MEDICINSKI GLASNIK

198
Medicinski Glasnik, Volumen 6, Number 2, August 2009
INTRODUCTION
During psychiatric treatment, body weight
usually increases and this is frequently accompanied
by an increase in appetite (1). This side effect,
which is difficult to foresee of its development and
timing, finally causes obesity and results in the
cessation of an effective treatment in some of the
patients. Obesity not only affects the psychological
state of the patient, but also increases the risk
of development of several chronic diseases such
as coronary artery disease, hypertension, hyperlipidaemia,
diabetes, some types of cancer, cerebrovascular
diseases, osteoarthritis, pulmonary diseases
and sleep apnoea (2-4). Therefore, reduction of
body weight plays a pivotal role in the prevention
of several chronic diseases and improvement of
the prognosis of an ongoing disease.
In this research, we aimed to compare the
changes in anthropometric and biochemical parameters
in patients treated with psychiatric drugs
with ones who did not, and to find out the contrubution
of a dietitian specialized in this area for the
treatment of nutrition related metabolic problems
arising out of psychiatric pharmacotherapies.
PATIENTS AND METHODS
In order to determine patients’ group for this
research the records of all patients who addmitted
to outpatient clinic of Psychiatric Department
in Cerrahpasa Medical Faculty University of Istanbul
in the 2004 to 2008 period retrospectively
analyzed. It has chosen two groups among 363
patients who suffer from obesity and were followed
by a dietician. All patients are informed
and accepted their inclusion in the research.
The study group included 102 (28.1%) adult
female patients taking psychiatric pharmacotherapies
and complained about increased body weight
within this period. The mean ±SD age of study
group was 40.9±12.44 years.
Medications that patients in the study group
have taken were antipsychotics 34 (38,2%), mood
stabilisers 36 (40,4%), antidepressants 72 (80,9%)
or anxiolytic 9 (10,1%) which were mostly taken
as combined pharmacotherapy.
The controls included 261 (71.9%) adult
females who had no endocrine, metabolic or
psychiatric disorders or history of drug use and
had been referred to dietitians due to exogenous
obesity. The mean ±SD age of control group was
39.8±13.0 years.
As body composition depends on age, sex
and severity of obesity (5, 6) both groups included
adult females with body-mass index (BMI) ≥25.
All patients underwent antropometric assessment,
body composition analysis using a Bioelectrical
Impedance Analyzer (Bodystat Quadscan 4000,
England). Biochemical parameters of patients
were studied with overnight fasting blood samples
taken from the antecubital vein. Biochemical parameters,
serum fasting blood glucose (FBG), total
protein, albumin, uric acid, triglyceride, and total,
HDL and LDL cholesterol were measured using an
Olympus AU 800 autoanalyzer (Olympus, Japan).
FBG was analysed using the hexokinase method.
The methods were biuret for total protein, BCG
for albumin and the uricase / PAP method for uric
acid. Levels of total, HDL cholesterols and triglycerides
were measured using enzymatic methods in
all samples. Serum hsCRP concentrations were
determined with immunonephelometry using the
BN II Systems Analyzer (Dade Behring, Malburg,
Germany). FT3, FT4, third-generation thyroid sitimulating
hormone (TSH) were measured on Immulite
2000 (DPC; LosAngeles,USA). FT3 and
FT4 were measured by a competitive analog-based
immunoassay. TSH levels were determined by
two-side chemiluminescent immunometric assay.
Insulin and cortisol were measured with Immulite
2000 analyzer (DPC,USA) by chemiluminescent
immunometric assay. Insulin resistance (IR) was
determined by HOMA- IR index, e.g. serum insulin
(mg/dl) x plasma glucose (mg/dl) / 405. Serum
B12, folic acid levels were measured by radioimmunoassay
(RIA) (DPC, USA). Plasma level of
homocysteine was determined by high-performance
liquid chromatography (HPLC Agilent 1100
Series), coupled with fluorescence detector. Plasma
fibrinogen levels were measured by BCT (Dade
Behring, Malburg, Germany) analyser. Serum zinc,
and copper concentrations were determined using
the standard atomic absorption spectrophotometry.