A study of prescription pattern in the drug therapy of acne vulgaris at a tertiary care hospital in Mangalore, India

Background: Acne Vulgaris is the most common skin disorder of the pilosebaceous unit with excess sebum production, follicular epidermal hyperproliferation, inflammation and Propionibacterium acnes activity, affecting about 80% of teenagers and has considerable psychological and social consequences and physical disability. Use of established topical and oral drugs assumes paramount importance in the treatment of acne vulgaris. Therefore, periodic auditing of prescription is necessary to increase therapeutic benefit and decrease adverse effects. Aim and objectives of the study was to evaluate the pattern of prescription and its rationale in the drug therapy of acne vulgaris. To monitor the adverse effects, if any.Methods: A prospective, hospital based, observational study. Data was collected for a period of 1 year from January 2015 to December 2015 from the outpatient records in the OPD of Dermatology at Justice K.S. Hegde Charitable Hospital, Deralakatte, Mangalore, in a specifically designed proforma.Results: The prescription data of 346 patients were analyzed of which 45.1% were males with an average age of 21.94±0.3 years. Among the four grades of Acne Vulgaris, Grade II (53.17%) was more prevalent followed by Grade I (26.58%), Grade III (13.87%) and Grade IV (6.35%). The number of drugs prescribed for topical use was 514 of which the most commonly prescribed drugs were Benzoyl Peroxide (19.46%), a combination of Tretinoin and Clindamycin (17.12%), Tretinoin alone (12.45%), Clindamycin alone (10.51%) etc. The number of drugs prescribed for systemic use was 98 consisting of Doxycycline (55.1%), Azithromycin (34.7%), Isotretinoin (6.12%) and Erythromycin (4.08%).Conclusions: There was rationality in most of the prescriptions giving no scope for polypharmacy

2-(2-Methoxy­phen­yl)-4,4-dimethyl-4,5-dihydro-1,3-oxazole

In the title mol­ecule, C12H15NO2, the oxazole ring adopts an envelope conformation. Overall, the mol­ecule is approximately planar, the dihedral angle between the mean plane through all but the methyl­ene C atom of the five-membered ring and the aromatic ring being 8.6 (1)°. A weak C—H⋯O inter­action contributes to the stabilization of the crystal structure

(2E)-1-(4-Methyl­phen­yl)-3-(2,3,5-trichloro­phen­yl)prop-2-en-1-one

In the title mol­ecule, C16H11Cl3O, the dihedral angle between the two benzene rings is 33.2 (1)°. The crystal packing is stabilized by C—H⋯O hydrogen bonds

4-(4-Bromo­benzyl­ideneamino)-3-{1-[4-(2-methyl­prop­yl)phen­yl]eth­yl}-1-(mor­phol­ino­meth­yl)-1H-1,2,4-triazole-5(4H)-thione

There are two mol­ecules (A and B) in the asymmetric unit of the title compound, C26H32BrN5OS, with almost identical geometry. The morpholine ring adopts the usual chair conformation in both mol­ecules. The triazole ring forms dihedral angles of 4.84 (6) and 74.19 (6)°, respectively, with the bromo­phenyl and isobutylbenzene rings in mol­ecule A, and angles of 16.68 (7) and 87.29 (6)°, respectively, in mol­ecule B. Intra­molecular C—H⋯S hydrogen bonds generate S(5) and S(6) ring motifs in both independent mol­ecules. The crystal structure is stabilized by C—H⋯N, C—H⋯Br and C—H⋯O hydrogen-bonding inter­actions, together with C—H⋯π inter­actions

4-[(E)-2,6-Dichloro­benzyl­ideneamino]-3-{1-[4-(2-methyl­prop­yl)phen­yl]eth­yl}-1H-1,2,4-triazole-5(4H)-thione

In the title Schiff base compound, C21H22Cl2N4S, the triazole ring makes dihedral angles of 2.15 (11) and 87.48 (11)° with the 2,6-dichloro­phenyl and methyl­propyl­phenyl rings, respectively. Weak intra­molecular C—H⋯S and C—H⋯Cl inter­actions generate S(6) and S(5) ring motifs, respectively. In the crystal structure, centrosymmetrically related mol­ecules are linked into dimers by N—H⋯S hydrogen bonds. These dimers are arranged into sheets parallel to the ab plane and are stacked along the c axis. C—H⋯π inter­actions involving the methyl­propyl­phenyl ring and π–π inter­actions involving the dichloro­phenyl ring [centroid–centroid distance = 3.5865 (3) Å] are also observed

β-catenin negatively regulates expression of the prostaglandin transporter PGT in the normal intestinal epithelium and colorectal tumour cells: A role in the chemopreventive efficacy of aspirin

Background: Levels of the pro-tumorigenic prostaglandin PGE 2 are increased in colorectal cancer, previously attributed to increased synthesis through COX-2 upregulation and, more recently, to decreased catabolism. The functionally linked genes 15-prostaglandin dehydrogenase (15-PGDH) and the prostaglandin transporter PGT co-operate in prostaglandin degradation and are downregulated in colorectal cancer. We previously reported repression of 15-PGDH expression by the Wnt/β-catenin pathway, commonly deregulated during early colorectal neoplasia. Here we asked whether β-catenin also regulates PGT expression. Methods: The effect of β-catenin deletion in vivo was addressed by PGT immunostaining of β-catenin/lox-villin-cre-ERT2 mouse tissue. The effect of siRNA-mediated β-catenin knockdown and dnTCF4 induction in vitro was addressed by semi-quantitative and quantitative real-time RT-PCR and immunoblotting. Results: This study shows for the first time that deletion of β-catenin in murine intestinal epithelium in vivo upregulates PGT protein, especially in the crypt epithelium. Furthermore, β-catenin knockdown in vitro increases PGT expression in both colorectal adenoma-and carcinoma-derived cell lines, as does dnTCF4 induction in LS174T cells.Conclusions:These data suggest that β-catenin employs a two-pronged approach to inhibiting prostaglandin turnover during colorectal neoplasia by repressing PGT expression in addition to 15-PGDH. Furthermore, our data highlight a potential mechanism that may contribute to the non-selective NSAID aspirins chemopreventive efficacy. © 2012 Cancer Research UK All rights reserved