Nifedipine Induced Gingival Hyperplasia in Pregnancy: A Case Report.

BACKGROUND: It is known that calcium channel blockers are associated with a risk of gingival hyperplasia. These drugs are widely used in the management of gestational hypertensive disorders. CASE: A 27-year-old G1 woman presented with gingival hyperplasia at 27 weeks gestation during a hospitalisation for preeclampsia. She had been on nifedipine for hypertension for the last 9 weeks. Nifedipine was discontinued and replaced by methyldopa and already after 48 hours the gingival hyperplasia improved. She delivered two weeks later and the gingival hyperplasia resolved completely without surgical intervention. The Naranjo's score was used to prove the nifedipine's imputability. CONCLUSION: This first case report of gingival hyperplasia induced by nifedipine in pregnancy could be used as a reference for clinicians in the management of this adverse effect during the pregnancy.

Invasion of hepatocytes by Plasmodium sporozoites requires cGMP-dependent protein kinase and calcium dependent protein kinase 4.

Invasion of hepatocytes by sporozoites is essential for Plasmodium to initiate infection of the mammalian host. The parasite's subsequent intracellular differentiation in the liver is the first developmental step of its mammalian cycle. Despite their biological significance, surprisingly little is known of the signalling pathways required for sporozoite invasion. We report that sporozoite invasion of hepatocytes requires signalling through two second-messengers - cGMP mediated by the parasite's cGMP-dependent protein kinase (PKG), and Ca2+ , mediated by the parasite's calcium-dependent protein kinase 4 (CDPK4). Sporozoites expressing a mutated form of Plasmodium berghei PKG or carrying a deletion of the CDPK4 gene are defective in invasion of hepatocytes. Using specific and potent inhibitors of Plasmodium PKG and CDPK4, we demonstrate that PKG and CDPK4 are required for sporozoite motility, and that PKG regulates the secretion of TRAP, an adhesin that is essential for motility. Chemical inhibition of PKG decreases parasite egress from hepatocytes by inhibiting either the formation or release of merosomes. In contrast, genetic inhibition of CDPK4 does not significantly decrease the number of merosomes. By revealing the requirement for PKG and CDPK4 in Plasmodium sporozoite invasion, our work enables a better understanding of kinase pathways that act in different Plasmodium stages.