[Crazy Paving Pattern of the Lung]. / Pflastersteine in der Lunge.

Pulmonary alveolar proteinosis (PAP) is a rare pulmonary disease. PAP results from impaired surfactant clearance. In adults, autoimmune pulmonary alveolar proteinosis is present in 90 - 95 % of the cases. In 5 - 10 %, other etiologies such as toxins and dust exposure, hematological disorders and infections have to be considered. Men between 30 - 60 years are commonly affected. Typical symptoms are cough, dyspnea and alteration in ventilatory function. CT scan of the lung is characterised by a crazy paving pattern. In serological testing, granulocyte macrophage colony-stimulation factor can be identified in most patients with autoimmune pulmonary alveolar proteinosis. Whole-lung lavage remains the therapy of choice. In the current case, treatment with whole-lung lavage resulted in clinical and functional improvement.

[A food cognition questionnaire]. / Elaboration d'un questionnaire sur les cognitions alimentaires.

BACKGROUND: Many authors evoke the role of cognition in the persistence of symptoms or in relapse. In pathology the cognitions produced by the patients are called dysfunctional or erroneous. The content of the cognitions are words or images issued from the treatment of information. In emotional disorders, the structure of thoughts named dysfunctional "schemata" involves a biased treatment of information and leads to erroneous cognitions. Several studies have attempted to elicit the most specific cognitions of different diseases. In this field, Hollon and Kendall found 36 cognitions specific to depression gathered in the automatic thoughts questionnaire (ATQ). In the same spirit, Beck et al. gathered 14 cognitions of anxiety and 12 depressed cognitions in the cognition check list (CCL). In the etiology and maintenance of eating disorders the cognitions take a large place. Around 1980 cognitive dysfunctioning was described and concerned food, interpersonal relationship and body shape. A few years later, some experimental studies explored these processes. The Stroop test, a categorization task, showed specific cognitive impairment in with patients eating disorders versus normal control subjects. It was then established that cognitive errors were based on food cognitions in restrictive patients, whereas they were based on body shape cognitions in bulimic patients. In several famous papers, Garner described typical cognitions of eating disorder patients and distinguished food-cognitions, eating-cognitions using case reports. As far as we know there is no clinical tool concerning such cognitions in France. That is the main motivation of the authors. AIM OF THE STUDY: The aim of this paper was to determine the characteristic cognitions of anorexic, anorexic-bulimic and bulimic patients and to compare them with those of normal control subjects. The goal of the study was to create a food cognition questionnaire. FIRST STEP METHODS: In the first step, food cognitions were collected among female eating disorder patients and normal female control subjects during systematic investigation. Ninety-two women were assessed and provided more than 3 000 food cognitions. Two independent psychologists identified the most frequent cognition per group and thus retained 115 food items. These items were randomly assigned. This provided the questionnaire. To illustrate the latter, here are the first five items: 1) Apricots are good for the health because they are rich in vitamins. 2) Pears are big fruit, difficult to digest. 3) Canned fruit is soaked with sugar. 4) Banana is a fruit which makes one put on weight. 5) White coloured food give the impression that it is not alive... The list of possible answers was: never, rarely, sometimes, often enough, often, always. SECOND STEP METHODS: In the second step, the food cognition questionnaire was proposed to 217 women including 131 eating disorder patients (53 anorexic, 50 anorexic bulimic, 28 bulimic) and 86 normal control subjects. The values of body mass index and the eating attitude test differed when we compared the two groups, and the mean age was close to 26 years in both groups. RESULTS: The statistic analysis highlighted six discriminative variables: two clinical criteria (weight and height) and four food-items given below: Q24: When I see food being fried, I feel the grease all over my body. Q76: When I start a cookie packet, I eat it up. Q102: When I feel anxious, I crave for food to fill my body. Q106: Eating pastry gives me heart-burn and makes me belch. The statistical model allowed us to differentiate eating disorder patients from normal control subjects. The content of the four food items is in agreement with experimental and clinical data. All these items included some aspects of the quality or quantity of food and also the negative consequences of food consumption on the body. CONCLUSION: To conclude, the model can help clinicians identify the patients and then initiate treatment. We also insist on the fact that this study is new and empirical, and should be extended by determining some food items for example, which would clarify the difference of behaviour between anorexics and bulimics.

[Cognitions in eating disorders and their assessment]. / Les cognitions et leur évaluation dans les troubles des conduites alimentaires.

UNLABELLED: Cognitions are of crucial importance in the -aetiology and the maintenance of eating disorders. Dysfunctional cognitions in eating disorders are related to body image, self-esteem and feeding. The aim of this paper is to review the actual knowledge in this area. First, we will display -cognitive models in eating disorders. Cognitive factors in -eating disorders are logical errors, cognitive slippage and conceptual complexity. Eating disorder patients seem to have a deficient cognitive development. Some cognitive models stipulate that eating disorder patients may develop organised cognitive structures schemas concerning the issues of weight and its implications for the self. These schemas can account for the persistence and for the understanding the "choice of the eating disorder symptomatology. Cognitive pheno-mena of interest are self-schema, weight-related schema and weight-related self-schema. The maintenance model of ano-rexia nervosa argued that, initially there is an extreme need to control eating which is supported by low self-esteem. The maintenance of the disorder is reinforced by three mechanisms: dietary restriction enhances the sense of being in control; aspects of starvation encourage further dietary restriction; concerns about shape and weight encourage restriction. The development and maintenance of bulimic symptomatology are explained by placing a high value on attaining an idealised weight and body shape accompanied by inaccurate beliefs. The cognitive model of specific family of origin experiences puts forward the development of -maladaptative expectancies for eating and thinness. Second, we discuss distortions in information processing. a) In feeding laboratories, bulimics show a wide range of caloric intake and a disruption of circadian feeding patterns. In overeating bulimics, large meals occurred mainly during afternoon and evening with high fat and carbohydrate intake, but the majority of meals were of normal size and frequency. Responsivity to food cues indicates that bulimics were more responsive to sight, smell and taste of their favourite binge food, and a greater responsivity was associated with increasing -cue salience. Eating disorder patients appear to have internalised a mediated social rule concerning "good food" and make drastic selections thus removing the possibility of choice of foodstuffs. b) Experimental processes: temporal factors in the processing of threat seem to be of importance in patients with high levels of eating psychopathology. There is no evidence for preattentive processing biases among anorectics. Changes in information processing speed after treatment were not linked to treatment condition or treatment response. c) Judgement and emotions: in eating disorder patients, distortions of depressogenic nature are found that influence the cognitive style; thoughts about eating, weight and shape are characterised by negative affective tone; negative emotions could account for bulimic behaviour; anxiety and distress are correlated to thought control strategies. Information treating seems to be impaired in a non-homogeneous way. d) Cognitive schemas are seriously maladaptive and not well investigated. In eating disorder patients, core beliefs are absolute, unconditional and dichotomous cognitions about oneself and the world. There are only few studies in this field moreover showing controversial results. Core beliefs can explain links between personality disorders and eating psychopathology. Pathological core beliefs have to be taken in to account because they influence the outcome and the efficacy of cognitive behavioural therapy. Third, the last part of this paper summarises actually available rating scales eva-luating distorted cognitions in eating disorders. There are different methods for evaluation: specific and non-specific self-report questionnaires, thought-sampling procedures, -methods derived from cognitive psychology. The Mizes Anorectic Cognition questionnaire (MAC) is a well-known self-rating scale with good psychometric properties. The revised form of the MAC appears to be an improvement in the area of internal consistency, sensitivity, and reliability. It is obvious that there is no particular rating scale referring to specific cognitions on food. IN CONCLUSION: the main result of this literature review reflects that the cognitive treatment in eating disorders is altered in a specific way on an emotional basis and on self-representation.

[Self-esteem: a comparison study between eating disorders and social phobia]. / Estime de soi: étude comparative entre patients avec troubles de conduites alimentaires et phobiques sociaux.

Eating disorder patients evidenced very often a low self-esteem. Self-esteem in eating disorder patients is excessively based on body dissatisfaction. In eating disorders there seems to be a link between body image dissatisfaction and social anxiety. We hypothesised: self-esteem would be as low in eating disorder patients as in social phobia patients; self-esteem would be lower in eating disorder patients with social phobia than in patients with social phobia alone; self-esteem would be lower in eating disorder patients with depressive cognitions than in social phobia patients with depressive cognitions; self-esteem could have different characteristics in the two disorders; self-esteem would be as low in anorexia as in bulimia; 103 eating disorder patients (33 restrictive anorectics, 34 anorectics-bulimics, 36 bulimics) and 26 social phobia patients diagnosed according to DSM IV and ICD-10 criteria have been investigated by the Self-Esteem Inventory of Coopersmith, the Assertiveness Schedule of Rathus, the Fear Survey Schedule of Wolpe (FSS III) and the Beck Depression Inventory (BDI). Patients were free of medication and presented no episode of major depression according to DSM IV criteria. Evaluations took place before any psychotherapy. Self-esteem in eating disorder patients is reduced at the same level as in social phobia patients; 86.1% of the total sample and 84.5% of the eating disorder patients have a very low self-esteem (score 33 in the SEI). Eating disorder patients have significantly higher scores in the Social (p=0.016) and Professional (p=0.0225) sub-scales of the SEI than social phobia patients. Eating disorder patients show higher scores on the Assertiveness Schedule of Rathus (p=0.0013) than social phobia patients. Eating disorder patients disclose higher scores on the BDI (p=0.0003) but eating disorder patients with depressive cognitions do not differ from social phobia patients with depressive cognitions in the level of self-esteem. The FSS III scores are significantly lower in eating disorder patients (p<0.0001). There is a difference in the nature of the deficit of self-esteem between the two patient populations. Self-esteem is not influenced by the Body Mass Index (BMI) and is identically reduced in all groups of eating disorder patients. Whereas eating disorder patients have the same complaints compared to social phobia, they differ significantly from social phobia patients in their characteristics of social phobia and self-esteem.

Reward craving and withdrawal relief craving: assessment of different motivational pathways to alcohol intake.

AIMS: Craving for the rewarding effects of alcohol may be evoked by conditioned alcohol-like effects whereas conditioned compensatory responses may induce withdrawal relief craving. We tested the hypothesis that drinking in positive emotional states is associated with appetitive reactions to alcohol-associated cues and contributes to reward craving, while conditioned withdrawal is associated with drinking in negative situations and distressful, obsessive preoccupations with alcohol. METHODS: In 38 detoxified alcoholics, the Obsessive Compulsive Drinking Scale was used to assess the craving factors 'impaired control', 'interference with social functioning' and 'obsession'. Affective responses to alcohol-associated visual stimuli were measured with the affect-modulated eyeblink startle reflex, positive and negative drinking situations with the Inventory of Drinking Situations (IDS) and withdrawal-like symptoms preceding alcohol intake with the revised Clinical Institute Assessment for Alcohol Scale (CIWA-Ar). RESULTS: Appetitive reactions to alcohol-associated cues correlated positively with drinking in positive situations and contributed significantly to the craving factor 'interference' with social and work functioning. The severity of withdrawal-like symptoms preceding alcohol intake contributed to the craving factor 'obsession'; however, contrary to our hypothesis, this measure of conditioned withdrawal correlated with drinking not only in negative but also in positive situations. CONCLUSIONS: Drinking in positive and negative situations, appetitive reactions to alcohol and withdrawal-like symptoms contributed differentially to the craving factors 'obsession' and 'interference', supporting the notion of different craving factors with separate underlying mechanisms.

[Actual approaches to post-psychotic depression]. / Approche actuelle des dépressions post-psychotiques: une mise au point.

Clinical features of post-psychotic depression in schizophrenia have been described since the beginning of the century. However, international nosographies mention this concept only since the ICD 10 and the DSM IV. In clinical practice, post-psychotic depression is a real challenge. Currently, the exact prevalence remains undetermined and is estimated about 25%, varying from 7 to 70% in the literature. The diagnostic criteria nowadays available will encourage searchers to determine the exact prevalence of post-psychotic depression. This is surely due to difficulties in the diagnostic approach. The clinical picture resembles that of major depression. However, there are confounding factors such as negative symptoms and extrapyramidal symptoms. With regard to psychometrics, two specific rating scales are thought to measure depressive symptoms in schizophrenia: the Calgary Depression Scale (CDS) and the Psychotic Depression Scale (PDS). Nonetheless, the scales are not specific for post-psychotic depression. Prognosis of an acute schizophrenia is linked among other factors with the emergence of a post-psychotic depression that is in turn influences suicidal risk and quality of life. Genetic, therapeutic, psychodynamic and psychological factors have been invoked in the etiopathogenesis of post-psychotic depression. In clinical practice, post-psychotic depression can be successfully treated with antidepressive medication. Some antidepressants have shown their efficacy.

[Correlation between eating disorders and sleep disturbances]. / Relations entre trouble des conduites alimentaires et perturbations du sommeil.

Anorectics and bulimics often complain sleep onset insomnia and disrupted sleep. During awakenings bulimics can have binges. Conversely, eating disorders can be a clinical expression of a concomitantly occurring sleep disorder. Two clinical entities have been recently described: the Night Eating Syndrome (NES) and the Sleep Related Eating Disorders. The main goal of this literature review was to better characterize the relationships between eating disorders and sleep disturbances. No specific EEG sleep pattern emerges in anorectic and bulimic patients. However, all studies include several methodological limitations: a few number of patients, heterogeneous patient groups, various diagnostic criteria. The results of studies evaluating the impact of depression on sleep EEG in eating disorder patients are also subject to controversy. The only study examining the relationship between sleep EEG and morphological alterations in anorectics and normal weight bulimics shows that patients with enlarged cerebrospinal fluid spaces spent more time in slow wave sleep and that the duration of rapid eye movement (REM) sleep was reduced. The ventricular brain ratio was negatively correlated with REM sleep. The Night Eating Syndrome consists in insomnia, binge eating and morning anorexia. Other criteria are proposed to characterize the NES: more than 50% of the daily energy intake is consumed after the last evening meal, awakenings at least once a night, repetition of the provisional criteria for more than 3 months, subjects do not meet criteria for bulimia nervosa or binge eating disorder. Patients have no amnesia nor alteration of alertness, and no other sleep disorder. There is no modification of sleep EEG except sleep maintenance. The prevalence of the NES is 1.5% in the general population. Some neuroendocrine disturbances have been found in the NES. The delimitation with eating disorders is not yet clearly established. If it shares the compulsive features with eating disorders, particularly the "Binge Eating Disorder", and occurs during full awakenings, the night eating syndrome may be recognized as a specific eating disorder. The sleep related eating syndrome is also characterized by compulsive binge eating during awakenings. But in this case, night eating is linked with a reduced consciousness and sleep disorders, mainly somnambulism. Patients never experience hunger, abdominal pain, nausea or hypoglycemia. Night-eating takes place invariant across weekdays, weekend and vacations. Patients consumed high caloric foods and fluids but never alcohol and purging does not occur. Diurnal bulimia is frequently associated with the sleep-related eating disorder. In conclusion, the sleep related eating disorder seems rather be a clinical subtype of sleep disorders whereas the NES could be considered as an eating disorder.

[Polysomnographic aspects of antidepressive therapy]. / Aspects polysomnographiques des thérapeutiques antidépressives.

Sleep disorders are very common in depression. They have been quantitatively and qualitatively described by polysomnographical recordings. It is of interest to know how treatments act on polysomnographical data. In this article, we propose to evaluate five treatment approaches proposed for depressive illness. Pharmacological treatment induces marked changes in sleep continuity, sleep architecture and REM sleep. However, no specific sleep profiles emerge neither for each treatment class nor for molecules within the same pharmacological class. But actually, sleep data cannot be viewed as markers of treatment response. Psychotherapeutic interventions have only few effects on sleep of depressed patients. Treatment efficiency does not seem to be correlated to abnormal sleep parameters. Sleep deprivation induces marked changes in nearly all sleep parameters and in temporal distribution of sleep stages during the night. Actually, the efficiency of sleep deprivation cannot longer be explained by suppression of REM sleep. Sleep deprivation has only a transient effect and treatment indications are therefore secondary. Sleep parameters do not distinguish responders from non-responders. Sleep deprivation shows that there is a depressogenic effect of sleep in the end of the night. Bright light therapy shows marked changes in sleep continuity parameters. Among all studies that examine the impact of treatment on sleep EEG, ECT has received little attention. The few studies available are either case studies or with poor effectifes++. For this reason and because of methodological bias, results are heterogeneous and no definite conclusions can be drawn. But all of them agree that ECT modifies sleep EEG. So, changes in polysomnographical data cannot predict response to any treatment. Prospective sleep studies are difficult to realise on a great number of patients explaining absence of treatment predictors.

[Sleep electroencephalography in depression and mental disorders with depressive comorbidity]. / La valeur de la polysomnographie dans la dépression et les pathologies mentales avec comorbidité dépressive.

Traditional scoring of sleep EEG in depressed patients shows abnormalities in sleep maintenance, sleep architecture, REM sleep, the distribution of slow wave and REM sleep during the night. Computerized analysis that comprises the period-amplitude analysis procedure and spectral analysis discloses changes in delta activity and distribution of delta activity. However, these methods of analysing EEG sleep are not able to distinguish the various concepts of depression: endogenous and non-endogenous depression, unipolar and bipolar depression, psychotic and non-psychotic depression. Polysomnographical data in patients with recurrent depression show alteration during remission suggesting trait-like abnormalities of sleep in depression illness. Shortened REM latency is not specific in depression. This sleep parameter is defined in many different ways explaining the heterogeneousness of study results and the failure of constituting a biological marker. Many sleep parameters are affected by several factors such as age, gender and severity. Several physiopathological hypotheses have been proposed to explain EEG sleep alterations. They refer either to circadian rhythms such as the two process model of Borbély, the phase advance hypothesis and the circadian amplitude hypothesis, or to neurotransmitter abnormalities such as the cholinergic hypothesis. None of them takes sufficient account of all the sleep abnormalities. Sleep abnormalities have also been described in other psychiatric disorders such as mania, panic and obsessional-compulsive disorders, generalized anxiety, phobias, post-traumatic stress disorder, eating disorders, borderline personality, schizophrenia and dementia. None of them have a particular sleep EEG profile which allows to differentiate between them. A concomitant episode of major depression cannot be uncovered by sleep recordings.

[Heroin abuse, autobiographical memory and depression]. / Héroïnomanie, mémoire autobiographique et dépression.

The early psychiatric interviews with opiate addicts are characterized by three features: 1) the patient has a very factual and objective conversation, 2) the evaluation of the autobiographical memory is very difficult, 3) there is a high prevalence of affective disorders responsible for an impairment in cognitive functions. Therefore we have two aims: First, to compare episodic and semantic autobiographical memory in opiate addicts and healthy controls. Autobiographical memory is the knowledge a person has about oneself and his past. Personal semantic memory is the knowledge of the biographical facts, general knowledge and beliefs about oneself. Autobiographical episodic memory concerns recollections of personal events clearly delineated in time and space. Second, to estimate the impact of depression on the ability to produce autobiographical recollection in a population of opiatre addicts. Participants were consecutive attenders of a methadone outpatient clinic who are multiple drug dependent patients consuming mainly heroine. The first investigation took place in entry and after two months. We have recruited 21 patients with a mean duration of intoxication of 11 years. Ten of these patients have been investigated again after 2 months and 8 of them have been included in a methadone maintenance program. The patients'investigation comprised two parts: first, the evaluation of autobiographical memory (only assessed at entry of the study) with an autobiographical fluency test and the semi-structured autobiographical memory interview of Kopelman; second, the psychiatric assessment included self-rating questionnaires and observer-rating questionnaires. Opiate addicts showed a decrease in episodic autobiographical memory but an increase in semantic affective memory and objective modalization. In the fluency test, there was no difference in the number of evoked items between opiate addicts and healthy controls. The educational level influences several results. The possible explanations of these results are the action of the toxic products and a particular psychic functioning. The lack of correlation between autobiographical memory and affective disorder suggests the implication of the drugs in the emergence of memory deficits. The improvement of depressive symptomatology after two months occurring without psychotropic drugs suggests the transient feature of depression and emphasises on non-pharmacological aspects of treatment.

[Associations and interactions: tricyclic antidepressants and selective serotonin reuptake inhibitors]. / Associations et interactions: les antidépresseurs tricycliques et les inhibiteurs spécifiques de la recapture de la sérotonine.

Following the commercialization of the SSRIs clinicians described cases of drug interactions with tricyclic antidepressants among their patients. When combining tricyclic antidepressants and SSRIs clinical side effects and elevated plasma levels of tricyclics appeared. A better knowledge of the cytochrome P450 system allows to understand the mechanism of such drug interactions. The cytochrome P450 is composed of a group of isoenzymes, which are classified, into families and subfamilies on the basis of amino acid sequence homology. A number of the cytochrome genes have a genetic polymorphism responsible for poor and extensive metabolisers. The clinical importance of genetic polymorphism is highly dependent upon the therapeutic index. Thus, poor metabolisers, will experience side effects and rapid metabolisers prone to therapeutic failure. Concerning pharmacological issues SSRIs have a great affinity for at least one of the isoenzymes which accounts for drug interactions. Due to the inhibitory potential of the SSRIs drug interactions occur with tricyclics that have a narrow therapeutic index. The SSRIs do not exert the same inhibitory effect on the various isoenzymes. The inhibitory activity for an isoenzyme depends on the molecule of the SSRIs. In clinical practice, the associations between tricyclics and SSRIs should be practiced with caution. It is recommended to decrease the tricyclic dose before administering the SSRI, to start with low doses of the SSRI and to take into account the therapeutic index. Although the coadministration of tricyclics and SSRIs can produce adverse reactions it has also two main interests in clinical practice. First, the drug combination enhances clinical response to treatment. Secondly, it converts non-responders of pharmacological treatment to responders. Used with caution the association of tricyclics and SSRIs is well tolerated. However, it should be kept in mind that a single drug therapy should be tried first. These data show the complexity of drug interactions.

Perioperative pattern of peritoneal interleukin 8, tumour necrosis factor-alpha, and granulocyte elastase release in human secondary peritonitis.

Cytokine levels during infection and sepsis have been extensively studied in the past. In contrast to the excellent data on tumour necrosis factor alpha (TNF-alpha), interleukin 8 (IL-8), and polymorphonuclear (PMN) granulocyte elastase (PMN-E) concentrations in blood, little is known about cytokine and PMN-E levels in tissue or local fluids like abdominal exudate in secondary, purulent peritonitis of man. Therefore, the authors studied perioperative intra-abdominal levels of TNF-alpha, IL-8 and PMN-E in 21 patients with severe purulent peritonitis. The average pre-operative levels of TNF-alpha were 694 +/- 239 pg/ml in exudate and 26 +/- 6 pg/ml in plasma, for IL-8 100 +/- 34 ng/ml and 0.7 +/- 0.5 ng/ml, and for PMN-E 68 +/- 14 microg/ml and 0.7 +/- 0.1 microg/ml, respectively. Standard surgical procedures reduced the intra-abdominal concentrations of cytokines and PMN-E to as low as one tenth of the pre-operative levels. Postoperatively, TNF-alpha and IL-8 levels recovered rapidly and pre-operative levels of IL-8 were reached again after 1 h and for TNF-alpha after 8 h. PMN-E concentration remained below the initial baseline within 8 h of observation. TNF-alpha concentration, but not IL-8 or PMN-E, depended on the microbiological load of the abdominal exudate (< or > 10(3) cfu/ml). There were no significant differences in the intra-abdominal or plasma levels of cytokines or PMN-E between survivors and non-survivors at any observation time.

Phobic symptoms, particularly the fear of blood and injury, are associated with poor glycemic control in type I diabetic adults.

OBJECTIVE: To investigate the presence of psychiatric disorders and symptoms in type I diabetic patients and to identify those that may influence metabolic control as assessed by GHb levels. RESEARCH DESIGN AND METHODS: This was a cross-sectional study. One hundred and two consecutive patients with type I diabetes who were regular outpatient visitors of a diabetology department were evaluated. The psychiatric assessments included self-rating questionnaires (General Health Questionnaire and Fear Questionnaire) and observer-rating questionnaires (Montgomery-Asberg Depression Rating Scale [MADRS] and Mini International Interview). Diabetic characteristics were assessed by a structured interview. The observer was blind to the diabetic characteristics of the patients. RESULTS: Type I diabetic patients with GHb levels > or = 8% had higher psychological distress, scored significantly higher for symptoms of agoraphobia and for fear of blood and injury, had substantially higher levels of anxiety-depression, and performed significantly fewer blood glucose measurements per day. They did not differ in MADRS score from patients with GHb levels < 8%. Multivariate analysis showed that GHb was positively associated with the total score of phobic symptoms and the level of anxiety-depression and inversely associated with the number of daily blood glucose measurements. These factors explained 41% of the variance of GHb. The inverse relationship between GHb and the number of blood glucose measurements per day was mainly influenced by the fear of blood and injury. Patients with high scores for the fear of blood and injury performed fewer blood glucose measurements and had poorer glycemic control; conversely, subjects without fear of blood and injury performed more daily blood glucose measurements and had better glycemic control. CONCLUSIONS: Phobic symptoms are frequent in patients with type I diabetes. The intensity of phobic symptoms and anxiety-depression negatively influences metabolic control. Increased fear of blood and injury may lead some patients to perform few home blood glucose measurements and may result in poorer glycemic control. This suggests that, by decreasing the fear of blood, injury, and injection, metabolic control may be improved.

[Insulin-dependent diabetes and psychiatric pathology: general clinical and epidemiologic review]. / Diabète insulino-dépendant et pathologie psychiatrique: revue générale clinique et épidémiologique.

Insulin dependent diabetes mellitus is one of the most common metabolic diseases and affects 150,000 persons in France. To achieve good metabolic control requires a strict daily management of the treatment by the patients themselves. Lack of active involvement can have direct consequences which underlines the importance of a good adherence to the treatment. About 50% of the patients do not obtain adequate metabolic control. The major problem of insulin treatment consists in the repeated occurrence of severe hypoglycemias which may be accompanied by an alteration of the perception of hypoglycaemic signs. On the other hand, when the risk of severe hypoglycaemia is removed, glycosylated haemoglobin levels rise. Permanent hyperglycaemia leads to numerous somatical complications. An extremely dramatic combination of these two types of metabolic unbalance is represented by the brittle diabetes characterised by very frequent and extreme oscillations between hypo and hyperglycaemia. This raises the question of the influence of psychopathological factors on metabolic control and the possibility of improving metabolic control by acting on these factors. Epidemiological studies in diabetic patients have established higher prevalence rates of psychiatric disorders, in particular mood and anxiety disorders. The current prevalence rate of depression was found to be homogeneous in the literature about 11% and life time prevalence rates of major depressive disorders vary between 24% and 29%. The symptom profile of depression in diabetic patients is similar to that in depressed non diabetic psychiatric patients and it has been shown that highly sensitive psychiatric diagnosis of depression can be made among diabetic patients. There is no specific personality pattern in diabetic patients. There seems to be a relationship between metabolic control as defined by glycosylated haemoglobin and psychiatric disorders. Indeed, high levels of glycosylated haemoglobin are found in patients with psychiatric disorders. There seems to be some evidence of an association between blood glucose levels and actual emotional states. Nothing is known about the specificity of the link between psychiatric disorders and insulin-dependent diabetes mellitus. No study has evaluated if the relationship between psychiatric disorders and insulin-dependent diabetes mellitus is due to the disease itself or to the chronic feature of diabetes.