Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029713 (immaturity)
 4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Necrotizing enterocolitis--a highly letal disease in the newborn period--is diagnosed in about 1--2% of the admissions to a nursery. The marcroscopic lesions are basically necroses predominantly found in the ileum, colon and jejunum. Untreated they lead to perforation, peritonitis and sepsis. The predisposing factors include such as perinatal complications, immaturity and umbilical vein catheterization; the main symptoms are bile stained vomiting and blood-streaked diarrhea, followed by signs of fulminant sepsis and peritonitis. The most typical roentgenographic findings are intramural air (pneumatosis intestinalis) and in more advanced cases pneumoperitoneum (free peritoneal air) and portal vein gas. The current plan of management--consisting of immediate withdrawal of oral feeds, gastric suction, intravenous fluid therapy, treatment of shock and administration of antibiotics--and the indication for operation are discussed. Perinatal stress and secondary bacterial invasion of the intestinal lesions seem to play an important role in the etiology of the disease. An early nutrition of the healthy immature with human breast milk seems to reduce the incidence of necrotizing enterocolitis or at least has a mitigating influence on the later course of the disease. The mortality in our own series--as reported--was high (6 patients: 1 survivor, mortality: 83%) as 4 of the patients were admitted with gross symptoms of intestinal perforation and severely shocked.
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PMID:[Necrotizing enterocolitis (pediatric review)]. 33 53

Sequential chemotherapeutic regimens, primarily used in the treatment of hematopoietic malignancies, and employing ara-C as a basic antineoplastic agent induce mucosal alterations in the entire gastrointestinal tract. These are characterized by surface and glandular epithelial atypia, immaturity, and necrosis. Glandular regeneration is characteristically delayed leading to a state of intestinal aproliferative cytopenia. Other toxic intestinal changes include telangiectasia of blood vessels and the formation of intramural hematomas. Intestinal infections develop frequently and are complicated by peritonitis, liver abscesses, pneumatosis cystoides in testinalis and sepsis. These intestinal lesions are accompanied by a predictable clinical syndrome which begins concomitantly with ara-C infusions and is characterized by diarrhea, ileus, abdominal pain, hematemesis and melena, severe hypokalemia, hypocalcemia and a protein-losing enteropathy. Additional toxic manifestations induced by ara-C include transient weight gains, fever elevations and severe bone marrow depression. The genesis of the intestinal lesions is linked to the three day dose schedule of ara-C infusions which insures both arrest of the cycling intestinal cells in the S-phase and a high cytotoxic index. The severity of these lesions is markedly augmented by prior treatment with ara-C and cyclophosphamide which causes synchronization and probable recruitment of intestinal stem cells, respectively.
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PMID:Cytosine arabinoside induced gastrointestinal toxic alterations in sequential chemotherapeutic protocols: a clinical-pathologic study of 33 patients. 70 32

To assess the influence of immaturity on the responsiveness of enterocytes to specific pathogens, a dose-response curve for cholera toxin (CT)-induced fluid secretion was determined in the proximal small intestine of rats at 2 and 4 wk of age. The suckling rat was approximately 50 times more sensitive to CT in triggering the secretory response than the weaned rat, when estimated by the medium-effective dose (ED50, 0.8 vs. 38.9 nM). Cortisone, known to promote enterocyte maturation, when injected into suckling rats, decreased host sensitivity approximately 1,000 times. Neither age nor cortisone decreased the receptor binding of 125I-labeled CT to intestinal microvillus membranes. In contrast, cortisone treatment caused a threefold increase in receptor density from 14.5 to 43.0 pmol/mg protein. The enzyme responsible for the sodium pump, Na+-K+-ATPase, showed a threefold increase in activity both after weaning and after a cortisone treatment. These data indicate that the immature gut exhibited an increased host sensitivity to CT stimulation that was not correlated with initial receptor binding but was related to a lowered Na+-K+-ATPase activity, suggesting that an underdeveloped sodium pump may be partially responsible for the high incidence of secretory diarrhea in neonates.
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PMID:Age and cortisone alter host responsiveness to cholera toxin in the developing gut. 253 37

We report a case of chronic diarrhea due to hypergastrinemia with achlorhydria but without gastritis in a five-year-old boy. Symptoms responded promptly to oral administration of hydrochloric acid and resolved completely after one year of treatment. The pathophysiologic situation in this patient closely resembled that normally seen in neonates, suggesting prolonged but nevertheless transient immaturity of gastric secretions.
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PMID:[Chronic diarrhea with hypergastrinemia and achlorhydria without gastritis in a 5-year-old child]. 274 10

An analysis is presented of data on all 30 129 inpatient admissions to a mission hospital in the West Nile District of Uganda in the 27 year period from July 1951 to August 1978. For most of this period the hospital was staffed by the same two doctors. For each patient admitted, a record was made of their age (adult or child), sex, place of residence, duration of stay in hospital, diagnosis and vital status at discharge. The annual number of admissions increased steadily from around 300 in 1952 to over 1600 in 1966 and subsequently declined to about 900 in 1977. Sixty-five per cent of admissions were medical, 12% surgical, 11% obstetric and 9% gynaecological. Thirty per cent of admissions were children (aged 0-9 years). Forty-five per cent of admissions were from those resident in the same county as the hospital and another 20% were from an immediately adjacent county. Infective and parasitic conditions (including respiratory diseases) accounted for over 60% of admissions among children and over 38% of admissions among adults (excluding obstetric patients). The six most common causes of admission were: uncomplicated delivery (2308 admissions), pneumonia (2020), hookworm (1999), malaria (1806), schistosomiasis (1742) and diarrhoea (1041). In total 1960 deaths were recorded (6.5% of all admissions). High case fatality rates were observed for tetanus (61%), immaturity (54%), meningitis (38%), kwashiorkor (21%), other malnutrition (19%) and anaemia (19%). A striking increase in the number of admissions for measles was observed in the period 1976 to 1978. Admission rates for schistosomiasis (S. mansoni) appeared to be highest from counties adjacent to the Nile and 104 deaths were recorded among the 1742 patients with this as the primary diagnosis. Admissions for diabetes, as a percentage of all admissions increased from 0.2% in 1951-54 to 1.5% at the end of the study period. Marked seasonal variations in admission patterns were found for diarrhoea, measles, meningitis and respiratory infections, the last two, but not diarrhoea, being most common in the wettest months. Admissions for malaria showed no strong seasonal associations. Despite the limitations of hospital-based data, it is argued that the data analysed provide a reasonable indication of the important causes of severe morbidity and mortality in the district. Furthermore, some of the changes in admission patterns over time are likely to represent true changes in disease rates rather than artefacts of diagnosis or referral. The analyses presented indicate the value of simple record systems, carefully maintained.
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PMID:Admissions to a rural hospital in the West Nile District of Uganda over a 27 year period. 378 13

We report an interesting case of congenital inflammatory bowel disease and intestinal epithelial immaturity that presented as secretory diarrhea. No infectious, metabolic, or anatomical basis for these findings was identified. As differentiated from previous reports of neonatal enteropathies, this infant demonstrated involvement of both the small and large intestine with histopathologic findings of acute and chronic inflammation, extensive submucosal fibrosis, and "flat" small intestine mucosa. In addition, this patient had a polyamine deficiency (a primary or secondary phenomenon), which may have contributed to delayed epithelial maturation. These findings suggest that the inflammatory bowel disease and altered epithelial maturation contributed to a fatal intractable diarrhea.
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PMID:Congenital diarrhea with intestinal inflammation and epithelial immaturity. 379 28

Mucin secretion was examined in three functional models relevant to human disease, using rat small intestinal rings or in situ loops, [3H]glucosamine precursor labelling, gel chromatography and a specific radioimmunoassay for mucin. As a model for acute bacterial secretory diarrhoea, tissues were exposed to cholera toxin for up to 4 h. Both stored and newly synthesized radioactive glycoproteins were secreted in amounts twofold to threefold above control levels. Immunoreactive mucin secretion increased fivefold to eightfold. Other agents known to raise cAMP levels did not stimulate mucin secretion, suggesting that cholera may release mucin by a non-cAMP-dependent mechanism. Sepharose 2B chromatography indicated that secreted mucin was smaller in size than intracellular mucin and had compositional differences suggestive of 'immaturity' or protein contamination. In chronically (seven days) reserpinized rats, used as a model of glycoprotein abnormalities relevant to cystic fibrosis, mucin secretion increased twofold to threefold, but the most prominent abnormality was a marked increase in [3H]glucosamine incorporation into all tissue glycoproteins. On purification, the intracellular mucin of reserpine-treated rats had the same composition as mucin from control rats, but the former was smaller in size and had a higher specific radioactivity. Mucin hypersecretion in reserpinized rats may therefore be secondary to a primary and chronic hyperstimulation of mucin biosynthesis. A model of intestinal 'anaphylaxis' or immune-mediated diarrhoea was created in Hooded Lister rats by immunizing with egg albumin (10 micrograms) and challenging with the same antigen in intestinal loops 14 days later. After 4 h, total protein, DNA and brush border sucrase were increased in the lumen. Enhancement of mucin secretion did not occur, however, and therefore does not seem to be a particular feature of the pathophysiology of this model.
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PMID:Acute and chronic models for hypersecretion of intestinal mucin. 656 39

Morbidity and mortality patterns were examined among 968 pediatric patients on the island of Dominica. These children, whose ages ranged from newborn to 13 years, were seen by the consulting pediatrician at Princess Margaret Hospital during a 9-month period in 1978-79; 852 children were seen as inpatients. A total of 477 cases of infectious disease were diagnosed among inpatients alone. Stool examination in a subsample of these children revealed parasites (mostly Trichuris) in roughly half. Also found was a relatively high prevalence of chronic health problems, especially rheumatic heart disease (34 cases), mental retardation (28 cases), epilepsy (31 cases), and sickle cell anemia (21 cases). Examination of the hospital records of 100 of the inpatients ages 6 months-5 years demonstrated that 34% were low weight-for-age according to the World Health Organization classification. There were 34 deaths (9 pediatric patients and 255 newborns). The high neonatal mortality is attributed to an unusually high incidence of immaturity and prematurity, irregular and insufficient hospital oxygen supply, and a septicemia epidemic. Although these findings reflect patterns of the more serious diseases, they could be useful in planning preventive health measures. The high prevalence of malnutrition points to a need for nutrition education, promotion of breastfeeding, promotion of vegetable growing, and the introduction of a home-based growth chart. The high incidence of diarrhea, typhoid fever, and helminthiases highlights problems with general hygiene, latrines, and water supply. There is also a need for follow-up facilities for children with rheumatic heart disease, epilepsy, and sickle cell anemia. It is suggested that hospital care could be improved by dividing pediatric and neonatology wards into 5 units: isolation ward, malnutrition ward, semi-intensive care unit, general pediatrics, and pediatric surgery.
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PMID:Morbidity and mortality patterns among pediatric patients in Dominica (West Indies). 662 10

Cow's milk protein sensitive enteropathy (CMPSE) is characterized by the following items: 1. The great majority of affected infants have not been breast fed or only for a few days. Additional risks are immaturity, preceding enteritis, trisomy 21, and abdominal operation in the newborn. 2. Half of the patients become ill during the first two weeks after starting cow's milk formula. The main symptoms are watery, mucus containing diarrhea, vomiting, abdominal distension, pallor and rapid weight loss. 3. In CMPSE the small intestinal mucosa shows varying degrees of inflammation and villous atrophy. Bloody stools refer to large bowel affection. 4. CMPSE is always transitory and usually persists for less than one year. Inadequate treatment leads to "severe protracted diarrhea" or "intractable diarrhea" syndrome. Soya-based formula should not be the diet of first choice, since secondary intolerance to soya proteins will frequently develop. Exclusive breast feeding during the first months of life is the best prophylaxis of CMPSE.
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PMID:[Cow's milk protein sensitive enteropathy]. 675 83

Bile salt metabolism was examined in 12 infants (ages 7 weeks to 10 months) who had recovered from protracted infantile diarrhea. Cholic acid kinetics were measured with the isotopic dilution technique. Cholate pool size was 938 +/- 89 mg/m2 (means +/- S.E.), synthetic rate was 478 +/- 52 mg/m2/day, and the fractional turnover rate was 0.537 +/- 0.060 day -1. Estimated chenodeoxycholate pool size was 607 +/- 103 mg/m2. similar cholic acid pool sizes were previously observed in older children; however, the synthetic and turnover rates were significantly lower, p less than 0.05 and 0.025, respectively. A significant inverse relationship between age and fractional turnover rate (r = -0.577, p less than 0.05) was observed in the first 10 months of life. Fasting serum cholylglycine measured by radioimmunoassay was significantly higher (p less than 0.01) in infants than in children. Peak postprandial concentrations were higher in infants than in older children. Accelerated hepatic bile salt synthesis rapidly increases the size of small pools at birth. Intraluminal bile salt concentrations concurrently increase, thereby normalizing fat solubilzation. Slow maturation of intestinal transport mechanisms may result in normal cycling of bile salts by 3 to 7 months of age. Persistent immaturity of hepatic uptake and/or excretion of bile salts leads to intrahepatic retention of a portion of the pool, with resultant regurgitation into the serum during the first months of life.
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PMID:Bile salt metabolism in the first year of life. 720 Oct


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