Abstract:The elimination of leprosy has been possible with the available anti-leprotic drugs. However, the lepra reactions usually occur months or years after multi-drug therapy completion, and continue to be a formidable challenge mainly owing to its role in causing nerve damage and disability. Corticosteroids are commonly used but they lead to systemic complications, and hence require dose reduction and adjunct therapy with a different target. Various drugs with different targets have been identified and are in practice to treat lepra reactions. The newer targets can include genetic and tissue targets in the skin and nerve. Thalidomide treatment reducing pentraxin-3, toll-like receptor antagonists, minocycline, apremilast, immunomodulators, and tenidap can be helpful in lepra reaction. Other modalities to manage lepra reactions include plasma exchange, intravenous immunoglobulins, and immunotherapy. Most of these treatments are based only on the pathological process of the reaction and tend to be incomplete leading to recurrence. Newer multimodal approaches are required based on various biomarkers (genetic, tissue, serological), which can be monitored to prevent the recurrence of reactions. Hence, there is a need for newer targets and drugs to be identified for the management of lepra reactions.

01 Jan 2020·Indian Dermatology Online Journal

What is new in the pathogenesis and management of erythema nodosum leprosum

Review

Author: Bhat, Ramesh M ; Vaidya, Tanvi P

Erythema nodosum leprosum (ENL) is a manifestation of type II lepra reaction, seen in lepromatous or borderline lepromatous leprosy. Although it is a common reaction encountered in clinical practice, there are an increasingly large number of newer updates in the pathophysiology and management of this condition. The treatment options have expanded far beyond just thalidomide and steroids and now extends to TNF-α inhibitors, thalidomide analogs, tenidap, cyclosporine A, plasma exchange, and even IVIG amongst others. These updates and the current knowledge of ENL are summarized in this review.

30 Dec 2019·CNS & Neurological Disorders - Drug Targets

Activation of Kir2.3 Channels by Tenidap Suppresses Epileptiform Burst Discharges in Cultured Hippocampal Neurons

Article

Author: Zhang, Lu ; Wang, Guoxiang ; Sun, Wanbing ; Wang, Yun ; Wu, Xunyi ; Zang, Kai ; Chen, Zhiyun ; Zhang, Yuwen

Background & Objective:Tenidap, a selective human inwardly rectifying potassium (Kir) 2.3 channel opener, has been reported to have antiepileptic effect in the pilocarpine temporal lobe epilepsy rat model in our previous study. However, the effect of tenidap on neurons and its relationship with the epileptiform bursting charges in neuron is still required to be explored.Methods:In this study, cyclothiazide (CTZ) induced cultured hippocampal neuron epileptic model was used to study the antiepileptic effect of tenidap and the relationship between Kir2.3 channel and the neuronal epileptiform burst.Results:Patch clamp recording showed that both acute (2h) and chronic (48h) CTZ pre-treatment all significantly induced robust epileptiform burst activities in cultured hippocampal neurons, and tenidap acutely application inhibited this highly synchronized abnormal activities. The effect of tenidap is likely due to increased activity of Kir2.3 channels, since tenidap significantly enhanced kir current recorded from those neurons. In addition, neurons overexpressing Kir2.3 channels, by transfection with Kir2.3 plasmid, showed a significant large increase of the Kir current, prevented CTZ treatment to induce epileptiform burst discharge.Conclusion:Our current study demonstrated that over activation of Kir2.3 channel in hippocampal neurons could positively interference with epileptiform burst activities, and tenidap, as a selective Kir2.3 channel opener, could be a potential candidate for seizure therapy.

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