OBJECTIVETo explore the clinical application of imiquimod for the treatment of infantile hemangiomas (IH).

METHODS320 children with IH, including 250 superficial cases, 20 deep cases, and 50 mixed cases, were treated with 5% imiquimod cream every other day for 16 weeks. The clinical efficacy and side effects were evaluated at one year of age.

RESULTSThe total effective rates of the superficial, deep, and mixed IH were 61.2% (153/250), 10.0% (2/20) and 60.0% (30/50) respectively, showing no statistical difference between superficial and deep type (P = 0.874), but significant difference between superficial and mixed (P < 0.01), deep and mixed type (P < 0.01). 56.0% (28/50) of mixed IH showed proliferation of its deep lesions. Slight skin erythema and crusting were the most common side effects.

CONCLUSIONS5% imiquimod cream is effective and safe in superficial IH and superficial lesions of mixed IH with minimal skin reactions. The dysplasia of local tissue and systemic growth retardation are not found. It should be avoided to apply the cream to IH located around the cavities and skin fold. Imiquimod cream is a simple and convenient home-nursing medication. It can reduce care burden of family. Thus topical use of imiquimod can be considered as a good clinical indication for the treatment of superficial lesions of IH.

Aminoquinolines ; therapeutic use ; Female ; Hemangioma ; drug therapy ; Humans ; Infant ; Male ; Skin Neoplasms ; drug therapy ; Treatment Outcome

Imiquimod (R-837) and Resiquimod (R-838), two novel small-molecular-weight immune response modifiers, have similar structure. They have anti-virus and anti-tumor activities and can be used as B lymphocyte activators and adjuvants. They are widely used in dermatology to treat virus dermatoses and cutaneous benign or malignant tumors.
Adjuvants, Immunologic ; therapeutic use ; Aminoquinolines ; therapeutic use ; Antineoplastic Agents ; therapeutic use ; Condylomata Acuminata ; drug therapy ; Humans ; Imidazoles ; therapeutic use ; Skin Neoplasms ; drug therapy

Humans ; Aminoquinolines/therapeutic use* ; Carcinoma, Non-Small-Cell Lung/genetics* ; Lung Neoplasms/genetics* ; Mutation/genetics* ; Standard of Care

Adult ; Aminoquinolines ; adverse effects ; therapeutic use ; Condylomata Acuminata ; drug therapy ; Female ; Humans ; Hypopigmentation ; chemically induced ; diagnosis ; Male ; Middle Aged ; Vitiligo ; chemically induced ; diagnosis

OBJECTIVE: Pyrotinib, a novel irreversible pan-ErbB receptor tyrosine kinase inhibitor, showed promising antitumor activity and acceptable tolerability in phase II and phase III randomized clinical trials. We assessed the activity and safety of oral pyrotinib for human epidermal growth factor receptor 2 (HER2) positive metastatic breast cancer patients in the real world. METHODS: We retrospectively analyzed 72 HER2 positive metastatic breast cancer (MBC) patients who received oral pyrotinib based regimens at Beijing Cancer Hospital and other four hospitals (Peking University First Hospital, China-Japan Friendship Hospital, General Hospital of PLA, Peking University Third Hospital) from August 2018 to September 2019. Progression free survival (PFS), objective response rate (ORR), adverse events (AE) of pyrotinib were investigated. RESULTS: Seventy-two patients with HER2 positive MBC were enrolled. The median age of the patients was 55 years (range: 32-79 years). Sixty-nine (95.8%) patients had received anti-HER2 treatment in the metastatic and/or (neo) adjuvant settings; 61 (84.7%) patients had received anti-HER2 treatments in the metastatic setting in terms of trastuzumab 56 (77.8%) patients, lapatinib 36 (50.0%) patients, and T-DM1 4 (5.6%) patients. Among these 72 patients who received oral pyrotinib based regimens, 62 (86.1%) patients received pyrotinib (±trastuzumab) in combination with chemotherapy, 6 (8.3%) patients received pyrotinib (± trastuzumab) in combination with endocrine therapy and 4 (5.6%) patients received pyrotinib (±trastuzumab). Sixty-five (90.3%) patients received 400 mg pyrotinib once daily as initial dose, and 7 (9.7%) patients received 320 mg. OBJECTIVE response and safety to pyrotinib based therapy were evaluable in all the 72 patients. One (1.4%) patient achieved complete response (CR), 18 (25.0%) patients achieved partial response (PR), 41 (56.9%) patients had stable disease (SD), and 12 (16.7%) patients had progressive disease (PD). The ORR (CR+PR) was 26.4% and the median PFS was 7.6 months (95%CI: 5.5-9.7 months). Among the 36 patients with prior lapatinib therapy, the median PFS was 7.9 months (95%CI: 4.1-11.7 months). Among the 15 patients with brain metastasis, the median PFS was 6.0 months (95%CI: 2.2-9.8 months). The main toxicities related to pyrotinib were diarrhea in 57 (79.2%) cases, and 48 (66.7%) cases with grade 1-2 as well as 9 (12.5%) cases with grade 3. CONCLUSION Pyrotinib based therapy is an effective treatment for patients with HER2 positive MBC, including patients with lapatinib treatment failure and brain metastasis, and the toxicities can be tolerated.
Acrylamides/therapeutic use* ; Adult ; Aged ; Aminoquinolines/therapeutic use* ; Antineoplastic Combined Chemotherapy Protocols ; Breast Neoplasms/drug therapy* ; China ; Humans ; Middle Aged ; Neoplasm Metastasis ; Receptor, ErbB-2 ; Retrospective Studies ; Trastuzumab ; Treatment Outcome

BACKGROUNDImiquimod is an imidazoquinoline, which class of compounds are known to have antiviral and antitumoural properties. In recent studies, it was shown that imiquimod modulates the T helper cell type Th1/Th2 response by inducing the production of Th1 cytokines like IFN-gamma, and by inhibiting the Th2 cytokines like interleukin (IL)-4. Several investigators have shown that T-bet and GATA-3 are master Th1 and Th2 regulatory transcription factors. This study investigated whether imiquimod treatment inhibited airway inflammation by modulating transcription factors T-bet and GATA-3.

METHODSThirty-six male SD rats were randomly divided into a control group, an asthmatic group, and an imiquimod group, which was exposed to an aerosol of 0.15% imiquimod. Twenty-four hours after the last ovalbumin (OVA) challenge, airway responsiveness was measured and changes in airway histology were observed. The concentrations of IL-4, IL-5 and IFN-gamma in bronchoalveolar lavage fluid (BALF) and serum were measured by enzyme linked immunosorbent assay (ELISA). The mRNA expressions of IL-4, IL-5, IFN-gamma, T-bet and GATA-3 in lung and in CD4(+) T cells were determined by reverse transcription polymerase chain reaction (RT-PCR). The protein expressions of T-bet and GATA-3 were measured by Western blot.

RESULTSIt was demonstrated that imiquimod 1) attenuated OVA induced airway inflammation; 2) diminished the degree of airway hyperresponsiveness (AHR); 3) decreased the Th2 type cytokines and increased Th1 type cytokines mRNA and protein levels; 4) modulated the Th1/Th2 reaction by inhibiting GATA-3 production and increasing T-bet production.

CONCLUSIONImiquimod treatment inhibits OVA induced airway inflammation by modulating key master switches GATA-3 and T-bet that result in committing T helper cells to a Th1 phenotype.

Administration, Inhalation ; Aminoquinolines ; administration & dosage ; therapeutic use ; Animals ; Asthma ; drug therapy ; metabolism ; Bronchi ; pathology ; Bronchial Hyperreactivity ; drug therapy ; metabolism ; Cytokines ; biosynthesis ; Eosinophils ; physiology ; GATA3 Transcription Factor ; genetics ; Gene Expression Regulation ; drug effects ; Lung ; pathology ; Male ; Ovalbumin ; immunology ; RNA, Messenger ; analysis ; Rats ; Rats, Sprague-Dawley ; T-Box Domain Proteins ; Transcription Factors ; genetics

Aminoquinolines ; pharmacology ; therapeutic use ; Animals ; Asthma ; drug therapy ; immunology ; pathology ; Bronchoalveolar Lavage Fluid ; cytology ; Cell Count ; Chemokine CCL17 ; Chemokine CCL22 ; Chemokines, CC ; analysis ; genetics ; Cytokines ; biosynthesis ; Flow Cytometry ; Interleukin-4 ; antagonists & inhibitors ; Male ; Mice ; Mice, Inbred BALB C ; RNA, Messenger ; analysis ; STAT6 Transcription Factor ; analysis ; antagonists & inhibitors ; genetics ; Signal Transduction ; drug effects