6 research outputs found

    INDUCED STEVENS-JOHNSON SYNDROME IN A HUMAN IMMUNODEFICIENCY VIRUS PATIENT: A CASE REPORT

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    ABSTRACTStevens-Johnson syndrome (SJS) is an acute life-threatening condition. In 95% of case reports, drugs were found to be an important cause for thedevelopment of SJS. About 100 drugs have been identified to causes of SJS. Very few reports were published on diclofenac-induced SJS. The incidencerate of SJS is approximately 1-2/1000 individuals with human immunodeficiency virus. In this case report, we present a 58-year-old female developedSJS after taking of diclofenac tablets.Keywords: Stevens-Johnson syndrome, Diclofenac, Human immunodeficiency virus patients

    CLINICAL OUTCOMES OF USE OF HYDROXYCHLOROQUINE IN PARADOXICAL TUBERCULOSIS-IMMUNE RECONSTITUTION INFLAMMATORY SYNDROME IN HIV-INFECTED PATIENTS.

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     Objective: Immune reconstitution inflammatory syndrome (IRIS) is an inflammatory reaction in HIV-infected patients after initiation of antiretroviral therapy (ART) resulting from restored immunity to specific infectious or non-infectious antigens. The most common condition where IRIS has been reported is tuberculosis (TB). Various mechanisms have been proposed and studied to account for the immune regulatory role of hydroxychloroquine (HCQ). This study is done to identify clinical outcome in HIV-TB patients with IRIS after given with HCQ.Methods: An uncontrolled longitudinal study was conducted among HIV-infected patients with TB initiated on ART and developed IRIS between July 2013 and June 2015 in a South Indian HIV care hospital.Results: A total of 40 patients have developed IRIS with mean age of 35.87 years and 77.5 % of them were males. At the time of IRIS occurrence, the mean body mass index was found to be 19.17 kg/m2 and CD4 count was 200 cells/mm3. The time duration took to get improvement in majority of the patients was 4–12 weeks.Conclusion: There was definite improvement seen in patients who received HCQ in TB-IRIS condition

    Effectiveness of isoniazid preventive therapy on incidence of tuberculosis among HIV-infected adults in programme setting

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    Background & objectives: As India and other developing countries are scaling up isoniazid preventive therapy (IPT) for people living with HIV (PLHIV) in their national programmes, we studied the feasibility and performance of IPT in terms of treatment adherence, outcome and post-treatment effect when given under programmatic settings. Methods: A multicentre, prospective pilot study was initiated among adults living with HIV on isoniazid 300 mg with pyridoxine 50 mg after ruling out active tuberculosis (TB). Symptom review and counselling were done monthly during IPT and for six-month post-IPT. The TB incidence rate was calculated and risk factors were identified. Results: Among 4528 adults living with HIV who initiated IPT, 4015 (89%) successfully completed IPT. IPT was terminated in 121 adults (3%) due to grade 2 or above adverse events. Twenty five PLHIVs developed TB while on IPT. The incidence of TB while on IPT was 1.17/100 person-years (p-y) [95% confidence interval (CI) 0.8-1.73] as compared to TB incidence of 2.42/100 p-y (95% CI 1.90-3.10) during the pre-IPT period at these centres (P=0.017). The incidence of TB post-IPT was 0.64/100 p-y (95% CI 0.04-1.12). No single factor was significantly associated with the development of TB. Interpretation & conclusions: Under programmatic settings, completion of IPT treatment was high, adverse events minimal with good post-treatment protection. After ruling out TB, IPT should be offered to all PLHIVs, irrespective of their antiretroviral therapy (ART) status. Scaling-up of IPT services including active case finding, periodic counselling on adherence and re-training of ART staff should be prioritized to reduce the TB burden in this community

    Mechanisms underlying metabolic disturbances associated with psychosis and antipsychotic drug treatment

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    The increase in cardiovascular disease and reduced life expectancy in schizophrenia likely relate to an increased prevalence of metabolic disturbances. Such metabolic risk factors in schizophrenia may result from both symptom-related effects and aetiological factors. However, a major contributory factor is that of treatment with antipsychotic drugs. These drugs differ in effects on body weight; the underlying mechanisms are not fully understood and may vary between drugs, but may include actions at receptors associated with the hypothalamic control of food intake. Evidence supports 5-hydroxytryptamine receptor 2C and dopamine D2 receptor antagonism as well as antagonism at histamine H1 and muscarinic M3 receptors. These M3 receptors may also mediate the effects of some drugs on glucose regulation. Several antipsychotics showing little propensity for weight gain, such as aripiprazole, have protective pharmacological mechanisms, rather than just the absence of a hyperphagic effect. In addition to drug differences, there is large individual variation in antipsychotic drug-induced weight gain. This pharmacogenetic association reflects genetic variation in several drug targets, including the 5-hydroxytryptamine receptor 2C, as well as genes involved in obesity and metabolic disturbances. Thus predictive genetic testing for drug-induced weight gain would represents a first step towards personalised medicine addressing this severe and problematic iatrogenic disease
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