Risk factors for eating disorders in Italian adolescents.
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Biomedical subjects
Publications and source records attributed to C Marchesi.
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OBJECTIVE: This study was undertaken to assess the prevalence of obsessive-compulsive symptoms in a population of Italian adolescents. METHOD: A sample of 2877 high-school students, 1463 males (51%) and 1414 females (49%), aged 16-21 years were assessed with the Leyton Obsessional Inventory--Child Version (LOI-CV). Two groups of subjects were defined as 'positive' on the screen: the high interference (HI) (i.e. all subjects who scored 25 or more in the interference score), and the supernormals (Sn). RESULTS: Females scored higher than males both on yes and interference scores. One hundred and nineteen (4.1%) and 87 (3.0%) constitute, respectively, the HI and the Sn groups. The most interfering symptoms were obsessions linked to dirt phobia, rumination and nail biting. CONCLUSION: The prevalence estimates of OCD symptoms confirmed the recent data of the literature that adolescent OCD symptoms are more frequent than was believed previously. Females showed more symptoms and more interference on personal functioning than males.
OBJECTIVE: To determine the circulating levels of nerve growth factor (NGF), neuropeptide Y (NPY), and vasoactive intestinal peptide (VIP) in systemic sclerosis (SSc), and to correlate these levels with clinical and laboratory features. METHODS: Forty four patients with SSc were evaluated for circulating NGF (immunoenzymatic assay), NPY and VIP (radioimmunoassay), anticentromere and antitopoisomerase I autoantibodies, lung disease (pulmonary function tests with carbon monoxide transfer factor (TLCO), ventilation scintiscan with 99mTc DTPA radioaerosol, high resolution computed tomography (HRCT), pulmonary pressure (echo colour Doppler)), heart disease (standard and 24 ECG, echocardiography), cutaneous involvement (skin score), joint involvement (evidence of tender or swollen joints, or both), peripheral nervous system (PNS) involvement (electromyography), rheumatoid factor, angiotensin converting enzyme (fluorimetric method), von Willebrand factor (ELISA), and erythrocyte sedimentation rate (ESR) (Westergren). RESULTS: Circulating NGF levels in SSc were significantly increased compared with controls (p<0.00001) and significantly higher in the diffuse than in the limited subset of patients (p<0.01). Patients with articular disease had significantly higher levels of NGF. A significant indirect correlation between NGF levels and TLCO was detected (p<0.01), but no correlation was found between NGF and HRCT, DTPA, skin score, PNS involvement and angiotensin converting enzyme and von Willebrand factor levels, antitopoisomerase or anticentromere antibodies, and ESR. NGF levels increased progressively as the disease worsened. Similarly, VIP circulating levels were significantly increased in patients with SSc (p<0.001), whereas the increase of NPY levels did not reach statistical significance. However, both neuropeptides, following the same trend as NGF, increased as the disease worsened (skin score and lung disease). CONCLUSIONS: The increase of NGF and VIP in patients with SSc, the former in the diffuse subset of the disease, and in patients with prominent articular disease, may suggest a link between neurotransmitters and the disease pathogenesis. Neuropeptide circulating levels seem to increase only in patients with the most severe disease.
OBJECTIVE: The present study examined patients during the year after the index hospitalization in an Emergency Ward (ED) to determine whether patients with depressive or anxiety disorders have a higher rate of readmission than patients without these conditions. METHOD: For this purpose, 165 subjects (85 diagnosed with DSM-IV depressive or anxiety disorders and 80 controls) were evaluated with the Hospital Anxiety and Depression Scale (HADS) and with the Duke Severity of Illness Scale both during the index hospitalization and one year later. Hospitalizations during the follow-up period were determined using the hospital database. RESULTS: During the follow-up period, depressed and anxious patients were more frequently rehospitalized in ED wards than controls (p = 0.006), after controlling for the effect of medical illnesses severity, marital status, living arrangement, and employment status. No difference was found regarding the admissions to wards different from ED. CONCLUSIONS: Patients with depressive or anxiety disorders use the ED ward more frequently than controls for the diagnosis and treatment of somatic symptoms.
OBJECTIVE: the present study was undertaken to gain a better insight into the relationship between alexithymia, anxiety, and depression. Two hypotheses were tested: (1) whether a depressive or anxiety disorder is associated with an elevation of one or more dimensions of alexithymia; and (2) whether alexithymia is an independent construct from depression and anxiety in patients with depressive or anxiety disorders. METHOD: a total of 113 patients with depressive or anxiety disorders (DSM-IV) and 113 control subjects completed the 20-item version of the Toronto alexithymia scale (TAS-20) and the hospital anxiety and depression scale (HADS). RESULTS: the TAS-20 total score was higher in depressed and anxious patients than in controls. This finding mainly depended on an increased score for "difficulty identifying feelings"(DIF), and (only in depressed patients) on an increased score for "difficulty communicating feelings" (DCF). The factor analysis of the TAS-20 and HADS items showed that depression is a construct different from alexithymia, whereas some overlap exists between anxiety and DIF dimension. CONCLUSION: our results suggest that in depressive and anxiety disorders, alexithymia and depression are separate constructs that may be closely related; in contrast, there are some overlaps between the DIF dimension and anxiety.
We analyzed the 1986-1997 mortality in a cohort of 2065 residents of an Italian municipality which had been exposed to drinking water with a high content of inorganic selenium over a long period of time, and compared it with mortality in the remainder of the municipal population. Mortality from malignant neoplasms increased [standardized mortality ratio (SMR) 1.17, 95% confidence interval (CI) 0.96-1.42], mainly due to an excess mortality from melanoma and colorectal cancer in both sexes, kidney cancer in men, and lymphoid malignancies in women. Overall cardiovascular mortality changed little (SMR 1.05, 95% CI 0.89-1.23), despite the higher cerebrovascular mortality (SMR 1.43, 95% CI 1.03-1.93). Coronary disease mortality slightly decreased (SMR 0.87, 95% CI 0.63-1.16), due to a low mortality among women. We also noted an excess mortality from Parkinson's disease in men and from motor neuron disease in women. Evaluation of these findings is, however, hampered by the lack of information about potential lifestyle confounders, the fact that the exposure could only be characterized by a simple dichotomization, and the inconsistencies of most estimates between the two sexes.
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OBJECTIVE: We tested the possibility that lysine vasopressin (LVP) changes the GH responsiveness to exogenously administered GH-RH (at its minimal and maximal doses), clonidine (which is thought to stimulate endogenous GH-RH release) and arginine (which is thought to inhibit somatostatin) in patients with type 1 diabetes mellitus and normal subjects. DESIGN AND PATIENTS: Normal male subjects (NC) and age- and weight-matched insulin-dependent diabetic men (DM) with good metabolic control were studied. An iv bolus of LVP at a dose (15 microg/kg body weight (BW)) lower than the minimal GH releasing effective dose was injected just before the I.V. injection of the minimal effective dose of GH-RH (0.035 microg/kg BW) in 10 NC and 10 DM, the I.V. injection of the maximal effective dose of GH-RH (100 microg) in 7 NC and 7 DM, the I.V. infusion of arginine (30 g over 30 min) in 7 NC and 8 DM or the oral administration of clonidine (150 microg) in 7 NC and 8 DM. On different occasions, GH stimuli, LVP or normal saline were given alone to the same normal and diabetic subjects. MEASUREMENTS: GH responses in the presence and absence of LVP were measured and compared within each group and between normal and diabetic groups. RESULTS: LVP or normal saline administration did not modify the basal concentrations of GH in any subject. The administration of GH-RH (at the minimal dose), arginine or clonidine alone induced significantly higher GH responses in the diabetic subjects than in the normal controls. At the maximal dose GH-RH induced similar GH responses in normal and diabetic subjects. The simultaneous administration of LVP did not change the GH response to any challenging stimulation in the normal controls; in contrast, GH-RH- (at both minimal and maximal dose), arginine- and clonidine-induced GH increments were significantly enhanced by LVP in the diabetic subjects. CONCLUSIONS: These data show that in diabetic, but not in normal subjects LVP enhances the GH responsiveness to secretagogues, such as GH-RH, clonidine and arginine, which act through three different mechanisms. These findings suggest that in diabetes mellitus, vasopressin functions as a primer for various GH responses.
This paper describes a system for electronic medical record (EMR) we have developed for use in our health care institution, mainly dealing with diagnosis and treatment of cardiovascular pathologies. This activity is part of the project SPERIGEST, supported by Health Ministry of Italy, for the management of health care delivery, as concerns both clinical and administrative aspects. A networked computer-based information system was realized to integrate the different heterogeneous sources of patient information. Both clinical and administrative patient relevant data are provided from the various systems and stored into a central database. The EMR system was designed using World Wide Web (WWW) technology (Java, HTML). The system is currently under clinical evaluation.
The effect of melatonin (MEL) (12 mg orally), pyridostigmine (60 mg orally), the combination of MEL and pyridostigmine, or placebo on growth hormone (GH) secretion was tested in seven normal men. In addition, MEL tests and pyridostigmine tests were repeated after pretreatment with naloxone (1.2-mg bolus followed by intravenous [i.v.] infusion of 1.6 mg/h for 3 hours). Serum GH levels increased fivefold after MEL and sixfold after pyridostigmine administration. The concomitant administration of MEL did not change the GH response to pyridostigmine. In the presence of naloxone, the GH response to MEL was completely abolished, whereas naloxone did not modify the pyridostigmine-induced GH increase. These data suggest that MEL and pyridostigmine stimulate GH secretion through a common mechanism, which is probably represented by the inhibition of somatostatin activity. However, in contrast to pyridostigmine, the action of MEL appears to be exerted through a naloxone-sensitive opioid mediation.
Primary organic disorders of the thyroid gland must be excluded in interpreting the thyrotropin (TSH)-releasing hormone (TRH) test in affective disease. Both endogenous depression and subclinical thyrotoxicosis are frequently associated with low basal TSH levels and a blunted (<5 mIU/L) TSH response to TRH despite thyroid hormone levels within the normal range. The present study was performed to establish whether a reduction of the hypothalamic somatostatinergic tone by treatment with the acetylcholinesterase inhibitor pyridostigmine before TRH might be useful to distinguish endocrine from affective diseases. Twelve male depressed patients (aged 41.4 +/- 3.1 years) and 12 men (aged 43.4 +/- 4.1 years) with subclinical thyrotoxicosis because of autonomous thyroid nodules were selected according to the presence of a low basal TSH level and a blunted TSH response to 200 microg TRH intravenously (IV) (TSH increment was <5 mIU/L at 30 minutes [peak] after TRH) but thyroid hormone levels within the normal range. All patients were tested again with TRH 60 minutes after treatment with 180 mg pyridostigmine orally. Eleven normal men served as controls. Basal TSH levels were 0.2 +/- 0.2 mIU/L (mean +/- SE) in depression and 0.1 +/- 0.2 in subclinical thyrotoxicosis (normal controls, 1.4 +/- 0.3). In both groups, the mean peak response to TRH was significantly higher than baseline; however, according to selection, the TSH increase was less than 5 mIU/L. Pyridostigmine did not change basal TSH levels in any group, but significantly enhanced the TRH-induced TSH increase in normal controls and in depressed subjects (TSH increment became >7 mIU/L in all depressed subjects). In contrast, no significant change in the TSH response to TRH was observed in subclinical thyrotoxicosis after pyridostigmine treatment. Basal and TRH- and pyridostigmine + TRH-induced TSH levels were significantly higher in the normal controls than in the other groups. These data show a cholinergic involvement in the blunted TSH response to TRH in patients with endogenous depression, but not in subjects with subclinical thyrotoxicosis, suggesting that these diseases could be separated on the basis of the pyridostigmine + TRH-induced TSH response test.
Whether fluoxetine (FX) is effective in the treatment of anxious depression is still debated. In the present study, after one week of placebo (single blind), 142 outpatients affected by major depression with relevant anxiety and agitation were randomly assigned (double blind) to either FX (20 mg/day) (n. 67) or amitriptyline (AM) (daily dose: 115+/-39.2mg) (n.75) for a period of 10 weeks. Between groups, the mean score of Hamilton Rating Scale for Depression (HRSD) was significantly different only after 3 weeks of treatment (AM 14.7+/-5.7 vs FX 17.3+/-6.2 (p = 0.02), whereas at the end of the trial it was similar (AM 8.15+/-6.9; FX 8.96+/-6.6). At each visit, no significant difference between groups was found regarding the scores of the HRSD items "psychic anxiety", "somatic anxiety", "agitation". Furthermore, the FIX treatment did not increase the scores of the items "suicide", "psychic anxiety", "somatic anxiety", "agitation" and "insomnia". These findings suggest that patients affected by major depression with anxiety and/or agitation were effectively and safely treated with FX without increasing risks.
The circadian secretion of beta-endorphin, adrenocorticotropic hormone (ACTH), and cortisol was evaluated in 14 non-cirrhotic alcoholic men after 7 and 28 days of abstinence and in 12 sex- and age-matched normal subjects. A significant decrease in plasma levels of beta-endorphin, reduced ACTH levels, and increased cortisol levels were observed in samples taken at 08.00 h, 12.00 h, 18.00 h, and 23.00 h both after 7 and 28 days of abstinence. These data suggest the presence of a strong negative feedback on pro-opiomelanocortin synthesis by cortisol hypersecretion in abstinent alcoholics, which might be due to long-term stimulation of adrenal function by alcohol. The decreased plasma beta-endorphin levels might predispose to relapse in alcohol abuse.
The present study was performed in order to establish whether melatonin (MEL) plays a role in the regulation of arginine vasopressin secretion (AVP) in normal human subjects. For this purpose, the effects of an oral administration of 6 or 12 mg MEL on basal and metoclopramide (MCP)- or hypoglycemia-stimulated AVP secretion was tested in 18 normal men. MCP was given at a dose of 20 mg as an intravenous (i.v.) bolus; hypoglycemia was induced with an i.v. bolus injection of 0.15 IU/kg body weight of insulin. In addition, in view of the well-known inhibitory effect of MEL on the growth hormone (GH) response to hypoglycemia, GH levels were measured during the insulin tolerance test (ITT), as an independent index of MEL activity. MEL did not produce any change in AVP secretory patterns in basal conditions or during the MCP test. In contrast, the mean peak AVP response to hypoglycemia was 2.33 times higher than baseline in the control ITT, whereas it was only 1.77 times higher than baseline in the ITT plus MEL tests. Also, the GH response to hypoglycemia was significantly lower in the presence than in the absence of MEL. For both AVP and GH, the inhibitory effect of MEL during ITT was similar, when either 6 or 12 mg MEL was given. These data indicate an involvement of MEL in the control of the AVP response to hypoglycemia, but not of basal and MCP-induced AVP secretion. In addition, the similar effects of MEL on GH and AVP secretions during ITT suggest that similar neuroendocrine mechanisms underlie these hormonal responses to hypoglycemia.
1. Plasma oxytocin (OX), vasopressin (VP), estrone (ES) and beta-endorphin (beta-end) levels were measured in 13 male non-chirrotic alcoholics, at 1, 4, 7, 15 and 28 days after alcohol withdrawal and only once in 9 sex- and age-matched normal controls. 2. At all examined time points, plasma OX and ES, but not VP, levels were significantly higher in alcoholics than in controls. Alcoholics showed plasma beta-end levels lower than normal. 3. A positive relationship was found between ES and OX levels suggesting that elevated estrogens levels in chronic alcoholics might exert a stimulatory effect on OX. 4. In light of the well-known effect of OX on learning and memory, an involvement of OX in alcohol-induced neuropsychological deficits may be supposed.
OBJECTIVE: Several alterations in hypothalamo-pituitary-thyroid (HPT) function have been described in diabetes mellitus and have been attributed to metabolic decompensation. The present study was performed in order to establish whether residual endogenous insulin secretion in patients with insulin-dependent diabetes mellitus (IDDM) may play a role in the control of HPT function. DESIGN: The nocturnal (2230 h-0200 h) serum TSH surge, the TSH response to TRH (200 microgram as an i.v. bolus) and serum free thyroid hormone levels were evaluated in C-peptide positive (CpP) (subjects with residual detectable endogenous pancreatic beta-cell activity) and C-peptide negative (CpN) patients both before and after optimization of metabolic status by 3 days of treatment with continuous subcutaneous insulin infusion, and in normal controls. TSH response to TRH and serum free thyroid hormone levels were assessed in the morning. SUBJECTS: Twenty male diabetic patients hospitalized to achieve a better control of hyperglycaemia were subdivided into 10 CpP (age: 33 +/- 1.5 years (mean +/- SE); body mass index (BMI): 22.6 +/- 0.3) and 10 CpN (age: 32 +/- 1.7 years; BMI: 22.5 +/- 0.4) patients. Nine normal men (age: 34.0 +/- 1.2 years; BMI: 23.1 +/- 0.4) served as controls. MEASUREMENTS: The nocturnal serum TSH peak was measured by dividing the highest night-time TSH value by the next morning TSH value and then multiplying by 100. Serum TSH levels were measured in samples taken just before (time 0) and 30 minutes, after TRH administration. Serum free thyroid hormone levels were measured in samples taken at time 0 of the TRH test. RESULTS: Before improvement of hyperglycaemia, CpP and CPN patients showed similar alterations in HPT function; i.e. serum free T3 levels and TSH responses to TRH were lower than normal; the nocturnal TSH surge was absent. Correction of hyperglycaemia normalized all examined HPT parameters in CpP diabetics, whereas normalization in serum free T3 levels and pituitary TSH responsiveness to TRH in CpN patients was not accompanied by restoration of the nocturnal TSH peak. CONCLUSIONS: These data indicate that the absence of residual pancreatic beta-cell function in patients with insulin-dependent diabetes mellitus is associated with neuroendocrine dysfunction in the regulation of circadian TSH secretion, which is not reversible after restoration of good glycaemic control.
Personality and temperament features, assessed with the Structured Interview for DSM-III-R Personality Disorders-Revised (SIDP-R) and the Tridimensional Personality Questionnaire (TPQ), respectively, were evaluated in 62 patients affected by panic disorder with (PD + MD) (n = 22) or without comorbid mood disorder (PD) (n = 40). A significant difference in the prevalence of personality disorders (PD + MD, 86% vs. PD, 62%; P < 0.05), particularly dependent (PD + DM, 50% vs. PD, 17%; P < 0.01) and borderline (PD + DM, 9% vs. PD, 0%; P = 0.05) personality disorders, was observed between the groups. Moreover, patients in the PD + MD group had higher scores for harm avoidance (PD + MD, 22.2 +/- 5.6 vs. PD, 26.9 +/- 5.1; P < 0.05) than patients in the PD group. The harm avoidance score in PD patients was significantly related to personality disorder and not to MD, suggesting that harm avoidance is not associated with greater severity of the illness. Our data confirm the hypothesis that subjects with higher harm avoidance scores have a greater probability of being affected by cluster C personality disorders and comorbid mood and anxiety disorders.
In order to evaluate the tuberoinfundibular endogenous dopaminergic tone in alcoholic subjects, the inhibitory effect of an infusion of dopamine (3 micrograms/kg/min for 2 h) on PRL secretion was tested in 11 alcoholics after 4 weeks of abstinence. On different days alcoholics were tested with TRH to evaluate possible alterations in the PRL pituitary reserve. Age-matched normal men participated as controls. In addition, the status of cerebral structures, such as the frontal-subcortical area, where dopamine plays an important role as neurotransmitter, was evaluated in all subjects by radiological (CT scan) and functional (neuropsychological tests) studies. The PRL response to TRH was similar in the two groups. In contrast, dopamine-induced PRL decrement was significantly lighter in alcoholics than in controls. Neuroradiological and neuropsychological parameters were abnormal in alcoholics. These data suggest an alteration in dopaminergic activity involving the tuberoinfundibular and probably the fronto-subcortical system in 4 weeks abstinent alcoholics.