ELISA (dsg1 and dsg3) is an efficient tool for confirming the diagnosis of PV. Specific antibody titers correlate with disease severity; however, desmoglein testing cannot differentiate between the various morphologic subtypes of PV.
Pemphigus vulgaris (PV) is classical example of antigen-driven severe autoimmune bullous skin disorder. Auto reactive T cells are critical for the induction and regulation of antibody production. With regard to cytokine production profiles, it has been reported that qualitative as well as quantitative alterations in cytokine production can result in activation of inefficacious effector mechanisms and therefore, complex and severe impairment in immune functions. The purpose of this study was to observe the alterations in the levels of T(H)1 [Interleukin-2 (IL-2), Interferon-gamma (IFN-gamma)] and T(H)2 (IL-4 and IL-10) cytokines in the sera from patients affected with PV and compared with Pemphigus foliaceus and healthy subjects. This work is aimed to comprehend the involvement of T(H)1 and T(H)2 cells as inflammatory infiltrate in the modulation of acantholysis and production of pemphigus lesions. Seventy PV, 13 PF and 50 healthy, age-matched individuals without any generalized skin diseases were included in this study. The diagnosis of PV and PF patients was confirmed by histopathology (hematoxylin and eosin) and / direct immunofluorescence. The levels of T(H)1 cytokines (IL-2 and IFN-gamma) and T(H)2 cytokine markers (IL-4 and IL-10) were estimated by high sensitivity ELISA kits. All patients with PV and PF showed significantly (p < 0.000) elevated levels of T(H)2 cytokines (IL-10 and IL-4) as compared with healthy controls. However, the mean concentration of T(H)1 cytokines (IL-2 and IFN-gamma) was significantly decreased in patients as compared to healthy individuals. Both T(H)1 and T(H)2 cytokines did not show any significant difference between PV and PF cases. Current concepts support the idea that PV, induced by autoantibodies against Dsg3, is the consequence of an imbalance between Dsg3-reactive T(H)2 and T(H)1 cells that may be critical for the maintenance of tolerance against Dsg3. Cytokine profile for confirmed PV cases showed direct evidences for involvement of T cell responses. Increase in IL-4 and IL-10 shows induction of T(H)2 cells in the pathogenesis of autoimmune disorders Pemphigus vulgaris. The decreased levels of IL-2 and IFN-gamma might demonstrate the inhibitory effects by IL-4 and IL-10, which suppress the expansion of T(H)1 population.
Drug-induced photosensitivity occurs when a drug is capable of absorbing radiation from the sun (usually ultraviolet A) leading to chemical reactions that cause cellular damage (phototoxicity) or, more rarely, form photoallergens (photoallergy). The manifestation varies considerably in presentation and severity from mild pain to severe blistering. Despite screening strategies and guidelines in place to predict photoreactive drugs during development there are still new drugs coming onto the market that cause photosensitivity. Thus, there is a continuing need for dermatologists to be aware of the different forms of presentation and the culprit drugs. Management usually involves photoprotection and cessation of drug treatment. However, there are always cases where the culprit drug is indispensable. The reason why some patients are susceptible while others remain asymptomatic is not known. A potential mechanism for the phototoxic reactions is the generation of reactive oxygen species (ROS), and there are a number of reasons why some patients might be less able to cope with enhanced levels of ROS.
Our understanding of the aetiology of androgenetic alopecia (AGA) has substantially increased in recent years. As a result, several treatment modalities have been tried with promising results especially in early stages of AGA. However, as far as has been ascertained, there is no comprehensive study comparing the efficacy of these agents alone and in combination with each other. One hundered male patients with AGA of Hamilton grades II to IV were enrolled in an open, randomized, parallel-group study, designed to evaluate and compare the efficacy of oral finasteride (1 mg per day), topical 2% minoxidil solution and topical 2% ketoconazole shampoo alone and in combination. They were randomized into four groups. Group I (30 patients) was administered oral finasteride, Group II (36 patients) was given a combination of finasteride and topical minoxidil, Group III (24 patients) applied minoxidil alone and Group IV (10 patients) was administered finasteride with topical ketoconazole. Treatment efficacy was assessed on the basis of patient and physician assessment scores and global photographic review during the study period of one year. At the end of one year, hair growth was observed in all the groups with best results recorded with a combination of finasteride and minoxidil (Group II) followed by groups IV, I and III. Subjects receiving finasteride alone or in combination with minoxidil or ketoconazole showed statistically significant improvement (p<0.05) over minoxidil only recipients. No signifcant side-effects related to the drugs were observed. In conclusion, it is inferred that the therapeutic efficacy is enhanced by combining the two drugs acting on different aetiological aspects of AGA.
The study indicates that levamisole is not as effective in arresting disease progression as was observed in a previous open study. A study with a larger sample size is necessary to determine if levamisole is truly superior to placebo in this respect.
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