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Results for “SIMMONDS' DISEASE”

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PubMed1989

Duodenopancreatic fistula accompanying Crohn's disease of the distal duodenum.

A 47-yr-old male with known Crohn's disease involving the third and fourth part of the duodenum and terminal ileum presented to hospital with nausea and vomiting due to duodenal obstruction. An upper gastrointestinal series revealed a clinically unsuspected fistula joining the duodenum and pancreatic duct. He subsequently underwent vagotomy and gastroenterostomy to bypass the obstructed segment of duodenum. The duodenopancreatic fistula was not disturbed. Post-operatively, his symptoms resolved, he gained 30 pounds of weight, and manifested no ill effect secondary to the fistula. A repeat upper gastrointestinal series 9 months postoperatively revealed the fistula to have closed, although marked duodenal narrowing remained.

Crohn Disease↗
PubMed1989

Weight in infancy and death from ischaemic heart disease.

Environmental influences that impair growth and development in early life may be risk factors for ischaemic heart disease. To test this hypothesis, 5654 men born during 1911-30 were traced. They were born in six districts of Hertfordshire, England, and their weights in infancy were recorded. 92.4% were breast fed. Men with the lowest weights at birth and at one year had the highest death rates from ischaemic heart disease. The standardised mortality ratios fell from 111 in men who weighed 18 pounds (8.2 kg) or less at one year to 42 in those who weighed 27 pounds (12.3 kg) or more. Measures that promote prenatal and postnatal growth may reduce deaths from ischaemic heart disease. Promotion of postnatal growth may be especially important in boys who weigh below 7.5 pounds (3.4 kg) at birth.

Adult↗
PubMed2002

Severe pyridine nucleotide depletion in fibroblasts from Lesch-Nyhan patients.

The relationship between a complete deficiency of the purine enzyme hypoxanthine-guanine phosphoribosyltransferase and the neurobehavioural abnormalities in Lesch-Nyhan disease remains an enigma. In vitro studies using lymphoblasts or fibroblasts have evaluated purine and pyrimidine metabolism with conflicting results. This study focused on pyridine nucleotide metabolism in control and Lesch-Nyhan fibroblasts using radiolabelled salvage precursors to couple the extent of uptake with endocellular nucleotide concentrations. The novel finding, highlighted by specific culture conditions, was a marked NAD depletion in Lesch-Nyhan fibroblasts. ATP and GTP were also 50% of the control, as reported in lymphoblasts. A 6-fold greater incorporation of [(14)C]nicotinic acid into nicotinic acid- adenine dinucleotide by Lesch-Nyhan fibroblasts, with no unmetabolized substrate (20% in controls), supported disturbed pyridine metabolism, NAD depletion being related to utilization by poly(ADP-ribose) polymerase in DNA repair. Although pyrimidine nucleotide concentrations were similar to controls, Lesch-Nyhan cells showed reduced [(14)C]cytidine/uridine salvage into UDP sugars. Incorporation of [(14)C]uridine into CTP by both was minimal, with more than 50% [(14)C]cytidine metabolized to UTP, indicating that fibroblasts, unlike lymphoblasts, lack active CTP synthetase, but possess cytidine deaminase. Restricted culture conditions may be neccesary to mimic the situation in human brain cells at an early developmental stage. Cell type may be equally important. NAD plus ATP depletion in developing brain could restrict DNA repair, leading to neuronal damage/loss by apoptosis, and, with GTP depletion, affect neurotransmitter synthesis and basal ganglia dopaminergic neuronal systems. Thus aberrant pyridine nucleotide metabolism could play a vital role in the pathophysiology of Lesch-Nyhan disease.

Adenosine Triphosphate↗
PubMed1997

Hepatitis C virus genotypes and liver disease in patients undergoing allogeneic bone marrow transplantation.

Hepatitis C virus (HCV) genotypes were investigated in 57 HCV-infected patients undergoing allogeneic BMT at four European BMT units where death resulting from liver failure (LF) in HCV-infected patients varied from < 1% to > 80%. The aim of the study was to determine whether differing HCV genotypes could account for the different severity of post-transplant liver disease (LD). Sera from patients with pre (n = 22) or post-BMT (n = 35) HCV infection were collected from Italy (Genova, Monza), Sweden (Huddinge) and Germany (Ulm). Patients were grouped as follows: LF: 19/57; acute hepatitis (AH): 10/57 or chronic hepatitis (CH): 22/57; no liver disease (LD): 6/57. HCV genotypes were identified by hybridisation of the 5'UTR amplified products with type-specific oligonucleotides probes according to Simmonds (Hepatology 1994; 19: 1321-1324). Genotype HCV 1 was identified in 34 patients (60%), HCV 2 in 15 (26%), HCV 3 in three (5%), mixed infection in three (5%) and undefined in two (3.5%). In the LF group HCV 1 was identified in 10/19 and other genotypes in 9/19. Median timing of LF was earlier in patients infected with HCV 1 compared to other genotypes (45 and 68 days, respectively), largely due to the cause of LF; death from veno-occlusive disease (VOD) and hepatitis occurred at 30 and 68 days post-BMT, respectively. Genotype 1 was also identified in cases with no LD. These data indicate that there was no evident correlation between HCV genotype and type or severity of post-transplant liver disease.

Adolescent↗
PubMed2004

Evaluation of porB PCR-amplicon restriction endonuclease analysis as a method to determine porB variable-region sequences in nonserotypeable meningococci.

porB PCR-amplicon restriction endonuclease analysis is a rapid, simple method developed to assess porB variation in nonserotypeable meningococci isolated during New Zealand's epidemic of meningococcal disease. Most nonserotypeable meningococci isolated between 1990 and 1999 inclusively either were type 4 (40.5%) or contained the porB variable region 1 (VR1)-19, VR2-D, VR3-7, and VR4-14a sequences (45.1%).

Amino Acid Sequence↗
PubMed1992

Chemiluminescence assay of mucosal reactive oxygen metabolites in inflammatory bowel disease.

Previous studies suggesting increased reactive oxygen metabolite (ROM) production in inflammatory bowel disease have been restricted to peripheral blood and isolated intestinal phagocytes. In the current study, chemiluminescence and the effect of various scavengers, enzymes, and enzyme inhibitors were used to show that ROMs account for the increased production of oxidants by colorectal mucosal biopsy specimens in inflammatory bowel disease. Luminol-amplified chemiluminescence was increased in active ulcerative colitis [macroscopic grade 1: 25 photons.mg-1.min.10(-3) (median), 8-47 (95% confidence intervals), n = 40; grade 2: 89, 65-156, n = 30; grade 3: 247, 133-562, n = 13] and Crohn's disease [mild: 9, 3-84, n = 6; severe: 105, 25-789 (range), n = 5] compared with normal-looking mucosa (ulcerative colitis: 0.8, 0.4-1.4, n = 22, P less than 0.01; Crohn's disease: 0.8, 0.1-2, n = 6, P less than 0.05) and controls (0.6, 0.04-1.4, n = 52, P less than 0.01). In ulcerative colitis, luminol chemiluminescence correlated with microscopic inflammation (Spearman's p = 0.74, P = 0.0001) and was decreased by sodium azide (-89%, P less than 0.05), taurine (-31%, P less than 0.05), catalase (-23%, P less than 0.05), and dimethyl sulfoxide (-29%, P less than 0.05). Superoxide dismutase and oxypurinol decreased lucigenin chemiluminescence in ulcerative colitis by -63% (P less than 0.05) and -27% (P less than 0.05), respectively. Luminol chemiluminescence correlated with lucigenin chemiluminescence (Spearman's rho = 0.72, P = 0.003). These results suggest that neutrophil-derived oxidants (superoxide, hydrogen peroxide, hydroxyl radical, and hypochlorite) are generated in colorectal mucosa in active inflammatory bowel disease and support the hypothesis that production of such metabolites by neutrophils is of major pathogenetic importance.

Acridines↗
PubMed2004

Pulmonary rehabilitation: analysis of a clinical service.

BACKGROUND AND PURPOSE: There is significant research supporting the role of pulmonary rehabilitation in chronic obstructive pulmonary disease (COPD). However, less is known about real-life clinical rehabilitation services. Data were analysed from a clinical pulmonary rehabilitation service provided in the UK, consisting of seven weeks' twice-weekly training and education. METHOD: A retrospective study. Baseline measures consisted of activity of daily living, mood state, spirometry, exercise tolerance using the Incremental Shuttle Walk Test (ISWT) and health status using the St George's Hospital Respiratory Questionnaire (SGRQ). Responders to pulmonary rehabilitation were defined as those with a mean reduction of four points on the SGRQ and a mean increase of 48 metres on the ISWT. RESULTS: One hundred and eight patients entered the programme and 91 completed it. All outcomes showed statistically and clinically significant change after the rehabilitation programme. Responder analysis showed that 37% of patients achieved benefits for both the SGRQ and the ISWT. Twenty-eight per cent of patients were non-responders for both; 17% benefited for the SGRO only and 14% improved their exercise tolerance. Patients with restrictive disease (n = 11) showed large mean ISWT score of 98.2 m (Standard deviation (SD) 69.4 m) (p < 0.01), as did patients with moderate COPD (n = 30), who scored a mean ISWT change of 77.3 m (SD 92.0 m) (p < 0.01) and a SGRQ score of -7.6 (SD 13.7) (p < 0.01), and those with mild COPD (n = 12), who scored a mean ISWT change of 62.5 m (SD 87.4 m) (p < 0.01) and a mean SGRQ change of -3. 7 (SD 8.1) (p < 0.01). Patients with severe COPD (n = 23) showed a smaller mean change in ISWT of 32.6 m (SD 79.4 m) and in SGRQ of -2.8 (SD 7.1). However, analysis of variance (ANOVA) showed no statistical differences between the groups (p = 0.13). CONCLUSIONS: Clinical pulmonary rehabilitation programmes are effective for most patients. However for patients with more severe impairment, maximal gains may be harder, or take longer, to achieve. Patients with restrictive disease appear to do well, although future trials will be needed to test this supposition.

Aged↗
PubMed2004

High levels of human immunodeficiency virus infection of CD8 lymphocytes expressing CD4 in vivo.

Human immunodeficiency virus (HIV)-infected CD8 lymphocytes have been reported in vivo, but the mechanism of infection remains unclear. Experiments using the thy/hu mouse model support export of intrathymically infected CD8 precursors, while recent in vitro data suggest that mature CD8 lymphocytes upregulate CD4 upon activation (generating a CD8bright CD4dim phenotype) and are susceptible to HIV infection. To determine whether these mechanisms operate in vivo and to assess their relative importance in the generation of circulating HIV-infected CD8 lymphocytes, we quantified HIV long terminal repeat (LTR) DNA in CD8+ CD4- and CD8bright CD4dim lymphocytes isolated from HIV-infected individuals by fluorescence-activated cell sorting. HIV infection of CD8 lymphocytes was demonstrated in 17 of 19 subjects, with a significant inverse relationship between level of infection and CD4 lymphocyte count (R = -0.73; P < 0.001). The level of HIV infection of CD8bright CD4dim lymphocytes was significantly higher (median, 1,730 HIV LTR copies/10(6) cells; n = 9) than that of CD8+ CD4- lymphocytes (undetectable in seven of nine individuals; P < 0.01) and approached that of CD4 lymphocytes from the same individuals (median, 3,660 HIV LTR copies/10(6) cells). CD8bright CD4dim lymphocytes represented 0.8 to 3.3% of total CD8 lymphocytes and were most prevalent in the memory subset. Thus, HIV-infected CD8 lymphocytes commonly circulate in HIV-infected individuals and are generated through infection of activated CD8 lymphocytes rather than through export of intrathymically infected precursors. The high level of infection of CD8bright CD4dim lymphocytes could have a direct role in the decline in CD8 lymphocyte function that accompanies HIV disease progression.

Adult↗
PubMed1991

A high performance liquid chromatographic assay for AMP-deaminase activity in the erythrocytes of healthy subjects and patients with inherited purine disorders.

A novel method for measuring AMP-deaminase activity in human erythrocytes is presented, based on the determination of the reaction product, IMP, using high performance liquid chromatography. IMP formation was found to be proportional both to the incubation time and the amount of haemolysate over a wide range. The minimal detectable AMP-deaminase activity was more than 1000 times lower than the mean activity found in healthy controls (1083 nmol/h/mg Hb). No marked difference of activity was found in the patients with the following inherited purine disorders: familial juvenile gouty nephropathy and deficiencies of adenosine deaminase, hypoxanthine-guanine phosphoribosyltransferase or adenine phosphoribosyltransferase. The activity in the erythrocytes of patients with chronic renal failure was also similar to controls. The existence of subjects with low erythrocyte AMP-deaminase activity in the population has been confirmed.

AMP Deaminase↗
PubMedDate not supplied

Incidence of localized cutaneous leishmaniasis (chiclero's ulcer) in Mexico.

Cutaneous leishmaniasis in Mexico was first described in 1912. Since then, its existence has been repeatedly confirmed in the forest regions of the peninsula of Yucatan. In order to obtain reliable knowledge about the magnitude of this problem, we questioned and skin-tested a sample of 449 persons randomly selected from men aged 15-45 years. We found a positivity rate of 24 to 90% (mean 43%) in the seven rural health posts studied. Furthermore, 72 patients were examined between January and December 1987 by parasitological investigation (smear, isolation, culture and/or biopsy) and the Montenegro skin test; 56 had acquired the disease in 1987. Based on these data, we found an annual incidence rate of 508 per 100,000 inhabitants. Further long-term studies are indicated to determine the incidence and prevalence rates for this disease in other parts of the country.

Adolescent↗
PubMed1983

Gout and uric acid nephropathy: some new aspects in diagnosis and treatment.

It has been recognized that primary disorders of uric acid metabolism result from impaired renal excretion or increased endogenous production of uric acid. It has also been found that these two mechanisms do not comprise two distinct syndromes, but may each constitute a group of syndromes. Contrary to earlier as well as currently published reports we conclude from our clinical and experimental experience that the fraction of so-called over-producers is less than 1% of all patients with primary hyperuricaemia and gout. A procedure for the diagnosis of uric acid overproduction is suggested. The manifestation of hyperuricaemia and gout mainly depends on renal uric acid clearance and is greatly influenced by dietary habits in most of the patients. An impaired renal uric acid excretion results in an increased intestinal excretion; this partly compensates for the defect. Normalization of serum uric acid should be achieved by dietary regimens with or without additional drug treatment, but not by drug treatment alone. With drug treatment xanthine oxidase inhibitors are preferable to uricosurics; no other xanthine oxidase inhibitor besides Allopurinol has been in clinical trial, however. Due to the enhancement of uric acid clearance with uricosurics, there are groups of patients who should not be treated with these drugs. Fixed combinations of Allopurinol and uricosurics should not be used. Drugs which have uricosuric as well as other pharmacologic properties are under investigation. So far they have not reached general clinical application.

Adult↗