Are calculated ratios and red blood cell and platelet distribution width really important for the laryngeal cancer and precancerous larynx lesions.

INTRODUCTION: In this research, it is planned to investigate the differences in neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio, lymphocyte-to-monocyte ratio, reticulocyte distribution width, and platelet distribution width values of groups of benign laryngeal lesion, precancerous laryngeal lesion, and laryngeal squamous cell carcinoma and among patients with different stages of tumors in laryngeal carcinoma and precancerous laryngeal lesion groups, and whether these values carry a prognostic features. MATERIALS AND METHODS: The investigated parameters determined from preoperative blood samples of patients have been compared among the groups and in the subgroups according to severity of illness in laryngeal carcinoma and precancerous laryngeal lesion groups. Also, the laryngeal carcinoma and precancerous laryngeal lesion groups were divided into two subgroups as good and poor prognosis and were compared with patients having good prognosis requiring no additional treatment during the follow-up, and the statistical significance of the differences was examined. RESULTS: On comparison, statistically significant differences were only observed between the gross larynx carcinoma group and other lesions. Apart from that, when the values were evaluated in terms of prognosis, no significant statistical results were found in any of the values. CONCLUSION: Despite the significant statistical results seen in the gross tumors, it is known that there are more objective methods for identifying those lesions in clinical use. We conclude that caution should be exercised when using these new hematological parameters, which can be affected by many factors.

Comparison of clinical outcomes of three different packing materials in the treatment of severe acute otitis externa.

OBJECTIVE: To analyse the clinical outcomes of biodegradable synthetic polyurethane foam versus ribbon gauze and ear wick in the treatment of severe acute otitis externa. METHODS: Ninety-two adults with severe acute otitis externa were randomly assigned to groups receiving ear wick (n = 28), ribbon gauze (n = 34) or biodegradable synthetic polyurethane foam (n = 30). Clinical efficacy, in terms of otalgia, oedema, erythema and tenderness of the external auditory canal, was assessed before packing was applied and at follow up on the 3rd and 7th days of presentation. RESULTS: All packing materials were associated with improved otalgia and oedema on the 3rd day; however, there were significant differences between biodegradable synthetic polyurethane foam and the other packing materials, and there was no significant reduction in tenderness in the biodegradable synthetic polyurethane foam group on the 3rd day. In the ribbon gauze and ear wick groups, improvements in all clinical efficacy scores were statistically significant for all pairwise comparisons. CONCLUSION: The three packing materials were all quite effective in treating severe acute otitis externa, but ear wick and ribbon gauze were superior to biodegradable synthetic polyurethane foam for relieving signs and symptoms, especially on the 3rd day.

Protective effect of CDP-choline on ischemia-reperfusion-induced myocardial tissue injury in rats.

BACKGROUND: CDP-choline exerts tissue protective effect in several ischemic conditions. Recently we have reported that the drug prevents cardiac arrhythmias and improves survival rate in short-term myocardial ischemia reperfusion in rats. AIM: In the current study, we determined the effect of intravenously administered CDP-choline on myocardial tissue injury induced by 30-min ischemia followed by 3-h reperfusion in anesthetized rats. METHODS: Myocardial ischemia was produced by ligature of the left main coronary artery. CDP-choline (100-500 mg/kg) was intravenously injected in the middle of the ischemic period. Cardiovascular parameters were recorded through the experimental period. At the end of the reperfusion period, the hearts of the animals were removed and stained for the investigation of tissue necrosis and apoptosis. The infarct size was evaluated as the ratio of the infarct area to the risk area. Apoptotic activation was assessed by TUNEL assay. Also the blood samples of rats were collected for the measurement of M30-M65, ADMA, homocysteine, and lactate levels. RESULTS: Ischemia/reperfusion caused serious injury in myocardium, increased blood ADMA and lactate levels without influencing other parameters. CDP-choline significantly reduced the infarct size and the number of apoptotic cells in the risk area. Blood pressure increased after CDP-choline injection; however, it returned back to the basal levels before the onset of reperfusion. CDP-choline failed to alter any other measured parameters. CONCLUSION: The present results demonstrate that intravenously administered CDP-choline is able to protect myocardium from injury induced by long-term coronary occlusion-reperfusion in rats. The inhibition of apoptosis by the drug may contribute to its protective effect. But neither the increase in blood pressure in response to CDP-choline injection nor changes in plasma ADMA concentration appear to mediate the attenuation of the myocardial injury.

Peripheral administration of CDP-choline, phosphocholine or choline increases plasma adrenaline and noradrenaline concentrations.

1 Intraperitoneal (i.p.) injection of 200-600 mumol/kg of cytidine-5'-diphosphocholine (CDP-choline) increased plasma adrenaline and noradrenaline concentrations dose- and time-dependently. 2 CDP-choline treatment caused several-fold increases in plasma concentrations of CDP-choline and its metabolites phosphocholine, choline, cytidine monophosphate (CMP) and cytidine. 3 Equivalent doses (200-600 mumol/kg; i.p.) of phosphocholine or choline, but not CMP or cytidine, increased plasma adrenaline and noradrenaline dose-dependently. 4 CDP-choline, phosphocholine and choline (600 mumol/kg; i.p.) augmented the increases in plasma adrenaline and noradrenaline in response to graded haemorrhage. 5 The increases in plasma adrenaline and noradrenaline induced by i.p. 600 mumol/kg of CDP-choline, phosphocholine or choline were abolished by pre-treatment with hexamethonium (15 mg/kg; i.p.), but not atropine (2 mg/kg; i.p.). 6 At 320-32 000 mum concentrations, choline, but not CDP-choline or phosphocholine, evoked catecholamine secretion from perfused adrenal gland. Choline (3200 mum)-induced catecholamine secretion was attenuated by the presence of 1 mum of hexamethonium or mecamylamine, but not atropine, in the perfusion medium. 7 Intracerebroventricular (i.c.v.) injection of choline (0.5-1.5 mumol) also increased plasma adrenaline and noradrenaline dose- and time-dependently. Pre-treatment with mecamylamine (50 mug; i.c.v.) or hexamethonium (15 mg/kg; i.p.), but not atropine (10 mug; i.c.v.), prevented i.c.v. choline (1.5 mumol)-induced elevations in plasma adrenaline and noradrenaline. 8 It is concluded that i.p. administration of CDP-choline or its cholinergic metabolites phosphocholine and choline increases plasma adrenaline and noradrenaline concentrations by enhancing nicotinic cholinergic neurotransmission in the sympatho-adrenal system. Central choline also activates the sympatho-adrenal system by increasing central nicotinic cholinergic neurotransmission.

Intraperitoneal administration of CDP-choline and its cholinergic and pyrimidinergic metabolites induce hyperglycemia in rats: involvement of the sympathoadrenal system.

CDP-choline is an endogenous metabolite in phosphatidylcholine biosynthesis. Exogenous administration of CDP-choline has been shown to affect brain metabolism and to exhibit neuroprotective actions. On the other hand, little is known regarding its peripheral actions. Intraperitoneal administration of CDP-choline (200-600 micromol/kg) induced a dose- and time-dependent hyperglycemia in rats. Hyperglycemic response to CDP-choline was associated with several-fold elevations in serum concentrations of CDP-choline and its metabolites. Intraperitoneal administration of phosphocholine, choline, cytidine, cytidine monophosphate, cytidine diphosphate, cytidine triphosphate, uridine, uridine monophosphate, uridine diphosphate and uridine triphosphate also produced significant hyperglycemia. Pretreatment with atropine methyl nitrate failed to alter the hyperglycemic responses to CDP-choline and its metabolites whereas hexamethonium, the ganglionic nicotinic receptor antagonist which blocks nicotinic cholinergic neurotransmission at the autonomic ganglionic level, blocked completely the hyperglycemia induced by CDP-choline, phosphocholine and choline, and attenuated the hyperglycemic response to cytidine monophosphate and cytidine. Increased blood glucose following CDP-choline, phosphocholine and choline was accompanied by elevated plasma catecholamine concentrations. Hyperglycemia elicited by CDP-choline and its metabolites was entirely blocked either by pretreatment with a nonselective -adrenoceptor antagonist phentolamine or by the 2-adrenoceptor antagonist, yohimbine. Hyperglycemic responses to CDP-choline, choline, cytidine monophosphate and cytidine were not affected by chemical sympathectomy, but were prevented by bilateral adrenalectomy. Phosphocholine-induced hyperglycemia was attenuated by bilateral adrenalectomy or by chemical sympathectomy. These data show that CDP-choline and its metabolites induce hyperglycemia which is mediated by activation of ganglionic nicotinic receptors and stimulation of catecholamine release that subsequently activates 2-adrenoceptors.