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E Standl

Publications and source records attributed to E Standl.

At least 55 records · Page 3Linked to original sources
PubMed1998

Course of islet autoantibody titers during Ig-immunoadsorption in a patient with newly diagnosed type 1 diabetes.

The purpose of this study was to determine whether and to what extent diabetes-specific autoantibodies can be removed from the plasma by Ig-immunoadsorption therapy. We followed the course of islet cell antibodies (ICA), insulin antibodies (I[A]A), glutamic acid decarboxylase antibodies (GADA) and antibodies to the protein tyrosine phosphatase IA-2 (IA2A) in a patient with newly diagnosed insulin-dependent diabetes mellitus (IDDM) under multiple immunoadsorption treatments over 6 months. Autoantibodies were not removed from the plasma as efficiently as expected when compared to the removal of total immunoglobulin (IgG). Whereas IgG levels were lowered by 70-90% through each immunoadsorption treatment, antibodies to insulin were reduced by an average of 83%, IA2A by 36% and GADA by only 9% directly after treatment. ICA were > 320 JDF U at diabetes onset and remained above this level. During the 6 months of multiple immunoadsorption therapies, I[A]A levels showed a 24-fold increase due to stimulation of insulin antibody production by exogenous insulin substitution, IA2A levels remained unchanged (average 6% increase), and GADA levels were reduced by an average of 39% compared to antibody titers at onset. All four antibodies were highly positive in the eluate from the immunoadsorption columns. We showed that antibodies to pancreatic islet cells can be reduced by immunoadsorption, but as for plasmapheresis the effect is incomplete and transient for most of the antibodies. If there is clinical benefit through immunoadsorption therapy--as has been shown for newly diagnosed IDDM patients treated with plasmapheresis--our data suggest that this may be due to factors other than the sufficient removal of antibodies.

Adult↗
PubMed1998

[Type 2 diabetes].

Explore the source record for details and available documents.

Combined Modality Therapy↗
PubMed1998

Delay of type I diabetes in high risk, first degree relatives by parenteral antigen administration: the Schwabing Insulin Prophylaxis Pilot Trial.

The Schwabing Insulin Prophylaxis Trial is a randomised, controlled pilot study designed to examine whether insulin therapy can delay or prevent the clinical onset of Type I diabetes in high risk first degree relatives of people with the disease. First degree relatives of patients with Type I diabetes, who were aged 4 years or more, had an islet cell antibody (ICA) value more than 20 Juvenile Diabetes Foundation Units (JDF-U), a reduced first phase insulin response (FPI) to an i.v. glucose tolerance test less than the 5th centile, and a normal oral glucose tolerance test were eligible for the trial. Between January 1989 and October 1995, 1736 relatives of patients with Type I diabetes were screened for ICA. We identified 64 cases (3.7%) with ICA values more than 20 JDF-U. Of ICA positive relatives, 17 (27%) had a low FPI and were eligible for enrolment. Of these 14 agreed to participate, of whom 7 were randomised to the treatment group and 7 to the control group. In the treatment group, human insulin was administered i.v. by continuous infusion for 7 days, followed by daily s. c. injections for 6 months. Intravenous insulin infusions were repeated every 12 months. In the treatment group 3 of the 7 individuals (follow-up from time of eligibility: 2.3 to 7.1 years) and in the control group 6 of the 7 untreated individuals (1.7 to 7.1 years) developed clinical diabetes. Life table analysis showed that clinical onset of Type I diabetes was delayed in insulin-treated subjects compared with control subjects (means+/-SEM diabetes-free survival: 5.0+/-0.9 years vs 2.3+/-0.7 years, p < 0.03). Insulin levels after i.v. glucose increased in the first year of intervention therapy. Titres of ICA, and antibodies to glutamic acid decarboxylase, and tyrosine phosphatase-like protein IA2 remained unchanged. These data suggest that insulin prophylaxis can delay the onset of overt diabetes in high risk relatives. This is encouraging in view of 1) the continuing American Diabetes Prevention Trial, which is currently testing the effect of parenteral insulin in a large nation-wide study and 2) the initiation of pilot trials to determine whether new antigen-specific intervention is more effective in delaying the clinical onset of Type I diabetes.

Adolescent↗
PubMed1998

On the prognosis of IDDM patients with large kidneys.

BACKGROUND: Approximately 10-30% of IDDM patients develop diabetic nephropathy depending on the metabolic control. Previous examinations on the significance of the kidney size prior to the manifestation of nephropathy produced varying results. METHODS: The present study, therefore, was designed to assess the correlation between sonographically determined kidney size and kidney function over 8 years in a follow-up examination, and to evaluate a potential risk pattern. Data could be collected from 73 (66%) of 110 IDDM patients with initially normal serum creatinine whose sonographically determined kidney volume (cm3 = L cm x W cm x D cm x pi/6) and kidney function (creatinine, albuminuria, beta2-microglobulin in serum) had been examined in 1986, and who had a diabetes duration of 1 month to 25 years at that time. RESULTS: 30% (11 of 37) patients with large kidneys (>170 cm3) reached at least one serious renal end-point (increase of serum creatinine by more than 50%, requirement of dialysis or kidney transplantation, or death in end-stage renal disease) versus one of 36 patients with normal kidney size (P<0.002). As many as 42% of patients with large kidneys developed abnormal creatinine values (>106 micromol/l) in contrast to only 20% of the patients with normal kidney volume (P<0.05). Six of seven patients with a more than 50% increase of serum creatinine from baseline showed large kidneys in 1986, but had a normal serum creatinine, and four also a normal urine albumin excretion. Furthermore all five patients with more severe end-points (two deaths in end-stage renal disease and three patients presently requiring dialysis) exhibited either an increased serum creatinine or large kidneys at baseline; four of these, however, were still in the normoalbuminuric state in 1986. CONCLUSIONS: These results indicate that large kidneys might be a morphological marker for subsequent diabetic nephropathy, and as a consequence, renal insufficiency.

Adult↗
PubMed1998

Humoral and cellular immune parameters before and during immunosuppressive therapy of a patient with stiff-man syndrome and insulin dependent diabetes mellitus.

OBJECTIVES: Humoral and cellular immune reactivity are reported for two neuroendocrine autoantigens-glutamic acid decarboxylase (GAD) and the protein tyrosine phosphatase IA-2-in a patient with the autoimmune type of stiff-man syndrome and insulin dependent diabetes (IDDM). METHODS: Antibodies and T cell proliferation against GAD and IA-2 and cytokine release of antigen stimulated T cells (IFN-gamma) were determined before and several times during immunosuppressive therapy with prednisolone. RESULTS: Raised GAD antibodies against full length GAD65 or chimeric constructs were detected before therapy and they remained at a high concentration despite a marked clinical improvement during cortisone treatment. Antibodies to IA-2 were undetectable, but weak T cell responses to both GAD and IA-2 were seen before therapy and once on reduction of high cortisone dosages when the patient showed signs of clinical deterioration. Cytokine profiles showed increased IFN-gamma production after stimulation with GAD or IA-2 suggesting increased activation of TH1 cells. CONCLUSION: Immunosuppressive therapy --even with extremely high doses of 500 mg a day--does not lead to the reduction of antibody concentrations in the periphery nor to a switch in epitope recognition of such antibodies despite clinical improvement. The amount of T cell reactivity to various antigens, however, may be a useful marker to monitor the effectiveness of immunotherapy.

Autoantibodies↗
PubMed1998

Successful treatment with insulin analog lispro in IDDM with delayed absorption of subcutaneously applied human regular insulin and complicated intraperitoneal insulin infusion. A case report.

OBJECTIVE: To subcutaneously administer the insulin analog lispro in a patient with delayed absorption of subcutaneously applied human regular insulin whose continuous intraperitoneal insulin infusion (CIPII) with a percutaneous access device had required multiple surgical interventions because of complications. RESEARCH DESIGN AND METHODS: In a 35-year-old woman with long-term IDDM and delayed absorption of subcutaneously applied human regular insulin, a 3-year CIPII with human regular insulin via a percutaneous access device was complicated by three catheter obstructions and one subcutaneous abscess. Each complication required the implantation of a new percutaneous access device. During a 2-day trial with continuous subcutaneous insulin infusion (CSII) of the insulin analog lispro at basal infusion rates of 0.5-1.1 U/h, stable metabolic control was achieved. A 5-h intermediate attempt with human regular insulin in CSII, however, increased blood glucose concentrations from 6.0 to 28.8 mmol/l, despite identical basal rates and additional injection of 16 U of human regular insulin. Restarting with CSII of the insulin analog lispro reinforced stable metabolic control. CONCLUSIONS: It is suggested that the insulin analog lispro is a promising approach in the treatment of IDDM with delayed absorption of subcutaneously applied human regular insulin and a suitable alternative therapy for patients with complications attributed to percutaneous access devices for CIPII.

Administration, Cutaneous↗
PubMed1998

Failure of reducing lower extremity amputations in diabetic patients: results of two subsequent population based surveys 1990 and 1995 in Germany.

BACKGROUND: A 50% reduction of lower extremity amputations during the subsequent 5 year period has been targeted by the St. Vincent-Declaration issued in 1989/90 for a better care of diabetic patients across Europe. PATIENTS AND METHODS: In two adjacent counties far off major city areas 10 hospitals without specialised diabetes centers in the area provide care to about 300,000 inhabitants. Based on the official operation books and verified by the individual patient file all patients amputated in the 10 hospitals during the years 1990 and 1995 were evaluated retrospectively. RESULTS: A total of 119 patients (66 males, 53 females, age median 72 years) were amputated in the 10 hospitals 1990, and 162 (89 males, 73 females, age median 74 years) in 1995. The proportion of diabetic amputees amounted to 70.6 and 62.3%, respectively. A trend towards more toe amputations in diabetic versus nondiabetic patients was seen in both surveys which reached significance in 1995 (59 vs. 41%; p < 0.05). Based on the total population and the estimated number of diabetic patients (5% of the population) 1.4 and 2/10,000 nondiabetics were amputated in 1990 and 1995, respectively, in contrast to 61 and 66/10,000 diabetic individuals, indicating a 44 fold and 33 fold excess risk of diabetic patients. CONCLUSION: It is concluded that these 2 surveys 5 years apart reveal a failure of reducing lower extremity amputations in people with diabetes--despite the objectives of the St. Vincent-Declaration.

Adolescent↗
PubMed1997

[Alström syndrome--a rare disease of diabetic association].

BACKGROUND: Alström's disease is a rare hereditary multiple-system illness, whereas a second-messenger defect can be assumed. CASE REPORT: We describe a case-the first in Germany of 15 known cases in the world literature-, who suffers from all clinical features, such as non-insulin-dependent diabetes mellitus, retinitis pigmentosa, pancochlear damage of the ears, hypogonadism, obesity and chronic nephropathy, with the exception of acanthosis nigricans. CONCLUSION: Because of the multiplicity of affected organs the diagnosis of Alström's disease is difficult.

Adult↗
PubMed1997

Partial restoration of scintigraphically assessed cardiac sympathetic denervation in newly diagnosed patients with insulin-dependent (type 1) diabetes mellitus at one-year follow-up.

Diabetic neuropathy is thought to comprise a reversible metabolic and an irreversible structural component of neuronal abnormality. To investigate whether the cardiac sympathetic denervation recently described in newly diagnosed, but metabolically stabilized, diabetic patients without myocardial perfusion abnormalities reflects transient or permanent sympathetic abnormalities, 123-I-metaiodobenzylguanidine (123-I-MIBG) scintigraphy was performed in 16 patients with insulin-dependent (Type 1) diabetes mellitus (IDDM) 1 year after initial assessment and diagnosis. All patients had been treated with an intensified insulin therapy for 1 year. HbA1c had fallen from 11.5 +/- 2.0% to 6.3 +/- 0.9% (p < 0.001). The global myocardial 123-I-MIBG uptake (score 1-6) had improved in 7 patients at 1 year, remained unchanged in 7, and deteriorated in 2 patients. Regionally, the myocardial uptake score of the posterior and septal regions had improved significantly (p < 0.01, p = 0.02) with a mean uptake score in the groups of 3.8 +/- 1.1 and 3.4 +/- 1.2 at diagnosis versus 2.6 +/- 0.5 and 2.5 +/- 0.9 at 1 year. Myocardial uptake scores of the anterior, lateral, and apical regions had also improved in 7, 6, and 9 patients, but the mean changes of these scores did not reach significance. The study demonstrates that scintigraphically assessed cardiac sympathetic denervation in newly diagnosed, but metabolically stabilized, IDDM patients is partially reversed with improved metabolic control after 1 year of intensified insulin therapy. We suggest that even in the early stage of IDDM, cardiac sympathetic dysfunction is composed of reversible and irreversible neuronal abnormalities.

3-Iodobenzylguanidine↗
PubMed1997

Antibodies to bovine serum albumin (BSA) in type 1 diabetes and other autoimmune disorders.

Clinical and experimental studies have delineated a link between dietary cow milk protein and the development of insulin-dependent diabetes mellitus (IDDM), and bovine serum albumin (BSA) was proposed as one candidate mediator of this effect. The demonstration of anti-BSA antibodies in new onset type 1-diabetic children from Finland initiated a controversial debate on the utility of BSA antibodies as a disease marker and on the role of BSA in IDDM. Here we analyzed BSA antibodies in newly diagnosed type 1-diabetic patients and their first degree relatives, patients with other autoimmune diseases, and children with Down's syndrome from Germany. Blinded serum samples (n = 308) were screened for IgG anti-BSA antibodies by particle concentration fluoroimmunoassay (PCFIA). The prevalence of elevated BSA antibodies in newly diagnosed type 1-diabetic patients was low (11%), although mean BSA antibody levels were significantly increased in diabetic patients as compared to controls (1.94 +/- 1.51 vs. 0.97 +/- 0.93 kFU, p < 0.0007). Mean BSA antibody levels were also increased in ICA+ and/or IAA+ first degree relatives (1.32 +/- 0.43, p < 0.002) and in children with Down's syndrome (3.01 +/- 1.93, p < 0.0007), but not in the other autoimmune disorders tested. The low prevalence of elevated anti-BSA levels in IDDM patients limits the clinical usefulness of this immune marker. We conclude that current anti-BSA assays do not substantially contribute to the prediction and diagnosis of IDDM.

Adolescent↗
PubMed1997

Prediction of type 1 diabetes postpartum in patients with gestational diabetes mellitus by combined islet cell autoantibody screening: a prospective multicenter study.

Women with gestational diabetes mellitus (GDM) have a considerable risk of developing diabetes later in life. To determine the predictive value of autoantibody markers in gestational diabetic pregnancy for the development of type 1 diabetes postpartum, we tested 437 patients with GDM (289 women treated with diet only [GDM-A] and 148 requiring insulin treatment during pregnancy [GDM-B]) for antibodies to islet cells (ICAs), GAD (GADAs), and tyrosine phosphatase ICA512/IA-2 (IA2As). We prospectively followed them with repeated oral glucose tolerance tests and antibody determinations for up to 7 years postpartum (mean, 1.6 years; range, 0-7.2 years). The cumulative risk of diabetes up to 5 years postpartum was 17% (95% CI 12-22%). The risk of type 1 diabetes was 3% (2-5%) by 9 months and 7% (4-9%) 2 years after delivery. At delivery, 8.5% of all patients were ICA+, 9.5% were GADA+, 6.2% were IA2A+, and 18.1% were positive for at least one antibody (12.6% for GDM-A vs. 30.4% for GDM-B, P < 0.0001). During follow-up, GADAs persisted in 75%, ICAs in 35%, and IA2As in 30% of the subjects positive for the respective marker at delivery. By 2 years postpartum, 29% (19-39%) of patients positive for at least one antibody developed type 1 diabetes, compared with 2% (1-4%) of antibody-negative patients (P < 0.0001). Thereby, the risk for type 1 diabetes 2 years postpartum increased with the number of antibodies present at delivery from 17% (6-28%) for one antibody, to 61% (30-91%) for two antibodies, and to 84% (55-100%) for 3 antibodies. Risk of progression to type 1 diabetes postpartum was also associated with the status of parity. Women with one or more pregnancies before the index pregnancy had a higher risk for type 1 diabetes 2 years after delivery (14.7% [4.9.-24.5%]) than women having their first (i.e., index) pregnancy (5% [2.9-7.1%]) (P < 0.006). A comparison of different prediction strategies showed that single antibody screening with GADA yielded the highest sensitivity of 63% (45-75%), compared with ICA (48% [31-65%]) and IA2A (34% [13-47%]). Combined screening with two autoantibodies increased sensitivity to 74% (58-90%) and 75% (60-92%) when using GADA plus ICA or GADA plus IA2A, respectively. Screening with all three markers improved sensitivity further to 82% (67-100%). Beta-cell autoantibodies determined at delivery in women with GDM are highly predictive for the development of type 1 diabetes postpartum. Autoantibody screening in pregnant women with GDM from populations at high risk for type 1 diabetes should therefore be considered to allow early diagnosis and appropriate therapy.

Adolescent↗
PubMed1997

Autoantibodies to sympathetic ganglia, GAD, or tyrosine phosphatase in long-term IDDM with and without ECG-based cardiac autonomic neuropathy.

OBJECTIVE: To evaluate the association of autoantibodies to complement-fixing sympathetic ganglia (CF-SG), and tyrosine phosphatase (IA-2) with electrocardiogram (ECG)-based cardiac autonomic neuropathy (CAN) in long-term IDDM. RESEARCH DESIGN AND METHODS: We examined the prevalence of autoantibodies to CF-SG (by complement-fixing indirect immunoflourescence), GAD, and IA-2 (by radioligand assay) and islet cells (by indirect immunofluorescence) in 96 long-term IDDM patients (41 with ECG-based CAN, > or = 2 of 5 cardiac reflex tests abnormal; 55 without ECG-based CAN). As a control group, 89 healthy nondiabetic subjects were investigated. RESULTS: CF-SG autoantibodies were observed more frequently in long-term IDDM patients than in the control group (25 vs. 4%, P = 0.0001). Of the IDDM patients, 14 (34%) with CAN and 10 (18%) without CAN presented with CF-SG autoantibodies (P = 0.06). GAD or IA-2 autoantibodies were detected in 14 (34%) and 17 (41%) IDDM patients with CAN, compared with 24 (44%) and 29 (53%) IDDM patients without CAN (P = 0.2, P = 0.2). Islet cell antibodies were observed in 6 (15%) IDDM patients with and in 9 (16%) IDDM patients without CAN (P = 0.5). CONCLUSIONS: In long-term IDDM, the role of CF-SG autoantibodies, which tend to be more frequent in patients with ECG-based CAN, requires further investigations. The persistence of GAD and IA-2 autoantibodies is not related to ECG-based CAN.

Adult↗
PubMed1997

High-dose intravenous insulin infusion versus intensive insulin treatment in newly diagnosed IDDM.

High-dose intravenous insulin infusion at the onset of IDDM has been suggested to improve beta-cell function during the 1st year of insulin treatment. To test this hypothesis, we randomly assigned newly diagnosed IDDM patients to receive either an experimental 2-week high-dose intravenous insulin infusion (n = 9; age, 25 +/- 7 years; HbA1e, 10.5 +/- 2.0%) or an intensive insulin therapy of four injections per day (n = 10; age, 28 +/- 7 years; HbA1c, 12.3 +/- 3.0%). The experimental-therapy group received three times more insulin (1.2 +/- 0.4 U.kg-1.day-1) than the intensive-therapy group (0.4 +/- 0.1 U.kg-1. day-1, P < 0.0005). By week 3, both groups were treated similarly with intensive insulin therapy and were followed for 1 year. beta-cell function was evaluated with fasting plasma C-peptide and glucagon-stimulated and mixed meal-stimulated C-peptide concentrations. In both groups, insulin doses were comparable, and HbA1c levels were near normal during follow-up. At diagnosis of IDDM, fasting C-peptide was 0.40 +/- 0.13 nmol/l in the experimental-therapy group and 0.39 +/- 0.23 nmol/l in the intensive-therapy group. Irrespective of treatment, a slight decline of fasting C-peptide was observed in sequential measurements up to 12 months in both groups (delta, -0.13 and -0.08 nmol/l, respectively; NS). Glucagon-stimulated C-peptide concentrations decreased from 0.54 +/- 0.18 and 0.70 +/- 0.39 nmol/l at month 0 to 0.41 +/- 0.20 and 0.61 +/- 0.52 nmol/l, respectively, at month 12. In the experimental-therapy group, mixed meal-stimulated C-peptide concentrations (area under the curve over 2 h) increased from 82.10 +/- 43.72 to 101.20 +/- 32.53 nmol/l and in the intensive-therapy group, from 75.05 +/- 46.01 to 107.20 +/- 102.51 nmol/l. Changes in stimulated C-peptide concentrations between month 0 and 12 were not significant in both groups. During follow-up, fasting and stimulated C-peptide concentrations were not significantly different between the experimental-therapy group and the intensive-therapy group. We conclude that as initial treatments of newly diagnosed IDDM, high-dose intravenous insulin infusion and intensive insulin therapy equally preserve beta-cell function during the 1st year of insulin therapy.

Adolescent↗
PubMed1996

[The diagnostic value of the rate-corrected QT interval in long-term type-1 diabetes mellitus].

OBJECTIVE: To assess the relationship between rate-corrected QT interval (QTc interval) and cardiac reflex tests in order to determine the value of QTc interval measurements in the diagnosis of diabetic cardiac autonomic neuropathy. INVESTIGATIONS: The QTc interval was measured in the resting ECG of 97 type 1 diabetics (58 women, 39 men; mean age 35 +/- 12 years; duration of diabetes 18 +/- 10 years; HbA1c 7.8 +/- 1.8%). Age-related results were compared with five cardiac function tests (heart rate variation at rest and on forced breathing; 30/15 ratio of heart rate; Valsalva manoeuvre; orthostasis). RESULTS: The QTc interval was not prolonged ( < or = 440 ms) in 68 patients (70%), while in 29 (30%) it was prolonged ( > 440 ms). No significant differences regarding QTc interval were found between patients with autonomic cardiac neuropathy ( > or = 2 abnormal function tests) and those without ( < 2 abnormal function tests) (QTc interval 436 +/- 25 vs 426 +/- 19 ms). QTc intervals correlated with the coefficients of variation for heart rate variation at rest and on forced breathing and the 30/15 ratio of heart rate (p = 0.001; p = 0.001; p = 0.03), but not with the results of the Valsalva manoeuvre and the orthostasis test. CONCLUSION: Prolongation of the QTc interval in longstanding type 1 diabetes does not provide a reliable indication of cardiac autonomic neuropathy and this measure cannot replace conventional reflex tests for its diagnosis.

Adult↗
PubMed1996

[Newly manifested type IIb diabetes presents with significant hyperinsulinemia].

BACKGROUND: Data concerning the insulin status in the early phase of NIDDM are controversial. PATIENTS AND METHOD: Since this has therapeutical implications, ten patients were identified with new-onset type 2 diabetes, defined by fasting blood glucose concentrations below 120 mg/dl, no previous history of diabetes and venous blood glucose concentrations at 120 min of an oral glucose tolerance test above 200 mg/dl (x 262 +/- 15 mg/dl) ("diabetic glucose tolerance"). Ten subjects with normal glucose tolerance and no familial history of NIDDM, who were matched for gender, age (n: 56 +/- 2 years, D: 61 +/- 5) and BMI (n: 28 +/- 1, D: 28 +/- 1), served as control group. Serum insulin was measured using a double-antibody sandwich-test (no cross-reaction with proinsulin and C-peptide) at 0, 30 and 120 min of an oGTT. RESULT: In the diabetic group, basal insulin levels were found to be elevated 1.7-fold (n: 7.9 +/- 1.4 uU/ml, D: 13.3 +/- 1.4, p = 0.03), 30 min values were the same in both groups and the 120 min value was 4.6-fold higher in the diabetic group (n: 33.9 +/- 8.7, D: 156.2 +/- 27.4, p = 0.0008). CONCLUSION: Thus, in new-onset diabetes, in the early phase of an oGTT (30 min) both insulin secretion and action are reduced, in the second phase (120 min) severe insulin resistance predominates at maximally stimulated secretion. These findings underline the therapeutical strategy in these patients, to reduce postprandial blood glucose increments and improve insulin resistance by diet and, if necessary, pharmacologically.

Blood Glucose↗
PubMed1996

Autoantibodies against sympathetic ganglia and evidence of cardiac sympathetic dysinnervation in newly diagnosed and long-term IDDM patients.

To investigate the presence of autoantibodies against sympathetic nervous tissue and their correlation with cardiac sympathetic dysinnervation in insulin-dependent diabetes mellitus (IDDM), 20 newly diagnosed (age 26 +/- 6 years) and 48 long-term IDDM patients (age 40 +/- 13 years, duration of diabetes 22 +/- 12 years) without myocardial perfusion abnormalities (normal 99mTC-methoxyisobutylisonitrile uptake) were assessed for myocardial 123I-metaiodo benzylguanidine (123I-MIBG) uptake and complement-fixing sympathetic ganglia (CF-SG) autoantibodies. Both groups of patients were also studied for islet cell antibodies (ICA) and ECG-based cardiac autonomic neuropathy. Eighty control subjects (age 18-49 years) were investigated for CF-SG autoantibodies. Eight newly diagnosed (40%) and 12 long-term (25%) IDDM patients exhibited CF-SG autoantibodies, compared to 4 control subjects (5%; p < 0.01, p < 0.05). In long-term diabetic patients, the reduction of global but not of regional myocardial 123I-MIBG uptake correlated with CF-SG autoantibodies (r = 0.34, p = 0.02). Newly diagnosed diabetic patients did not show an association between CF-SG autoantibodies and global or regional myocardial 123I-MIBG uptake. ECG-based cardiac autonomic neuropathy (> or = two of five cardiac reflex tests abnormal) was present in 22 and absent in 26 long-term IDDM patients, of whom 9 (41%) and 3 (12%), respectively were positive for CF-SG autoantibodies (p = 0.02). Only 1 newly diagnosed IDDM patient demonstrated ECG-based cardiac autonomic neuropathy and was also positive for CF-SG autoantibodies. Although they are somewhat suggestive, results concerning autoantibodies against sympathetic nervous tissue and cardiac sympathetic dysinnervation do not strongly support the view that autoimmune mechanisms play a major role in the pathogenesis of cardiac sympathetic neuropathy in IDDM.

3-Iodobenzylguanidine↗
PubMed1996

Predictors of 10-year macrovascular and overall mortality in patients with NIDDM: the Munich General Practitioner Project.

The 10-year follow-up of the Munich General Practitioner Project was designed as a long-term prospective study to evaluate factors predicting macrovascular and overall mortality in a random cohort of non-insulin-dependent diabetic (NIDDM) patients. Of the original 290 patients (103 males, 187 females, median age 65 years) 92.5% could be assessed, 103 subjects had died, 58 from macrovascular causes. In an univariate analysis of baseline data, deceased patients, and especially those who died from macrovascular causes had significantly higher fasting blood glucose, HbA1c, von Willebrand-factor protein, urine albumin excretion, and serum beta 2-microglobulin, were significantly older, exhibited significantly more ischaemic heart disease (abnormal ECG Minnesota codes), carotid artery and peripheral vascular disease (both determined by ultrasound-Doppler), and had significantly inferior knowledge about diabetes and its treatment. No significant differences were seen for gender, blood pressure, smoking, total cholesterol, triglycerides, HDL-cholesterol, or the use of antidiabetic, antihypertensive or coronary drugs. In a multiple logistic regression analysis, the risk factors for macrovascular death were age, HbA1c and von Willebrand-factor protein. When baseline macrovascular disease was taken into account, carotid artery disease was also a determinant. The main variables from the metabolic syndrome (blood pressure, dyslipidaemia, body mass index) did not enter a multiple logistic regression analysis. The data suggest that age and haemoglobin A1c are major determinants, and that in addition von Willebrand-factor associated endothelial damage is a risk factor for macrovascular mortality in NIDDM patients.

Age Factors↗