METHODS: Clarithromycin susceptibility of H pylori isolates was determined by E test. Analyses for point mutations in the domain V of 23S rRNA genes in clarithromycin-resistant and -sensitive strains were performed by sequence analysis of amplified polymerase chain reaction products. Restriction fragment length polymorphism was performed using BsaI and MboII enzymes to detect restriction sites that correspond to the mutations in the clarithromycin-resistant strains.
RESULTS: Of 187 isolates from 120 patients, four were resistant to clarithromycin, while 183 were sensitive. The MIC of the resistant strains ranged from 1.5 to 24 microg/mL. Two isolates had an A2142G mutation and another two had A2143G mutations. A T2182C mutation was detected in two out of four clarithromycin-resistant isolates and in 13 of 14 clarithromycin-sensitive isolates. Restriction enzyme analyses with BsaI and MboII were able to detect the mutations.
CONCLUSION: Clarithromycin resistance is an uncommon occurrence among Malaysian isolates of H pylori strains and the mutations A2142G and A2143G detected were associated with low-level resistance.
Case presentation: We report a case 41 years old female presented with lesion on the scalp and sternal mass, increasing in size with itchiness and erythematous for 6 months duration. Further CECT scan of brain and neck shows features of malignant left frontal scalp lesion with poor plane with overlying skin and underlying skull bone and CECT of thorax shows a large, irregular heterogeneously enhancing mass with necrotic center noted at right hilar within superior segment of right lower lobe, encasing right middle and lower lobe bronchi. Wedge biopsy of scalp lesion showed an intradermal lesion extensively infiltrating by malignant gland accompanied by desmoplasia and the tumor cells are seen extending into the surgical margins suggestive of ductal eccrine carcinoma.Clinical Discussion:This case highlights the importance and challenges in achieving early diagnosis coupled with the scarcity of information on these leads to difficulty in managing this patient.
Conclusion: In managing Ductal Eccrine Carcinoma tumor, standard method of treatment for has not been established. However, wide surgical excision is the treatment of choice for localized lesions. Regarding prognosis, there is conflicting data published which we describe in this article.
METHODS: We performed a randomized, double-blind, placebo-controlled trial of consecutive adults with biopsy-proven NASH and a NAFLD activity score (NAS) of 4 or more at a tertiary care hospital in Kuala Lumpur, Malaysia, from November 2012 through August 2014. Patients were randomly assigned to groups given silymarin (700 mg; n = 49 patients) or placebo (n = 50 patients) 3 times daily for 48 weeks. After this 48-week period, liver biopsies were repeated. The primary efficacy outcome was a decrease of 30% or more in NAS; findings from 48-week liver biopsies were compared with those from the baseline biopsy. Secondary outcomes included changes in steatosis, lobular inflammation, hepatocyte ballooning, NAS and fibrosis score, and anthropometric measurements, as well as glycemic, lipid, and liver profiles and liver stiffness measurements.
RESULTS: The percentage of patients achieving the primary efficacy outcome did not differ significantly between the groups (32.7% in the silymarin group vs 26.0% in the placebo group; P = .467). A significantly higher proportion of patients in the silymarin group had reductions in fibrosis based on histology (reductions of 1 point or more; 22.4%) than did the placebo group (6.0%; P = .023), and based on liver stiffness measurements (decrease of 30% or more; 24.2%) than did the placebo group (2.3%; P = .002). The silymarin group also had significant reductions in mean aspartate aminotransferase to platelet ratio index (reduction of 0.14, P = .011 compared with baseline), fibrosis-4 score (reduction of 0.20, P = .041 compared with baseline), and NAFLD fibrosis score (reduction of 0.30, P < .001 compared with baseline); these changes were not observed in the placebo group (reduction of 0.07, P = .154; increase of 0.18, P = .389; and reduction of 0.05, P = .845, respectively). There was no significant difference between groups in number of adverse events; adverse events that occurred were not attributed to silymarin.
CONCLUSIONS: In a randomized trial of 99 patients, we found that silymarin (700 mg, given 3 times daily for 48 weeks) did not reduce NAS scores by 30% or more in a significantly larger proportion of patients with NASH than placebo. Silymarin may reduce liver fibrosis but this remains to be confirmed in a larger trial. It appears to be safe and well tolerated. ClinicalTrials.gov: NCT02006498.