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Anup K Sharma

Publications and source records attributed to Anup K Sharma.

4 recordsLinked to original sources
PubMed2006

Current use of antibiotic prophylaxis in breast surgery: a nationwide survey.

There is currently no consensus regarding the use of antibiotic prophylaxis in breast surgery. This postal survey aimed to establish the current practice in perioperative antibiotic use for breast surgery in the United Kingdom. Questionnaires were sent to 406 breast surgeons, enquiring about antibiotic use for common breast procedures. A total of 266 completed questionnaires were returned (65.5%). Over 80% of surgeons who performed breast augmentations, myocutaneous flap reconstructions and implant reconstructions used antibiotic prophylaxis. Up to 33% used antibiotic prophylaxis for wide local excisions (WLEs), mastectomies and axillary surgery for breast cancer, while 62% and 45% used antibiotics for breast reductions and duct excisions, respectively. The most common antibiotic used was co-amoxiclav. The variation in practice regarding antibiotic prophylaxis in breast surgery reflects the lack of reliable evidence for its efficacy. Further randomised controlled trials are required, taking into consideration specific risk factors affecting postoperative infection rate for breast surgery.

Antibiotic Prophylaxis↗
PubMed2006

The relationship between the insulin-like growth factor-1 system and the oestrogen metabolising enzymes in breast cancer tissue and its adjacent non-cancerous tissue.

AIMS: Previous studies have shown that oestrogen and Insulin-like Growth Factor-1 (IGF-1) act synergistically and cross-stimulatory while the oestrogen receptor (ER) and IGF-1R downstream signalling pathways interact at many levels. We investigate the relationship between the ER, and IGF-1R and their ligands in a series of human breast cancer tissue and adjacent non-cancerous tissue (ANCT). METHODS: A series of 139 pairs of breast cancer tissue and ANCT were obtained and divided into ER positive and ER negative groups based on tumour ER alpha immunostaining. All samples were processed for real-time quantitative-PCR to measure IGF-1, IGF-1R, ER alpha, STS and Cyp-19 mRNA levels. In addition, ER positive MCF-7 and ER negative MDA-MB-231 cell lines were treated separately with IGF-1 and an IGF-1R inhibitor called Tyrphostin AG1024 to see the effects of stimulating and inhibiting the IGF-1R. MCF-7 cell line was also treated with 4-hydroxytamoxifen. The mRNA levels of IGF-1, IGF-1R, ER alpha, STS and Cyp-19 of treated cell lines were measured and compared to those of non-treated controls. Data generated was normalised to Cytokeratin-19 mRNA levels. RESULTS: IGF-1R expression was higher in tumour tissue compared to ANCT (P = 0.038) while IGF-1 expression was marginally higher in ANCT compared to tumour tissue only in the ER positive samples (P = 0.098). ER positive tumours had a higher expression of IGF-1 compared to ER negative tumours (P = 0.001) while IGF-1R, STS and Cyp-19 expression were higher in ER negative tumours (P = 0.000, 0.000 and 0.006 respectively). There was no difference in STS or Cyp-19 expression in tumours or ANCT. Using Spearman's Correlation test, IGF-1 positively correlated with STS, Cyp-19 and ER alpha in ER positive and negative groups (Coefficient = +0.497, +0.662 and +0.651 respectively, P = 0.000 in all). IGF-1R correlated with IGF-1, STS, Cyp-19 and ER alpha only in the ER negative tumours (Coefficient = +0.620, +0.394, +0.692 and +0.662 respectively, P = 0.000, 0.012, 0.000 and 0.000 respectively). In cell lines, IGF-1 treatment led to an increase in the mean expression of IGF-1, IGF-1R, STS and Cyp-19 in both cell lines while ER alpha expression increased only in MCF-7. IGF-1R inhibition caused a decrease in expression of all five genes in MDA-MB-231 but not in the MCF-7 cell line. Treatment with 4-hydroxytamoxifen caused a decrease in expression of all five genes. CONCLUSIONS: IGF-1R is over-expressed in malignant tissue. IGF-1 is expressed at higher levels in ER positive tumours probably as a result of oestrogen stimulation while IGF-1R expression is higher in ER negative samples as an adaptation to lower local IGF-1 levels. An IGF-1 paracrine relationship may exist between tumour and ANCT but for STS and Cyp-19, there may be an autocrine-paracrine relationship. The IGF-1 ligand-receptor system is an important regulator of oestrogen production while oestrogen may be involved in stimulating IGF-1 expression. The expression of oestrogen synthesising enzymes is higher in ER negative breast cancers which may be due to the lack of oestrogen negative feedback or contribution from the overexpression of IGF-1R.

Adult↗
PubMed2004

Hypothesis: the case for quaternary hyperparathyroidism.

We report the case of a young woman with hyperparathyroidism due to a large parathyroid adenoma associated with severe vitamin D deficiency. The case is noteworthy for the size of the parathyroid adenoma and for the young age at presentation, and is more typical of the presentation of hyperparathyroidism seen in developing countries where the prevalence of vitamin D deficiency is high. Vitamin D is known to have a suppressive effect on parathyroid cell proliferation and parathyroid hormone synthesis. Vitamin D deficiency may result in a compensatory increase in the secretion of parathyroid hormone (secondary hyperparathyroidism) which involves hyperplasia of all four parathyroid glands. Secondary hyperparathyroidism can become autonomous and this has been termed tertiary hyperparathyroidism, the underlying pathology of which has been variably described in the literature as adenoma formation or four gland hyperplasia. The pathogenesis of parathyroid adenoma formation in vitamin D deficiency remains unclear. It is possible that a proportion of cases represent the coincidence of primary hyperparathyroidism in patients with vitamin D deficiency. Alternatively, we hypothesise that autonomous four gland hyperplasia or tertiary hyperparathyroidism may progress to adenoma formation and that this should be termed 'quaternary hyperparathyroidism'.

Adenoma↗