Given the longevity achievable with current prophylactic and therapeutic strategies for persons with HIV infection, quality of life (QOL) has emerged as a significant medical outcome measure, and its enhancement has an important goal. This review highlights the relevance and complexity of physical, psychological, and social factors as determinants of health-related quality of life in HIV-infected persons. Existing data suggest that physical manifestations, antiretroviral therapy, psychological well-being, social support systems, coping strategies, spiritual well-being, and psychiatric comorbidities are important predictors of QOL in this population. Consequently, the impact of HIV infection on the dimensions of QOL, including physical and emotional well-being, social support systems, and life roles, has emerged as a key issue for persons infected with HIV.
Psoriasis is a common skin disorder; knowledge of the factors that may induce, trigger, or exacerbate the disease is of primary importance in clinical practice. Drug intake is a major concern in this respect, as new drugs are constantly being added to the list of factors that may influence the course of this disease. Drug ingestion may result in exacerbation of pre-existing psoriasis, in induction of psoriatic lesions on clinically uninvolved skin in patients with psoriasis, or in precipitation of the disease in persons without family history of psoriasis or in predisposed individuals. In view of their relationship to drug-provoked psoriasis, therapeutic agents may be classified as drugs with strong evidence for a causal relationship to psoriasis, drugs about which there are considerable but insufficient data to support the induction or aggravation of the disease, and drugs that are occasionally reported to be associated with aggravation or induction. This review focuses on the most common causative agents for drug-induced, drug-triggered, or drug-aggravated psoriasis, such as β-blockers, lithium, synthetic antimalarial drugs, nonsteroidal anti-inflammatory agents, and tetracyclines, and the mechanisms of action of these drugs in the pathogenesis of psoriasis.
Psoriasis is a common, chronic skin disorder, the pathogenesis of which is incompletely understood. Results from various clinical and experimental studies indicate that psoriasis is a complex, multifactorial disease with a genetic predisposition. Factors such as climate, physical trauma, drug, stress and infections (Streptococcus, human immunodeficiency virus) are known to trigger psoriasis. The success of treatment of psoriasis with T-cell depletion and antitumour necrosis factor (TNF)-alpha treatment is explained by the involvement of T cells and TNF- alpha in the pathogenesis of psoriasis. The biochemical basis for the pathogenesis of psoriasis can be attributed to both overexpression and underexpression of certain proteins in psoriatic lesions. The anomalies in protein expression can be classified as abnormal keratinocyte differentiation, keratinocyte hyperproliferation and inflammation. Oxidative stress (OS) and increased free-radical generation have been linked to skin inflammation in psoriasis. The review presents evidence for various markers of psoriasis that can be targeted for effective treatment, including biomarkers of inflammation, keratinocyte hyperproliferation and abnormal differentiation, and stress.
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