Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Necrotizing fasciitis is a rapidly progressive soft tissue infection, involving the skin, subcutaneous tissue, and superficial fascia. It is a rare but life-threatening complication in the postoperative patient. In the last 7 years, we have treated four children in whom necrotizing fasciitis developed after appendectomy for ruptured appendix, bilateral inguinal herniorrhaphy, or gastrostomy closure. These four patients and seven well-described children from the literature with necrotizing fasciitis following surgery form the basis of this review. The ages ranged from six days to 15 years (mean 4.5 years). There were eight boys and three girls. There were five clean, five clean-contaminated, and one contaminated surgical procedures. No patient had evidence of malignancy or diabetes. Two of our four patients had evidence of failure to thrive. Only one patient had an intraabdominal abscess. In ten, the infection started in the abdominal wall; in one, the infection started in the chest wall. In our four patients, three had neutropenia and fever, four had tachycardia, and two had wound crepitation and radiographic evidence of subcutaneous gas. Cultures of all ten wounds were positive for bacteria; six were positive for more than one organism. Blood culture results were positive in five of five patients who died and in only two of five patients who survived. All survivors had wide surgical debridement and were treated with broad-spectrum antibiotics. The mortality rate was 45% in the whole series.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Postoperative necrotizing fasciitis in children. 305 88

A 16-year-old boy with Prader-Labhart-Willi syndrome (PLWS) had hypotonia, feeding difficulties, failure to thrive, strabismus and bilateral inguinal hernias with cryptorchidism during infancy followed by hyperphagia, marked early-onset obesity with insulin-dependent diabetes mellitus and necrobiosis lipoidica diabeticorum, short stature, hypogonadotropic hypogonadism and some of the facial characteristics of the individuals with the PLWS. IQ is estimated around 90. Cytogenetic studies showed mosaicism: 45,X, t(Y;15) with partial deletion 15 (15pter----15q12); 46,X, t(Y;15), dic (15)(15pter----15q12::15q12----15pter) and 47, X, t(Y;15), dic(15), dic(15). The dic(15) was bisatellited, NOR-positive on both arms and represented inv dup(15). Thus, the 2 lines with the dic(15) showed partial trisomy 15 (15pter----15q12) and partial pentasomy 15 (15pter----15q12), respectively. The cell line ratios were different in lymphocyte and fibroblast cultures. The unique cytogenetic findings in this patient, the reports of a variety of chromosome 15 aberrations in PLWS, as well as aberrations of other chromosomes, suggest that the condition is a contiguous gene syndrome rather than an aneuploidy syndrome.
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PMID:Unique mosaicism in Prader-Labhart-Willi syndrome--a contiguous gene or aneuploidy syndrome? 368 18

We report a patient with a clinical picture consisting of small birth weight, connatal hypoplastic anaemia, vacuolised bone marrow precursors, failure to thrive, and, subsequently, by insulin-dependent diabetes, renal Fanconi syndrome, lactic acidosis, complex organic aciduria, and elevation of haemoglobin F and of adenosine deaminase activity. The clinical course was progressive and death occurred at age 19 months. A high proportion of mitochondrial (mt) DNA molecules with a deletion of nucleotides 9238 to 15575 were identified in several tissues; about half of the shortened mtDNA molecules were concatenated to form circular dimers. The clinical and laboratory findings support recent conclusions that Pearson syndrome is not confined to bone marrow and pancreas, as originally described, but is a multi-organ disorder associated with deletions in part of the mtDNA molecules. The tissue distribution and the relative proportions of the abnormal mtDNA molecules apparently determine the phenotype and clinical course.
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PMID:Pearson bone marrow-pancreas syndrome with insulin-dependent diabetes, progressive renal tubulopathy, organic aciduria and elevated fetal haemoglobin caused by deletion and duplication of mitochondrial DNA. 768 Mar 15

The 6-year follow-up of a patient affected by Wolfram's syndrome, a rare disease characterized by diabetes insipidus (DI), diabetes mellitus (DM), optic atrophy (OA), neurosensory deafness (D), atony of the urinary tract and other abnormalities (DIDMOAD or Wolfram's syndrome), is described. Our patient has diabetes insipidus, diabetes mellitus, abnormal audiograms, without subjective evidence of hearing loss, and dilatation of the urinary tract. Diagnosis was suspected at the age of 8 years. Diabetes mellitus was the first manifestation and treatment with insulin was necessary. Desmopressin therapy decreased dramatically the daily urinary output. In view of the significant morbidity and mortality from renal failure associated with recurrent urinary infections, we have drawn special attention to the urological manifestations of the syndrome. During the follow-up, the patients underwent some investigations, such as renal ultrasound and echotomography and cystourethroscopy. Outstanding results of these studies are severe bilateral hydronephrosis with dilatated ureters and loss of renal tissue. The particular finding is the presence of posterior urethral valves with obstructed bladder. The anatomical outlet obstruction are variable and may be disastrous. There may be failure to thrive, sepsis, anemia be disanal failure. In such instances corrective surgery could improve bladder and ureteral functions.
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PMID:[Wolfram syndrome. Peculiar urologic aspects]. 779 16

We report a classical case of Prader-Willi syndrome (PWS) in an adult with typical interstitial deletion of chromosome 15, and emphasize the study of hormonal change. This 21-year-old female had PWS face characteristics, small hands and feet, marked obesity, mental retardation, growth retardation, absence of puberty and amenorrhea. She also had the characteristic history of infantile hypotonia, poor feeding, failure to thrive and then improved appetite, followed by obesity from the age of four years. She had compulsive hyperphagia, to the extent of stealing and lying to take food. Chromosome study with high resolution banding technique revealed a small interstitial deletion at band q12 of chromosome 15, which is characteristically found in a majority of patients with PWS. Hormonal study revealed hypogonadism and growth hormone deficiency of supposed hypothalamic origin. She also had non-insulin-dependent diabetes mellitus with decreased pancreatic insulin reserve.
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PMID:Hormonal change in an adult with Prader-Willi syndrome: report of a case. 791 75

The classical clinical picture of coeliac disease includes prolonged diarrhoea with failure to thrive. During the past two decades this type of active presentation of coeliac disease has decreased in many European countries, giving the impression that coeliac disease is a disappearing disease. However, this is not true. The disease can be found in older children with a more or less silent presentation. Silent coeliac disease can be detected by active screening with serological tests. Coeliac disease can be suspected in children suffering from mild gastrointestinal symptoms, such as abdominal pain, and in those with signs of nutritional deficiencies, as well as in children of first-degree relatives of already diagnosed coeliacs, patients with IgA-deficiency, patients suffering from dental enamel hypoplasia or dermatitis herpetiformis, and patients with some other disease known to be associated with coeliac disease, such as diabetes mellitus. According to the fundamental criteria of coeliac disease, the intestinal mucosa is flat when the individual is eating gluten-containing foods. However, this is not strictly true. Intolerance to gluten is obviously variable and the intestinal mucosa may be normal. This type of latent coeliac disease can be detected by analysing genetic markers, measuring antibodies in intestinal fluid or counting the density of intra-epithelial gamma/delta T cells which are increased greatly even in the latent phase of coeliac disease. Thus the general concept of the natural history of coeliac disease is changing.
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PMID:Changing clinical features of coeliac disease. 802 51

This study was designed to investigate the outcome of all elderly patients older than 65 who started peritoneal dialysis (PD) between January 1989 and December 1992. One hundred and twenty end-stage renal disease (ESRD) patients commenced PD at our institution between January 1989 and December 1992. All the patients who started, completed PD training, and remained on PD for more than one month were included in the study. Of these, 30 patients were elderly (more than 65 years old) with a mean age of 72 years (range 66-81 years). The total number of patient-months observed was 2035, of which the elderly represented 454 patient-months. Twenty-five percent (30 of 120 patients) were elderly. The causes of ESRD were diabetes mellitus in 6 patients (20%), glomerulonephritis in 6 (20%), atheroembolic disease in 4 (13.3%), hypertension in 2 (6.7%), and unknown etiology in 10 (33.3%) patients. Sixteen patients performed continuous ambulatory peritoneal dialysis (CAPD) and 14 patients continuous cycling peritoneal dialysis (CCPD). Five patients required private home nurses for multiple medical problems and for PD. Mean duration of peritoneal dialysis per patient was 15 months. Four patients were transferred to incenter hemodialysis, one each because of failure to thrive, insurance, catheter malfunction, and fungal peritonitis. One patient recovered renal function after 22 months of PD. Twenty-one episodes of peritonitis occurred over 454 patient-months (1 episode/22 patient-months). In conclusion, the elderly patients on PD have a favorable outcome even with multiple comorbid conditions.
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PMID:Peritoneal dialysis in elderly end-stage renal disease patients. 810 7

A number of studies have found a relationship of lower all-cause mortality risk for ESRD patients treated with increasing dose of dialysis. The objective of this study was to determine the relationship of delivered dose of dialysis with cause-specific mortality. Data from the USRDS Case Mix Adequacy Study, which includes a national random sample of hemodialysis patients, were utilized. To minimize the contribution of unmeasured residual renal function, the sample used in this analysis (N = 2479) included only patients on dialysis for one year or more. Cox proportional hazards models, stratified for diabetes, were used to analyze the effect of delivered dose of dialysis (measured and reported by both Kt/V and URR) on major causes of death and withdrawal from dialysis, adjusting for other covariates including demographics, comorbid diseases present at start of study, functional status, laboratory values and other dialysis parameters. Patient follow-up for mortality was censored at the earliest of time of transplantation, 60 days after a switch to peritoneal dialysis or at the time of data abstraction. For each 0.1 higher Kt/V, the adjusted relative risk of death due to coronary artery disease was 9% lower (RR = 0.91, P < 0.05), due to other cardiac causes was 12% lower (RR = 0.88, P < 0.01), due to cerebrovascular disease (CVD) was 14% lower (RR = 0.86, P < 0.05), due to infection was 9% lower (RR = 0.91, P = 0.05), and due to other known causes was 6% lower (RR = 0.94, P < 0.05). There was no statistically significant relationship of Kt/V and risk of death among patients who died of malignancy (RR = 0.84, P = 0.10) or among patients whose death cause was missing (RR = 0.95, P = 0.41). The risk of withdrawal from dialysis prior to death due to any cause was 9% lower (RR = 0.91, P < 0.05) for each 0.1 higher Kt/V. The relationships of delivered dose of dialysis, as measured by URR, and cause-specific mortality were essentially similar in relative magnitude and statistical significance as the relationships observed using Kt/V as the measurement of dialysis dose, with the exception that the relationship was less significant for cerebrovascular disease and withdrawal from dialysis. The relationship of dialysis dose with risk of death due to each cause of death category except other cardiac causes and "other" causes appeared to be of greater magnitude and of greater statistical significance among diabetics than non-diabetics. These results indicate that low dose of dialysis is not associated with mortality due to just one isolated cause of death, but rather is due to a number of the major causes of death in this population. This study is consistent with hypotheses that low doses of dialysis may promote atherogenesis, infection, malnutrition and failure to thrive through a variety of pathophysiologic mechanisms. Further study is necessary to confirm these results and to test hypotheses that are developed.
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PMID:Relationship of dose of hemodialysis and cause-specific mortality. 884 Feb 86

Over the last several years, the authors have studied the relationship of insulin-like growth factors (IGFs) and the insulin-like growth factor binding proteins (IGFBPs) in the circulation in a number of clinical settings. Patterns have emerged that seem to be characteristic of various conditions. In aging, there are marked decreases in IGF-I and -II, normal levels of IGFBP-3, and marked increases in IGFBP-1 in serum. Using ligand blotting and an IGFBP-3 proteolysis assay, BP-3 is intact. Based on native gel electrophoresis, IGFBP-1 is in its most highly phosphorylated state in those elders who have high IGFBP-1 levels. This pattern is slightly different in catabolic conditions such as AIDS (wasting in adults; failure to thrive in children), uncontrolled diabetes mellitus, trauma, and severe burns. In these conditions, serum levels of IGF-I and -II are markedly diminished, IGFBP-3 levels are also decreased, and IGFBP-1 levels are markedly increased. In addition, there is increased proteolysis of IGFBP-3 (AIDS failure to thrive, uncontrolled diabetes mellitus) and disruption of the ternary complex with decreased levels of ALS (AIDS wasting and burns). IGFBP-1 is in its most highly phosphorylated state in all catabolic conditions studied. Thus, the alterations in the circulating levels of IGFs and the changes in the physical state of the IGFBPs may lead to decreased anabolic activity and be a part of the mechanism of increased catabolism and wasting.
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PMID:IGFBP-3. Functional and structural implications in aging and wasting syndromes. 944 38

Weaning is the cause of much concern among first-time mothers. A milk-only diet is advised until 3-4 months of age. Health professionals should ensure the baby receives a sufficient and balanced diet during the weaning period, to meet the needs for energy and growth. Breast milk or infant formula should continue up to the age of at least one year. The weaning period is a good time to educate parents in good nutrition. A wide variety of foods should be the aim in child nutrition, but each different type needs to be started separately during weaning. Care is needed to ensure vegetarian babies receive enough proteins, vitamins and minerals (especially iron). Failure to thrive has a multitude of causes, and treatment must be that of the cause. Strictly vegan children who eat no dairy products will need added synthetic vitamin B12. Failure to thrive may be due to physical problems (eg choanal atresia), infection, vomiting, diarrhoea, anorexia, parental ignorance or poverty. Other causes include coeliac disease, cow's milk protein allergy, cystic fibrosis, severe eczema or asthma, or diabetes.
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PMID:Common feeding problems in babies and children: 2. 981 53


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