What is known and objective: The clinical features of terlipressin-induced ischemic skin necrosis are unknown. The purpose of this study is to explore the clinical features of terlipressin-induced skin necrosis.Methods: We searched Chinese and English databases to collect case reports of terlipressin-induced skin necrosis for retrospective analysis.Results and discussion: A total of 42 patients (31 males and 11 females) from 35 studies were included, with a median age of 54 years (range 0.17-84). The onset of skin ischemia ranged from a few hours to 21 days. The most common clinical manifestations were bulla (15 cases, 35.7%), cyanosis (12 cases, 28.6%), necrosis (11 cases, 26.2%), and purpura (10 cases, 23.8%). The following were often affected: the legs (26 cases), 61.9%), abdomen (13, 31.0%), scrotum (10 cases, 23.8%), feet (10 cases, 23.8%), upper extremities (8 cases, 19.0%), and hands (7 cases, 16.7%).Skin biopsy showed fibrin thrombus (7 cases, 38.9%), nonspecific inflammation
<b><i>Background:</i></b> Trimethoprim-sulfamethoxazole (TMP/SMX) causes hyperkalemia, and hyponatremia caused by TMP/SMX is a challenge for clinicians. We described the clinical features of hyponatremia induced by TMP/SMX after collecting cases. <b><i>Summary:</i></b> The median age of the 24 patients (10 males and 14 females) was 67 years (range: 28–90 years). Hyponatremia induced by TMP/SMX manifested as nausea (41.7%) and vomiting (29.2%) or asymptomatic hyponatremia (20.8%). The median duration of hyponatremia was 5 days (range: 3–10 days). The median serum sodium concentration was 118 mmol/L (range: 101–128.1 mmol/L). The serum sodium levels gradually returned to the normal range at 4 days (median; range: 2–14 days) after withdrawing TMP/SMX. <b><i>Key Messages:</i></b> TMP/SMX-induced hyponatremia is a rare and serious adverse reaction. Clinicians should be aware of electrolyte disturbances caused by TMP/SMX and should always consider electrolyte monitoring.
A novel series of silibinin and 2,3-dehydrosilybin derivatives bearing carbamate groups were designed, synthesized and their in vitro anticancer activities were screened against human cancer cell lines including MCF-7, NCI-H1299, HepG2 and HT29 by CCK-8 assay. The results showed that most of the compounds significantly suppressed the proliferation of tested cancer cells. Among them, compounds 2h, 3h and 3f demonstrated markedly higher antiproliferative activity on MCF-7 cells with IC 50 values of 2.08, 5.54 and 6.84 µM, respectively. Compounds 3e, 3g and 2g displayed better cytotoxic activity against NCI-H1299 cells with IC 50 values of 8.07, 8.45 and 9.09 µM, respectively. Compounds 3g, 3c and 3h exhibited a promising inhibitory effect against HepG2 cells with IC 50 values of 8.88, 9.47 and 9.99 µM, respectively. Compounds 3e, 2e and 3c revealed effective biological potency on HT29 cells with IC 50 values of 6.27, 9.13 and 9.32 µM, respectively. In addition, the outcomes of the docking studies between compounds 2f, 2h, 3e, 3g and Hsp90 receptor (PDB ID: 4AWO) suggest the possible mechanism of inhibition against MCF-7 cell lines.
A series of 7-O-aminoalkyl-2,3-dehydrosilibinin derivatives were synthesized and evaluated for their antiproliferative activities against several cancer cell lines. A number of them exhibited greatly enhanced potency with 50% growth inhibition at low micromolar concentrations. Structure activity study indicated that the distance between N and 7-O on the side chain has a limited influence on the antiproliferative activity, while the presence of a morpholino group decreases the antiproliferative activities dramatically. Flow cytometry based assays on human colon cancer HCT116 cells revealed that 6a and 6c, two of the most potent derivatives, effectively arrest the cell cycle in the G2 phase and stimulate cell apoptosis. Our findings suggest that attaching an appropriate tertiary amino alkyl side chain through 7-O-alkylation on 2,3-dehydrosilibinin, would be a viable strategy for the development of silibinin derivatives as anticancer agents.
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