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K D Palitzsch

Publications and source records attributed to K D Palitzsch.

At least 37 records · Page 2Linked to original sources
PubMed1999

The human apM-1, an adipocyte-specific gene linked to the family of TNF's and to genes expressed in activated T cells, is mapped to chromosome 1q21.3-q23, a susceptibility locus identified for familial combined hyperlipidaemia (FCH).

The human adipocyte-specific apM-1 gene encodes a secretory protein of the adipose tissue that has been suggested to play a role in the pathogenesis of obesity. The regulation of apM-1 was studied along adipocyte differentiation. While apM-1-mRNA and apM-1 protein were absent in preadipocytes and in 48 h differentiated adipocytes, they were found upregulated from day 4 to day 9 of adipocyte differentiation as shown by RNase protection assay and Western blot analysis. These data indicate that apM-1 may be a late marker of adipocyte differentiation. In human sera apM-1 protein is also detectable by Western blots using a polyclonal antibody raised against a synthetic peptide sequence of the human apM-1. The genomic structure of the human apM-1 gene together with a total of 2.7 kb of the 5'-flanking region with putative transcription factor binding sites is presented. Interestingly, sequence comparisons link the apM-1 gene to the family of TNF's and to genes expressed in activated T-cells. The chromosomal localization of apM-1 was investigated by FISH and mapped to human chromosome 1q21.3-1q23, a region that was identified as a susceptibility locus for Familial Combined Hyperlipidaemia (FCH) and polygenic NIDDM. These data and the chromosomal localization on chromosome 1q21.3-q23 raises the possibility that apM-1 as an adipocyte-specific secretory protein may play a role in the pathogenesis of FCH and associated insulin resistance. Exon- and intron-specific primer sequences are presented as a basis for mutation screening of patients affected with FCH.

3T3 Cells↗
PubMed1999

[Fatal liver failure after corticosteroid treatment of a hepatitis B virus carrier].

HISTORY AND ADMISSION FINDINGS: A 69-year-old man, a known carrier of hepatitis B virus (HBV) after blood transfusion, developed increasingly severe jaundice with high transaminase levels after receiving steroids in high doses. Significant preceding conditions included chronic obstructive pulmonary disease, coronary heart disease, ulcerative colitis in remission and diabetes mellitus. On admission he was jaundiced and experienced pain on pressure below the right costal margin. INVESTIGATIONS: Serology demonstrated reactivated hepatitis B with an increase of the HBV-DNA concentration in serum, as well as seroconversion with HBe antigen, anti-HBc-IgM antibodies and absence of anti-HBe antibodies. DIAGNOSIS, TREATMENT AND COURSE: The history and serological findings indicated reactivation of the hepatitis B by the steroid treatment. Progressive liver failure developed. A marked reduction of virus particles in the blood occurred after a therapeutic trial with the nucleoside analog lamivudine, but the patient died of liver failure 30 days after admission. CONCLUSION: Steroids should be given to known hepatitis B carriers only if strictly indicated, because of the danger of acute deterioration of liver functions by reactivation of the disease with possibly fatal consequences. If steroids are administered, liver functions and serological hepatitis markers should be closely monitored so that any necessary treatment can be quickly initiated.

Adrenal Cortex Hormones↗
PubMed1999

[A 63-year-old patient with worsening general condition, bone demineralization, hypocalcemia and excess parathyroid hormone: late manifestations of pseudohypohyperparathyroidism].

HISTORY AND CLINICAL FINDINGS: A 63-year-old man was hospitalized because of his worsening general condition and weight loss. Physical examination revealed marked thoracic kyphosis with impaired mobility of his back and restricted walking because of pain in the right hip. He also had other bone pains. INVESTIGATIONS: Serum calcium was reduced (1.60 mmol/l) and there was generalized bone demineralization. Subsequently an increased parathormone (PTH) level was noted (499.0 ng/l) as well as markedly increased activity of enzymes involved in bone metabolism, decreased renal excretion of phosphates (4.76 mmol/24 h) and multiple pathological fractures. TREATMENT AND COURSE: The listed abnormalities indicated the diagnosis of pseudohypoparathyroidism (PHP), type 1 b. After treatment had been started with vitamin D (calcitriol 2 x 0.25 micrograms/d) and calcium (calcium gluconate, 3 x 500 mg/d), the levels of calcium, PTH and enzymes in bone metabolism gradually became normal. A cataract operation had to be performed because of calcification of the lens. CONCLUSION: The level of PTH should be determined in patients with extensive bone demineralization and hypocalcaemia. If PTH is raised, PHP should be included in the differential diagnosis. Normalization of serum calcium by calcium substitution and vitamin D administration will normalize PTH and improve mineralization of the skeleton. In this way the debilitating effects of osteodystrophia cystica generalisata (OCG) (Engel von Recklinghausen syndrome) can be prevented. Also, the consequences of extraosseous calcification, such as extrapyramidal symptoms of calcification of the brain-stem ganglia can be avoided if treated in time.

Bone Demineralization, Pathologic↗
PubMed1999

[Unusual case of disseminated sarcoidosis with prominent gastrointestinal symptoms].

HISTORY AND ADMISSION FINDINGS: A 63-year-old man had for 10 months suffered from marked weight loss, night sweats, diffuse abdominal pain and increased stool frequency. He was admitted to evaluate an ultrasonically abnormal focus in the liver parenchyma and elevated liver function parameters. His sclerae were obviously icteric and he looked under-weight. INVESTIGATIONS: He had a hypochromic microcytic anemia and abnormal liver and pancreatic function tests: total bilirubin 3.11 mg/dl, direct bilirubin 2.21 mg/dl, GOT21U/l, gamma-GT 422 U/l, alkaline phosphatase 1449 U/l, alpha-amylase 481 U/l, lipase 2827 U/l. The serum creatinine level was elevated to 1.47 mg/dl. Computed tomography revealed enlarged liver and spleen as well as an enlargement of intraabdominal lymph nodes, chest radiogram and endoscopic cholangio-pancreatography were unremarkable. Biopsies from the lower duodenum, large intestine, bone marrow and liver showed inflammatory changes with Langhans-type mononuclear granulomas. Together with these findings an increased activity of the angiotensin-converting-enzyme (ACE) indicated sarcoidosis, other causes having been excluded. TREATMENT AND COURSE: All signs and symptoms rapidly improved under prednisolone, and 4 weeks after begin of treatment the biochemical abnormalities had clearly regressed. The raised serum levels of soluble IL-2 receptors and of neopterin, measures of sarcoidosis activity, had decreased. Activity of ACE had fallen. CONCLUSION: Sarcoidosis can present with diverse clinical signs and symptoms. In a case of multi-system disease that cannot be readily classified, sarcoidosis should be included in the differential diagnosis.

Anti-Inflammatory Agents↗
PubMed1999

Glucocorticoid receptors are down-regulated in inflamed colonic mucosa but not in peripheral blood mononuclear cells from patients with inflammatory bowel disease.

BACKGROUND: Growing evidence indicates that the immune system and the hypothalamic-pituitary-adrenal system are linked by several mechanisms, for example intracellular glucocorticoid receptors (hGR). Glucocorticoids are the standard treatment of acute attacks of inflammatory bowel disease (IBD). Binding of glucocorticoids to hGR down-regulates the transcription of inflammatory genes that can propagate IBD. PATIENTS AND METHODS: IBD patients were either treated with 5-60 mg of prednisolone for more than 1 week or were without glucocorticoid treatment for more than 4 weeks. hGR levels were determined from isolated cytosol of peripheral blood mononuclear cells (PBMCs) or mucosal biopsies using a radioassay with [3H]-dexamethasone. Interleukin (IL) 6 levels were determined by enzyme-linked immunosorbent assay (ELISA). RESULTS: The systemic (PBMC) hGR levels of corticosteroid-treated IBD patients were significantly lower than those of control subjects (59.6 +/- 57.1 dpm mg-1 cytosol protein vs. 227.0 +/- 90.8 dpm mg-1 cytosol protein, P = 0.007) and IBD patients not receiving glucocorticoid treatment (179.7 +/- 171.3 dpm mg-1 cytosol protein, P = 0.002). Systemic hGR levels in untreated IBD patients did not differ significantly from those in control subjects. In patients with connective tissue diseases, systemic hGR levels were also found to be decreased in the absence of glucocorticoid treatment. Systemic hGR levels in patients with Crohn's disease (CD) treated with steroids (66.6 +/- 61.0 dpm mg-1 cytosol protein) were not different from those in patients with ulcerative colitis (UC) (56.1 +/- 51.6 dpm mg-1 cytosol protein). In contrast to these findings, mucosal hGR levels were significantly decreased in both steroid-treated (18.0 +/- 15.5) and not steroid-treated (37.8 +/- 30.5) patients compared with control subjects (125.6 +/- 97.1; P = 0.00009 and P = 0.0008 respectively). IL-6 levels in all IBD groups with and without steroids were significantly different from those in control subjects. CONCLUSION: In IBD there is no difference in systemic hGR levels between not steroid-treated patients and control subjects, in spite of inflammatory activity (IL-6). Mucosal hGR levels were decreased independently of treatment, probably leading to a decreased protection against NF-kappaB action in the intestinal mucosa.

Binding, Competitive↗
PubMed1999

Frequency and significance of the A-->G (-3826) polymorphism in the promoter of the gene for uncoupling protein-1 with regard to metabolic parameters and adipocyte transcription factor binding in a large population-based Caucasian cohort.

BACKGROUND: The recently described A-->G (-3826) point mutation within the distal region of the UCP-1 promoter is possibly involved in the development of obesity, diabetes and related metabolic disorders. It was the aim of this study to examine the allelic frequency and the prevalence of the three UCP-1 genotypes in a broad caucasian cohort and to investigate the significance of this polymorphism for obesity and diabetes. METHODS: 1020 subjects were randomly chosen from 6450 participants in the Diabetomobile Study. The UCP-1 genotype was determined by genomic PCR and Bcl-I-RFLP analysis in 1020 subjects and tested for association with a variety of metabolic parameters. In addition, the influence of this mutation on adipocyte nuclear factor binding was investigated by electrophoretic mobility shift assays (EMSA). RESULTS: The genotype frequencies in 1020 subjects were: AA genotype, 57.0%; AG genotype, 35.4%; GG genotype, 7.6%; with allelic frequencies of 0.75 for allele A and 0.25 for allele G. No significant differences between the genotypes and age, gender, BMI, leptin, glucose, fasting insulin, C-peptide, HbA1c, diabetes manifestation, total cholesterol, and HDL cholesterol were found. Analysis of the Trp64Arg polymorphism of the beta3-adrenergic receptor in a subgroup of 343 subjects revealed no additive effect to the UCP-1 polymorphism. An yet unknown adipocyte-specific factor of nuclear extracts from 3T3-L1 adipocytes during differentiation is able to bind specifically to the distal UCP-1 promoter region and this binding ability can not be abolished by the mutation. CONCLUSIONS: We determined the genotype and allelic frequency of the UCP-1 promoter polymorphism in the largest known population-based study. The results from genotyping demonstrate clearly that this polymorphism does not play a major role in the pathogenesis obesity and diabetes. A yet unknown adipocyte derived and differentiation-dependent regulated transcription factor is able to bind to the distal UCP-1 promoter surrounding -3826 bp. This binding is not affected by presence of the mutation.

Adipocytes↗
PubMed1999

Cardiovascular autonomic dysfunction and hemodynamic response to anesthetic induction in patients with coronary artery disease and diabetes mellitus.

UNLABELLED: Autonomic neuropathy is a major complication of diabetes mellitus and is reported to be associated with increased perioperative hemodynamic instability. We investigated the relationship between autonomic dysfunction and hemodynamic response to anesthetic induction in diabetic and nondiabetic patients with coronary artery disease. We studied 60 patients scheduled for coronary artery surgery, 30 suffering from diabetes mellitus. Preoperative evaluation included traditional cardiovascular autonomic function tests (coefficient of variation of 150 beat-to-beat intervals in heart rate at rest, heart rate response to deep breathing, and heart rate and arterial blood pressure response to standing), spectral analysis of blood pressure and heart rate variability (HRV), and the computation of spontaneous baroreflex sensitivity. After premedication with clorazepate, anesthesia was induced with sufentanil (0.5 microg/kg), etomidate (0.1-0.2 mg/kg), and vecuronium (0.1 mg/kg). Heart rate and blood pressure before anesthetic induction and before and after tracheal intubation were compared between groups. Autonomic function tests, spectral analysis of HRV, and spontaneous baroreflex sensitivity revealed significant differences between patient groups. Most diabetic patients (n = 23) had one or more abnormal test results, in contrast to most nondiabetic patients, who did not show signs of autonomic neuropathy (n = 23). There was no relationship between cardiovascular autonomic function and hemodynamic behavior during anesthetic induction. The blood pressure response to anesthetic induction was not different between patient groups, even when comparing the subgroups with and without abnormal autonomic function tests. These findings indicate that increased hemodynamic instability during anesthetic induction is not obligatory in patients with diabetes mellitus and autonomic dysfunction. IMPLICATIONS: This study indicates that increased hemodynamic instability during anesthetic induction is not obligatory in patients with coronary artery disease and autonomic dysfunction.

Adult↗
PubMed1999

Prevalence of antibodies against hepatitis C virus in the adult German population.

OBJECTIVE: The prevalence of anti-HCV in Germany has been determined for blood donors and certain risk groups, but the burden of disease in the general population remains unknown. The aim of this study was to determine the prevalence of anti-HCV in a study group representing the normal adult German population. DESIGN: A total of 5312 individuals aged 18-70 years were randomly selected from small, middle-sized and big cities in five different German states. Sera were tested for anti-HCV by enzyme immunoassay and immuno dot assay, as well as for anti-HBc and, in the case of a positive result, for anti-HBs and HBsAg. Serological typing was performed in anti-HCV-positive persons. RESULTS: Thirty-nine individuals were anti-HCV positive; indeterminate results (with antibodies against the viral core protein only) were obtained in 20. There was a tendency to higher prevalence rates with increasing age as well as to a higher prevalence in women. Serological typing revealed the presence of genotype 1 in the vast majority of participants (82%); only a minority showed genotype 3 (7.2%) or other genotypes (7.2%). Markers of HBV were seen in 43.6% of the anti-HCV positive individuals, with nearly one third (29.4%) of the double-infected showing anti-HBc as the only marker for HBV. CONCLUSIONS: According to our data, an anti-HCV prevalence of 0.63% (95% confidence interval, CI, 0.42-0.84%) can be assumed in the general adult German population, with higher values in older people and women. Nearly half of the anti-HCV positive individuals also show markers of hepatitis B virus.

Adolescent↗
PubMed1998

Identification and characterization of the human adipocyte apM-1 promoter.

The human adipocyte-specific apM-1 gene encodes a secretory protein of the adipose tissue and seems to play a role in the pathogenesis of obesity. A 1.3 kb amount of the proximal promoter region has been cloned and analyzed for the presence of putative transcription factor binding sites. Several binding sites known to be involved in adipogenesis and regulation of adipocyte-specific genes (C/EBP, SREBP) are present. No TATA box, but a classical CCAAT box could be identified. To confirm functionality and cell specificity of the 1.3 kb promoter, a series of 5'-deleted fragments were ligated in front of the luciferase gene and the constructs were transfected into 3T3-L1 adipocytes. The reporter gene was effectively transcribed, as demonstrated by the expression of enzyme activity. The 5'-end of the human cDNA was completed by 5'-RACE-PCR. Several alternative transcription start sites were detected by RNase protection assay and primer extension analysis. In addition, an exon/intron boundary was mapped at the extreme 5'-end of the cDNA sequence. Genomic Southern blotting suggests that the human apM-1 gene is a single copy gene.

Adipocytes↗
PubMed1998

Coexistent thyroiditis is associated with lower tumour stage in thyroid carcinoma.

BACKGROUND: Microsatellite instability (MSI) is a new mechanism described in carcinogenesis of several tumours and seems to predispose for cancer in some chronic inflammatory diseases. As thyroiditis is thought to be both the cause and the consequence of thyroid carcinoma, it was the aim of this retrospective study to investigate the epidemiology and the influence of a coexistent thyroiditis on prognosis and clinicopathological parameters in an iodine-deficient area. METHODS: The grade of lymphocytic infiltration (LI) of 153 thyroid carcinomas was determined in paraffin-embedded tissues: G0 = no LI, G1 = peritumoral LI, G2 = peritumoral LI with follicle, G3 = diffuse LI. A non-radioactive PCR-based screening method was used for detection of MSI. RESULTS: Twenty-seven (17.7%) out of 153 carcinomas were accompanied by thyroiditis (G1, 16; G2, 5; G3, 6). Ten cases fulfilled the criteria necessary for diagnosing Hashimoto's thyroiditis. Nine out of 10 (90%) Hashimoto's cases and 16 out of 17 (94%) other thyroiditis cases were associated with a significantly (chi2 < 0.01) lower pT stage (pT1, pT2) than cases without thyroiditis. No statistical association was found by comparing multifocality or sclerosing variants with the grade of lymphocytic infiltration. MSI was detected neither in patients with severe inflammation nor in the absence of thyroiditis. CONCLUSIONS: MSI does not seem to play a role in the pathogenesis of thyroid carcinoma. Coexistent thyroiditis is associated with a lower pT stage and thus could be an indicator of a better prognosis.

Adult↗
PubMed1998

Lactulose and neomycin attenuate leukocyte-endothelial cell adhesion in an animal model of inflammatory bowel disease.

OBJECTIVE: The role of intestinal flora in the pathogenesis of inflammatory bowel disease is under discussion. The objective of this study was to assess the effect of lactulose (Lac) and neomycin (Neo), both of which are used clinically for changing or reducing intestinal flora, on leukocyte-endothelial cell interaction in an indomethacin (Indo)-induced long-lasting ileitis in Sprague-Dawley rats. METHODS: Two doses of Indo (7.5 mg/kg, s.c.) were given 24 h apart. Animals were fed with standard rat chow for 10 days until 12 h prior to the experiment. Solutions of Lac (1.0 mg/kg b.w.) or Neo (0.1 g/kg) were gavaged daily for 10 days between Indo administration and the experiment. Ten mesenteric venules (30 microm diameter) per animal (n = 5 per group) were observed using intravital microscopy, and the following parameters were monitored: number of adherent and emigrated leukocytes, leukocyte rolling velocity, erythrocyte velocity, venular blood flow, and shear rate. Macroscopically visible injury was scored 0 to 5, and faecal pH was measured in the distal 20 cm of ileum. RESULTS: Ten days after Indo treatment leukocyte adherence and emigration were increased (2.2-fold and 3.3-fold vs. control, respectively) while leukocyte rolling velocity and venular wall shear rate were reduced (both parameters to 81% of control). Lac and Neo attenuated microcirculatory parameters to a similar extent while macroscopic damage was prevented only by Neo but not by Lac. The effects of both substances were accompanied by a normalization of faecal pH to control level which had been lowered by Indo. CONCLUSION: The Indo-induced increase in leukocyte-endothelial cell interaction is blunted by Lac and Neo. At the same time the Indo-induced lowering of faecal pH is normalized by both substances. The reduction of macroscopic injury by Neo but not by Lac in the chronic phase of Indo inflammation might be due to additional effects on other inflammatory cells such as macrophages.

Animals↗
PubMed1998

Healing response to non-surgical periodontal therapy in patients with diabetes mellitus: clinical, microbiological, and immunologic results.

The aim of the present study was to monitor clinical, microbiological, medical, and immunological effects of non-surgical periodontal therapy in diabetics and healthy controls. 20 IDDM (insulin dependent, n = 7) or NIDDM (non-insulin dependent, n = 13) diabetic patients (median duration 11.5 years, range of HbA1C: 4.4-10.6%) with moderate to advanced periodontal disease and 20 matched healthy control patients, were subjected to supragingival pretreatment and subsequent subgingival therapy. Periodontal examinations (API, PBI, BOP, PPD, PAL), microbiological examinations (culture), medical routine examinations, and immunological examinations (oxidative burst response of PMNs to TNF-alpha and FMLP) were performed at baseline, 2 weeks after supragingival, and 4 months after subgingival therapy. 4 months after completion of non-surgical therapy, the following compared to baseline significant (p < or = 0.05) changes (delta) of clinical parameters (median) were found in diabetic patients versus control patients: deltaAPI (30.4% versus 36.3%), deltaPBI (22.9% versus 24.2%), deltaBOP (39.5% versus 46.9%). The median % per patient of pockets with PPD > or = 4 mm decreased from 41.9% to 28.3% in diabetics, and from 41.6% to 31.8% in controls. Microbiologically, similar reductions of periopathogenic bacteria were found in diabetics and controls. Neither periodontal data nor the oxidative burst response of PMNs showed any significant difference (p > 0.05) between diabetics and control patients. In this study, periodontal therapy had no significant influence on medical data of diabetics. In conclusion, this study indicates that metabolically well-controlled diabetics might respond to non-surgical periodontal therapy as well as healthy control patients.

Adult↗
PubMed1998

Leucocyte endothelial cell adhesion in indomethacin induced intestinal inflammation is correlated with faecal pH.

BACKGROUND: Recent studies indicate that faecal pH is acidified in patients with inflammatory bowel disease compared with healthy controls. In healthy volunteers, stool pH, faecal flora, and bile acid concentration could be affected by means of elemental diets. AIMS: To assess the role of variations of faecal pH on leucocyte endothelial cell adhesion in indomethacin induced long lasting ileitis in rats. METHODS: Indomethacin (7.5 mg/kg subcutaneously) was injected twice, 24 hours apart. Rats were either fed with the identical diet before and 10 days after the induction of inflammation until the experiment, or the diet was changed at the time of induction. Ten postcapillary mesenteric venules (30 microns diameter) per animal were observed using intravital microscopy. Macroscopic visible intestinal ulceration was scored and faecal pH of different sections of the small bowel was determined. RESULTS: Small intestinal faecal pH was 8.5 in controls and 8.0 in indomethacin treated animals. Indomethacin significantly changed microcirculatory parameters: there was a 2.3-fold increase in leucocyte adherence, a 3.2-fold increase in leucocyte emigration, and a 20% reduction in shear rate. Application of various diets or diet combinations resulted in variations in faecal pH ranging from 7.8 to 8.8 which were inversely correlated with macroscopic ulcerations (r = -0.67). Leucocyte adherence was attenuated with increased pH and augmented with decreased pH (r = -0.55). Venular wall shear rate was positively correlated with faecal pH (r = 0.48) while leucocyte emigration showed no correlation. Leucocyte rolling velocity was not significantly altered. Normalisation of faecal pH by different alkalising drugs induced a significant decrease in leucocyte adherence in standard fed, indomethacin treated rats. CONCLUSIONS: Faecal pH is lowered in the indomethacin model of long lasting ileitis in rats, which is similar to human inflammatory bowel disease. Alkalisation of faecal pH due to different diets or alkalising drugs reduces indomethacin induced leucocyte endothelial cell adhesion and macroscopic intestinal damage. These results may provide a rationale for the therapeutic effect of enteral diets in Crohn's disease.

Animals↗
PubMed1998

The Trp64Arg polymorphism of the beta 3-adrenergic receptor gene is not associated with obesity or type 2 diabetes mellitus in a large population-based Caucasian cohort.

The beta3-adrenergic receptor (3-BAR) is assumed to play a role in the regulation of energy balance by increasing lipolysis and thermogenesis. A recently detected allelic polymorphism (Trp64Arg polymorphism) has been suggested to contribute to the development of obesity and non-insulin-dependent diabetes mellitus. We examined the prevalence of the two 3-BAR alleles in Germany and looked for associations between 3-BAR genotype and metabolic disorders (obesity and type 2 diabetes mellitus). From over 6450 participants in the Diabetomobile Study, a nationwide epidemiologic study on the prevalence of metabolic disorders (carried out from 1993 to 1996 in Germany), 1259 participants were randomly chosen. The 3-BAR genotype status was determined by 3-BAR gene-specific genomic PCR and consecutive restriction fragment length polymorphism analysis. The frequencies of the different genotypes in the examined cohort were as follows: Trp64/Trp64, 88.3%; Trp64/Arg64, 10.8%; and Arg64/ Arg64, 0.8%. No significant differences between the different genotypes were found when comparing age, body mass index, weight, total and high-density lipoprotein (HDL) cholesterol, fasting insulin, HbA11, and blood pressure; neither did the type 2 diabetes mellitus participants in the different genotype groups differ significantly in terms of age of diabetes onset or HbA11. This is the largest population-based study on the Trp64Arg polymorphism reported yet. The Arg64 allele of the 3-BAR gene was found commonly in Germany. In our cohort, no significant associations between the Arg64 allele and metabolic disorders (e.g. obesity, type 2 diabetes mellitus, dyslipidemia, or hypertension) were detected.

Adult↗
PubMed1997

[Cardiovascular and pupillary autonomic and somatosensory neuropathy in chronic diseases with autoimmune phenomena. A comparative study of patients with Crohn disease, ulcerative colitis, systemic lupus erythematosus, progressive systemic sclerosis and type I diabetes mellitus].

BACKGROUND: During the last years, examination of autonomic nervous function and of autonomic neuropathy has attracted attention not only in diabetes mellitus research but also in other areas of internal medicine. However, patients with various chronic diseases with autoimmune phenomenons have never been investigated in a comparative study with standardized examination techniques. Hence, the aim of the study was to examine the prevalence and the severity of autonomic neuropathy in patients with the following chronic diseases. PATIENTS AND METHODS: We investigated 28 patients with Crohn's disease (CD: age: 32.4 +/- 2.0 y), 17 patients with ulcerative colitis (UC: 39.7 +/- 3.6 y), 39 patients with systemic lupus erythematosus (SLE: 34.9 +/- 2.0 y), 38 patients with progressive systemic sclerosis (pSS; 51.5 +/- 2.4 y) and 65 patients with insulin-dependent diabetes mellitus (IDDM: 35.5 +/- 1.6 y). Cardiovascular autonomic (cANP), pupillary autonomic (pANP), and sensorimotor (ssNP) neuropathy were assessed by standardized techniques. RESULTS: Prevalence rates for cANP, pANP and ssNP were found to be 0%, 19%, and 7% in CD, 6%, 25%, and 18% in UC, 5%, 29%, and 10% in SLE, 11%, 16%, and 32% in pSS, and 26%, 66%, and 29% in IDDM, respectively. CONCLUSION: The study demonstrated patients with IDDM to have the highest prevalence rates of cANP and pANP. Patients with other chronic diseases, particularly SLE, pSS and UC, had high prevalence rates of pANP. This may be due to alterations of structures of the central nervous system in these patients. cANP was rare in patients with inflammatory bowel disease and ssNP was found very often in patients with pSS, probably due to local fibrotic lesions. The various disease groups differ in the pattern and severity of autonomic and sensorimotor neuropathy, which indicates that different structures and neuropathogenic mechanisms may be involved.

Adult↗
PubMed1997

Acute and chronic effects of different bile acids on indomethacin-induced intestinal inflammation.

The role of bile acids in the pathogenesis of bowel inflammation is unknown. The objective of this study was to determine whether urso- (UDC), cheno- (CDC), and taurochenodeoxycholic acid (TCDC) exert a pro- or antiinflammatory action in the acute and chronic phase of the indomethacin model of a long lasting ileitis in rats. Short-term and long-term inflammatory responses (48 h and 10 days, respectively) after two subcutaneous indomethacin (Indo) injections were elicited in rat small bowel and mesentery. To distinguish between common and model-specific effects bile acids were tested also in another model of acute inflammation induced by mesenteric superfusion with leukotriene B4(LTB4). The number of adherent and emigrated leukocytes, leukocyte rolling velocity, and venular wall shear rate were monitored in normal and inflamed postcapillary venules, and fecal pH of ileal contents which has been shown to correlate with degree of inflammation was measured, 6.5- and 2.3-fold increases in leukocyte adherence and comparable increments in leukocyte emigration were observed 48 h and ten days after indomethacin treatment, respectively. UDC, CDC, and TCDC (10 mg/kg) given daily from Indo administration until the experiment attenuated the leukocyte adherence and emigration responses elicited by indomethacin in short- and long-term inflammation. This effect was accompanied by a significant increase of fecal pH which had been lowered by indomethacin. None of the bile acids reduced the LTB4-induced increases in adherence and emigration. Oral administration of UDC, CDC, and TCDC reduces leukocyte adhesion and emigration in acute and chronic stages of Indo-induced inflammation. This could be due to the alkalizing effect of these bile acids on fecal pH which has been shown to correlate with a decrease of leukocyte-endothelial cell interactions but--according to the missing effectiveness in another model of intestinal inflammation--not to specific influences on leukocyte-endothelial cell adhesion.

Animals↗
PubMed1996

Association between eating behaviour and current glycaemic control, body mass or autonomic nervous function in long-term type I and type II diabetic patients.

This cross-sectional study was aimed at investigating the association between eating behaviour and current glycaemic control, body mass or autonomic nervous function in patients with type I and type II diabetes mellitus (DM). In 72 patients (31 type I DM, 41 type II DM) we investigated body mass index (BMI), serum cholesterol, serum triglycerides, haemoglobin A1c (HbA1c) and autonomic nervous function (seven standardized tests). The three-factor eating questionnaire was used to investigate cognitive control of eating behaviour (CC) and susceptibility to eating problems (SEP). The mathematical product of CC and SEP provides information about disinhibition of eating control (DEC). In type I DM, there was a correlation between SEP and age (r = -0.536, P < 0.01), SEP and HbA1c (0.438, P < 0.05), and between DEC and duration (-0.371, P < 0.05) and DEC and HbA1c (0.376, P < 0.05). In type II DM, there was a correlation between SEP and BMI (0.401, P < 0.01) and between DEC and BMI (0.429, P < 0.01). Low CC was associated with autonomic nervous dysfunction in type I DM (P = 0.022). In type II DM, autonomic nervous dysfunction was associated with high SEP (P = 0.044). In conclusion, the correlation between eating behaviour and HbA1c or triglycerides in type I DM indicates that the questionnaire is able to address current parameters of diabetes control. Self-assessment of eating behaviour in type I and type II diabetic patients reveals associations between eating behaviour and autonomic nervous function.

Adult↗