Inflammatory choroidal neovascularization in Indian eyes: Etiology, clinical features, and outcomes to anti-vascular endothelial growth factor.

BACKGROUND AND OBJECTIVES: The aim was to study the clinical profile of inflammatory choroidal neovascularization (CNV) and its treatment response to intravitreal bevacizumab or ranibizumab on pro re nata (PRN) basis in Indian eyes. MATERIALS AND METHODS: This was a retrospective case series of consecutive patients with inflammatory CNV treated with anti-vascular endothelial growth factor (anti-VEGF) in a tertiary eye care center in Eastern India between 2009 and 2014. The data about clinical features, investigations, treatment, and outcomes were obtained from the medical records. We included patients with active inflammatory CNV but with no evidence of inflammation and were treated with anti-VEGF alone, with a minimum follow-up of 6 months. Main outcome measures were a clinical and etiological profile of inflammatory CNV in Indian eyes and their response to treatment. RESULTS: Thirty eyes of 28 patients were included in the study. The mean follow-up was 17.93 ± 14.28 months (range 6-53 months). In our cohort, seven (23.33%) eyes had inflammatory CNV secondary to idiopathic choroiditis, four (13.33%) eyes had toxoplasmosis, idiopathic panuveitis, and Vogt Koyanaki Harada's disease each. Three (10%) eyes had geographic helicoid peripapillary choroidopathy and tubercular choroiditis each. Remaining two (6.66%) eyes had punctate inner choroidopathy, while multifocal choroiditis with panuveitis, resolved endogenous endophthalmitis and Hansen's diseases were the etiology in one (3.33%) case of inflammatory CNV each. The mean number of injections were 2.76 (range 1-5). Among thirty eyes of inflammatory CNV, 16 (53.3%) eyes showed improvement, eight (26.6%) maintained the same vision, whereas six (20%) eyes showed deterioration of vision. Interpretations and Conclusion: Idiopathic choroiditis was the most common cause of inflammatory CNV and PRN intravitreal anti-VEGF (ranibizumab or bevacizumab) appears to have effective treatment response.

Steven's Johnson syndrome with toxic epidermal necrolysis due to thalidomide in a case of multiple myeloma.

Thalidomide developed in 1954 for morning sickness had proven to be a teratogen and hence was withdrawn from market. Resurgence of thalidomide began as an immunomodulator when it was shown to be effective in the management of multiple myeloma and many conditions like erythema nodosum leprosum, graft versus host disease, recurrent aphthous ulcers etc. We report a case of Stevens Johnson syndrome-toxic epidermal necrolysis developing in an elderly male who was prescribed thalidomide after being diagnosed with multiple myeloma.

Leukocytoclastic vasculitis due to thalidomide in multiple myeloma.

Thalidomide is successfully used in the treatment of multiple myeloma, leprosy and various autoimmune diseases due to its anti-angiogenic, immunomodulatory and anti-inflammatory effects. Thalidomide's most common side effects are constipation, neuropathy, fatigue, sedation, rash, tremor and peripheral edema. We achieved complete response with a 400 mg/day dose thalidomide therapy in a 58-year-old male patient diagnosed with relapsing refractory multiple myeloma. While continuing thalidomide for sustainable response, the therapy was terminated at the ninth month due to development of leukocytoclastic vasculitis. We describe the case and discuss the place of thalidomide in the treatment of multiple myeloma and the rare occurrence of leukocytoclastic vasculitis during thalidomide therapy in multiple myeloma, since only one such case has been reported in the literature thus far.

Development of leukocytoclastic vasculitis in a patient with multiple myeloma during treatment with thalidomide.

Thalidomide, an agent with antiangiogenic and immunomodulatory properties, is therapeutically effective in multiple myeloma, leprosy, and autoimmune diseases. The most common clinical toxicities of thalidomide are constipation, neuropathy, fatigue, sedation, rash, tremor, and edema. We here describe for the first time a patient who developed leukocytoclastic vasculitis during therapy with thalidomide. Of the 260 patients treated with thalidomide in our institution, this is the first patient who developed autoimmune disease. We conclude that patients with malignant disorders who are treated with thalidomide should be carefully monitored for the development of autoimmune disorders. Whether autoimmune phenomena also occur during treatment with new drugs such as PS-341 or potent immunomodulatory agents remains to be evaluated.

Dermatologic side effects of thalidomide in patients with multiple myeloma.

BACKGROUND: Thalidomide, an antiangiogenic agent, was approved by the Food and Drug Administration in 1998 for the treatment of erythema nodosum leprosum. Although its teratogenic and neurologic side effects are well known, its dermatologic side effects continue to be defined. OBJECTIVE: We report the dermatologic side effects in 87 patients with multiple myeloma enrolled in a comparative, open-label, clinical trial treated with thalidomide alone (50 patients) or thalidomide and dexamethasone (37 patients). METHOD: We reviewed the records of all patients enrolled in the clinical trial. The frequency, type, severity, and time of onset of all skin eruptions that were temporally related to thalidomide treatment were recorded. RESULTS: Minor to moderate skin eruptions were noted in 46% of patients taking thalidomide alone and in 43% of those taking thalidomide and dexamethasone. These included morbilliform, seborrheic, maculopapular, or nonspecific dermatitis. Severe skin reactions (exfoliative erythroderma, erythema multiforme, and toxic epidermal necrolysis) that required hospitalization and withdrawal of thalidomide developed in 3 patients receiving thalidomide and dexamethasone. CONCLUSION: The prevalence of dermatologic side effects of thalidomide appear to be higher than previously reported. Although in most patients they were minor, in a few patients they were quite severe, particularly when given in conjunction with dexamethasone for newly diagnosed myeloma. Further studies are needed to verify the extent of the interaction between thalidomide and dexamethasone in this group of patients.