Light stability of molsidomine in infusion fluids

Abstract— The influence of artificial light, daylight or stimulated sunlight on the stability of molsidomine was investigated. In static experiments an 80 μg mL^?1 solution of molsidomine in saline was stored in an unprotected infusion bag. During dynamic experiments the molsidomine solution (80 μg mL^?1) was dropped at 12·5 mL h^?1 from an unprotected infusion bag, from an infusion bag covered with aluminium-foil, or from an infusion bag protected with a UV-cover. Either unprotected infusion tubing or infusion tubing with a UV-filter were connected to the infusion bags. Static as well as dynamic experiments showed a half-life of about 20 min for the unprotected molsidomine solutions, when placed behind a window during a sunny day. Protection from light of the infusion bag but not of the infusion tubing had only a minor influence on the drug half-life. Protection of the infusion bag and the infusion tubing with a UV-filter increased the half-life to several days. These results confirm that both the infusion bag and the infusion tubing need adequate light protection during molsidomine administration.     

Extracorporeal photochemotherapy induces apoptosis of infiltrating lymphoid cells in patients with mycosis fungoides in early stages. A quantitative histological study

Extracorporeal photochemotherapy (ExP) is a well-tolerated new form of chemoimmunotherapy, which is considered to be effective for cutaneous T-cell lymphoma (CTCL) and the treatment of choice for Sézary syndrome. Improvements have also been seen in patients with non-erythrodermic mycosis fungoides (MF) in the early stages, even when tumour cells are not detectable in the peripheral blood. In this study, we used ExP as a monotherapy in seven patients who had early stage (Ib) MF, and who were no longer responsive to or had contraindications for other therapies. We observed a clinical improvement in the disease after 12 months of treatment: one patient showed a complete response, five a partial response, and one remained stable. In each patient we compared skin biopsies of large plaque lesions before and after the treatment. We undertook a histological evaluation of the infiltrate. The lymphoid cell proliferation and death rates were quantified using the following parameters: lymphoid cell density (LCD), Ki67+ lymphoid cell nuclei percentage (Ki67+ Lcn percentage), and apoptotic index (AI). Significant decreases in the lymphoid cell infiltrate and in cell proliferation, and a significant increase in AI were observed after therapy. The mean LCD decreased from 187 ± 33 to 34 ± 17·7, Ki67+ Lcn mean percentage decreased from 16·9 ± 3·9 to 4·9 ± 2·4, and the AI mean value increased from 0·05 ± 0·03 to 2·41 ± 1·54. Our results suggest a role for apoptosis in the improvement of the skin lesions and are in line with some reports on the mode of action of ExP. Although the way in which ExP works needs to be clarified further, it does seem to stimulate a CD8+ cell-mediated anticlonotypic activity against circulating pathogenic clones. Furthermore, a release of tumour necrosis factor α (TNF-α) by circulating monocytes has been demonstrated after ExP. Both are known to induce cell death by apoptosis.