Morphine inhibits indolactam V-induced U937 cell adhesion and gelatinase secretion.

We demonstrate that indolactam V, a non-phorbol protein kinase C activator, promotes U937 cell attachment to fibronectin, type IV collagen and laminin. In the absence of indolactam V, 2-4% of U937 cells attach to all test substrates, however, in the presence of 100 nM indolactam V, 25, 16 and 11% of U937 cells attach to fibronectin, type IV collagen and laminin, respectively. When added concomitantly, 90 microM H-7, a protein kinase C inhibitor, reduces indolactam V-induced U937 cell adhesion to fibronectin by 91%. Monoclonal antibodies directed against both the beta1 and alpha 5 integrin subunits inhibit indolactam V-induced U937 cell adhesion to fibronectin by 62 and 52%, respectively. Indolactam V also promotes homotypic aggregation in U937 cells, which is blocked with either anti-ICAM or anti-LFA-1 antibodies. In addition, indolactam V promotes U937 cell secretion of a 92 kDa gelatinase as demonstrated by zymography. In the presence of low levels of morphine (10 nM-1.0 microM), the U937 cell attachment to matrix proteins was not significantly affected. However, in the presence of 10 microM morphine, the indolactam V treated cells exhibit a 71-74% reduction in cell adhesion to the matrix proteins. Further, 10 microM morphine also blocks indolactam V-induced homotypic aggregation and gelatinase secretion. The inhibitory effect of morphine on cell-matrix adhesion and gelatinase secretion was not inhibited by the opiate receptor antagonist naloxone (1 microM). While 10 microM naloxone did partially counteract the effect of 10 microM morphine on U937 cell attachment, this effect was likely non-specific since 10 microM naloxone alone increased cell adhesion. Supporting this conclusion, PCR analysis revealed that U937 cells do not express the mu high affinity morphine receptor. Also, indolactam V did not induce mu receptor expression, suggesting that morphine acts on U937 cells in a non-specific fashion.

Successful delivery in a pregnant woman with lupus anticoagulant positive systemic lupus erythematosus treated with double filtration plasmapheresis.

The case was a 29 year old female who has suffered from systemic lupus erythematosus (SLE) since 15 years of age. The activity of SLE was low, and she took prednisolone orally. Her first pregnancy failed after 14 weeks. In the second pregnancy, she had thrombocytopenia, prolonged activated partial thromboplastin time (APTT), positive lupus anticoagulant (LAC) and thus was diagnosed with antiphospholipid antibody syndrome (APS). Combination therapy with steroids and aspirin was started, and she underwent treatment of double filtration plasmapheresis (DFPP) in the early stage of pregnancy. Her platelet count increased, and the value of APTT has normalized with DFPP treatment. She delivered successfully on the 32nd week of pregnancy. We think that DFPP is an effective and safe treatment in patients with an LAC positive pregnancy.

Lidocaine and prilocaine toxicity in a patient receiving treatment for mollusca contagiosa.

We describe a 3-year-old child with mollusca contagiosa whose caregiver applied a eutectic mixture of 5% lidocaine and prilocaine (EMLA) in excessive amounts with the subsequent development of adverse reactions, including methemoglobinemia and hypoxemia. Because of the significant systemic absorption of lidocaine and prilocaine, the patient required overnight admission to the pediatric intensive care unit for close monitoring. A brief description of the proper dosing, pharmacokinetics, and possible side effects of EMLA cream are reviewed.