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Sodium fluorescein may cause serious intolerance reactions: these are always unpredictable but are more common amongst patients who have experienced a poorly tolerated injection of the product (except for symptoms of nausea and vomiting) or who present with a history of allergy: food or drug-induced urticaria , asthma, eczema, hay fever ; those intolerance reactions may not be detected by a fluorescein test, which is of no value and may even be dangerous. A visit with a specialist in allergy may clarify the diagnosis.

Oral theophylline initially seemed promising in the prophylactic treatment of childhood asthma. When compared with placebo, it significantly increased the mean morning peak expiratory flow rate and reduced the mean number of acute nighttime attacks and doses of bronchodilator used. 37 However, it proved to be less promising when its use over one year was compared with the use of inhaled corticosteroids. Although there was no significant difference between theophylline and inhaled corticosteroids in reduction of asthma symptoms, there was an increased use of short-acting beta 2 agonists and oral corticosteroids in children receiving theophylline. 38 In summary, its use in children cannot be recommended because of the potential for serious side effects, such as cardiac arrhythmias or convulsions, if therapeutic blood levels are exceeded. 39

Gonadal steroids ( estrogens and androgens) generally have negative feedback effects on GnRH-1 release at the level of the hypothalamus and at the gonadotropes, reducing their sensitivity to GnRH. Positive feedback by estrogens also occurs in the gonadal axis of female mammals and is responsible for the midcycle surge of LH that stimulates ovulation. Although estrogens inhibit kisspeptin (Kp) release from kiss1 neurons in the ARC, estrogens stimulate Kp release from the Kp neurons in the AVPV. As estrogens' levels gradually increase the positive effect predominates, leading to the LH surge. GABA -secreting neurons that innervate GnRH-1 neurons also can stimulate GnRH-1 release. These GABA neurons also possess ERs and may be responsible for the GnRH-1 surge. Part of the inhibitory action of endorphins on GnRH-1 release is through inhibition of these GABA neurons. Rupture of the ovarian follicle at ovulation causes a drastic reduction in estrogen synthesis and a marked increase in secretion of progesterone by the corpus luteum in the ovary, reinstating a predominantly negative feedback on hypothalamic secretion of GnRH-1. [11]

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