ABSTRACT
Background: Background: There are few studies of depression in Indian population which have looked at depression comprehensively covering various facets in a sample population. The objective of the current study was to recognize the clinical features and comorbidities of depression among inpatients in a tertiary care centre. Method: This was an observational study in which 50 patients admitted with ICD-10 diagnosis of depression were assessed for clinical symptomatology and comorbidity. Results: The mean number of somatic symptoms was 11.44 (SD 6.66), and the mean number of stressful life events over lifetime and in past 1 year were 8.02 (SD 3.8) and 1.44 (SD 1.18), respectively. One fifth of the sample (20%) had personality disorder; among them, mixed personality disorder (12%) was the most common diagnosis. Most of the patients had suicidal ideation (62%) and 26% had attempted suicide during their lifetime. Majority (60%) had atleast one psychiatric comorbidity; the most common being anxiety disorder (46%). Physical comorbidity was present in 54% of the patients; the common diagnoses were hypertension (18%), diabetes mellitus (14%) and ischaemic heart disease (12%). Conclusion: The current study found somatic symptoms and suicide ideation to be frequent in the sample. Also, comorbid conditions including personality disorders are frequent in patients with depression.
ABSTRACT
The study was designed to investigate the role of hepatic metabolic activity on body burden of HCH residue. Male albino rats were orally administered 0, 5, and 10 mg/kg HCH for 90 days, followed by either sodium phenobarbital or carbon tetrachloride treatment for 0, 15 and 30 days after withdrawal of their respective HCH administration. The liver weight was significantly increased at 30 days after the administration of phenobarbital and carbon tetrachloride in both 5 mg and 10 mg/kg HCH withdrawal groups when compared to control. HCH residue was maximum in fat followed by adrenal > thymus > liver > kidney > spleen > tests > brain > plasma. Carbon tetrachloride caused an accumulation of HCH residues in the liver 15 and 30 days after administration of both doses of HCH. Phenobarbital did not show significant variation in HCH residues in hepatic tissue. Phenobarbital treatment caused significant induction of hepatic RED, APD, AHH, GST and QR activities. Significant decreases in activities were observed by carbon tetrachloride when compared to animals treated with HCH alone. The overall results clearly suggest the role of P450 protein on the body burden of HCH residues.