Corneal Leproma : A Rare Ocular Manifestation in Leprosy

A leproma is a discrete granulomatous nodule rich in lepra bacilli and is a rare yet characteristic finding seen in the lepromatous spectrum of Hansen’s disease. Majority of the ocular lepromas reported in the literature so far arise from uveal tissue and sclera with an incidence of 0.75 to 1%. Exclusive corneal leproma associated with multibacillary leprosy is an extremely rare finding. It is painless and silent nature in earlier stages because of that it may remain unattended for several years until significant visual loss, disease progression and transmission may continue to occur. We report a case having corneal leproma, the detection of which led to the uncovering of advanced cutaneous involvement. The patient had chosen not to disclose his skin involvement and disability possibly due to social stigma and partly due to ignorance. The presence of such untreated multi-bacillary forms in the community may present a significant hurdle for a country like ours, aiming to eliminate this chronic disease. Public awareness through health education coupled with early detection remains the cornerstone in tackling this multi-system disorder which has implications both from disability and transmission angles

Aggravating action of hydralazine on ethanol-induced gastric lesions.

Endogenous nitric oxide has been proposed as one of the mediators of gastric cytoprotection. We studied the effect of the vasodilator hydralazine which acts via nitric oxide and thus is expected to have a gastroprotective action. However, hydralazine aggravates ethanol-induced gastric lesions. This effect is not influenced by pretreatment with the selective alpha 1 adrenergic antagonist prazosin but is abolished by the angiotensin converting enzyme inhibitor, captopril suggesting the involvement of the renin-angiotensin system.

Protective effect of propranolol on ethanol-induced gastric lesions in rats: probable mechanism of action.

The non-selective beta-adrenoceptor antagonist, propranolol, has been reported to protect against gastric injury in mice, an effect only partly due to prostaglandin release. This study was designed to confirm the gastric cytoprotective effect of propranolol in another species of animal, the rat, and investigate further its mechanism of action. Our results show that propranolol prevents both ethanol-induced gastric lesions as well as ethanol-induced contraction of the circular muscle of rat fundic strip. The local anaesthetic, lignocaine also inhibited the effect of ethanol on circular muscle. However, timolol, another non-selective beta-adrenoceptor antagonist, failed to produce such an action. The effect of propranolol was abolished by the cyclooxygenase inhibitor, indomethacin and a high dose of the guanylate cyclase inhibitor, methylene blue. The results suggest that in addition to prostaglandins, endogenous nitric oxide and the membrane stabilising action of propranolol may also be involved in its gastroprotective action.

Aggravating action of clonidine on ethanol-induced gastric lesions: probable mechanism of action.

Large doses of the imidazoline alpha 2 adrenoreceptor agonist clonidine aggravate ethanol-induced gastric lesions. The alpha 2 adrenoceptor antagonist phentolamine, the opioid antagonist naloxone and the H2 antagonist cimetidine do not prevent this action of clonidine suggesting that it is not mediated by alpha 2, opioid or H2 receptors. Further, like clonidine, high doses of phentolamine and cimetidine aggravate gastric lesions per se, suggesting that all three may be acting at a common 'receptor' site, possibly the imidazoline-preferring receptor (IPR).