Sudden bilateral hearing loss after spinal anaesthesia.

BACKGROUND: Spinal anaesthesia is one of the most widely used regional anaesthesia techniques. Sudden bilateral hearing loss following spinal anaesthesia has only been reported in a few cases. CASE REPORT: This paper reports the case of a 50-year-old woman who developed sudden bilateral hearing loss following spinal anaesthesia for hallux valgus orthopaedic surgery. This is followed by a literature review. RESULTS: The patient's hearing improved almost completely on the morning of the 3rd day following surgery. No recurrence of hearing loss, tinnitus or vertigo was reported during the six-month follow-up period. CONCLUSION: Some complications regarding hearing may emerge after spinal anaesthesia. The possibility of hearing loss after spinal anaesthesia should be taken into consideration. Complaints such as hearing loss, tinnitus or vertigo should be taken seriously when reported, and the patient should be referred to an ENT clinic. This will ensure early diagnosis and treatment.

Investigation of zinc and copper levels in methimazole-induced hypothyroidism: relation with the oxidant-antioxidant status.

Thyroid hormones are associated with the oxidative and antioxidative status of the organism. Depression of metabolism by hypothyroidism has been reported to decrease oxidant production and thus protect tissues against oxidant damage. The purpose of the present study was to investigate Zn and Cu levels in MMI-induced hypothyroidism and to show whether there is a connection between these trace elements and the oxidant-antioxidant status in experimental hypothyroidism. 3-Nitrotyrosine was measured as a marker of nitro-oxidative stress. In order to examine the antioxidant status of MMI-induced hypothyroidism in rats, GSH and SOD levels were determined as well. Significantly decreased 3-nitrotyrosine, Cu and Zn levels were observed in our experimental model when compared with the controls. On the other hand, GSH and SOD levels remained constant. It may be suggested that Cu and Zn serve as antioxidant molecules and exert their effects in an indirect manner to reduce oxidative stress in experimental hypothyroidism.

The effects of experimental hyperthyroidism on hemorheology and plasma fibrinogen concentration.

The present study in female rats determined the effects of experimental hyperthyroidsm on hemorheological parameters and fibrinogen concentration. To induce experimental hyperthyroidism L-thyroxine (0.4 mg/100 g fodder) was added to the fodder of the experimental group rats for 20 d. After experimental duration, T3, T4, and TSH levels, plasma and blood viscosity, hematocrit, erythrocyte rigidity index, and plasma fibrinogen concentration values of both the control and the experimental group animals were determined and evaluated. In the experimental group, T3 and T4 levels were higher and TSH levels lower than that of the control rats (respectively, p < 0.01, p < 0.001, p < 0.001). Plasma viscosity and fibrinogen concentration of hyperthyroid group were found significantly higher than controls (p < 0.01). However there was no significant difference found in blood viscosity, hematocrit, and erythrocyte rigidity index between control and experimental groups. Thus, hyperthyroidism induced increased fibrinogen concentration can alter the rheological structure of blood by inducing increase in plasma viscosity.

Oxidative stress in heart tissue of hyperthyroid and iron supplemented rats.

This study was designed to investigate the effect of hyperthyroidism and/or iron supplementation or cardiac oxidative stress parameters--the lipid peroxidation end product glutathione (GSH), glutathione peroxidase (CSH-Px), and superoxide dismutase (CuZnSOD)--in rats. In plasma, ferritin as an indicator of iron status and glutamate oxaloacetate transaminase (GOT) as an indicator of damage to the heart tissue were analyzed. Our findings show that hyperthyroidism increased lipooxidative damage as reflected by higher lipid peroxidation end product levels and elevated antioxidant defense parameters-GSH and GSH-Px. Iron supplementation per se does not affect oxidative stress parameters studied in the euthyroid state. Although iron increased lipid peroxidation in the hyperthyroid state, this effect was less than that seen in euthyroidism. Iron supplementation to hyperthyroid rats significantly lowered plasma ferritin levels, suggesting increased iron elimination with consequently reduced oxidative stress.

Evaluation of oxidative stress in experimental colitis: effects of L-arginine-nitric oxide pathway manipulation.

In this study it was of interest to evaluate the impact of nitric oxide (NO) modulation by administration of arginine/NAME, on oxidative stress in experimental colitis induced by 2,4,6-trinitrobenzenesulfonic acid. Arginine was used to increase NO levels while NAME lowered oxidant levels. Histopathological findings of colon revealed mucosal inflammation in all groups but significantly higher with arginine alone. The levels of NO and of thiobarbituric acid-reactive substances (TBARS, a marker of lipid peroxidation) were observed to be significantly higher in the arginine-administered group compared to glycine, and these levels were found to decrease on administration of NAME to both glycine- and L-arginine-administered groups. Glutathione peroxidase (GSH-Px) activity and glutathione (GSH) levels were significantly higher in arginine administered group compared to glycine. Significantly higher CuZn superoxide dismutase (CuZn-SOD) activity was observed in the L-arginine + L-NAME group compared to arginine. Data show that NO plays a role in oxidant damage found in experimental colitis and that the use of NAME may potentially inhibit injury.

Evaluation of antioxidant status in liver tissues: effect of iron supplementation in experimental hyperthyroidism.

The antioxidant defense system in liver tissue in experimental hyperthyroidism and/or in iron supplementation was investigated. Thyroid hormones (T3, T4, TSH), ferritin (marker of iron status), antioxidant status components (glutathione [GSH], glutathione peroxidase [GSH-Px], superoxide dismutase [SOD]), and serum transaminases (GOT and GPT, both of which are known to be released from damaged hepatocytes), were measured. Hyperthyroidism in rats, induced by L-thyroxine administration, significantly raised SOD activity (p < 0.05), but significantly decreased GSH-Px activity and GSH values (p < 0.001) in the liver. In the L-thyroxine administered and iron supplemented (TI) group, GSH and GSH-Px values of liver tissues were significantly lower than those of control rats (p < 0.05). GSH-Px levels of the TI group were higher (p < 0.001), and SOD levels significantly lower (p < 0.001) than those of the L-thyroxine administered group. We conclude that hyperthyroidism induces SOD activity in liver; ferritin levels increase in hyperthyroidism, contributing to the antioxidant defense system; GSH-Px and GSH levels are decreased significantly in hyperthyroidism either due to inactivation due to increased oxidative stress or to insufficient synthesis; iron supple- and GPT analysis); iron decreases the effect of T4. This must be taken into consideration during iron supplementation.

The effect of iron supplementation on GSH levels, GSH-Px, and SOD activities of erythrocytes in L-thyroxine administration.

Our aim was to study the effect of iron supplementation on the following aspects of erythrocyte metabolism in experimental hyperthyroidism: glutathione (GSH) levels, glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD) activities. Hyperthyroidism induced by L-thyroxine administrations significantly raised erythrocyte GSH, GSH-Px and SOD levels of the rats (P < 0.001). Likewise, we observed that iron supplementation induced significant rises in erythrocyte GSH, GSH-Px and SOD levels (P < 0.001) as compared with the control group. The erythrocyte GSH, GSH-Px and SOD levels of hyperthyroidism-induced iron-supplemented animals were significantly higher when compared with either the iron-supplemented group (P < 0.001) or the only L-thyroxine-administered hyperthyroid group (P < 0.001, P < 0.05, P < 0.01, respectively). The results of this study show that L-thyroxine administration and/or iron supplementation increases GSH, GSH-Px and SOD levels of erythrocytes.

Calcium, magnesium, and zinc status in experimental hyperthyroidism.

In this study, experimental hyperthyroidism was established and used to investigate possible alterations in the calcium (Ca), magnesium (Mg), and zinc (Zn) homeostasis by assessing their concentrations in plasma and erythrocytes. In the L-thyroxine-induced hyperthyroidism condition, the experimental animals show a significant decrease in erythrocyte Ca, Mg, and Zn concentrations, and a significant decrease in plasma Mg concentration. Significant positive correlations were found for Mg and Zn both in plasma and in erythrocytes. The results suggest that the homeostasis of Ca, Mg, and Zn is altered during experimental hyperthyroidism.

Calcium, magnesium, and zinc status in experimental hypothyroidism.

In this study, experimental hypothyroidism was established and used to investigate possible alterations in the calcium, magnesium, and zinc homeostasis by assessing their concentration in plasma and erythrocytes. Hypothyroidism was induced by administration of methimazole an iodine blocker at a dose of 75 mg/100 g food for 3 wk. In the methimazole-induced hypothyroid state, the experimental animals showed a significant decrease in plasma zinc concentration, whereas a significant increase in plasma magnesium concentration occurred. No change was observed in plasma calcium concentration. The erythrocyte zinc and calcium concentrations were found to be increased, whereas magnesium concentration decreased. Erythrocyte magnesium concentration showed a significant positive correlation with T4 values. The study provides evidence for marked alterations in homeostatis of zinc, magnesium, and calcium.

Antioxidant status in experimental hyperthyroidism: effect of vitamin E supplementation.

Free radical-mediated oxidative stress has been implicated in the genesis and exacerbation of degenerative diseases. In view of the role of oxidative processes in hyperthyroidism, in this study, we investigated the antioxidant status of erythrocytes in experimental hyperthyroidism and the effect of vitamin E supplementation on defense systems. Our findings of significantly increased T4 and T3 and undetectable TSH values in thyroxine administered rats confirmed the establishment of hyperthyroidism. Superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and glutathione (GSH) values were found to be significantly increased in hyperthyroid rats in comparison to the control group. Vitamin E supplementation to hyperthyroid rats induced a significant decrease in GSH-Px activity and a significant increase in GSH level. These findings show that hyperthyroidism increases the components of the antioxidant system in the erythrocytes. Furthermore, vitamin E supplementation reduces the burden of oxidative stress in hyperthyroidism.