Nutritional assessment of failure to thrive

Failure to thrive is a common problem that is met by pediatricians all over the world. 40 cases of children with FTT aged 1-5 years and 10 normal children of the same age as a conttrol group were studied. All were subjected to comperhensive history taking, through physical examination including anthroprometric assessment [weight, height, head and mid-arm circumferences] and laboratory investigations with particular to estimation of nutritional markers [plasma prealbumin, fibronectin and retinal binding protein]. Our results showed a statistically, significant difference with [P<0.001] in the weight and mid-arm circumference between cases of FTT and control group.Statistical non significan't difference between control group and cases in respect to supine length or height and head circumference [All parameters as a percentage of 50[th] percentile of normal Egyptian growth curves] there was statistical difference in the control levels and our cases of FTT in all nutritional markers. The mean prealbumin level in the control group was 25.4 +/- 9.2 mg/dL compared to the organic group 9.57 mg/dL with P value <0.0001 and in non-organic cases was 12.1 mg/dL with P -value [< 0.005] which is highly significant. The mean plasma fibronectin level in the control group was 21.5 +/- 6.8 mg/dL compared to the mean level in FTT cases 11.7 +/- 4.18 mg/dL with P-value [<0.05]. In the organic group mean level was 10. 15 +/- 3.2 mg/dL with P value [< 0.0005] and in non-organic group the mean fibronectin level was 12.68 +/- 2.3 mg/dL with P-value [< 0.05] compared to control group. Retinol binding protein mean level in control group was 3.82 +/- 1.1 mg/dL while in FTT cases was 1.81 +/- 0.69 mg/dL with statstically non-stignificant difference P-value [< 0.25]. We concluded that the incidence of non-organic failure to thrive cases was higher than the organic causes, most likely in children < 5 years. Ignorance, poverty, frequent infections, cultural customs or unstable families are the main causes in our developing countries

Effect of a single dose of clonidine and guanfacine on the content of norepinephrine and GABA in rat brain

This work aimed at studying the pattern of GABA and norepinephrine in Egyptian strain of male albino rats in normotensive and DOCA/ Salt hypertensive rats. Moreover, the effect of two centrally acting antihypertensive drugs namely clonidine and quanfacine upon the contents of neurotransmitters in whole brain as well as cerebral cortex, thalamus and hypothalamus, mid brain and hind brain was investigated. The data revealed that, the highest levels of norepinephrine and GABA were in hind brain of normotensive rats. Hypertensive rats showed significant increase in norepinephrine concentration in whole brain and specified areas.The concentration of GABA in hind brain of DOCA/Salt hypertensive rats was significantly raised. On the other hand, it was significantly decreased in other areas of brain. The agonistic effect of clonidine caused a significant rise in norepinephrine concentration in hind brain. Other brain areas showed significant decrease. The findings in the work showed that guanfacine is a weaker agonist than clonidine as it failed to raise norepinephrine concentration in hind brain. This may explain the lack of sedation after guanfacine treatment, while clonidine has a powerful sedative effect

Effect of clonidine and guanfacine on dopamine and serotonin level in rat brain

In the present work, the pattern of dopamine and 5-HT in whole and different areas of brain of Egyptian strain of male albino rats both in normotensive and DOCA and salt hypertensive rats has been determined. Moreover, the effects of two centrally acting antihypertensive drugs, namely clonidine [0.1 mg/kg] and guanfacine [1 mg/kg], have been analyzed using biochemical fluorescent techniques. The findings revealed that in normotensive rats the highest level of dopamine was in the cerebral cortex compared with the midbrain for serotonin. Hypertensive rats showed rise in dopamine level in whole and specified areas of brain. This may be due to increase in dopamine synthesis or inhibition of its release. Serotonin level was also elevated which can be due to enhancement in its synthesis secondary to its influence on other neurotransmitters as well as adaptation to stress. On the other hand, clonidine and guanfacine normalized the dopamine level in hypertensive rats to the values of controls. This may be attributed to increased dopamine release. On the other hand, clonidine and guanfacine increased serotonin level in hind brain possibly due to reduction in its release. This may explain the central hypertensive role of serotonin. The quantitative differences in the action of clonidine and guanfacine can be explained by their relative concentration and effectiveness in different areas of rat brain