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Adriaan Honig

Publications and source records attributed to Adriaan Honig.

At least 19 recordsLinked to original sources
PubMed2005

Inflammatory markers in depressed post-myocardial infarction patients.

BACKGROUND: Depressive disorder in the post-myocardial infarction (MI) period has been associated with increased cardiac morbidity and mortality. Possible pathophysiological mechanisms behind this association are not clear. Major depression in physically healthy subjects has been related to immune abnormalities including increased plasma levels of interleukin-6 (IL-6), tumor necrosis factor alfa (TNF-alpha) and C-reactive protein (CRP). In patients with MI, increased inflammatory markers, such as CRP and TNF-alpha, have been associated with increased cardiovascular events. It was the aim of this study to test the hypothesis that depression in post-MI patients is associated with increased inflammation as compared to non-depressed post-MI patients. METHODS: The cytokines IL-6 and TNF-alpha ; the soluble cytokine receptors sIL-6R, sTNF-RI and sTNF-RII; neopterin; and the inflammation-sensitive plasma proteins (ISPs) CRP and haptoglobin were assessed in a group of 57 patients with a diagnosis of depression post-MI and in a control group of 46 non-depressed post-MI patients, matched for age, gender and time elapsed since MI. RESULTS: Cytokine, neopterin and ISP levels were not statistically different in the depressed post-MI group as compared to the non-depressed post-MI group. Several inflammatory markers were however elevated in both cohorts when compared with levels reported in healthy subjects, indicating persistent inflammation several months after MI. CONCLUSIONS: There was no indication of increased inflammation in depressed post-MI patients as compared to non-depressed post-MI patients.

Adult↗
PubMed2004

Whole blood serotonin and platelet activation in depressed post-myocardial infarction patients.

Depression is an independent risk factor for post myocardial infarction (MI) mortality. Abnormalities in platelet function have been proposed as one of the mechanisms involved in increased cardiovascular risk among patients with depression post-MI. Depression in somatically healthy patients has been associated with increased platelet activation. Some but not all studies showed changes in blood serotonin level. Increased platelet activation and blood serotonin level have been associated with increased risk of cardiac events in patients with MI. The goal of this study was to investigate whether 1) depressed post-MI patients have higher markers of platelet activation as measured by plasma levels of beta-thromboglobulin (betaTG), platelet factor 4 (PF4) and soluble CD40 ligand (sCD40L) and higher serotonin (5-HT) levels than non-depressed post-MI patients and 2) treatment with the antidepressant mirtazapine decreases platelet activation. In this study, 25 depressed post-MI patients were asked for blood collection before start as well as after 8 weeks treatment with mirtazapine or placebo. The control group (n=22) consisted of non-depressed post-MI patients, matched for age, gender and time elapsed since MI. Plasma levels of betaTG, PF4 and sCD40L were not statistically different between the groups, but 5-HT levels were significantly higher in depressed patients. Treatment with mirtazapine resulted in a non-significant decrease in betaTG and PF4 and platelet 5-HT levels. Platelet and whole blood 5-HT, but not platelet activation was significantly increased in depressed post-MI patients. Treatment with mirtazapine showed a non-significant decrease in platelet activation and platelet 5-HT.

Adult↗
PubMed2004

Brain- and heart-type fatty acid-binding proteins in the brain: tissue distribution and clinical utility.

BACKGROUND: Detection of brain injury by serum markers is not a standard procedure in clinical practice, although several proteins, such as S100B, neuron-specific enolase (NSE), myelin basic protein, and glial fibrillary acidic protein, show promising results. We investigated the tissue distribution of brain- and heart-type fatty acid-binding proteins (B-FABP and H-FABP) in segments of the human brain and the potential of either protein to serve as plasma marker for diagnosis of brain injury. METHODS: B-FABP and H-FABP were measured immunochemically in autopsy samples of the brain (n = 6) and in serum samples from (a) patients with mild traumatic brain injury (MTBI; n = 130) and (b) depressed patients undergoing bilateral electroconvulsive therapy (ECT; n = 14). The protein markers S100B and NSE were measured for comparison. Reference values of B-FABP and H-FABP were established in healthy individuals (n = 92). RESULTS: The frontal, temporal, and occipital lobes, the striatum, the pons, and the cerebellum had different tissue concentrations of B-FABP and of H-FABP. B-FABP ranged from 0.8 microg/g wet weight in striatum tissue to 3.1 microg/g in frontal lobe. H-FABP was markedly higher, ranging from 16.2 microg/g wet weight in cerebellum tissue to 39.5 microg/g in pons. No B-FABP was detected in serum from healthy donors. H-FABP serum reference value was 6 microg/L. In the MTBI study, serum B-FABP was increased in 68% and H-FABP in 70% of patients compared with S100B (increased in 45%) and NSE (increased in 51% of patients). In ECT, serum B-FABP was increased in 6% of all samples (2 of 14 patients), whereas H-FABP was above its upper reference limit (6 microg/L) in 17% of all samples (8 of 14 patients), and S100B was above its upper reference limit (0.3 microg/L) in 0.4% of all samples. CONCLUSIONS: B-FABP and H-FABP patterns differ among brain tissues, with the highest concentrations in the frontal lobe and pons, respectively. However, in each part of the brain, the H-FABP concentration was at least 10 times higher than that of B-FABP. Patient studies indicate that B-FABP and H-FABP are more sensitive markers for minor brain injury than the currently used markers S100B and NSE.

Adult↗
PubMed2004

Fatty acid profile and affective dysregulation in irritable bowel syndrome.

Irritable bowel syndrome (IBS) is a functional gastrointestinal disorder with a high co-occurrence with affective dysregulation. Affective disorders have been associated with specific changes in the PUFA and cholesterol profile. In IBS, similar changes may be present as have been reported in patients with affective disorders. This exploratory study investigates (i) the level of affective dysregulation (AD) in IBS patients and healthy controls; (ii) PUFA and cholesterol profiles in IBS patients compared with controls; and (iii) associations between PUFA and cholesterol parameters with the level of AD. Blood samples were obtained for determination of the FA composition of plasma phospholipids and serum cholesterol in 23 diarrhea-predominant IBS patients and 23 healthy matched controls. AD was scored using the Symptom Check List depression scale, the Hospital Anxiety and Depression Scale, and the Hamilton Depression Rating Scale. The level of AD was higher in IBS patients compared with controls. PUFA and cholesterol profiles did not differ significantly between groups. Total n-3 PUFA and cholesterol were significantly negatively associated and the ratio of n-6 to n-3 PUFA and the ratio of arachidonic acid to EPA were significantly positively associated with the level of AD. The findings of the present study reveal that AD was higher in IBS patients compared with healthy controls and that changes in PUFA and cholesterol profiles were significantly associated with the level of AD. These results warrant further studies regarding the role of PUFA and cholesterol status in the co-occurrence of AD and functional gastrointestinal disorders.

Adult↗
PubMed2004

One year cumulative incidence of depression following myocardial infarction and impact on cardiac outcome.

BACKGROUND: Major depression has been identified as an independent risk factor for increased morbidity and mortality in mixed patients populations with first and recurrent myocardial infarction (MI). The aim of this study was to evaluate whether incidence of major and minor depression is as high in a population with merely first-MI patients as in recurrent MI populations. Furthermore, it was evaluated whether in first-MI patients major and minor depression, and depressive symptoms, had an impact on cardiac mortality and morbidity up to 3 years post MI. METHODS: A consecutive cohort of 206 patients with a first MI were included in this study. One month following MI, all patients were interviewed using the Structured Clinical Interview for DSM-IV (SCID-I-R). Three, six, nine and twelve months following MI, patients filled out three psychiatric self-rating scales for depression, the Beck Depression Inventory (BDI), the Hospital Anxiety and Depression Scale (HADS), and the 90-item Symptom Checklist (SCL-90). Patients, exceeding a previously defined cut-off value on at least one of these scales, were reinterviewed using the SCID. The BDI was applied to assess depressive symptoms in relation to cardiac outcome as the SCL-90 and HADS showed similar results. Cardiac outcome was defined as major cardiac event, i.e., death or recurrent MI, and health care consumption, i.e., cardiac rehospitalisation and/or frequent visits at the cardiac outpatient clinic. Depression outcome was assessed from 1 month post MI up to 1 year post MI whereas cardiac outcome was assessed between 1 month and 3 years post MI. RESULTS: A 1-year incidence of 31% of major and minor depression was found in first-MI patients. The highest incidence rate for both major and minor depression was found in the first month after MI. Compared with nondepressed patients, depressed patients were younger (P=.001), female (P=.04) and were known with a previous depressive episode (P=.002). Neither major/minor depression nor depressive symptoms significantly predicted major cardiac events, but did predict health care consumption (P=.04 and P<.001, respectively). CONCLUSIONS: Incidence of major and minor depression is similar in this first-MI patients population as in recurrent MI populations. Major/minor depressive disorder nor depressive symptoms predicted neither mortality nor reinfarction.

Cohort Studies↗
PubMed2004

Development and feasibility of a nurse administered strategy on depression in community-dwelling patients with a chronic physical disease.

This contribution reports on the acceptability and feasibility to nurses and patients of an intervention to ameliorate minor depression among patients with chronic physical diseases. Elderly patients with chronic obstructive pulmonary disease (COPD) and type II Diabetes Mellitus were recruited from 10 general practices. All eligible patients were screened. Twenty-nine patients with minor depression gave their informed consent to participate in this feasibility study. The nurses spent an average of 70 min per visit. Our intervention appeared feasible and acceptable to patients and nurses. For the nurses, it provided an additional tool for a well-known problem. The majority of the patients regarded the intervention as worthwhile and effective. Patients had difficulties in understanding the link between physical complaints and symptoms of depression. The intervention has been further improved on the basis of our experiences, and is now ready to be tested in an effectiveness study.

Aged↗
PubMed2003

Comparing symptoms of depression and anxiety as predictors of cardiac events and increased health care consumption after myocardial infarction.

OBJECTIVES: We sought to compare symptoms of depression and anxiety as predictors of incomplete recovery after a first myocardial infarction (MI). BACKGROUND: Depressive symptoms have been related to post-MI mortality and health care consumption, but little is known about the effect of anxiety. We wanted to examine the effect of emotional distress on health care consumption and whether depressive symptomatology is a better predictor of prognosis than anxiety. METHODS: Subjects were 318 men (mean age 58 years) who completed the depression, anxiety, and hostility scales from the 90-item symptom check list after they survived a first MI. RESULTS: After an average follow-up of 3.4 years, there were 25 cardiac events (fatal or non-fatal MI). Symptoms of both depression (hazard ratio [HR] 2.32, 95% confidence interval [CI] 1.04 to 5.18; p = 0.039) and anxiety (HR 3.01, 95% CI 1.20 to 7.60; p = 0.019) were associated with cardiac events, adjusting for age, left ventricular ejection fraction, and use of antidepressants. However, a multivariate analysis including all three negative emotions indicated that symptoms of anxiety (HR 2.79, 95% CI 1.11 to 7.03; p = 0.029) explained away the relationship between depressive symptoms and cardiac events. Regarding health care consumption, anxiety (OR 2.00, 95% CI 1.24 to 3.22; p = 0.005), but not depression/hostility, was a predictor of cardiac rehospitalization and frequent visits at the cardiac outpatient clinic. CONCLUSIONS: Symptoms of depression and anxiety were associated with cardiac events. Anxiety was an independent predictor of both cardiac events and increased health care consumption and accounted for the relationship between depressive symptoms and prognosis. Symptoms of anxiety need to be considered in the risk stratification and treatment of post-MI patients.

Aged↗
PubMed2003

Fluvoxamine versus fluoxetine in major depressive episode: a double-blind randomised comparison.

A double-blind, multinational study was conducted to compare the efficacy and safety of fluvoxamine and fluoxetine in outpatients with major depressive episode; 184 patients were randomised to fluvoxamine (100 mg/day) or fluoxetine (20 mg/day) for 6 weeks. Both drugs were effective and there were no statistically significant differences between them in the area under the curve of change from baseline in the Hamilton depression rating scale (HAMD) total score. However, the percentage of HAMD responders (>or= 50% decrease in HAMD total score) at week 2, the clinical global improvement severity of illness score at week 2 and the depression subscale of the irritability, depression and anxiety scale at weeks 1, 2 and 4, all showed significant advantages for fluvoxamine. During the last 2 weeks, fluvoxamine was significantly more effective in improving the HAMD sleep disturbance scale. Both drugs were well tolerated and there were no marked differences in their side effect profiles which were typical of SSRIs. Fluvoxamine and fluoxetine have similar efficacy and safety profiles in the treatment of major depressive episode; the findings of this study indicate that fluvoxamine may have a faster onset of action with respect to resolution of depressive symptoms and result in a better improvement in sleep quality.

Adolescent↗
PubMed2003

[Depression after first myocardial infarction. A prospective study on incidence, prognosis, risk factors and treatment].

In these studies patients with first myocardial infarction (MI) were selected for studies focusing on epidemiology, risk factors and treatment of depression post-MI. Two consecutive cohorts of first MI patients were included. The first cohort was selected between May 1994 and May 1997 (n = 206), and the second between May 1997 and October 1999 (n = 206). All patients were screened every 3 months for depression using the SCL-90 and the Zung (cohort 1) or SCL-90, BDI and HADS (cohort 2) until 12 months post-MI. Patients scoring above the cut-off of one of the questionnaires were interviewed using a standardised interview in order to evaluate whether DSM-IV criteria for major depression were met; patients of the second cohort were also interviewed 1 month post-MI, independently of the score of the questionnaires. Of both cohorts data concerning major cardiac events and increased health care consumption were assessed during a 1 to 6 years follow-up period. Patients with major depression were offered treatment in the double-blind placebo-controlled trial with fluoxetine (n = 54). Depression appeared to be a predictor of increased health care consumption, but not of major cardiac events such as cardiac death and recurrent infarction in first myocardial infarction (MI) patients up to 6 years post-MI. This finding is in contrast to findings in the literature indicating that in patient populations with mixed first and recurrent MI, depression is a risk factor for cardiac mortality. In contrast to depression, symptoms of anxiety do predict cardiac mortality and recurrent MI in patients following first MI independently of other risk factors of cardiac mortality. Recognition of risk factors for post-MI depression may help the cardiologist to identify patients at risk for depression. Examples of such risk factors are, according to our studies, complications during admission, such as arrhythmic disorders and recurrent angina pectoris, and prescription of benzodiazepines. Patients at risk can be screened for depression using a 4-item questionnaire, and, if scoring is positive, be referred for psychiatric evaluation. Although the effectivity of antidepressive treatment in MI patients has as yet not been proven, we found that fluoxetine is a cardiac-safe antidepressive agent, but only in mild depression more effective than placebo. The positive effect of antidepressive treatment on cardiac prognosis has as yet not been shown.

Antidepressive Agents, Second-Generation↗
PubMed2002

Atypical cognitive profile in patients with depression after myocardial infarction.

BACKGROUND: We evaluated the cognitive profile of 48 patients with major depression following their first myocardial infarction (MI). METHODS: The cognitive performance of the patients was compared with the performance of 48 non-depressed MI patients and 48 healthy controls. RESULTS: Depressed MI patients performed slower on a simple cognitive speed related measure compared with non-depressed MI patients and healthy controls. Attention and speed-related aspects of cognitive functioning were not affected. Surprisingly, (depressed) MI patients showed even better performances with respect to memory function. LIMITATION: No patients with non-MI-related depression were included. CONCLUSIONS: The cognitive profile of major depression after MI differs from that of non-cardiac-related depressive disorder, as described in the literature. This may reflect a different etiology of post MI depression from non-cardiac-related depression.

Adult↗
PubMed2002

Mood, prolactin and cortisol responses following intravenous L-tryptophan challenge: evidence for serotonergic vulnerability in first-degree relatives of bipolar patients.

Central serotonergic vulnerability indicated by altered mood and neuroendocrine responses to an intravenous (i.v.) tryptophan (Trp) challenge was assessed in healthy adult unaffected first-degree relatives of bipolar disorder (BD) patients (n = 30) (family history; FH). The effects of a single dose of 7.0 g Trp on mood, cortisol and prolactin (Prl) in FH subjects were compared with healthy matched controls (n = 15) in a placebo-controlled, double blind cross-over design. Prl and cortisol responses increased following Trp. Overall, Trp lowered mood. Hormonal and mood effects did not differ between FH and controls. Results show some evidence for differences in serotonergic vulnerability between relatives of type I BD patients and relatives of type II BD patients.

Adult↗
PubMed2002

Personality and vulnerability to depression in stroke patients: a 1-year prospective follow-up study.

BACKGROUND AND PURPOSE: Depression is a frequent sequela of stroke that negatively interferes with rehabilitation outcome. Personality traits have been neglected as potential vulnerability factors for poststroke depression (PSD). In a 1-year prospective study, the influence of the 5 main personality traits (ie, neuroticism, extraversion, openness, agreeableness, and conscientiousness) on the development of PSD was studied. METHODS: One month after stroke, 190 consecutive patients with a first-ever supratentorial infarct were asked to complete a personality inventory, the NEO-Five Factor Inventory, which is based on the Five Factor Model of personality. Depressive symptoms were assessed 1, 3, 6, 9, and 12 months after stroke with 3 self-rating questionnaires as screening instruments for depression. PSD was diagnosed as major or minor depression through the use of the Structured Clinical Interview from the Diagnostic and Statistical Manual of Mental Disorders. RESULTS: The 1-year cumulative incidence of depression was 38.7%. Cox regression analysis showed that patients with high neuroticism scores had a 4.6-times-higher risk of developing PSD than patients with low neuroticism scores (P=0.001) regardless of lesion location. Level of handicap was the only other factor that showed an independent effect on the occurrence of PSD. CONCLUSIONS: Neuroticism is an important predictor of PSD, a finding that emphasizes the need to take personality into account as a potential vulnerability factor for depression in stroke patients. Research on PSD should aim at delineating the interplay between neurological and psychological factors in the development of PSD.

Adult↗
PubMed2002

Treatment of depression after myocardial infarction and the effects on cardiac prognosis and quality of life: rationale and outline of the Myocardial INfarction and Depression-Intervention Trial (MIND-IT).

BACKGROUND: Patients with a depressive disorder after myocardial infarction (MI) have a significantly increased risk of major cardiac events. The Myocardial INfarction and Depression-Intervention Trial (MIND-IT) investigates whether antidepressive treatment can improve the cardiac prognosis for these patients. The rationale and outline of the study are described. METHODS: In this multicenter randomized clinical trial, 2140 patients admitted for MI are screened for depressive symptoms with a questionnaire 0, 3, 6, 9, and 12 months after MI. Patients with symptoms undergo a standardized psychiatric interview. Those with a post-MI depressive episode are randomized to intervention (ie, antidepressive treatment; n = 190) or care-as-usual (CAU; n = 130). In the intervention arm, the research diagnosis is to be confirmed by a psychiatrist. First-choice treatment consists of placebo-controlled treatment with mirtazapine. In case of refusal or nonresponse, alternative open treatment with citalopram is offered. In the CAU arm, the patient is not informed about the research diagnosis. Psychiatric treatment outside the study is recorded, but no treatment is offered. Both arms are followed for end points (cardiac death or hospital admission for MI, unstable angina, heart failure, or ventricular tachyarrhythmia) during an average period of 27 months. Analysis is on an intention-to-treat basis. CONCLUSION: The MIND-IT study will show whether treatment of post-MI depression can improve cardiac prognosis.

Adult↗
PubMedDate not supplied

Increased coronary events in depressed cardiovascular patients: 5-HT2A receptor as missing link?

OBJECTIVE: Major depressive disorder and depressive symptoms have been identified as independent risk factors for cardiac morbidity and mortality in patients with ischemic heart disease. Increased susceptibility to platelet activation has been proposed as one of the mechanisms by which depression acts as a significant risk factor for thrombotic events. In this review, data on platelet activation and platelet aggregation measures in depressed patients with or without concomitant cardiovascular disease are given. Data on the influence of antidepressants on parameters of platelet activation are summarized. METHODS: A literature search was done by checking MEDLINE Advanced and PsycInfo from 1990 to 2003 and through checking the bibliographies of these sources. The following key words were used for this search: platelet activation, platelet aggregation, depression, depressive disorder, ischemic heart disease, calcium, and serotonin. RESULTS: There is an indication of enhanced platelet activation and aggregation in depressed patients. Next, patients with a depressive disorder show signs of a hyperactive platelet 5-HT2A receptor signal transduction system as measured by increased platelet calcium mobilization after stimulation of platelets with serotonin. CONCLUSIONS: Depression appears to be associated with an increased susceptibility for serotonin-mediated platelet activation. Upregulation and/or increased sensitivity of 5-HT2A/1B receptors and downregulated 5-HT transporter receptors in the periphery may contribute to increased risk of thromboembolic events in patients with depression and cardiovascular disease. Increased platelet reactivity based on a hyperreactive 5-HT2A receptor signaling system might be influenced by antidepressive medication that antagonizes platelet 5-HT2A receptors.

Antidepressive Agents↗
PubMedDate not supplied

Validity of the beck depression inventory, hospital anxiety and depression scale, SCL-90, and hamilton depression rating scale as screening instruments for depression in stroke patients.

Most instruments used to assess poststroke depression have never been specifically validated in stroke patients. This study evaluated the depression screening abilities of three questionnaires and one observer-rated scale in 202 consecutive patients 1 month after they experienced their first-ever ischemic stroke. At their respective optimum cutoff values, the sensitivity of the self-rated scales varied between 80% and 90%, while the specificity was about 60%. For the observer-rated scale (Hamilton Depression Rating Scale), sensitivity was 78.1%, and specificity was 74.6%. The instruments clearly performed better in men than in women. Despite this difference, it was concluded that all scales were acceptable screening instruments for poststroke depression.

Aged↗