Neosensitization to Multiple Drugs Following Valproate-Induced Drug Reaction with Eosinophilia and Systemic Symptoms Syndrome

Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS) syndrome is associated with severe skin eruptions, fever, hematological abnormalities, and multi-organ involvement. Although aromatic anticonvulsant drugs have been frequently associated with the manifestation of DRESS syndrome, its induction following treatment with nonaromatic anticonvulsants, such as valproate, has rarely been reported. Moreover, there are limited data regarding the development of neosensitization related to chemically unrelated drugs following an episode of DRESS syndrome. Here, a case of neosensitization to multiple drugs is described. The present case report describes a female patient who experienced neosensitization to amoxicillin, olanzapine, and quetiapine following the manifestation of DRESS syndrome induced by valproate.

Influence of GnRH Agonist and Neural Antagonists on Stress-blockade of LH and Prolactin Surges Induced by 17 beta-estradiol in Ovariectomized Rats

In our previous study, we demonstrated that immobilization stress blocked estrogen-induced luteinizing hormone(LH) surge possibly by inhibiting the synthesis and release of gonadotropin-releasing hormone (GnRH) at the hypothalamic level and by blocking estrogen-induced prolactin (PRL) surge by increasing the synthesis of dopamine receptor at the pituitary level in ovariectomized rats. The present study was performed to determine whether immobilization stress affects pituitary LH responsiveness to GnRH, and whether endogenous opioid peptide (EOP) and dopamine systems are involved in blocking LH and PRL surges during immobilization stress. Immobilization stress was found to inhibit basal LH release and to completely abolish LH surge. However, the intravenous application of GnRH agonist completely restored immobilization-blocked LH surge and basal LH release. Treatment with naloxone did not exert any effect on immobilization-blocked LH surge but increased basal LH release during immobilization stress. Pimozide did not affect immobilization-blocked LH surge or basal LH release. Naloxone also decreased immobilization-induced basal PRL release, but had no effect on immobilization-blocked PRL surge. Immobilization-increased basal PRL levels were augmented by pimozide treatment and immobilization-blocked PRL surge was dramatically restored by pimozide. We conclude that immobilization stress does not impair pituitary LH response to GnRH, and that the immobilization stress-induced blockage of LH surge is probably not mediated by either the opioidergic or the dopaminergic system. However, immobilization-blockade of PRL surge may be partly mediated by the dopaminergic system.

Regulation of FSH Gene Expression and Release in Cultured Rat Anterior Pituitary Cells / 대한내분비학회지

BACKGROUND: FSH is a heterodimeric glycoprotein and is composed of alpha and beta subunits. alpha subunit is common to FSH and LH, while an unique beta subunit determines the biological specificity of each hormone. The synthesis of beta subunit is the primary rate-limiting step in the synthesis of each hormone. Although FSH plays a pivotal role in folliculogenesis and ovulation, very little studies have been performed on the regulation of FSH beta gene expression. Therefore, the present study attempted to examine the effect of GnRH or activin on the expression of FSH beta mRNA as well as FSH release and signaling pathway involved in their actions. METHODS: The primary cultures of rat anterior pituitary were used for this study. To determine FSH beta mRNA levels, northern blotting method was used. The concentration of FSH in the culture medium was evaluated by using a specific radioimmunoassay for rat FSH. RESULTS: PMA, an activator of PKC, increased FSH beta mRNA levels and FSH release, whereas forskolin, an activator of adenylate cyclase, showed no effect. The application of GnRH augmented FSH release, but not FSH beta mRNA levels. However, the administration of activin increased FSH beta mRNA levels as well as FSH release. Staurosporine, an inhibitor of PKC, suppressed activin-induced increment of FSH beta mRNA levels and FSH release. CONCLUSION: The present study demonstrated that activin rather than GnRH is a major regulator for FSH beta mRNA expression, and suggest that PKC-dependent pathway is also involved in the action of activin on the expression of FSH beta mRNA and FSH release.

Clinical significance of urinary growth hormone measurement in patients with growth hormone deficiency

Urinary growth hormone (GH) excretion was quantitated in 12-hr overnight urine collections obtained from 13 children with complete growth hormone deficiency (CGHD). 6 children with partial growth hormone deficiency (PGHD), 5 children with short stature and normal GH provocation tests (NSC), and 5 normal control children (NC) to investigate whether the measurement of urinary GH can clearly separate the PGHD and CGHD groups from the NSC and NC groups. In addition, the urinary excretion of GH was measured in CGHD after sc injections of 0.1 IU/kg GH three times a week and daily in an attempt to determine the optimal replacement dose. The results were as follows. 1) The 12-hr urinary GH excretion cleary separated the CGHD (1.2+/-1.1 ng/12 hr; range, 0.3-3.1, n=13) and PGHD (3.7+/-2.4 ng/12 hr; range, 0.9-6.8 n=6) groups from the NSC (14.0+/-3.6 ng/12 hr; range, 8.5-18.2 n=5) and NC (12.7+/-5.8 ng/12 hr; range, 6.9-20.8, n=5) groups without any overlap. 2) There were significant difference in 12-hr urinary GH excretion between CGHD and PGHD, but the higher values in CGHD groups overlapped some of the lower values in PGHD group. 3) There were no differencies in 12-hr urinary GH excretion between NC and NSC. 4) A 12-hr urinary GH values less than 6.9 ng/12 hr suggested GH deficiency. 5) The CGHD patients who received o.1 IU/kg GH. sc. daily GH levels within the range of the mean +/-SD in NC. but those who received theree times a week had daily variable urinary GH levels. These results suggest that the measurement of 12-hr nocturnal urinary GH excretion monitering of GH therapy response.