell overgrowth syndrome is a condition characterized by large numbers of bacteria, often anaerobes, in the upper intestine. Steatorrea, carbohydrate malabsorption and abdominal pain are frequently present. Predisposing conditions are localized anatomic disorders (surgical blind loops, small bowel strictures caused by surgery or Crohn's disease, short-gut syndrome without ileocaecal valve), motility derangements or reduction of gastric acidity. Diagnosis of the overgrowth syndrome is often difficult and quantitative cultures of jejunal-aspirated fluid is the best diagnostic test. Antimicrobial therapy directed against anaerobes is often successful, but the best therapeutic approach is the correction of predisposing conditions, if present.
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PMID:[Infected bowel syndrome]. 866 82

Breath tests are quick, noninvasive, simple to perform and reliable. In particular in patients with diarrhea, bloating, nausea and uncharacteristic abdominal symptoms, the H2 breath test is highly useful. Using this procedure, malabsorption of various different carbohydrates, the absorptive performance of the upper abdominal tract, the orocecal transit time, or bacterial overgrowth in the small bowel, can be determined. Using 24-hour pH-metry, the acidity in the stomach and esophagus can be measured, and reflux disease, for example, diagnosed. Today, elevated fat in the stool is detected on the basis of the beta carotene level in the serum. Further function tests for the detection of pancreatic insufficiency, such as the determination of fecal pancreatic elastase, are also available.
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PMID:[Gastroenterological function tests in the GP's office]. 1661 63

In this communication, we describe the isolation of a Lactobacillus delbrueckii subsp. bulgaricus 92063 mutant strain named pH-P11, which differed from the parent strain by low proteolytic activity and altered regulation of expression of lacZ in the presence of glucose or lactose. In the presence of lactose, beta-galactosidase activity was approximately twice as high in pH-P11 than in the wild type. pH-P11 exhibited protosymbiosis together with Streptococcus thermophilus. Yoghurt produced with pH-P11 was characterized by low acidity and little post-acidification during storage. The organoleptic properties (absence of bitterness and other off-flavors, weak sourness, and clear yoghurt taste) were those of a typical "yoghurt mild". This mild flavor was achieved at rather high cell counts of lactobacilli even at the end of shelf-life. High cell counts in conjunction with high beta-galactosidase activity make pH-P11 an interesting strain for application in yoghurt especially designed for consumers with lactose malabsorption. In contrast to "yoghurt mild", which is predominantly produced with Lactobacillus acidophilus together with Streptococcus thermophilus, the product obtained by fermentation with pH-P11 and Streptococcus thermophilus concurs with international standards for yoghurt. During frequent sub-culturing, strain pH-P11, which is supposed to differ from the wild type by one or a few so-far-not-characterized mutations, showed sufficient stability for application in industrial production.
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PMID:Production of yoghurt with mild taste by a Lactobacillus delbrueckii subsp. bulgaricus mutant with altered proteolytic properties. 1726 Mar 32

Over the past two decades, proton pump inhibitors (PPIs) have emerged as highly effective and relatively safe agents for the treatment of a variety of gastrointestinal disorders. Unfortunately, this desirable pharmacological profile has also contributed to superfluous and widespread use in both the inpatient and outpatient settings. While generally well-tolerated, research published over the last decade has associated these agents with increased risks of Clostridium difficile disease, fractures likely due to calcium malabsorption and both community-acquired (CAP) and hospital-acquired pneumonias (HAP). The mechanism behind PPI-associated pneumonia may be multifactorial, but is thought to stem from compromising the stomach's "acid mantle" against gastric colonization of acid-labile pathogenic bacteria which then may be aspirated. A secondary postulate is that PPIs, through their inhibition of extra-gastric H(+)/K(+)-ATPase enzymes, may reduce the acidity of the upper aerodigestive tract, thus resulting in increased bacterial colonization of the larynx, esophagus and lungs. To date, several retrospective case control studies have been published looking at the association between PPI use and CAP. Some studies found a temporal relationship between PPI exposure and the incidence of pneumonia, but only two could define a dose-response relationship. Furthermore, other studies found an inverse correlation between duration of PPI use and risk of CAP. In terms of HAP, we reviewed two retrospective cohort studies and one prospective study. One retrospective study in a medical ICU found no increased association of HAP in PPI-exposed patients compared to no acid-lowering therapy, while the other in cardiothoracic surgery patients showed a markedly increased risk compared to those receiving H(2)RAs. The one prospective study in ICU patients showed an increased risk of HAP with PPIs, but not with H(2)RAs. In conclusion, the current literature shows a slight trend toward an association between PPI use and pneumonia and an increased risk with PPIs over H(2)RAs, but the findings are not consistent across all studies. Larger controlled trials still need to be done to better identify the risk that PPIs impart towards patients contracting CAP or HAP. Until these are completed, we will have to continue to extrapolate across smaller controlled trials to predict the associated risks in our respective patient populations. In the interim, it appears prudent to limit the use of PPIs to situations where they are clinically indicated and, in such cases, use them at the lowest effective dose. In the case of prescribing for stress ulcer prophylaxis in ICU patients, perhaps H(2)RAs should be used as the preferred agents over PPIs.
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PMID:Proton pump inhibitor-associated pneumonia: Not a breath of fresh air after all? 2173 13

Renal stone disease may ensue from either derangements of urine biochemistries or anatomic abnormalities of kidneys and urinary tract. Genetic, environmental and dietary factors may also cooperate in the pathophysiology of nephrolithiasis. An adequate metabolic evaluation should focus on the urinary excretion of promoters and inhibitors of stone formation as well as on the occurrence of systemic diseases potentially related to secondary nephrolithiasis (i.e., endocrine disturbances, malabsorption, bone diseases). Moreover, metabolic investigations should provide reliable information on patient's dietary habits, guide towards the best therapeutic approach and enable the physician to verify patient's compliance to prescribed therapies.AN EXTENSIVE METABOLIC EVALUATION IS RECOMMENDED IN PATIENTS WITH ACTIVE STONE DISEASE (NAMELY, AT LEAST ONE NEW STONE WITHIN THE LAST TWO YEARS), OR IN THOSE HAVING HAD A SINGLE STONE EPISODE OCCURRED IN PECULIAR CONDITIONS: familial history of disease, childhood, menopause, pregnancy, systemic diseases. Simplified protocols may be adequate in non-active nephrolithiasis or in patients with single stone and no relevant risk factors.In our Stone Centre, a so-called "first level screening" is performed by routine, in order to assess urinary supersaturation with stone forming salts and evaluate the excretion of dietary-related metabolites in urine. Relative blood and urine determinations are reported below.IN VENOUS BLOOD: urea, creatinine, uric acid, Na, K, total and ionised Ca, Mg, P, Cl, alkaline phosphatase, gas analysis. In 24-hr urine samples: urea, creatinine, uric acid, Na, K, Ca, Mg, P, Cl, oxalate, inorganic sulphate, citrate, pH, ammonia and titratable acidity. IN FASTING URINE SAMPLES: Ca, citrate, creatinine, hydroxyproline, Brand's test for cistinuria, urine sediment, urine culture. If the first-level evaluation suggested an abnormal bone turnover, then further determinations are warranted, namely, calciotropic hormones (blood Vitamin D and PTH), markers of bone resorption (urine pyridinium crosslinks, serum crosslaps) and formation (serum osteocalcin) bone mineral density.EVENTUALLY, MORE SOPHISTICATED INVESTIGATIONS ARE REQUIRED TO IMPROVE THE DIAGNOSIS OF PECULIAR DISEASES: serum oxalate and glycolate, urine glycolate and L-glycerate, hepatic AGT activity (primary hyperoxalurias); genetic tests (hereditary nephrolithiasis); acidification tests (renal tubular acidosis).
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PMID:Biochemical evaluation in renal stone disease. 2246 Sep 94


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