Biomedical subjects

R H Straub

Publications and source records attributed to R H Straub.

At least 91 records · Page 5Linked to original sources

PubMed1997

Esophageal manometry in systemic sclerosis: screening procedure or confined to symptomatic patients?

The predictive value of esophagus-related symptoms for the diagnosis of esophageal dysmotility induced by systemic sclerosis (SSc) was prospectively evaluated in 50 consecutive patients with SSc. Patients were classified as symptomatic when either dysphagia or repeated episodes of heartburn were present. All patients underwent esophageal manometry; SSc-induced esophageal dysfunction was diagnosed when there was aperistalsis or marked hypocontractility of the distal two-thirds of the esophageal body. Twenty-nine patients (58%) had a history of esophagus-related symptoms, while 21 patients (42%) were asymptomatic. Compared to esophageal manometry, esophagus-related symptoms had a sensitivity of 64%, a specificity of 52%, a negative predictive value of 50% and a positive predictive value of 62% for the diagnosis of SSc-induced esophageal dysfunction. In conclusion, the association of esophagus-related symptoms and esophageal motility pattern is poor. As clinical management strategies depend on proof of esophageal dysfunction, screening examinations are mandatory in all patients with SSc.

Adult↗

PubMed1997

Association of autonomic nervous hyperreflexia and systemic inflammation in patients with Crohn's disease and ulcerative colitis.

The autonomic nervous system modulates gastrointestinal motility, secretion and mucosal immunity. Its dysfunction may be of pathogenetic importance in inflammatory bowel disease (IBD). This study aimed at investigating the autonomic nervous function in patients with IBD. Forty-seven patients with IBD, 28 with Crohn's disease (CD) and 19 with ulcerative colitis (UC), were investigated by means of 5 cardiovascular and 2 pupillary standardized autonomic nervous function tests. In CD and UC, cardiovascular autonomic neuropathy was very rare (0%, 5%), whereas pupillary autonomic neuropathy was more prevalent (21%, 21%). In contrast to autonomic neuropathy, overall cardiovascular (CD: 29%, UC: 26%) and pupillary autonomic hyperreflexia (46%, 37%) were found more often. Patients with CD and UC demonstrated elevated percentiles in the respiratory sinus arrhythmia test as compared to controls (RSA: 82.3 +/- 3.9%, 80.0 +/- 5.9%, controls: 50.0% +/- 1.5%, p < 0.0001). CD patients with, as compared to patients without, RSA hyperreflexia had significantly higher CDAIs (p < 0.001), increased erythrocyte sedimentation rates (p < 0.005) and more often extraintestinal disease manifestations (p < 0.001). UC patients with, as compared to patients without, pupillary latency time hyperreflexia had lower hemoglobin (p < 0.05), lower albumin (p < 0.01) and increased erythrocyte sedimentation rates (p < 0.05). Autonomic hyperreflexia was significantly associated with more severe inflammation and systemic disease in IBD. Hyperreflexia may be a response to inflammation or a pathogenetic element that drives mucosal inflammation.

Adolescent↗

PubMed1997

Neuronal regulation of interleukin 6 secretion in murine spleen: adrenergic and opioidergic control.

The PNS was anticipated to be involved in the modulation of immune responses. To study aspects of this neuronal-immune communication, a recently developed tissue slice method was used to study the effects of adrenergic and opioidergic transmitters on interleukin 6 (IL-6) secretion in the spleen. The alpha 2-adrenergic agonist p-aminoclonidine (10(-7) M) inhibited IL-6 secretion (control vs. p-aminoclonidine, 100.0 +/- 4.76 vs. 59.3 +/- 6.6% of control values; p < 0.001). The alpha 1-adrenergic agonist methoxamine (10(-8) M) also inhibited IL-6 secretion (100.0 +/- 4.8 vs. 71.5 +/- 3.8%; p < 0.001). The endogenous opioids beta-endorphin (10(-10) M), methionine-enkephalin (10(-9) M), and leucine-enkephalin (10(-9) M) inhibited IL-6 secretion as well (p = 0.0051, p = 0.0337, and p = 0.0226, respectively). Electrical stimulation of spleen slices inhibited IL-6 secretion (100.0 +/- 4.3 vs. 56.7 +/- 4.6% of control values; p < 0.001). The involvement of alpha-adrenergic and opioidergic molecules in this electrically induced inhibition was shown by the use of antagonists. Electrical inhibition of IL-6 secretion was attenuated by phentolamine (10(-7) M; p = 0.0345), by naloxone (10(-6) M; p = 0.0046), by cyprodime (10(-8) M; p = 0.0014), and by the combination of cyprodime (10(-7) M) plus phentolamine (10(-8) M; p < 0.0001). We conclude from the complementary studies that the inhibition of IL-6 secretion induced by electrical pulses was mostly mediated by alpha-adrenergic and mu-opioidergic endogenous transmitters.

Adrenergic alpha-Agonists↗

PubMed1997

Decrease of interleukin 6 during the first 12 months is a prognostic marker for clinical outcome during 36 months treatment with disease-modifying anti-rheumatic drugs.

The aim of this study was to determine prognostic markers for the outcome after 36 months of therapy with disease-modifying anti-rheumatic drugs (DMARDs) in patients with rheumatoid arthritis (RA) and to study serial cytokine serum levels. During 36 months, 20 patients receiving DMARDs (nine patients gold sodium thiomalate and 11 patients methotrexate, no comparison undertaken) were followed for clinical and laboratory data. Investigation at baseline, 12, 24 and 36 months, included clinical, radiological and laboratory parameters such as erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), and interleukin (IL)-1 beta, IL-6, tumor necrosis factor alpha (TNF-alpha), IL-1 receptor antagonist (IL-1RA) and IL-2. During the 3 yr of therapy, the patients showed significant clinical improvement and decline of ESR, CRP, and serum levels of IL-6 and IL-2. The decrease in IL-6 serum levels during the first year of therapy correlated significantly with the decrease, after 36 months, in the number of inflamed joints (r = 0.7608, P < 0.005), Lansbury index (r = 0.6642, P < 0.005) and morning stiffness (r = -0.6561, P < 0.005). In contrast to IL-6 or IL-2, TNF-alpha and IL-1RA did not vary significantly during the 3 yr of therapy. During 36 months of therapy, patients treated with DMARD showed significant improvement of clinical parameters and a trend for delayed progression of radiographic damage. The decrease in IL-6 concentration in serum during the first 12 months was the best prognostic marker for the clinical outcome after 36 months of DMARD therapy.

Aged↗

PubMed1997

High prolactin and low dehydroepiandrosterone sulphate serum levels in patients with severe systemic sclerosis.

The aim was to determine serum levels of prolactin (PRL) and dehydroepiandrosterone sulphate (DHEAS), and to demonstrate a link between PRL or DHEAS and soluble immune mediators in patients with systemic sclerosis (SSc) with different degrees of disease-induced organ involvement. Thirty-one patients with SSc were studied to evaluate 18 possible disease manifestations. In the serum, PRL, DHEAS and soluble immune mediators were determined by ELISA. Compared to SSc with <9 disease manifestations, patients with > or =9 disease manifestations had higher PRL (P = 0.044), higher soluble interleukin 2 receptor (sIL-2R, P = 0.004) and vascular cell adhesion molecule (sVCAM, P = 0.044), and lower DHEAS (P = 0.029). PRL (R(Rank) = 0.490, P = 0.003) and DHEAS (R(Rank) = -0.399, P = 0.013) were significantly correlated with the number of disease manifestations. The inverse correlation between PRL and DHEAS showed a trend (P = 0.059). PRL correlated with sIL-2R (R(Rank) = 0.553, P = 0.001) and sVCAM (R(Rank) = 0.520, P = 0.002). The number of disease manifestations and sIL-2R correlated significantly (R(Rank) = 0.463, P = 0.006). Psychometric variables to examine the presence of depression were not measured, but from the general aspect, the patients were not suffering from major depression which may have influenced our results. In conclusion, this study demonstrates the close association between DHEAS and, particularly, PRL and SSc severity and T-lymphocyte mechanisms.

Adult↗

PubMed1997

Elevated anticardiolipin antibodies in autoimmune haemolytic anaemia irrespective of underlying systemic lupus erythematosus.

In patients with systemic lupus erythematosus (SLE) and concomitant Coombs positive autoimmune haemolytic anaemia (AIHA) anticardiolipin antibodies (aCL) are found more frequently and at higher titres than in SLE patients without AIHA. In order to assess if aCL elevation is primarily associated with the underlying SLE, or with AIHA itself, we examined AIHA patients with and without underlying SLE for the presence of aCL. aCL (IgG and IgM) were determined by ELISA in 74 SLE patients without AIHA, 22 SLE patients with AIHA, 50 patients with idiopathic AIHA (warm-reactive autoantibodies), 52 patients with idiopathic AIHA (cold-reactive autoantibodies) and 50 healthy controls. The mean IgG and IgM aCL titres in SLE patients without AIHA (IgG 37.0 U/ml, IgM 8.9 U/ml) were significantly elevated compared with the values in healthy controls (IgG 9.1 U/ml, IgM 3.2 U/ml; P < 0.005). The mean aCL levels in SLE patients with AIHA (IgG 53.2 U/ml, IgM 28.2 U/ml) were higher than in SLE patients without AIHA (P = 0.09 for IgG, P < 0.005 for IgM). Interestingly, the mean aCL levels of patients with idiopathic AIHA (warm-reactive autoantibody type: IgG 29.2 U/ml, IgM 19.3 U/ml; cold-reactive autoantibody type: IgG 27.4 U/ml, IgM 18.9 U/ml) were also significantly elevated compared with healthy controls P < 0.001). As aCL are elevated not only in SLE (with and without concomitant AIHA) but also in idiopathic AIHA it can be speculated that aCL are involved in the pathomechanism of autoantibody-induced erythrocyte destruction per se irrespective of an underlying SLE.

Anemia, Hemolytic, Autoimmune↗

PubMed1997

Relapsing polychondritis: clinical and immunogenetic analysis of 62 patients.

OBJECTIVE: In this study we describe clinical and immunogenetic findings in 62 unselected patients with relapsing polychondritis. METHODS: In a multicenter study, clinical data of 26 (41.9%) female and 36 (58.1%) male patients were collected. HLA-DR specificities were identified in 60, and the frequencies were compared with those in healthy controls. RESULTS: The median age at the time of diagnosis was 46.6 years (range 17 to 86). 58 (93.5%) patients had auricular chondritis, 31 (50.0%) ocular symptoms, 35 (56.5%) nasal involvement. Involvement of joints (53.2%), respiratory system (30.6%), skin (24.2%), cardiovascular system (22.6%), central nervous system (9.7%), and kidneys (6.5%) was found as well. 22 (35.5%) patients had associated diseases such as systemic lupus erythematosus or rheumatoid arthritis. Susceptibility to relapsing polychondritis was significantly associated with HLA-DR4 (p < 0.001). There was no difference in the frequency or distribution of DRB1*04 subtype alleles between patients and healthy controls. The extent of organ involvement was negatively associated with HLA-DR6 (p < 0.011). CONCLUSION: Immunogenetic findings as well as similarities and overlapping clinical symptoms with other autoimmune or rheumatic diseases suggest that immunological mechanisms play a major role in the pathogenesis of relapsing polychondritis.

Adolescent↗

PubMed1996

Neuroimmune control of interleukin-6 secretion in the murine spleen. Differential beta-adrenergic effects of electrically released endogenous norepinephrine under various endotoxin conditions.

In a previous study we demonstrated a superfusion technique which allows for investigation of nerve-immune cell interaction in murine spleen. We demonstrated that under septic-like conditions in the presence of bacteria and lipopolysaccharide (LPS), electrically induced inhibition of interleukin 6 (IL-6) secretion was attenuated by the beta-adrenergic antagonist propranolol. This effect was now investigated more closely under various endotoxin conditions in order to dissect effects of bacteria and endotoxin: (A) bacteria-rich conditions (without penicillin/streptomycin [P/S] and without LPS), (B) LPS-enriched conditions (with P/S and with LPS), and (C) bacteria-free conditions (with P/S and without LPS). Under bacteria-rich conditions, norepinephrine (Emax = 10(-6) M, p = 0.012) and isoproterenol (Emax = 10(-6) M, p = 0.048) concentration-dependently inhibited IL-6 secretion from murine spleen slices in contrast to bacteria-free conditions. In a bacteria-free environment the beta-adrenergic antagonist propranolol did not attenuate the electrically induced inhibition of splenic IL-6 secretion. The insertion of bacterial filters in front of the superfusion chambers to avoid direct contact between bacteria and cells increased the electrically-induced inhibition of IL-6 secretion (p = 0.0036). Added LPS did not change the electrically-induced release of norepinephrine from presynaptic nerve terminals in murine spleen. The study demonstrates two different beta-adrenergic effects on IL-6 secretion of murine spleen slices under bacteria-rich or bacteria-free conditions.

Adrenergic beta-Antagonists↗

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↗

PubMed1996

Atrial natriuretic factor and digoxin-like immunoreactive factor in diabetic patients: their interrelation and the influence of the autonomic nervous system.

In diabetic patients, several factors contribute to volume expansion and have to be counteracted by humoral and neuronal feedback control systems. We investigated N-terminal proatrial natriuretic factor (ANF1-98) and digoxin-like immunoreactive factor (DLIF), which are two counteracting hormones, and their interrelationship, with additional consideration given to autonomic nervous function in diabetic patients. ANF1-98 and DLIF were measured in 64 diabetic patients. Autonomic nervous function was assessed using nine autonomic nervous function tests. The patients were subdivided into two groups, one with four or more (group 1) and one with less than four abnormal results in autonomic function tests (group 2). Compared with group 2, group 1 demonstrated detectable DLIF levels less often (17.2 vs. 45.7, P = 0.0195) and increased levels of ANF1-98 (mean +/- SEM: 850.0 +/- 108.8 vs. 554.8 +/- 45.9 pmol/L, P = 0.0099). However, the groups did not differ in blood pressure, daily sodium, and daily potassium excretion. The number of abnormal autonomic function tests correlated significantly with ANF1-98 (P = 0.0002). In patients with detectable DLIF, DLIF correlated with ANF1-98 (P = 0.0080). These results demonstrate close interactions between the autonomic nervous system and the two natriuretic hormones. In patients with autonomic nervous dysfunction, higher levels of ANF may possibly compensate for the lack of the natriuretic DLIF to counteract hypertension and chronic volume expansion.

Adult↗

PubMed1996

Impact of disease duration on cardiovascular and pupillary autonomic nervous function in IDDM and NIDDM patients.

OBJECTIVE: To determine the age-independent impact of disease duration on autonomic nervous function in diabetic patients and to compare it with other disease-related complications. RESEARCH DESIGN AND METHODS: Of the patients with diabetes, 166 (66 IDDM, 100 NIDDM) were investigated using standardized cardiovascular and pupillary test procedures, which provide 10 age-independent percentile values for each patient. Sensorimotor neuropathy was assessed using a standardized clinical examination, retinopathy by fundoscopy, and nephropathy using daily urinary protein excretion and creatinine clearance. RESULTS: The duration of the disease did not correlate with the results of any one of six standard cardiovascular tests (P > 0.15). Pupillary parameters showed a weak negative correlation with disease duration (P < 0.04). Prevalence of cardiovascular autonomic dysfunction was not different in five different subgroups subdivided according to disease duration (0-6, 7-12, 13-18, 19-24, and > or = 25 years), whereas prevalence of pupillary dysfunction changed significantly with disease duration (P = 0.016). In contrast, the prevalence of sensorimotor neuropathy (P = 0.006), retinopathy (P < 0.001), and proteinuria (P = 0.010) was significantly higher in patients with long-standing disease. Disease duration was not significantly different in patients without overall cardiovascular dysfunction, as compared with patients with dysfunction (15.6 +/- 1.0 vs. 16.5 +/- 1.5 years, P = 0.626). This was also found when considering overall pupillary dysfunction (14.5 +/- 1.4 vs. 17.2 +/- 1.0 years, P = 0.125). CONCLUSIONS: Disease duration was not correlated with cardiovascular autonomic nervous function, whereas a correlation was observed with pupillary autonomic nervous function, sensorimotor neuropathy, retinopathy, and proteinuria. This may indicate that cardiovascular autonomic nervous function does not markedly change during the course of the disease. The question arises whether cardiovascular autonomic neuropathy may be more a functional abnormality than a structural lesion of the autonomic nervous system, which may be already present at the beginning, or even before, the manifestation of diabetes.

Adolescent↗

PubMed1996

Dehydroepiandrosterone sulfate is positively correlated with soluble interleukin 2 receptor and soluble intercellular adhesion molecule in systemic lupus erythematosus.

OBJECTIVE: To determine whether dehydroepiandrosterone sulfate (DHEAS) is linked with soluble immune mediators in systemic lupus erythematosus (SLE). METHODS: DHEAS and various soluble immune mediators were measured by ELISA in the serum of 35 patients with SLE (26 women, 9 men) and in 41 control subjects. RESULTS: DHEAS was lower in patients with SLE compared to controls (male 1.29 +/- 0.32 vs 3.04 +/- 0.33 micrograms/ml, p < 0.001; female 0.75 +/- 0.12 vs 2.16 +/- 0.18 micrograms/ml, p < 0.001). The DHEAS reduction was in part dependent on prior glucocorticosteroid treatment (p < 0.02). After adjustment for multiple comparisons, there was significant negative correlation between steroid dose and DHEAS (RRank = -0.426, p = 0.005), but with none of the soluble immune mediators. No significant difference in the percentage of steroid treated male and female patients was found (p = 0.220). However, there was positive correlation between DHEAS and soluble interleukin 2 receptor in women, but not in men, with SLE [RRank = 0.747 (n = 26, p < 0.0001) vs RRank = -0.1333( n = 9, p = 0.366)] and between DHEAS and soluble intercellular adhesion molecule in women, but not in men, with SLE [RRank = 0.509 (n = 26, p = 0.005) vs RRank = 0.4833 (n = 9, p = 0.094)]. CONCLUSION: These data demonstrate positive interrelation between DHEAS and soluble immune mediators involved in leukocyte function and leukocyte adhesion only in female patients with SLE.

Adult↗

PubMed1996

Autonomic and sensorimotor neuropathy in patients with systemic lupus erythematosus and systemic sclerosis.

OBJECTIVE: To determine and compare the prevalence and degree of autonomic (ANP) and sensorimotor neuropathy (SNP) in patients with systemic lupus erythematosus (SLE) and systemic sclerosis (SSc). METHODS: Thirty-one patients with SLE and 19 with SSc were investigated. Pupillary ANP was assessed by pupillometry, cardiovascular ANP using a standardized test battery, and SNP by a standardized clinical examination. RESULTS: In patients with SLE (SSc), 26% (10.5%) had a pathological pupillary latency time and 6.5% (13.7%) had an abnormal maximal pupillary area (p for the difference between latency time and maximal pupillary area in SLE = 0.040). Thus, patients with SLE had more often lesions of the pupillary parasympathetic portion of the autonomic nervous system. Overall prevalence of ANP was not different between the 2 groups; 29.0% in SLE and 21.1% in SSc for pupillary ANP and 9.7 and 15.7% for cardiovascular ANP, respectively. Overall prevalence of SNP was 6.5% in SLE and 21.1% in SSc. Disease activity was correlated with ANP (p = 0.008) and SNP (p = 0.020) in SLE. Kidney involvement was associated with more severe ANP in patients with SSc (p = 0.031). Duration of the disease did not correlate with any type of neuropathy. CONCLUSION: ANP and SNP are often present in SLE and SSc. SLE and SSc differ in the pattern of ANP and SNP, which indicates that different structures and neuropathogenic mechanisms may be involved. Patients with SLE had severe pupillary ANP, probably a sign of central nervous system involvement.

Adult↗

PubMed1995

In vitro superfusion method for the investigation of nerve-immune cell interaction in murine spleen.

Immune defence mechanisms can be modulated by brain function. To study such interactions, an in vitro method was developed to examine the release of cytokines and norepinephrine (NE) after electrical stimulation. Slices of mouse spleen were placed in chambers with a volume of 80 microliters and superfused with culture medium. To characterize electrically evoked NE release and cell viability a suitable stimulation protocol was developed using of [3H]NE. As parameter for immune function, modulation of interleukin-6 (IL-6) release by the spleen cells brought about by electrical stimulation was investigated. Splenic [3H]NE overflow was calcium-dependent, tetrodotoxin-sensitive and elicited by 54 mM potassium. Electrically evoked [3H]NE release at 22 h was about 80% of the release at 5.3 h. Electrical stimulation substantially reduced IL-6 secretion at 6 h (control: 143.4 +/- 14.3 vs. electrical: 71.3 +/- 7.9 pg/ml/10(6) leukocytes, P = 0.0001). This effect was inhibited in a concentration-dependent manner by the beta-adrenergic antagonist propranolol (P = 0.0298, EC50 approx. 10(-7) M). In conclusion, this new technique allows long-term investigation of cell function in slices of murine spleen. In addition, these are the first in vitro data indicating the presence of a functional neuroimmunological link in murine lymphoid tissue.

Adrenergic beta-Antagonists↗

PubMed1994

Valid parameters for investigation of the pupillary light reflex in normal and diabetic subjects shown by factor analysis and partial correlation.

Pupillary test data of 103 normal and 119 diabetic subjects (47 IDDM, 72 NIDDM) were evaluated by factor analysis. From a total of nine pupillary parameters three factors were extracted in the analysis. Factor 1 represents maximal pupillary area, contraction velocity at 1 s, dilation velocity at 6 s and minimal pupillary area--static and simple dynamic parameters; factor 2 amplitude of pupillary unrest, area under the detrended curve of pupillary unrest and period of pupillary unrest--parameters of pupillary unrest; factor 3 fusion frequency of pupillary response following flicker stimuli and latency time of pupillary light reflex--second order dynamic parameters. Factor analysis was then applied to investigate diabetic patients with a high percentage of autonomic neuropathic participants (about 39% had pupillary and about 35% had cardiorespiratory function disorders), which revealed the same three factors as those identified in normal subjects. Furthermore, an age-related database of parameters of pupillary unrest is given. It demonstrates that normal subjects and diabetic patients did not differ in the period of pupillary unrest (normal vs diabetic (mean +/- SEM): 1550 +/- 29 vs 1536 +/- 27 ms; 2p > 0.5). The difference in amplitude (47.8 +/- 2.8 vs 41.0 +/- 2.6% percentile; 2p = 0.071) and area under the detrended curve of pupillary unrest (47.9 +/- 2.8 vs 40.8 +/- 2.6% percentile, 2p = 0.062) seems to show a trend but was not significant. In conclusion, factor analysis revealed three different pupillary test factors.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1994

Influence of digoxin-like immunoreactive factor on late complications in patients with diabetes mellitus.

The aim of this study was to compare the intensity of typical late complications in diabetic patients (n = 65, 28 type I, 37 type II) who were not on glycoside drugs with low vs. high serum levels of digoxin-like immunoreactive factor (DLIF: group I, n = 42, DLIF < or = the detection limit of 0.2 ng ml-1; and group II, n = 23, mean +/- SEM: 1.17 +/- 0.31 [0.25-4.96] ng ml-1). For detection of nephropathy, urinary albumin excretion (24 h) and creatinine clearance tests were used. For coronary heart disease a questionnaire and standard ECG; for peripheral occlusive vascular disease a questionnaire; for eye disease a fundoscopy; for neuropathy a neurological score system; and for autonomic neuropathy a standardized test battery was employed. Patients with high DLIF levels showed better test results in vibratory perception (95.7 +/- 1.5 vs. 82.8 +/- 3.8%, normal finding = 100%, 2p = 0.016), had better percentile localizations concerning maximal pupillary area in darkness (28.4 +/- 6.6 vs. 8.1 +/- 1.8%, 2p = 0.0004), contraction velocity at 1 s (21.5 +/- 5.8 vs. 8.0 +/- 2.2%, 2p = 0.012), and dilation velocity at 6 s (23.0 +/- 6.8 vs. 10.5 +/- 2.5%, 2p = 0.041), had less retinopathy (with retinopathy: 26.1% vs. 64.3%, 2p = 0.0028), and better percentile localizations in the respiratory sinus arrhythmia test (68.4 +/- 7.3 vs. 44.1 +/- 4.9%, 2p = 0.0064). There was no difference concerning nephropathy, blood pressure, coronary heart disease and peripheral vascular disease. Separate analysis according to the type of diabetes confirmed the results in each group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1994

Impact of obesity on neuropathic late complications in NIDDM.

OBJECTIVE: This cross-sectional study was aimed to investigate the isolated influence of obesity on peripheral sensorimotor and autonomic neuropathy in patients with long-term non-insulin-dependent diabetes mellitus (NIDDM). RESEARCH DESIGN AND METHODS: Ninety-one long-term NIDDM patients with a mean duration of 13.6 +/- 1.0 years and a mean age of 60.4 +/- 1.0 years were divided into two groups according to their body mass index (BMI) (lean with a BMI < 26.5: n = 41, age = 58.6 +/- 1.7 years, BMI = 23.7 +/- 0.3 kg/m2; and obese with a BMI > or = 26.5: n = 50, age = 61.9 +/- 1.2 years, BMI = 30.5 +/- 0.5 kg/m2). The two groups were not different in age, duration, gender, current parameters of glycemic control, number of smokers, cholesterol, triglycerides, and systolic and diastolic blood pressure. Neuropathic late complications were scrutinized by a standardized clinical examination that delivers a neuropathy score, pupillary autonomic neuropathy assessed by pupillometry, and cardiovascular autonomic neuropathy using a standardized test battery. RESULTS: One-way analysis of variance revealed that obese patients had poor results in the clinical neuropathy test (overall score in obese vs. lean: 71.1 +/- 2.9 vs. 80.6 +/- 3.0 points, 2P = 0.0266; 100 points were absolutely normal). This was particularly true for the discrimination perception (obese vs. lean: 67.0 +/- 4.0 vs. 81.7 +/- 3.3 points, 2P = 0.0073) and the reflex status (obese vs. lean: 57.4 +/- 4.0 vs. 71.8 +/- 4.3 points, 2P = 0.0164). Furthermore, obese patients had a poor result in the respiratory sinus arrhythmia (RSA) test, one of six autonomic function tests (RSA: obese vs. lean in average RSA percentile: 36.9 +/- 4.9 vs. 54.0 +/- 5.9%, 2P = 0.0264). CONCLUSIONS: Obesity influences sensorimotor and autonomic neuropathic late complications. The poor result in RSA in obesity may indicate an interrelation between pathogenesis of obesity and disorders of the respiratory and heart rhythm-generating control centers in the brain stem. Moreover, it could be due to intrathoracic fat deposits that alter lung mobility. Body mass control may be an important approach to reduce neuropathic complications. Beyond that, it seems necessary to control for body mass when comparing neuropathy in two groups of patients with NIDDM.

Adult↗

PubMed1993

[Patients with type-II diabetes mellitus and neuropathy have no deficiency of vitamins A, E, beta-carotene, B1, B2, B6, B12 and folic acid].

The present study was aimed to determine the vitamin status of vitamins A, E, beta-carotene, B1, B2, B6, B12 and folate in plasma using HPLC and vitamins B1, B2 and B6 in erythrocytes using the apoenzyme stimulation test with the Cobas-Bio analyzer in 29 elderly type II diabetic women with (G1: n = 17, age: 68.6 +/- 3.2 years) and without (G2: n = 12, age: 71.8 +/- 2.7 years) diabetic polyneuropathy. The basic parameters as age, hemoglobin A1c, fructosamine and duration of the disease did not differ in both groups. Furthermore, retinopathy was assessed with fundoscopy and nephropathy with creatinine clearance. The creatinine clearance (G1: 50.6 +/- 3.4 vs. G2: 63.6 +/- 3.7 ml/min, 2p < 0.025) and the percentage of retinopathy (G1: 76.5% vs. G2: 16.7%, 2p = 0.002) were different indicating that G1 had significantly more severe late complications than G2. Current plasma levels of all measured vitamins (A, E, beta-carotene, B1, B2, B6, B12 and folate) and the status of B1, B2 and B6 in erythrocytes did not vary between the two groups (2p > 0.1). In summary, we found a lack of association between the actual vitamin condition in plasma and erythrocytes and diabetic neuropathy.

Aged↗