Objectives To describe the clinical profile of Asian Indian patients with Takayasu’s arteritis (TAK) and to compare clinical features and outcome of childhood-onset Takayasu’s arteritis (cTAK) with adult-onset TAK (aTAK). Methods Data related to clinical features and response to treatment of patients with cTAK (age of onset <16 years) and aTAK from a large observational cohort in our tertiary care teaching hospital were noted and compared. Results Altogether, 602 patients (cTAK = 119; aTAK = 483) were studied. Patients with cTAK had a blunted female: male ratio; but fever, elevated acute phase reactants, involvement of abdominal aorta or its branches, hypertension, abdominal pain, elevated serum creatinine and cardiomyopathy were more common in cTAK as compared with aTAK. Patients with aTAK were more likely to have aortic-arch disease and claudication than cTAK. During follow-up, complete remission was more common in cTAK (87% vs 66%; P < 0.01), but subsequent relapses were equally common (30% vs 27%; P = 0.63). Independent associations of disease duration at presentation with disease extent [Disease Extent Index in TAK (DEI.Tak)] and damage [TAK Damage Score (TADS)] were observed (P ≤ 0.01). Moreover, 54% of patients with symptom duration of >5 years at presentation still continued to have elevated CRP suggesting continued and active inflammation warranting escalation or inititation of immunosuppression. Conclusion Patients with cTAK are more likely to have arterial disease below the diaphragm, systemic inflammation and achieve remission. Disease of the aortic arch is more common in patients with aTAK. Longer duration of symptoms prior to initiation of immunosuppression, thereby leading to extensive disease and damage, reflects ongoing disease activity as the rule rather than exception in untreated TAK.
This study examined the pathological complete response (pCR) rate and safety of sequential gemcitabine-based combinations in breast cancer. We also examined gene expression profiles from tumour biopsies to identify biomarkers predictive of response. Indian women with large or locally advanced breast cancer received 4 cycles of gemcitabine 1200 mg m À2 plus doxorubicin 60 mg m À2(Gem þ Dox), then 4 cycles of gemcitabine 1000 mg m À2 plus cisplatin 70 mg m À2 (Gem þ Cis), and surgery. Three alternate dosing sequences were used during cycle 1 to examine dynamic changes in molecular profiles. Of 65 women treated, 13 (24.5% of 53 patients with surgery) had a pCR and 22 (33.8%) had a complete clinical response. Patients administered Gem d1, 8 and Dox d2 in cycle 1 (20 of 65) reported more toxicities, with G3/4 neutropenic infection/febrile neutropenia (7 of 20) as the most common cycle-1 event. Four drug-related deaths occurred. In 46 of 65 patients, 10-fold cross validated supervised analyses identified gene expression patterns that predicted with X73% accuracy (1) clinical complete response after eight cycles, (2) overall clinical complete response, and (3) pCR. This regimen shows strong activity. Patients receiving Gem d1, 8 and Dox d2 experienced unacceptable toxicity, whereas patients on other sequences had manageable safety profiles. Gene expression patterns may predict benefit from gemcitabine-containing neoadjuvant therapy.
Background:Arterial inflammation Takayasu arteritis (TA) is an outcome of balance between pro- and anti-inflammatory cytokines. Comprehensive assessment of these cytokines is important for understanding pathogenesis and assessing disease activity.Objective:To study pro- and anti-inflammatory cytokines representing different T-helper cell pathway in serum samples of Asian Indian patients with TA and to assess their association with disease activity.Methods:Consecutive Indian patients with TA were assayed for serum interferon-γ, interleukin-6, interleukin-23, interleukin-17, interleukin-10 and transforming growth factor- β levels at baseline and follow up visit. Patients were grouped into active and stable disease based on Indian Takyasu Arteritis clinical Activity Score-2010. Serum levels of these cytokines between active and stable disease and between baseline and follow up visits were compared by non-parametric tests.Results:Among 32 patients enrolled, 15 were classified as active while 17 as stable disease at baseline. IFN-γ levels were significantly higher in active disease than stable disease (p=0.0129) while other cytokines did not differ significantly between 2 groups. Serum levels of none of the cytokines changed significantly over 2 visits in both responders and non-responders. IL23 levels positively correlate with disease duration ((r=0.999; p<0.005). Modest correlation was observed between IFN-γ and IL23 levels at both baseline and follow up and between IFN-γ and IL-6 and CRP at follow up.Conclusion:IFN-γ levels are raised in active disease in TA and correlates well with other biomarkers of disease activity and proinflammatory cytokines. There is also a direct correlation between Il-23 levels and disease duration.
Chikungunya virus (CHIKV) has been involved in epidemics in African and Asian subcontinents and, of late, has transcended to affect the Americas. Aedes aegypti and Aedes albopictus are the major vectors for CHIKV infection, which results in dissemination of virus to various vital organs. Entry of virus into these tissues causes infiltration of innate immune cells, monocytes, macrophages, neutrophils, natural killer cells, and adaptive immune cells. Macrophages bearing the replicating virus, in turn, secrete pro-inflammatory cytokines IL-1β, TNF-α, and IL-17. Together, this pro-inflammatory milieu induces osteoclastogenesis, bone loss, and erosion. CHIKV is characterized by fever, headache, myalgia, rash, and symmetric polyarthritis, which is generally self-limiting. In a subset of cases, however, musculoskeletal symptoms may persist for up to 3-5 years. Viral culture and isolation from blood cells of infected patients are the gold standards for diagnosis of CHIKV. In routine practice, however, assays for anti-CHIKV IgM antibodies are used for diagnosis, as elevated levels in blood of infected patients are noted from 10 days following infection for up to 3-6 months. Early diagnosis of CHIKV is possible by nucleic acid detection techniques. Treatment of acute CHIKV is mainly symptomatic, with analgesics, non-steroidal anti-inflammatory agents (NSAIDs), and low-dose steroids. No vaccines or anti-viral medicines have been approved for clinical therapy in CHIKV as yet. Hydroxychloroquine and methotrexate have been used in chronic CHIKV infection with variable success.
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