Acute de Garengeot Hernia Masquerading as a Recurrent Inguinal Hernia – A Diagnostic Dilemma.

A de Garengeot hernia is a femoral hernia in which the sac contains the vermiform appendix. herein, we report an interesting case of a de Garengeot hernia with secondary appendicitis presenting acutely in a male patient with previous history of inguinal hernia repair. We discuss the diagnostic dilemmas involved and present a review of current literature.

A rare case of dual obstruction of the colon.

The commonest cause of large bowel obstruction is colorectal malignancy. Volvulus of the colon is a rare cause and caecal volvulus accounts for less than 1% of all cases of intestinal obstruction. Reports of concurrent occurrence of obstructing lesions of the right and left colon are rare and anecdotal. We report a case of Caecal volvulus and carcinoma of the rectosigmoid in a 70-year-old lady.

Cutaneous histiocytic lesions: a clinical dilemma.

The diagnosis of malignant histiocytosis requires a high index of clinical suspicion, awareness of its atypical features and availability of various tissue samples for morphological and special studies. The case reported here highlights the diagnostic difficulties encountered in a patient diagnosed as malignant histiocytosis who presented with cutaneous lesions in multiple foci, which included the face, groin and forearm. Only after repeated biopsies and special stains, a diagnosis of malignant histiocytosis was arrived at. Chemotherapy with CHOP regimen (cyclophosphamide, doxorubicin, vincristine and prednisone) was initiated. The response to chemotherapy was good and the patient is doing well eleven months after initial diagnosis.

Pharmacokinetic study of niosome encapsulated insulin.

Pharmacokinetic profile and hypoglycemic effect, after intraperitoneal injection of insulin and insulin encapsulated in niosomes were determined in diabetic rats. Niosomes (non-ionic surfactant vesicles) of different doses and different lipid compositions were prepared by lipid layer hydration method. Plasma samples were collected at specified time intervals and plasma concentration of insulin was determined by HPLC. Blood glucose level was estimated spectrophotometrically using commercial glucose assay kit. In vitro release and pharmacokinetic profile of niosomal formulation and free insulin were evaluated. Though there was a slight delay in the in vitro drug release due to cholesterol content in the niosomes, there was no difference between the two preparations when plasma levels were compared in vivo. Niosomes significantly reduced the blood glucose level in diabetic rats. Fall in blood glucose level was almost 92% of initial value. In case of the niosomal form the half-life of insulin was prolonged by 4 -5 hr in contrast to 2 hr for free drug. Niosomes maintained the plasma insulin level up to 12 hr, but free drug was cleared quickly. The area under the plasma concentration-time curve for niosomal forms was, 26.07 degrees +/- 0.99 mIU. hr/ml and for free insulin was 11.722 +/- 1.00 mIU. hr/ml. More than 80% of the drug was successfully encapsulated to give a formulation with sustained release characteristics. Entrapment efficiency increased with increasing lipid concentration and decreased with increasing drug concentration. The results showed that insulin entrapped in niosomes prolongs the existence of drug in the body therefore increasing its therapeutic value.

Effect of antihypertensive drugs on ethanol induced gastric lesions: is there a correlation with mucosal blood flow?

We studied the effect of five antihypertensive drugs on ethanol-induced gastric haemorrhagic lesions in rats. While hydralazine aggravates these lesions, nifedipine and propranolol have a protective action. On the other hand, enalapril and prazosin have no effect. Thus the effects of antihypertensive drugs on ethanol-induced lesions do not always correlate with their reported actions on gastric mucosal blood flow.

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.

Gastric cytoprotection.

The term 'cytoprotection' means protection against gastric mucosal injury by a mechanism other than inhibition or neutralisation of gastric acid. Several mechanisms of gastric cytoprotection have been proposed like increased mucus and bicarbonate secretion, strengthening of gastric mucosal barrier, increased gastric mucosal blood flow, decreased gastric motility, increased formation of prostaglandins and sulfhydryls, scavenging of free radicals, stimulation of cellular growth and repair, decreased release of leukotrienes etc. Some of the drugs widely used in therapy of peptic ulcer are cytoprotective e.g. sucralfate, colloidal bismuth and aluminium containing antacids. As the concept of gastric cytoprotection is becoming widely accepted, the list of drugs which have shown a cytoprotective action in animal experiments is growing rapidly. This list includes zinc sulphate, meciadanol, propranolol, dipyridamole etc.

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).

Comparison of the effects of captopril and enalapril on oxyphenbutazone and ethanol-induced gastric lesions in rats.

We have compared the effect of the converting enzyme inhibitors, captopril and enalapril, on two models of gastric ulcers, viz; ethanol and oxyphenbutazone-induced lesions in rats. Both captopril and enalapril did not affect ethanol-induced lesions. While captopril significantly protected against oxyphenbutazone-induced lesions, enalapril aggravated the lesions. This difference is probably due to the lack of the protective sulfhydryl group in the chemical structure of enalapril.

Vascular desensitisation--possible role of prostaglandins.

Prolonged exposure to noradrenaline (NA) brings about an increase in the release of prostaglandin (PG)-like material from rat aortic strip. The release is greater with oxymetazoline while methoxamine decreases it. These effects are blocked by yohimbine and prazosin respectively. Pretreatment with 6-OHDA or reserpine diminishes the release of PG-like material. Barium chloride, a non-specific spasmogen, does not affect the release significantly. It appears therefore that the source of PG-like material is presynaptic and that its release mechanism is linked to an alpha 2 (alpha 2) adrenoceptor. It is proposed that this release of PG-like material contributes to the development of desensitisation in vascular tissue.