(1) Although GORD is primarily a motor disorder, the injurious effects of gastric acid are central to the pathogenic process of oesophagitis, and the severity of disease correlates with the degree and duration of oesophageal acid exposure.
(2) The ambulatory 24 hour pH test may have rendered the AP test obsolete in the assessment of GORD as the cause of NCCP.
(3) Epidemiological studies of gastro-oesophageal reflux disease (GORD) are confounded by the lack of a standardized definition and a diagnostic 'gold-standard' for the disorder.
(4) Using 24 hour pH monitoring as a reference standard, the usefulness of the acid perfusion (AP) test in predicting gastro-oesophageal reflux disease (GORD) was assessed in 71 non-cardiac chest pain (NCCP) patients and 23 endoscopic oesophagitis patients.
(5) This may be made worse by relative gastric acid hypersecretion in some patients with severe GORD.
(6) The aim of this study was to investigate the association of gastro-oesophageal reflux disease (GORD) with radiographic pulmonary changes.
(7) The pathogenesis of GORD depends on a mix of factors which vary amongst individual patients.
(8) In the NCCP population with a normal oesophageal examination (1) AP test reproduction of chest pain is poorly predictive of GORD; (2) AP test reproduction of heartburn is more predictive of GORD but does not ensure that the chest pain is caused by GORD; (3) a negative AP test does not exclude GORD and (4) only 48% of AP test positive patients have demonstrable acid mediated chest pain.
(9) Although these data are not conclusive, it seems prudent, if possible, to avoid the use of NSAIDs in patients with GORD, particularly those with oesophageal stricture.
(10) In patients with more severe grades of oesophagitis, there are abnormally high levels of nocturnal acid exposure, with the intra-oesophageal pH being less than 4.0 for 36% of the time, compared with 5% of the time in patients with mild GORD.
(11) In Western countries, 20-40% of the adult population experience heartburn, which is the cardinal symptom of GORD, but only some 2% of adults have objective evidence of reflux oesophagitis.
(12) Of patients with oesophagitis 29% had no typical symptoms of GORD; only 24% of patients with regurgitation had oesophagitis.
(13) Although GORD causes substantial morbidity, the annual mortality rate due to GORD is very low (approximately 1 death per 100,000 patients), and even severe GORD has no apparent effect on longevity, although the quality of life can be significantly impaired.
(14) A third of the patients reported such inconclusive symptomatology at history-taking that no preliminary diagnosis about the presence or absence of GORD could be made.
(15) The limited information available about salivation in GORD patients suggests that salivary secretion is no different from that of age-matched controls, but that there is an age-dependent loss of the salivary response to oesophageal acidification.
(16) The long duration of action and effective inhibition of meal-stimulated acid secretion probably explains the superiority of omeprazole in treating GORD.
(17) In the 105 of these patients in whom there was any suspicion of GORD, 24-hour pH monitoring was carried out.
(18) When patients were divided according to their symptoms suggestive of GORD, lower VC%, FVC%, and FEV1% were found in patients with than in those without symptoms (87 vs 102, p = 0.0018; 76 vs 91, p = 0.0099; 80 vs 93, p = 0.0026).
(19) The signs and symptoms of GORD often wax and wane in intensity, and spontaneous remissions have been reported.
(20) Of several symptoms thought to be related to gastrooesophageal reflux disease (GORD), only heartburn (68% vs 48%) and acid regurgitation (60% vs 48%) occurred in more of the patients with GORD (as determined by pH monitoring) than of those with normal pH monitoring.
Sord
Definition:
(n.) See Sward.
Example Sentences:
(1) Whether or not there were carriers for either amorphous or hypomorphous alleles of the SORD locus in the population studied could not be defined in terms of enzymatic activity levels.
(2) Each plasmid contained the structural genes sorA for an Enzyme II of the phosphoenolpyruvate-dependent carbohydrate:phosphotransferase system, sorD for a D-glucitol 6-phosphate dehydrogenase, sorE for an L-sorbose 1-phosphate reductase, and the corresponding regulator gene sorR.
(3) New descriptions of three species and one subspecies of larvae of T. semenovi Ols., T. regularis Jaenn., T. laetetinctus laetetinctus Beck., and T. l. sordes Bog.
(4) Biochemical studies showed that thiol groups participate in the mobility of the SP fast band; furthermore, an interchange of the bands of SP-SORD was observed which suggests that the isozymes are due to conformational isomerism or to molecular aggregates.
(5) An electrophoretic study of sorbitol dehydrogenase (SORD) in sperm and seminal plasma (SP) was realized.
(6) In SP, three phenotypes (one slow band, one fast, and both bands) were observed, corroborating the electrophoretic variability of SP-SORD formerly reported by us, while, in sperm, SORD showed a phenotype of one band faster than the one of SP.
(7) The structural genes sorD, sorA and sorE code for a D-glucitol-6-P dehydrogenase (27 kilodalton (kD)), an Enzymell (EllSor) activity specific for L-sorbose and an L-sorbose-1-P reductase (45kD).
(8) The chromosomal locations for these 23 loci were determined as follows: GOT1 on rat chromosome 1; HAGH on 2; ACP2, ADA, GANC, ITPA, and SORD on 3; LDHB on 4; PEPB on 7; GLB1 and HEXA on 8; IDH1 on 9; UMPH2 on 10; GUSB on 12; FH and PEPC on 13; PEPS on 14; ESD and NP on 15; DIA4 on 19; and PP on 20.
(9) The linkage of NP, IDH2, SORD, MPI, and PKM2 was confirmed, and three other independently segregating markers (MDH1, ACY1, and PEPB) were identified.
(10) A wide variability in RBC-SORD activity in controls and patients was observed.
(11) They form an operon (gene order sorCpCDFBAME) inducible by L-sorbose, and their products have the following functions: SorC (36 kDa), regulatory protein with repressor-activator functions; SorD (29 kDa), D-glucitol-6-phosphate dehydrogenase; SorF and SorB (14 and 19 kDa, respectively), and SorA and SorM (27 and 29 kDa, respectively), two soluble and two membrane-bound proteins, respectively, of an L-sorbose phosphotransferase transport system; SorE (45 kDa), sorbose-1-phosphate reductase.
(12) A screening for both thermostability and electrophoretic red blood cell sorbitol dehydrogenase (RBC-SORD) variants in blood donors was performed.
(13) A computer program was developed for on-line analysis of nystagmus parameters using a microcomputer (SORD M243EX).
(14) Of the 15 loci, three genes, HK1, PEPC, and SORD, were newly assigned to chromosomes 1, 5, and 6, respectively, while ENO1, PGD, and PGM1 were assigned to the long arm of chromosome 2, in the segment 2q113----qter.
(15) Quantitative screening for red blood cell sorbitol dehydrogenase (RBC-SORD) deficiency in 111 patients with juvenile onset diabetes, 92 patients with adult onset diabetes, 42 patients with idiopathic cataracts and 192 professional blood donors was performed.
(16) Linkage group 3 comprises PEP-B (peptidase B), MPI-1 (mannosephosphate isomerase), SORD (sorbitol dehydrogenase), and mIDH-2 (mitochondrial isocitrate dehydrogenase).
(17) No significant differences in SORD activity either between patients with diabetes and patients with idiopathic cataracts or between diabetics with and without cataracts were observed.