scholarly journals Prolonged treatment of hypertensive patients with low dose HCTZ improves arterial elasticity but not if they have niddm or ifg. treatment with full dose HCTZ (25 mg/d) aggravates metabolic parameters and arterial stiffness

2004 ◽  
Vol 17 (5) ◽  
pp. S138 ◽  
Author(s):  
R ZIMLICHMAN
Keyword(s):  
Arterial Stiffness ◽  
Low Dose ◽  
Metabolic Parameters ◽  
Prolonged Treatment ◽  
Arterial Elasticity ◽  
Hypertensive Patients ◽  
Full Dose

scholarly journals Low-Dose Rosuvastatin Improves Arterial Stiffness in High-Risk Japanese Patients With Dyslipdemia in a Primary Prevention Group

2011 ◽  
Vol 75 (11) ◽  
pp. 2660-2667 ◽  
Author(s):  
Minoru Hongo ◽  
Setsuo Kumazaki ◽  
Atsushi Izawa ◽  
Hiroya Hidaka ◽  
Takeshi Tomita ◽  
...  
Keyword(s):  
Primary Prevention ◽  
High Risk ◽  
Arterial Stiffness ◽  
Low Dose ◽  
Japanese Patients

scholarly journals A Phase 2 Clinical Trial of Trametinib and Low-Dose Dabrafenib in Patients with Advanced Pretreated NRASQ61R/K/L Mutant Melanoma (TraMel-WT)

Cancers ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 2010
Author(s):  
Gil Awada ◽  
Julia Katharina Schwarze ◽  
Jens Tijtgat ◽  
Giuseppe Fasolino ◽  
Hendrik Everaert ◽  
...  
Keyword(s):  
Clinical Trial ◽  
Low Dose ◽  
Objective Response ◽  
Braf Inhibitor ◽  
Skin Toxicity ◽  
Mek Inhibitor ◽  
Phase 2 ◽  
Cutaneous Toxicity ◽  
Full Dose ◽  
Phase 2 Clinical Trial

Background: MEK-inhibitor monotherapy has activity in advanced NRASQ61R/K/L mutant melanoma but is associated with dose-limiting cutaneous toxicity. The combination of a BRAF- with a MEK-inhibitor at their full dose (as in BRAFV600E/K mutant melanoma) has low cutaneous toxicity. It is unknown whether a low dose of BRAF-inhibitor can mitigate the skin toxicity associated with full-dose MEK-inhibitor treatment in patients with advanced NRASQ61R/K/L mutant melanoma. Methods: This two-stage phase 2 clinical trial investigated trametinib 2 mg once daily in patients with advanced NRASQ61R/K/L mutant melanoma who were pretreated with immune checkpoint inhibitors. In case of trametinib-related cutaneous toxicity, low-dose dabrafenib (50 mg twice daily) was added to prevent recurrent cutaneous toxicity (pre-amendment). Following an amendment, trametinib was combined upfront with low-dose dabrafenib (post-amendment). Objective response rate (ORR) served as the primary endpoint. Results: All 6 patients enrolled pre-amendment developed trametinib-related cutaneous toxicity, necessitating treatment interruption. Combining trametinib with low-dose dabrafenib prevented recurrent skin toxicity thereafter. Trametinib-related skin toxicity was effectively mitigated in all 10 patients post-amendment. In all 16 included patients, the ORR and disease control rate was 6.3% (1 partial response) and 50.0%, respectively. The trial was halted after the first stage. Conclusions: Combining full-dose trametinib with low-dose dabrafenib can mitigate MEK-inhibitor-related skin toxicity but was insufficiently active in this patient population. This combination can be of further interest for the treatment of MEK-inhibitor-sensitive tumors.

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