Laparoscopic Management of Prosthetic Infections Following Laparoscopic Groin Hernioplasty — Experiences from a Tertiary Care Center

Hellenic Journal of Surgery - Despite increasing trends towards laparoscopic groin hernioplasty, its early prosthesis-related complications have hardly been addressed. Although conventionally...     

Harnessing hyperuricemia to atherosclerosis and understanding its mechanistic dependence

Atherosclerosis is regarded as the disease of the arterial vasculature. The main characteristics of atherosclerosis are the abnormal accumulation of lipids, increased inflammatory cells, matrix deposits, and proliferation of smooth muscle cells. Diabetes mellitus, obesity, and hyperlipidemia are the most studied risk factors of atherosclerosis. One least studied risk factor is the uric acid (UA), a high UA in circulation is interlinked with many pathological processes. Several epidemiological studies suggest elevated UA levels as an essential biomarker in the forecast of several cardiovascular diseases. Available evidence claims that UA upholds the atherosclerosis process via disturbing lipid metabolism, reducing the nitric oxide synthesis in endothelial cells, promoting the proliferation of vascular smooth muscle cells, and overwhelms inflammation. In endothelial dysfunction and coronary artery lesions, UA is considered as an independent predictor. The updated studies on the involvement of hyperuricemia in atherosclerosis prove that treatment with xanthine oxidase (XO) inhibitors not just benefits the treatment of hyperuricemia but also reduces the burden of atherosclerosis to a greater extent. In this review, we highlight how the hyperuricemia affects vascular integrity, causes atherosclerosis, and the mechanism of action of XO inhibitors on atherosclerosis.     

A multiplanar three dimensional echocardiographic study of mitral valvar annular function in children with normal and regurgitant valves

INTRODUCTION: The mitral valvar complex is difficult to visualise accurately in only two dimensions. Three-dimensional echocardiography gives new insight into the dynamic changes of intra-cardiac structures during the cardiac cycle. The aim of this study was to study the mitral annulus in systole and diastole in normal children using three-dimensional echocardiography, and to analyse the effect of regurgitation on annular function. MATERIALS AND METHODS: Three-dimensional echocardiographic datasets, acquired in 11 consecutive subjects with mitral regurgitation, and 20 normal subjects, were analysed offline using simultaneous multiplanar review. RESULTS: The mitral valvar annular area decreased in diastole, and increased in systole, in both groups. The annulus in patients with mitral regurgitation is dilated compared to normal subjects, the systolic value for those with regurgitation having a mean of 6.79 plus or minus 2.55 centimetres2/metres2, and the diastolic value a mean of 5.01 plus or minus 1.78 centimetres2/metres2, as opposed to a systolic mean value of 5.28 centimetres2/metres2 plus or minus 1.68, p = 0.091, and diastolic mean value of 3.05 centimetres2/metres2 plus or minus 0.90, in normal subjects (p less than 0.0001). The proportional change in mitral valvar annular area from systole to diastole showed a trend towards being smaller in those with mitral regurgitation, although this did not reach significance (24.8% versus 41.13%, p equal to 0.249). Analysis of subgroups of patients with moderate or severe mitral regurgitation showed mitral excursion, expressed as percentage of left ventricular length, to be significantly less than in normal subjects, at 12.78 plus or minus 5.10% versus 15.84 plus or minus 4.23% (p equal to 0.012). CONCLUSIONS: Mitral valvar annular area in children decreases in diastole, and increases in systole. In those with mitral regurgitation, the annulus is dilated and the dynamic annular function is depressed.     

Elevated Liver Enzymes along with Comorbidity Is a High Risk Factor for COVID-19 Mortality: A South Indian Study on 1,512 Patients

Background and Aims: Liver enzyme abnormalities in coronavirus 2019 (COVID-19) are being addressed in the literature. The predictive risk of elevated liver enzy...     

Perforation of Jejunal Diverticula in Steroids and Nonsteroidal Anti-Inflammatory Drug Abusers: A Case Series

INTRODUCTION: Jejunal diverticula are rare lesions, and when complications arise, they pose diagnostic difficulties. Perforation is a common complication resulting in an acute abdomen, although preoperative diagnosis is usually not possible. The "gold standard" for management for patients with complications is surgery. We present a series of patients with perforated jejunal diverticula who were on prolonged treatment with nonsteroidal anti-inflammatory drugs (NSAIDs) and steroids for Chikungunya fever. METHODS: There were a total of six patients, all of them presenting with perforative peritonitis, with or without shock. Plain abdominal radiogram and ultrasonogram confirmed this, although the exact site of the perforation was not diagnosed preoperatively. All patients underwent exploratory laparotomy and perforated jejunal diverticulum was found. Resection and anastomosis was performed in all cases. RESULTS: The mean operating time was 113.5 minutes, and the blood loss was not significant. Postoperative course was uneventful except wound infection in two patients. There was no mortality. CONCLUSIONS: Prolonged NSAID and steroid use are known to cause ulceration/perforation of the upper digestive tract and colonic diverticula. This seems to be the most likely cause for the perforation of jejunal diverticula in our series of patients. This view is supported by the absence of inflammation and infiltration of neutrophils on histopathological examination of the diverticula.     

Laparoscopic right hemicolectomy for mucocele due to a low-grade appendiceal mucinous neoplasm.

Tumors of the appendix are rare entities causing mucoceles. The majority of them are discovered incidentally during investigation for other conditions. Laparoscopic surgery for appendiceal tumors is still controversial, as inadvertent rupture of the lesion due to improper handling will cause pseudomyxoma peritonei. The patient was incidentally discovered to have an appendiceal tumor and referred to us for laparoscopy. Because the tumor involved the entire appendix, a laparoscopic right hemicolectomy was performed without directly handling the tumor. Postoperative recovery was uneventful. Pathological diagnosis was low-grade appendiceal mucinous neoplasm. The safety of laparoscopic appendectomy for the management of incidentally discovered appendiceal tumors has not yet been established. Several reports in the literature support both laparoscopic and open surgery. The main concerns to be addressed are the adequacy of resection and intraperitoneal rupture of the tumor. Our patient successfully underwent laparoscopic surgery without any complications. A formal right hemicolectomy was performed because the tumor involved the entire appendix. We now think laparoscopic surgery for appendiceal tumors is safe, feasible, and even may be beneficial.     

Detection of novel coupled mutations in the katG gene (His276Met, Gln295His and Ser315Thr) in a multidrug-resistant Mycobacterium tuberculosis strain from Chennai, India, and insight into the molecular mechanism of isoniazid resistance using structural bioinformatics approaches

This study reports on the structural basis of drug resistance targeting the katG gene in a multidrug-resistant Mycobacterium tuberculosis (MDR-TB) strain with two novel mutations (His276Met and Gln295His) in addition to the most commonly reported mutation (Ser315Thr). A structural bioinformatics approach was used to predict the structure of the mutant KatG enzyme (MT). Subsequent molecular dynamics and docking studies were performed to explain the mechanism of isoniazid (INH) resistance. The results show significant conformational changes in the structure of MT leading to a change in INH binding residues at the active site, with a significant increase in the inhibition constant (Ki) of 5.67 μm in the mutant KatG-isoniazid complex (MT-INH) compared with the wild-type KatG-isoniazid complex (WT-INH). In the case of molecular dynamics studies, root mean square deviation (RMSD) analysis of the protein backbone in simulated biological conditions revealed an unstable trajectory with higher deviations in MT throughout the simulation process (1 ns). Moreover, root mean square fluctuation (RMSF) analysis revealed an overall increase in residual fluctuations in MT compared with the wild-type KatG enzyme (WT), whilst the INH binding residues of MT showed a decreased fluctuation that can be observed as peak deviations. Hence, the present study suggests that His276Met, Gln295His and Ser315Thr mutations targeting the katG gene result in decreased stability and flexibility of the protein at INH binding residues leading to impaired enzyme function.