Metabolic Disturbances In Patients Research Articles

Metabolic dysregulation in first-episode schizophrenia patients with respect to genetic variation in one-carbon metabolism

The aim of this study was to investigate the prevalence of metabolic disturbances in patients with first-episode schizophrenia (FES) and test the hypothesis that genetic variation in one-carbon metabolism may account for metabolic dysregulation in early psychosis. We measured fasting glucose, lipid profile parameters, homocysteine, folate and vitamin B12 in 135 patients with FES and 146 healthy controls (HCs). Polymorphisms in the following genes were determined: MTHFR (C677T and A1298C), MTHFD1 (G1958A), MTRR (A66G) and BHMT (G742A). Serum levels of folate and high-density lipoproteins (HDL) were significantly lower in patients with FES compared to HCs. In turn, serum levels of homocysteine and triglycerides were significantly higher in patients with FES than in HCs. Prevalence of hyperhomocysteinemia, low folate and HDL levels together with dyslipidemia was significantly higher in patients with FES compared to HCs. Higher homocysteine levels, lower vitamin B12 levels and the presence of metabolic syndrome were associated with higher severity of negative symptoms. None of studied polymorphisms was associated with schizophrenia risk. Several associations between studied polymorphisms and cardio-metabolic parameters were found. None of them remained significant after Bonferroni correction. Our results indicate that metabolic dysregulation in patients with FES is not associated with genetic variation in one-carbon metabolism.

Metabolic disturbances in patients with cerebral palsy and gastrointestinal disorders

Under nutrition and growth failure are common findings in children with cerebral palsy (CP) and neurologically impairments. Electrolyte and micronutrient abnormalities have also been documented. Gastrointestinal (GI) diseases like gastro esophageal reflux disease (GERD), feeding difficulties and constipation have been associated with increased frequency of these derangements. The goal of this study was to determine the prevalence of malnutrition, metabolic and electrolyte abnormalities in pediatric patients with cerebral palsy and gastrointestinal disorders. A retrospective review of 172 medical records was performed out of which 45 subjects did not have any GI problem, 69 patients had constipation and 58 patients either had GERD, esophagitis, gastrostomy and feeding difficulties. Data collected included: weight, length and body mass index, pre-albumin, albumin, vitamin D, potassium, chloride, bicarbonate, calcium, magnesium (Mg), phosphorus. The results demonstrate a significant difference (p=0.0126) in the values of albumin in children with CP with GI disorders vs. those without. Additionally, a significant difference (p=0.0129) was found in Mg levels between CP children with constipation vs. GERD/esophagitis/feeding issues/gastrostomy. Results suggest that children with CP and GI disorders have decreased levels of albumin, but normal pre-albumin. The mechanism for this is not completely clear and although we acknowledge importance of nutritional intake for albumin level support, other mechanisms such as low grade chronic inflammation and increased gut and vascular permeability may play a role. The lower levels of Mg in children with CP and constipation could be secondary to the use of laxatives. Further prospective studies looking at nutritional protein intake, gut and vascular permeability and laxative use in this patient population are important for future optimization of health care management.

Metabolic disturbances and ways of their pharmacological correction in acute poisoning with ethanol in patients with chronic alcoholism

To study an influence of chronic alcoholism on the clinical course and severity of metabolic disturbances in patients with acute poisoning with ethanol and to improve the treatment. Authors examined 93 patients stratified into three groups (acute poisoning with ethanol in patients with chronic alcoholism, without chronic alcoholism and those treated with reamberin). The presence of chronic alcoholism significantly augmented metabolic disturbances and influenced the disturbance of oxygen-transport function and free-radical processes in patients with acute intoxication with ethanol. Using of reamberin in the complex intensive therapy led to the decrease in metabolic disorders, which improved the clinical course of acute poisoning with ethanol in patients with chronic alcoholism.

No association between genetic or epigenetic variation in insulin growth factors and antipsychotic-induced metabolic disturbances in a cross-sectional sample.

Second-generation antipsychotics (SGA) are known to induce metabolic disturbances. Genetic pathways, such as the IGF pathway could be associated with increased metabolic syndrome (MetS). Additionally, IGF2 methylation varies as a function of environmental influences and is associated with schizophrenia and MetS. The current study aims to evaluate whether genetic and epigenetic variation in genes of the IGF pathway are associated with metabolic disturbances in patients under treatment with SGAs. Cross-sectional metabolic data from 438 patients with schizophrenia spectrum disorder was analyzed. Using the Sequenom MassARRAY iPLEX(TM) platform, 27 SNPs of the IGF1 and IGF2 genes and the IGF receptors IGF1R and IGF2R were genotyped. Methylation status of seven IGF2 CpG dinucleotides was evaluated using a Sequenom MALDI-TOF spectrometer. There was a significant association between IGF2 methylation and genotype, but no significant association between genetic or epigenetic variability and metabolic parameters in the present study.

Prolactin hyperproduction does not predict the risk of glucose metabolic disturbances in patients with acromegaly

Prolactin hyperproduction does not predict the risk of glucose metabolic disturbances in patients with acromegaly

Primary hyperparathyroidism and metabolic risk factors, impact of parathyroidectomy and vitamin D supplementation, and results of a randomized double-blind study

BackgroundVitamin D insufficiency may increase the risk for cardio metabolic disturbances in patients with primary hyperparathyroidism (PHPT).ObjectiveTo analyze the vitamin D status and indices of the metabolic syndrome in PHPT patients and the effect of vitamin D supplementation after parathyroid adenomectomy (PTX).Design and methodsDouble-blinded, randomized clinical trial (ClinicalTrials.gov Identifier: NCT00982722) performed at Karolinska University Hospital, Sweden, April 2008 to November 2011. One hundred and fifty consecutive patients with PHPT (119 women) were randomized after PTX, 75 to oral treatment with calcium carbonate 1000 mg daily and 75 to calcium carbonate 1000 mg and cholecalciferol 1600 IU daily over 12 months. Changes in metabolic profile and ambulatory blood pressure (BP) were analyzed. Main outcome measures were changes in metabolic factors, BP, and body composition.ResultsThe 25-hydroxyvitamin D (25-OH-D)-level was <50 nmol/l in 76% of the patients before PTX. After PTX, glucose, insulin, and IGF1 decreased, while the 25-OH-D and the IGF-binding protein 1 increased and remained unchanged at follow-up after study medication. One year of vitamin D supplementation resulted in lower parathyroid hormone (PTH) (40 (34–52) vs 49 (38–66) ng/l) and higher 25-OH-D (76 (65–93) vs 49 (40–62) nmol/l; P<0.05). Other laboratory parameters were stable compared with after PTX. Systolic BP decreased and total bone mineral content increased in both groups.ConclusionExcept for the lowering of the PTH level, no additive effect of vitamin D supplementation was seen. However, PTX proved effective in reducing insulin resistance.

Protein-Bound Uremic Toxins…New Targets to Prevent Insulin Resistance and Dysmetabolism in Patients With Chronic Kidney Disease

The retention of p-cresyl sulfate (PCS), the prototype of protein-bound uremic toxins that is produced by the gut microbiota and normally excreted by the kidney, may contribute to the development of insulin resistance in patients with chronic kidney disease. In a recent study, we demonstrated in mice, as in cultured muscle cells, that PCS interferes with intracellular insulin signaling pathways and triggers insulin resistance. The treatment of CKD mice with a prebiotic that reduces the intestinal production and decreases blood levels of PCS prevented insulin resistance and lipid abnormalities, suggesting new opportunities to prevent metabolic disturbances in patients with CKD. This study highlights the uremic toxins as new actors in metabolic alterations associated with CKD and allows for the consideration of new therapeutic approaches (e.g., prebiotics, probiotics, adsorbents) to better prevent them.

The Clinical Course and Correction of Metabolic Disturbances in Patients with Severe Methadone Poisoning

Objective: to study the clinical patterns due to course of severe methadone poisoning and to assess the results of reamberine use in the complex of intensive therapy for this condition. Subjects and methods. Sixty-eight patients with acute severe methadone poisoning were examined and treated. The clinical manifestations of intoxication and impairment in the tissue component of oxygen transport were evaluated. Results. The severity of its clinical picture, besides directly toxic effect of methadone was characterized by the depth and magnitude of hypoxia that clinically manifested both as cerebral edema/swelling and pulmonary edema and, in cases of hyperhypoxia, as severest disorders in the cardiovascular system. The incorporation of the antihypoxant reamberine into an intensive care program for severe acute methadone poisoning was found to result in a rapider reduction of tissue hypoxia, which substantially diminished the degree of occurring complications and improved the clinical course of acute intoxications. Conclusion. Thus, correction of metabolic aftereffects and alleviation of hypoxic lesions result in a reduction in the duration of coma, the length of stay on mechanical ventilation, the rate and severity of secondary pulmonary complications and mortality rates.

Genotype–phenotype correlations of PCOS susceptibility SNPs identified by GWAS in a large cohort of Han Chinese women

Are there any correlations between the phenotypes of polycystic ovary syndrome (PCOS) and the genotypes of the PCOS susceptibility single nucleotide polymorphisms (SNPs) in THADA, DENND1A and LHCGR? The PCOS susceptibility genes, THADA and DENND1A, carry risk alleles that are associated with endocrine and metabolic disturbances in patients with PCOS. PCOS is a heterogeneous endocrinopathy characterized by oligo-anovulation, hyperandrogenism and polycystic ovaries. In a previous genome-wide association study, the SNP variants rs13429458, rs12478601, rs2479106, rs10818854 and rs13405728 in the THADA, DENND1A and LHCGR genes were identified as being independently associated with PCOS. The aim of this study was to identify any additional correlations between the phenotypes of PCOS and genotypes of the five SNPs described in the previous study. In the present cross-sectional study, a total of 1731 PCOS patients and 4964 controls were enrolled. Patients were diagnosed according to Rotterdam criteria. Clinical information was collected from the patients and controls. Endocrine and metabolic parameters were evaluated for phenotype-genotype correlation analyses. Using a recessive model, the AA group for rs13429458 in THADA was associated with increased luteinizing hormone (LH) (P < 0.01) and testosterone (T) (P = 0.02) levels in subjects with PCOS; the LH/follicle-stimulating hormone ratio was also higher in the AA group (P < 0.01). Also using a recessive model, the CC genotype of rs12478601, also in THADA, was associated with increased levels of low-density lipoprotein (P = 0.02). Using a dominant model, the GG + AG group for rs2479106 in DENND1A was associated with elevated serum insulin levels 2 h after a glucose load in the patients with PCOS (P = 0.02). All of the comparisons were adjusted for age and BMI. The relatively younger age of the participants may represent a considerable bias when evaluating metabolic alterations as a function of different genotypes, as significant metabolic disturbances may emerge later in life. Furthermore, the sample sizes of several sub-genotype groups were relatively small; to some extent this limited the statistical power of the analysis. The PCOS susceptibility genes, THADA and DENND1A, carry risk alleles that are associated with endocrine and metabolic disturbances in PCOS patients of Han Chinese descent. The findings have shown genuine heterogeneity, stratified on the basis of both clinical findings and genotypes. Replication of these results is expected in other ethnic groups.

Role of Omega-3 fatty acids in preventing metabolic disturbances in patients on olanzapine plus either sodium valproate or lithium: a randomized double-blind placebo-controlled trial

BackgroundMetabolic and cardiovascular side effects have been noted with the use of second generation antipsychotics (SGAs) and mood stabilizers. Since Omega-3 fatty acids have been known to prevent some cardiovascular risks, this preliminary study was designed to evaluate the cardiovascular benefits of omega-3 when added to the combinations of olanzapine with mood stabilizers.MethodsThis study was a randomized, double-blind, placebo-controlled, within-subject trial in adult psychiatric patients who were receiving olanzapine combined with lithium (Li) or valproate sodium (VPA). Omega-3 as fish oil with less than 1 g/day of EPA/DHA or its placebo was added to patients’ olanzapine and mood stabilizer regimens for 6 weeks. Metabolic parameters including anthropometric variables, lipid profile, metabolic syndrome indices, C-reactive protein, fibrinogen and lipoprotein (a) [(Lp) (a)] were assessed for participants.ResultsForty one participants completed this study; 20 patients received omega-3 and 21 patients received placebo, added to their regimen of SGA and mood stabilizer. Omega-3 addition did not modulate anthropometric, metabolic syndrome and lipid parameter changes in 6 weeks. However, fibrinogen levels significantly decreased, Lp (a) did not increase and non-high-density lipoprotein cholesterol (non-HDL-C) did not go beyond its target level after omega-3 supplementation. Additionally, a significant inter-group effect was noted for Lp(a).ConclusionsThis study suggests that use of short-term omega-3 supplementation added to a combined regimen of olanzapine and mood stabilizer may have a small modulating effect on some cardiovascular risk factors. Trials in longer periods of time and with larger number of patients are needed to further evaluate the effects of omega-3 supplements on preventing cardiovascular risk factors.This trial is registered at irct.ir and its Identifier is as following: IRCT138712231764N1

Have Main Types of Primary Aldosteronism Different Phenotype?

Primary aldosteronism (PA) is the most common cause of endocrine hypertension with a high frequency of cardiovascular complications. We found in our previous study higher occurrence of metabolic disturbances in patients with idiopathic hyperaldosteronism (IHA) compared to subjects with aldosterone-producing adenoma (APA). The aim of our present study is to evaluate potential differences in the frequency of end-organ damage (arterial stiffness and microalbuminuria) between two main types of PA. The diagnosis of the particular form of PA was based on adrenal venous sampling and/or histopathological examination. We analyzed clinical and laboratory data from 72 patients with PA (36 with IHA, 36 with APA). The arterial stiffness was expressed as the carotid-femoral pulse wave velocity (PWV) and the renal damage as urinary albumin excretion levels (UAE). Patients with IHA had significantly (p<0.03) higher prevalence of metabolic syndrome (17 % in APA, 35 % in IHA), higher triglycerides (1.37+/-0.71 mmol/l in APA, 1.85+/-0.87 mmol/l in IHA), lower HDL cholesterol (1.25+/-0.28 mmol/l in APA, 1.06+/-0.25 mmol/l in IHA), higher PWV (7.91+/-1.61 m/s in APA, 8.99+/-1.77 m/s in IHA) and higher UAE (12.93+/-2.21 mg/l in APA, 28.09+/-6.66 mg/l in IHA). It seems that patients with IHA may have a slightly different phenotype compared to APA.

Effect of Combination Therapy with Coenzyme Q10 on Functional and Metabolic Parameters in Patients with Type 1 Diabetes Mellitus

Functional state of the kidneys, severity of metabolic disturbances, intensity of LPO, and activity of the antioxidant system in 30 patients (18-36 years old) with type 1 diabetes mellitus and diabetic nephropathy of different compensation were studied before and after standard therapy or combination treatment with coenzyme Q10. Similar parameters were evaluated in 20 healthy subjects of the same age group. The development of metabolic disturbances in patients with type 1 diabetes mellitus (decompensated form) was accompanied by activation of LPO and inhibition of the antioxidant system. These patients were characterized by oxidative stress, diabetic nephropathy with associated proteinuria, and impairment of water excretion, electrolyte excretion, and nitrogen excretion in the kidneys. Combination therapy with coenzyme Q10 had a positive effect on LPO and antioxidant system. This treatment was followed by the relief of hyperglycemia, decrease in the concentrations of glycosylated hemoglobin and LDL cholesterol, and improvement of nitrogen metabolism.

Polymorphisms of INSIG2, MC4R, and LEP Are Associated With Obesity- and Metabolic-Related Traits in Schizophrenic Patients

Schizophrenic patients have a high prevalence of metabolic adversities. Previous studies have suggested some candidate genes for obesity- and metabolic-related traits, including the insulin-induced gene (INSIG2), melanocortin 4 receptor gene (MC4R), and leptin and leptin receptor genes (LEP and LEPR). We aimed to investigate the associations between these genes and metabolic disturbances in patients with schizophrenia in Taiwan. Patients with a diagnosis of schizophrenia or schizoaffective disorder according to the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, were recruited from 36 community psychiatric rehabilitation centers or hospitals in Taipei. A total of 650 subjects were enrolled, and 577 were included in the genetic analyses. The anthropometric (body mass index, waist circumference [WC], and blood pressure) and biochemical measurements (fasting plasma glucose, insulin, triglyceride, high-density lipoprotein cholesterol, and Homeostasis Model of Assessment - Insulin Resistance index [HOMA-IR]) were assessed. Seven loci in the 4 genes were genotyped using standard TaqMan assays. Genetic association analyses were conducted for binary and quantitative measurements of the previously mentioned traits. Obese patients with schizophrenia exhibited more metabolic disturbances than nonobese patients. Our data showed that INSIG2 was significantly associated with fasting plasma glucose (for rs17587100, P < 0.0001), MC4R was associated with WC (for rs2229616, P = 0.005), and LEP was associated with body mass index and WC (for rs7799039, P < 0.01). In addition, these loci showed suggestive associations with traits including high-density lipoprotein cholesterol and triglyceride, metabolic syndrome, insulin level, and HOMA-IR index (P = 0.05). In addition to the effect from antipsychotic medications and an unhealthy lifestyle, genetic factors also contribute to the high prevalence of obesity and metabolic disturbances in patients with schizophrenia, especially genes involved in metabolic-related pathways.

Targeted Intervention to Improve Monitoring of Antipsychotic-Induced Weight Gain and Metabolic Disturbance in First Episode Psychosis

International guidelines recommend monitoring for weight gain and metabolic disturbance in patients prescribed second generation antipsychotics. We aimed to investigate whether a targeted intervention could improve levels of monitoring in a first episode psychosis clinic. A pre-intervention audit of both metabolic screening rates and specific monitoring of weight and metabolic indices following the initiation of antipsychotic medication was performed in our first episode psychosis clinic. This was repeated 18 months later, following an intervention that included a number of targeted improvement strategies based on an analysis of barriers and enablers to performing monitoring within the clinic. The intervention included provision of monitoring equipment, interactive educational events, reminders and prompts and embedding processes for monitoring within team structure. There were significant improvements in both the screening of metabolic indices and the monitoring of indices following initiation of antipsychotic medications. There were also improvements in the number of active interventions offered to clients by clinicians. However, the level of guideline concordant monitoring remains low within our service. A comprehensive programme of implementation strategies can improve both screening and monitoring of the metabolic side-effects of antipsychotic medications. Further focused strategies are necessary to continue to improve monitoring to guideline concordant levels.

A mathematical model of calcium and phosphorus metabolism in two forms of hyperparathyroidism

Parathyroid hormone (PTH) plays a critical role in calcium and phosphorus metabolism. Interestingly, in two forms of hyperparathyroidism (excessive amount of PTH in the serum), the metabolic disturbances in patients with chronic kidney disease (CKD) significantly differ from those with primary hyperparathyroidism (PHP). Since an intuitive understanding of these PTH-linked regulatory mechanisms are hardly possible, we developed a mathematical model using clinical data (1586 CKD and 40 PHP patients). The model was composed of a set of ordinary differential equations, in which the regulatory mechanism of PTH together with other key factors such as 1,25-Dihydroxyvitamin D (1,25(OH)₂D) and calcium was described in the tissues including bone, the kidney, the serum, and the parathyroid glands. In this model, an increase in PTH was induced by its autonomous production in PHP, while PTH in CKD was elevated by a decrease in feedback inhibition of 1,25(OH)₂D in the serum, as well as an increase in stimulation by phosphorus in the serum. The model-based analysis revealed characteristic differences in the outcomes of hyperparathyroidism in CKD and PHP. The calcium exchange in bone, for instance, was predicted significantly higher in PHP than CKD. Furthermore, we evaluated the observed and predicted responses to the administration of calcimimetics, a recently developed synthetic drug that modulated efficacy of calcium-sensing receptors. The results herein support the notion that the described model would enable us to pose testable hypotheses about the actions of PTH, providing a quantitative analytical tool for evaluating treatment strategies of PHP and CKD.

Relaxin polymorphisms associated with metabolic disturbance in patients treated with antipsychotics

People with schizophrenia have an increased risk of metabolic syndrome, with consequent elevated morbidity and mortality, largely due to cardiovascular disease. Metabolic disorders comprise obesity, dyslipidemia and elevated levels of triglycerides, hypertension, and disturbed insulin and glucose metabolism. The elevated risk of metabolic syndrome in individuals suffering from schizophrenia is believed to be multifactorial, related to a genetic predisposition, lifestyle characteristics and treatment with antipsychotic medications. Relaxin 3 (RLN3, also known as INSL7) is a recently identified member of the insulin/relaxin superfamily that plays a role in the regulation of appetite and body weight control. RLN3 stimulates relaxin-3 receptor 1 (relaxin/insulin-like family peptide receptor 3, RXFP3) and relaxin receptor 2 (relaxin/insulin-like family peptide receptor 4, RXFP4). We have investigated the role of ten polymorphisms in these genes (RLN3 rs12327666, rs1982632, and rs7249702, RLN3R1 rs42868, rs6861957, rs7702361, and rs35399, and RLN3R2 rs11264422, rs1018730 and rs12124383) in the occurrence of metabolic syndrome phenotypes (obesity, diabetes, hypercholesterolemia, hypertrigyceridemia, and hypertension) in a cross-sectional cohort of 419 US Caucasian patients treated with antipsychotic drugs. We found several associations between relaxin polymorphisms and hypecholesterolemia, obesity and diabetes, suggesting a role for the relaxin/insulin pathway in the development of metabolic disturbance observed in patients treated with antipsychotics.

Perioperative Correction of Metabolism in Patients with Lung Cancer

Objective: to reveal the features of perioperative metabolic disturbances in patients with lung cancer after pulmonectomy and a possibility of their correction with perioperative «Standard» formula sipping and with postoperative intravenous cytoflavin. Subjects and methods. The paper presents the results of a prospective randomized study of the efficiency of correction of metabolic disturbances in patients with lung cancer with perioperative enteral «Standard» formula sipping (5 days before surgery and 12 days after surgery). The study was conducted in 326 men aged 36 to 68 years. Arterial blood metabolic parameters (glucose, lactate, and pyruvate) and daily urine urea were estimated. Results. There was an association of preoperative metabolic disturbances with body mass index (BMI). Inclusion of sipping into perioperative therapy did not exert a considerable impact on the cause of postoperative metabolic disturbances. Key words: lung cancer, pul-monectomy, body mass index, sipping, cytoflavin.

Glutathione-dependent enzymes and glucose-6-phosphate dehydrogenase of blood in patients with lymphosarcoma (non-hodgkin's disease)

Activities of glutathione-dependent enzymes and glucose-6-phosphate dehydrogenase (GPDH) were studied in blood of the patients with lymphosarcoma (LS). The activity of glutathione reductase (GR), glutathione dehydroascorbate reductase (GDAR), gamma-glutamyltranspeptidase (GGT) and G6PDH in plasma, leucocytes, lymphocytes and erythrocytes of peripheral blood in 30 patients (42-56 years) with LS and in 20 healthy have been determined with spectrophotometric methods (Humalyzer 2000 DE). Leucocytes and lymphocytes were separated from blood using Boyum method. Spearmen method used for correlative analysis. The levels of enzymes activity and results of correlative analysis showed an imbalance of antioxidative system defense and metabolic disturbances in patients with LS. The strong functional interrelation was estimated only between GR and G6PDH in the patients' lymphocytes (r=+0,716; p<0.0005). Interrelation was found between the levels of activity of antioxidative enzymes and activity (stage) of pathologic process, this may be used as the additional biochemical test for differential diagnostics of LS and estimation of the cells proliferative activity.

MTHFR genotype and differential evolution of metabolic parameters after initiation of a second generation antipsychotic: an observational study

Most second-generation antipsychotics (SGAs) induce metabolic disturbances, but large differences exist in the degree to which individual patients develop these. Little is known about genetic factors associated with differential liability. Cross-sectional studies suggested an association between polymorphisms in 5,10-methylenetetraydrofolate reductase (MTHFR) and metabolic syndrome in patients with schizophrenia. This study aimed to assess whether the C677T (rs1801133) or A1298C (rs1801131) polymorphism in the MTHFR gene predict differential evolution of metabolic parameters over the course of a 3-month follow-up period after initiation of an SGA. One hundred and four patients with schizophrenia initiated on a SGA were measured at baseline, 6 weeks and 3 months. MTHFR A1298C, but not C677T, genotype predicted pos-baseline increases in weight [beta=2.5, standard error (SE)=0.92, P=0.006], waist circumference (beta=2.0, SE=1.0, P=0.050), fasting glucose (beta=2.8, SE=1.2, P=0.024) and glucose at 120 min during the Oral Glucose Tolerance Test (beta=10.7, SE=4.5, P=0.018) following a de novo metabolic challenge with a specific SGA. A1298C allele carriers consistently displayed the most unfavorable evolution of metabolic parameters. Thus, MTHFR A1298C genotype may explain part of the individual liability to metabolic disturbances in patients with schizophrenia.

Metabolic disturbances in patients with paranoid schizophrenia treated with atypical antipsychotic drugs

Цель. Изучение влияния терапии классическими и атипичными антипсихотическими препаратами (АА) на динамику толерантности к глюкозе и некоторых показателей липидного обмена. Материалы и методы. Обследовано 50 больных с развившимся впервые в жизни психотическим эпизодом, отвечающим критериям па- раноидной шизофрении (МКБ ? 10). В первую группу вошли больные, получающие галоперидол, вторую группу составили пациенты, по- лучающие атипичные антипсихотические препараты (АА). Использовались биохимический, антропометрический, статистический методы. Результаты. У 12% пациентов, получавших АА, выявлено нарушение толерантности к глюкозе на 8 неделе терапии, у 4% больных ? сахарный диабет (СД). Заключение. Терапия с использованием атипичных антипсихотических препаратов оказывает существенное влияние на состояние уг- леводного обмена у больных параноидной шизофренией по сравнению с галоперидолом.