Background:Depression and obesity are disorders of stress with a dose dependent relationship between the both. The adverse health and social consequences are significant, when depression and obesity co-exist. This study aimed to examine the prevalence of depression among overweight and obese patients in a large station of Armed Forces and associate other risk factors of depression.Methods:This cross sectional descriptive study was conducted in the general OPD of large Station medicare centre (SMC) on overweight and obese personnel. Data was collected by self-administered Patient Health Questionnaire (PHQ-9) to assess the risk for depression over a period of one month.Results:In this study, out of 106 individuals, 71 (67%) were overweight and 35 (33%) were obese, as per WHO criteria. Of the individuals assessed, 13 (12%) individuals were found to have risk of moderate depression, 58 (54%) for mild depression and 35 (33%) individuals had no risk for clinically significant depression. The likelihood of depression was most strongly associated with BMI followed by age, status of living with family and habit of drinking alcohol.Conclusion:Obesity and depressive disorders are common comorbidities with overlapping pathophysiology whose co-existence leads to exponential adverse health outcomes. The outcome of depression and obesity is to be managed comprehensively by psychological counseling and life style modification.
Objective: Parkinson's disease (PD) is a chronic progressive neurodegenerative disorder characterized by rest tremors, bradykinesia, rigidity, postural instability, gait dysfunction, and several non-motor symptoms. The marked difference in drug response and adverse effect profile among patients led to search of genetic markers and polymorphism associated with response to antiparkinsonian drugs which will enable us to predict an individual's response to drugs in terms of both efficacy and toxicity. Hence, efforts to define the role of genetic polymorphism in optimizing pharmacotherapy of PD have been undertaken and some promising genetic loci for the treatment have been determined. Therefore, we aim to present a critical review of pharmacogenetic aspects of levodopa, dopamine agonists (DAs), and catecol-O-methyltransferase (COMT) inhibitors and describe gene polymorphism of interest for future research.
Methods:The PubMed database was searched using the keywords "parkinsonism," "antiparkinsonian drugs," "levodopa," "DAs," "COMT inhibitors," "pharmacogenomics," and "polymorphism." Abstracts and review articles were included for the study.
Results and Conclusion:Studies conducted in different settings suggest that pharmacogenomics plays a significant role in Parkinsonism drug therapy. The gene/drug pairings with the strongest potential for pharmacogenetic recommendations include COMT allele/levodopa and entacapone, dopamine D2 receptor (DRD2)/ropinirole, pramipexole, and DRD3/ropinirole and pramipexole. It can be concluded that with the rapid development of genotyping platforms, genome-wide association study can be performed to analyze polymorphism associated with inefficient treatment or adverse effects. Hence, individualized therapy of PD for better patient care can be achieved by targeted genetic testing.
INTRODUCTIONPrecise regulation of body fluid osmolality is essential. It is controlled by a finely tuned, intricate homeostatic mechanism that operates by adjusting both the rate of water intake and the rate of solute-free water excretion by the kidney, i.e., water balance. Abnormalities in this homeostatic system can result from genetic diseases, acquired diseases, or drugs and may cause serious and potentially life-threatening deviations in plasma osmolality. Anti-diuretic hormone (ADH) released from posterior pituitary has a crucial role in the control of water content of the body through its actions on the cells of the distal part of nephron and collecting tubules in the kidney. One of the main stimulus to ADH release is an increase in plasma osmolality which produces a sensation of thirst. A decrease in circulating blood volume, i.e., hypovolemia is another stimulus and here the stimuli arise from baroreceptors in cardiovascular system or from angiotensin release. ADH binds to the V 2 receptors in basolateral membrane of cells of distal tubule and collecting ducts of the nephron. Its main effect in collecting duct is to increase the rate of insertion of water channels into luminal membrane thus increasing the permeability of membrane to water thereby leading to water reabsorption from the nephron. Several drugs affect the action of ADH.Diabetes insipidus (DI) is either due to deficient secretion of arginine vasopressin (AVP), also known as ADH by the pituitary gland (central DI) or due to renal tubular unresponsiveness to AVP (nephrogenic DI). This leads to polyuria, polydipsia with hyposthenuria, causing dehydration and hypernatremia if the patient is deprived of water.
2Vasopressin acts as an anti-diuretic by reabsorbing water via the principle cells of collecting ducts and the thick ascending loop of Henle, thereby increasing the plasma blood volume and decreasing the plasma osmolality.
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ABSTRACTBackground: Diabetes insipidus is a disease characterized by high amounts of urine excretion. Antidiuretic drugs are used to treat this condition. Hence, our study intends to evaluate the anti-diuretic effect of fluvoxamine, a selective serotonin reuptake inhibitors in albino rats. Methods: Albino rats were divided into three groups of six animals each. The control group was fed with distilled water 10 ml/kg body weight, standard group received 4 units of vasopressin and test group received fluvoxamine 18 mg/kg body weight. On the day of experiment, diuresis was induced in all the groups by giving frusemide in a dose of 20 mg/kg body weight after loading with saline at 25 ml/kg body weight. The animals were confined in diuretic cage for a period of 5 hrs and urine output was noted. Urine was analyzed for electrolyte concentration (Na
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