Biomedical subjects

J B Prins

Publications and source records attributed to J B Prins.

At least 19 recordsLinked to original sources

PubMed2007

Symptoms in the palliative phase of children with cancer.

BACKGROUND: The aim of the study was to make a comprehensive inventory of the physical, psychological, and social symptoms of children with cancer and their parents during the palliative phase and the extent to which health professionals address those symptoms. PROCEDURE: Forty parents of children who died 1-3 years prior to data collection (structured questionnaire) were invited to participate in the study. RESULTS: The response rate was 32 out of 40 parents (80%). Most frequently mentioned physical symptoms were pain, poor appetite, and fatigue. The children's most mentioned psychological symptoms were sadness, difficulty in talking to their parents about their feelings regarding illness and death and fear of being alone. The symptoms of fear of death of the child and fear of physical symptoms were most frequently mentioned parents' psychological symptoms. Health professionals addressed 82% of the children's physical symptoms, 43% of the children's psychological symptoms, and 56% of the parents' psychological symptoms. Parents indicated that after professional attention the proportion of children's physical symptoms that were completely or partially resolved was 18 and 26%, respectively. For children's psychological symptoms the figures were 9 and 25%, respectively, and for parents' psychological symptoms 2 and 23%, respectively. CONCLUSIONS: The burden of symptoms of the child with cancer during the palliative phase and their parents is high. Health professionals focus mainly on the physical symptoms of the child. Relief of symptoms could not be achieved for a large proportion of symptoms. Further prospective research is necessary to investigate the kind, frequency and intensity of symptoms in order to tailor optimal palliative care to the needs of both child and parent.

Adolescent↗

PubMed2006

Adiponectin--a key adipokine in the metabolic syndrome.

Adiponectin is a recently described adipokine that has been recognized as a key regulator of insulin sensitivity and tissue inflammation. It is produced by adipose tissue (white and brown) and circulates in the blood at very high concentrations. It has direct actions in liver, skeletal muscle and the vasculature, with prominent roles to improve hepatic insulin sensitivity, increase fuel oxidation [via up-regulation of adenosine monophosphate-activated protein kinase (AMPK) activity] and decrease vascular inflammation. Adiponectin exists in the circulation as varying molecular weight forms, produced by multimerization. Recent data indicate that the high-molecular weight (HMW) complexes have the predominant action in the liver. In contrast to other adipokines, adiponectin secretion and circulating levels are inversely proportional to body fat content. Levels are further reduced in subjects with diabetes and coronary artery disease. Adiponectin antagonizes many effects of tumour necrosis factor-alpha(TNF-alpha) and this, in turn, suppresses adiponectin production. Furthermore, adiponectin secretion from adipocytes is enhanced by thiazolidinediones (which also act to antagonize TNF-alpha effects). Thus, adiponectin may be the common mechanism by which TNF-alpha promotes, and the thiazolidinediones suppress, insulin resistance and inflammation. Two adiponectin receptors, termed AdipoR1 and AdipoR2, have been identified and these are ubiquitously expressed. AdipoR1 is most highly expressed in skeletal muscle and has a prominent action to activate AMPK, and hence promote lipid oxidation. AdipoR2 is most highly expressed in liver, where it enhances insulin sensitivity and reduces steatosis via activation of AMPK and increased peroxisome-proliferator-activated receptor alpha ligand activity. T-cadherin, which is expressed in endothelium and smooth muscle, has been identified as an adiponectin-binding protein with preference for HMW adiponectin multimers. Given the low levels of adiponectin in subjects with the metabolic syndrome, and the beneficial effect of the adipokine in animal studies, there is exciting potential for adiponectin replacement therapy in insulin resistance and related disorders.

Adiponectin↗

PubMed2006

Influence of melatonin on fatigue severity in patients with chronic fatigue syndrome and late melatonin secretion.

The effect of melatonin, a chronobiotic drug, was explored in 29 patients with chronic fatigue syndrome (CFS) and Dim Light Melatonin onset (DLMO) later than 21.30 hours, reflective of delayed circadian rhythmicity. The patients took 5 mg of melatonin orally, 5 h before DLMO during 3 months. Their responses to the checklist individual strength (CIS), a reliable questionnaire measuring the severity of personally experienced fatigue, were assessed twice with a 6-week interval immediately before the treatment and once after 3 months treatment. In the pre-treatment period the fatigue sub-score improved significantly. After treatment, the total CIS score and the sub-scores for fatigue, concentration, motivation and activity improved significantly. The sub-score fatigue normalized in two of the 29 patients in the pre-treatment period and in eight of 27 patients during treatment. This change was significant. In the patients with DLMO later than 22.00 hours (n=21) the total CIS score and the sub-scores for fatigue, concentration and activity improved significantly more than in the patients (n=8) with DLMO earlier than 22.00 hours. Melatonin may be an effective treatment for patients with CFS and late DLMO, especially in those with DLMO later than 22.00 hours.

Circadian Rhythm↗

PubMed2006

Familial isolated hyperparathyroidism is linked to a 1.7 Mb region on chromosome 2p13.3-14.

BACKGROUND: Familial isolated hyperparathyroidism (FIHP) is an autosomal dominantly inherited form of primary hyperparathyroidism. Although comprising only about 1% of cases of primary hyperparathyroidism, identification and functional analysis of a causative gene for FIHP is likely to advance our understanding of parathyroid physiology and pathophysiology. METHODS: A genome-wide screen of DNA from seven pedigrees with FIHP was undertaken in order to identify a region of genetic linkage with the disorder. RESULTS: Multipoint linkage analysis identified a region of suggestive linkage (LOD score 2.68) on chromosome 2. Fine mapping with the addition of three other families revealed significant linkage adjacent to D2S2368 (maximum multipoint LOD score 3.43). Recombination events defined a 1.7 Mb region of linkage between D2S2368 and D2S358 in nine pedigrees. Sequencing of the two most likely candidate genes in this region, however, did not identify a gene for FIHP. CONCLUSIONS: We conclude that a causative gene for FIHP lies within this interval on chromosome 2. This is a major step towards eventual precise identification of a gene for FIHP, likely to be a key component in the genetic regulation of calcium homeostasis.

Chromosome Mapping↗

PubMed2005

A report of a national mutation testing service for the MEN1 gene: clinical presentations and implications for mutation testing.

INTRODUCTION: Mutation testing for the MEN1 gene is a useful method to diagnose and predict individuals who either have or will develop multiple endocrine neoplasia type 1 (MEN 1). Clinical selection criteria to identify patients who should be tested are needed, as mutation analysis is costly and time consuming. This study is a report of an Australian national mutation testing service for the MEN1 gene from referred patients with classical MEN 1 and various MEN 1-like conditions. RESULTS: All 55 MEN1 mutation positive patients had a family history of hyperparathyroidism, had hyperparathyroidism with one other MEN1 related tumour, or had hyperparathyroidism with multiglandular hyperplasia at a young age. We found 42 separate mutations and six recurring mutations from unrelated families, and evidence for a founder effect in five families with the same mutation. DISCUSSION: Our results indicate that mutations in genes other than MEN1 may cause familial isolated hyperparathyroidism and familial isolated pituitary tumours. CONCLUSIONS: We therefore suggest that routine germline MEN1 mutation testing of all cases of "classical" MEN1, familial hyperparathyroidism, and sporadic hyperparathyroidism with one other MEN1 related condition is justified by national testing services. We do not recommend routine sequencing of the promoter region between nucleotides 1234 and 1758 (Genbank accession no. U93237) as we could not detect any sequence variations within this region in any familial or sporadic cases of MEN1 related conditions lacking a MEN1 mutation. We also suggest that testing be considered for patients <30 years old with sporadic hyperparathyroidism and multigland hyperplasia.

Australia↗

PubMed2005

Cognitive behaviour group therapy for chronic fatigue syndrome: a non-randomised waiting list controlled study.

BACKGROUND: It has been demonstrated that individual cognitive behaviour therapy is an effective treatment for chronic fatigue syndrome (CFS). The aim of the present study was to investigate the effectiveness of cognitive behaviour group therapy (CBGT) in an unselected group of CFS patients. Additionally, pretreatment characteristics of CFS patients who improve after CBGT were explored. METHODS: In a non-randomised waiting list controlled design, 31 patients were allocated to CBGT and 36 to the waiting list condition. CBGT consisted of 12 two-hour sessions during 6 months. Main outcome measures were fatigue (Checklist Individual Strength) and functional impairment (Sickness Impact Profile). RESULTS: A moderate effect on fatigue in favour of CBGT was found. For functional impairment, the effect was opposite to what was expected. Patients who improved after CBGT had less complaints at baseline compared to patients who did not improve. CONCLUSIONS: An explanation for the moderate effect might be that during CBGT, rest and relaxation were too much emphasised. Furthermore, an unselected group of CFS patients and therapists inexperienced in CB(G)T for CFS participated. Suggestions to improve CBGT for future research are given.

Adult↗

PubMed2004

Cost-effectiveness of cognitive behaviour therapy for patients with chronic fatigue syndrome.

BACKGROUND: There is some evidence that cognitive behaviour therapy (CBT) is efficacious in chronic fatigue syndrome (CFS), but little data on its cost-effectiveness. DESIGN: Prospective economic analysis alongside a randomized clinical trial. METHODS: CFS patients were randomly assigned to CBT, guided support groups (SG), or the 'natural course' (NC, no protocol-based interventions). Patients were treated for 8 months and followed-up for another 6 months. Costs per patient showing clinically significant improvement, based on the CIS fatigue scale, and costs per quality-adjusted life year, were determined for a time period of 14 months. RESULTS: Data were available for 171 patients at 8 months and for 128 at 14 months. At 8 and 14 months, the percentages of improved patients were 31% and 27% for CBT, 9% and 11% for SG, and 12% and 20% for NC. Mean QALYs gained at 14 months were, for CBT, SG and NC, respectively, 0.0737, -0.0018 and 0.0458. CBT and SG mean treatment costs were euro1490 and euro424. Other medical costs for CBT, SG, and NC, respectively, were euro324, euro623 and euro412 for the first period, and euro232, euro561 and euro378 for the second period. Non-medical costs for these periods for CBT, SG and NC were euro262, euro550, euro427 and euro226, euro439, euro287, respectively. Productivity costs were considerable, but not significantly different between groups. DISCUSSION: CBT was less costly and more effective than SG. Compared to NC, the baseline incremental cost-effectiveness of CBT was euro20 516 per CFS patient showing clinically significant improvement, and euro21 375 per QALY. The bootstrap ratios showed considerable uncertainty regarding the results. Future research should focus on productivity costs, and follow patients prospectively over a longer period.

Adolescent↗

PubMed2004

Modest weight loss and physical activity in overweight patients with chronic liver disease results in sustained improvements in alanine aminotransferase, fasting insulin, and quality of life.

BACKGROUND AND AIM: Obesity is a risk factor for progression of fibrosis in chronic liver diseases such as non-alcoholic fatty liver disease and hepatitis C. The aim of this study was to investigate the longer term effect of weight loss on liver biochemistry, serum insulin levels, and quality of life in overweight patients with liver disease and the effect of subsequent weight maintenance or regain. PATIENTS: Thirty one patients completed a 15 month diet and exercise intervention. RESULTS: On completion of the intervention, 21 patients (68%) had achieved and maintained weight loss with a mean reduction of 9.4 (4.0)% body weight. Improvements in serum alanine aminotransferase (ALT) levels were correlated with the amount of weight loss (r = 0.35, p = 0.04). In patients who maintained weight loss, mean ALT levels at 15 months remained significantly lower than values at enrollment (p = 0.004), while in regainers (n = 10), mean ALT levels at 15 months were no different to values at enrollment (p = 0.79). Improvements in fasting serum insulin levels were also correlated with weight loss (r = 0.46, p = 0.04), and subsequent weight maintenance sustained this improvement. Quality of life was significantly improved after weight loss. Weight maintainers sustained recommended levels of physical activity and had higher fasting insulin levels (p = 0.03) at enrollment than weight regainers. CONCLUSION: In summary, these findings demonstrate that maintenance of weight loss and exercise in overweight patients with liver disease results in a sustained improvement in liver enzymes, serum insulin levels, and quality of life. Treatment of overweight patients should form an important component of the management of those with chronic liver disease.

Adult↗

PubMed2004

Genetic testing in familial isolated hyperparathyroidism: unexpected results and their implications.

Familial hyperparathyroidism is not uncommon in clinical endocrine practice. It encompasses a spectrum of disorders including multiple endocrine neoplasia types 1 (MEN1) and 2A, hyperparathyroidism-jaw tumour syndrome (HPT-JT), familial hypocalciuric hypercalcaemia (FHH), and familial isolated hyperparathyroidism (FIHP). Distinguishing among the five syndromes is often difficult but has profound implications for the management of patient and family. The availability of specific genetic testing for four of the syndromes has improved diagnostic accuracy and simplified family monitoring in many cases but its current cost and limited accessibility require rationalisation of its use. No gene has yet been associated exclusively with FIHP. FIHP phenotypes have been associated with mutant MEN1 and calcium-sensing receptor (CASR) genotypes and, very recently, with mutation in the newly identified HRPT2 gene. The relative proportions of these are not yet clear. We report results of MEN1, CASR, and HRPT2 genotyping of 22 unrelated subjects with FIHP phenotypes. We found 5 (23%) with MEN1 mutations, four (18%) with CASR mutations, and none with an HRPT2 mutation. All those with mutations had multiglandular hyperparathyroidism. Of the subjects with CASR mutations, none were of the typical FHH phenotype. These findings strongly favour a recommendation for MEN1 and CASR genotyping of patients with multiglandular FIHP, irrespective of urinary calcium excretion. However, it appears that HRPT2 genotyping should be reserved for cases in which other features of the HPT-JT phenotype have occurred in the kindred. Also apparent is the need for further investigation to identify additional genes associated with FIHP.

Australia↗

PubMed2003

Greater replication and differentiation of preadipocytes in inherited corticosteroid-binding globulin deficiency.

Glucocorticoids are pivotal for adipose tissue development. Rodent studies suggest that corticosteroid-binding globulin (CBG) modulates glucocorticoid action in adipose tissue. In humans, both genetic CBG deficiency and suppressed CBG concentrations in hyperinsulinemic states are associated with obesity. We hypothesized that CBG deficiency in humans modulates the response of human preadipocytes to glucocorticoids, predisposing them to obesity. We compared normal preadipocytes with subcultured preadipocytes from an individual with the first ever described complete deficiency of CBG due to a homozygous null mutation. CBG-negative preadipocytes proliferated more rapidly and showed greater peroxisome proliferator-activated receptor-gamma-mediated differentiation than normal preadipocytes. CBG was not expressed in normal human preadipocytes. Glucocorticoid receptor number and binding characteristics and 11beta-hydroxysteroid dehydrogenase activity were similar for CBG-negative and normal preadipocytes. We propose that the increased proliferation and enhanced differentiation of CBG-negative preadipocytes may promote adipose tissue deposition and explain the obesity seen in individuals with genetic CBG deficiency. Furthermore, these observations may be relevant to obesity occurring with suppressed CBG concentrations associated with hyperinsulinemia.

11-beta-Hydroxysteroid Dehydrogenase Type 2↗

PubMed2003

Effects of rosiglitazone and linoleic acid on human preadipocyte differentiation.

BACKGROUND: Peroxisome proliferator activated receptor gamma (PPARgamma) is a ligand-activated transcription factor known to be central to both adipose tissue development and insulin action. Growth of adipose tissue requires differentiation of preadipocytes with acquisition of specific cellular functions including insulin sensitivity, leptin secretion and the capacity to store triglyceride. Dietary fatty acids and members of the thiazolidinedione class of compounds have been reported to influence adipogenesis at the transcriptional level. Here, we compare the effects of a dietary fatty acid, linoleic acid, and a thiazolidinedione, rosiglitazone, on biochemical and functional aspects of human preadipocyte differentiation in vitro. MATERIALS AND METHODS: Human omental and subcutaneous preadipocytes were subcultured 2-3 times and subsequently differentiated for 21 days in the presence of either linoleic acid or rosiglitazone. Differentiation was assessed using a number of biochemical and functional parameters. RESULTS: Omental and subcutaneous preadipocytes differentiated in the presence of linoleic acid showed marked cytoplasmic triacylglycerol accumulation however, no biochemical markers of differentiation (LPL expression, G3PDH gene expression and enzyme activity and leptin expression or secretion) were detected. In contrast, treatment of these cells with rosiglitazone induced full biochemical differentiation as judged by all markers assessed, despite comparatively little lipid accumulation. The rosiglitazone effects were subcutaneous depot-specific. Cells treated with linoleic acid showed decreased glucose uptake cf rosiglitazone-treated cells. A luciferase reporter assay demonstrated that rosiglitazone potently activates h-peroxisome proliferator activated receptor gamma while linoleic acid had no effect. CONCLUSIONS: These studies demonstrate that (a) human preadipocytes have the potential to accumulate triacylglycerol irrespective of their stage of biochemical differentiation; (b) while omental preadipocytes are refractory to biochemical differentiation in vitro, they are able to accumulate triacylglycerol; and (c) rosiglitazone and linoleic acid may exert their effects via different biochemical pathways.

Adipocytes↗

PubMed2003

Fatigue, burnout, and chronic fatigue syndrome among employees on sick leave: do attributions make the difference?

BACKGROUND: Persistent fatigue among employees, burnout, and chronic fatigue syndrome (CFS) are three fatigue conditions that share some characteristics in theory. However, these conditions have not been compared in empirical research, despite conceptual similarities. METHODS: This cross sectional study aimed to investigate relations between persistent fatigue, burnout, and CFS by describing the clinical features of a sample of 151 fatigued employees on sick leave. Using validated instruments, subgroups based on research criteria for CFS and burnout within the sample of fatigued employees and a reference group of 97 diagnosed CFS patients were compared. Analyses of covariance were performed. RESULTS: A total of 66 (43.7%) fatigued employees met research criteria for CFS (except symptom criteria) and 76 (50.3%) met research criteria for burnout. "CFS-like employees" (fatigued employees who met CFS criteria) reported stronger somatic attributions than "non-CFS-like employees". Burnt out CFS-like employees were more depressed and distressed than CFS-like employees who were not burnt out. Burnout cases among the non-CFS-like employees had stronger psychological attributions than fatigued employees who were not burnt out. Compared to diagnosed CFS patients, CFS-like employees merely had a shorter duration of fatigue complaints. Burnt out CFS-like employees had stronger psychological attributions and were more distressed than CFS patients. CONCLUSIONS: Fatigued employees shared many important characteristics with CFS patients, regardless of burnout status, and many fatigued employees met CFS criteria and/or burnout criteria. Differences however concerned the causal attributions that were made. This raises questions about the role of causal attributions: are they modified by fatigue complaints or do they determine illness outcome?

Adult↗

PubMed2003

Autosomal dominant hypocalcemia: a novel activating mutation (E604K) in the cysteine-rich domain of the calcium-sensing receptor.

We report a novel activating mutation (E604K) of the calcium-sensing receptor in a family with autosomal dominant hypocalcemia. Whereas all affected individuals exhibited marked hypocalcemia, some cases with untreated hypocalcemia exhibited seizures in infancy, whereas others were largely asymptomatic from birth into adulthood. The missense mutation E604K (G2182A; GenBank accession no. U20759), which affects an amino acid residue in the C terminus of the cysteine-rich domain of the extracellular head, cosegregated with hypocalcemia in all seven individuals for whom DNA was available. Two unaffected, normocalcemic members of the family did not exhibit the mutation. The molecular impact of the mutation on two key components of the signaling response was assessed in HEK-293 cells transiently transfected with cDNA corresponding to either the wild-type calcium-sensing receptor or the E604K mutation derived by site-directed mutagenesis. There was a significant leftward shift in the concentration response curves for the effects of extracellular Ca(2+) on both intracellular Ca(2+) mobilization (determined by aequorin luminescence) and MAPK activity (determined by luciferase expression). The C terminus of the cysteine-rich domain of the extracellular head may normally act to suppress receptor activity in the presence of low extracellular Ca(2+) concentrations.

Adult↗

PubMed2003

Diagnosing chronic fatigue syndrome: comparison of a protocol and computerised questionnaires.

BACKGROUND: In the context of outpatient care and within the framework of scientific research, guidelines and measuring instruments have been developed to help improve CFS diagnostics. The purpose of this study was to measure the agreement between the evaluations of chronically fatigued patients by physicians using a CFS protocol and by researchers using computerised questionnaires. METHODS: The sample consisted of 516 patients referred to an internal medicine outpatient clinic with complaints of chronic fatigue. Retrospectively the medical records and the computerised questionnaires were checked separately and compared to see whether the criteria for diagnosis of CFS had been met. In addition, the reasons for not diagnosing CFS were evaluated. RESULTS: Agreement between the physicians' and the researchers' evaluations was 84%. Disagreement mostly concerned severity of fatigue and functional impairment, or premorbid exclusion criteria. A physical cause for the chronic fatigue was only found in 3% of the cases. CONCLUSIONS: For physicians, questionnaire assessment may be complementary to the CFS protocol in optimising the process of diagnosing CFS.

Adult↗

PubMed2002

Effect of weight reduction on liver histology and biochemistry in patients with chronic hepatitis C.

BACKGROUND: Steatosis occurs in more than 50% of patients with chronic hepatitis C and is associated with increased hepatic fibrosis. In many of these patients the pathogenesis of steatosis appears to be the same as for patients with non-alcoholic fatty liver disease-that is, related to visceral adiposity and obesity. METHODS: The effect of a three month weight reduction programme on liver biochemistry and metabolic parameters was examined in 19 subjects with steatosis and chronic hepatitis C. Paired liver biopsies were performed in 10 subjects, prior to and 3-6 months following the intervention, to determine the effect of weight loss on liver histology. RESULTS: There was a mean weight loss of 5.9 (3.2) kg and a mean reduction in waist circumference of 9.0 (5.0) cm. In 16 of the 19 patients, serum alanine aminotransferase levels fell progressively with weight loss. Mean fasting insulin fell from 16 (7) to 11 (4) mmol/l (p<0.002). Nine of 10 patients with paired liver biopsies had a reduction in steatosis irrespective of viral genotype. In these subjects the median modified Knodell fibrosis score decreased from 3 to 1 (p=0.04) and activated stellate cells significantly decreased (p<0.004). CONCLUSIONS: Weight loss in patients with chronic hepatitis C may be associated with a reduction in steatosis and abnormal liver enzymes and an improvement in fibrosis, despite the persistence of the virus. Weight reduction may provide an important adjunct treatment strategy for patients with chronic hepatitis C.

Adult↗

PubMed2002

Dyspnoea perception during clinical remission of atopic asthma.

Symptoms of atopic asthma often disappear around puberty. The authors recently demonstrated that this clinical remission is accompanied with ongoing airways inflammation in most subjects. The discrepancy between lack of symptoms and persistent airway inflammation suggests that perception of the symptoms is unclear. In the present study, young adults in clinical remission of atopic asthma assigned themselves a modified Borg score during methacholine and adenosine-5'-monophosphate induced bronchoconstriction. Borg scores of subjects in clinical remission were compared with those of symptomatic asthmatic subjects. A marked variation in the Borg scores at a 20% fall in the forced expiratory volume in one second was found. Significant differences in Borg scores between remission patients and asthmatics could not be detected. It was concluded that perception of dyspnoea, induced with methacholine and adenosine challenge, is similar in young adults in clinical remission of atopic asthma compared to that of patients with symptomatic asthma. Hence, an unclear perception seems to be an unlikely explanation for the discrepancy between lack of symptoms and ongoing inflammation. Other factors, including both physical and psychological ones, may play a role in the apparent absence of symptoms, thereby potentially leading to undertreatment.

Adenosine Monophosphate↗

PubMed2001

Airway inflammation is present during clinical remission of atopic asthma.

Symptoms of atopic asthma often disappear at puberty. However, asthmatic subjects in clinical remission will frequently have a relapse later in life. The aim of this study was to investigate whether subjects in clinical remission of atopic asthma have persistent airway inflammation and/or airway remodeling. Bronchial biopsies were obtained from subjects in clinical remission, asthmatic subjects, and healthy control subjects. The presence and/or activation state of eosinophils, mast cells, macrophages, T lymphocytes, interleukin (IL)-5, eotaxin, and inducible nitric oxide synthase (iNOS) were analyzed. Results were compared with less invasive indicators of airway inflammation. Also aspects of airway remodeling were determined. Eosinophils, T cells, mast cells, and IL-5 were significantly elevated in the airway mucosa of subjects in remission compared with control subjects. Also, blood eosinophil cell counts were significantly higher in subjects in clinical remission. Blood eosinophil cell counts, exhaled nitric oxide (eNO) levels, and bronchial response to adenosine-5'-monophosphate correlated significantly with the quantity of tissue eosinophils. Significant airway remodeling was found in subjects in clinical remission. Our study has shown ongoing airway inflammation and airway remodeling in adolescents in clinical remission of atopic asthma. Subclinical airway inflammation may well determine the risk of an asthma relapse later in life.

Adenosine Monophosphate↗

PubMed2001

Segmental bronchoprovocation in allergic rhinitis patients affects mast cell and basophil numbers in nasal and bronchial mucosa.

Mast cells and basophils are cells that play an important role in the initiation and control of allergic inflammation in asthma and rhinitis. This study was undertaken to determine the presence and dynamics of mast cells and basophils in the nasal and bronchial mucosa of allergic rhinitis patients after segmental bronchial provocation (SBP). Eight nonasthmatic, grass pollen-allergic rhinitis patients and eight healthy controls were included. Bronchial and nasal biopsies, as well as blood samples, were taken before (T(0)) and 24 h (T(24)) after SBP. Immunohistochemical staining was performed for mast cells (tryptase and chymase; phenotypes MC(T), MC(TC), MC(C)) and basophils (BB1). In the bronchial mucosa, the number of BB1(+) cells increased significantly (p < 0.05) in allergic rhinitis patients after SBP. In the nasal mucosa, the numbers of MC(C) and MC(TC) cells decreased significantly, whereas the numbers of [BB1(+)] cells increased significantly in allergic rhinitis patients after SBP (p < 0.05). In blood, the number of basophils decreased (p < 0.05) and the level of interleukin (IL)-5 increased (p < 0.05) in atopic patients after SBP. No significant changes could be observed in healthy controls. This study shows that SBP in nonasthmatic allergic rhinitis patients reduces numbers of mast cells in the nose as a result of enhanced degranulation. At the same time, there is evidence for an influx of basophils from the blood into the nasal and bronchial mucosae.

Adolescent↗