Nephrotoxicity

Molecular profiles of hepatotoxicity and nephrotoxicity markers in dysmenorrheic (on treatment or not) students

Published on: 18th February, 2020

OCLC Number/Unique Identifier: 8550958914

Background: Dysmenorrhea is menstrual disorder that affects about 40% - 90% of women worldwide, it is associated with oxidative stress. The current treatment of this condition is administration of non-steroidal anti-inflammatory drugs, which when frequently used, may affect organs. Objective: Assess the hepatotoxicity and nephrotoxicity side effects related to dysmenorrhea and its treatment Materials and methods: A survey (questionnaire) was designed and implemented on 689 female students of the University of Dschang. After this, and following the inclusion criteria, 191 blood samples were collected for assay of hepatotoxicity markers (transaminases, albumin), nephrotoxicity indicators (creatinine, urea, total protein) and the inflammation associated indicators. The measurements were performed on fully automated Olympus AU 400 Analyzer, using standard reagent kits. Results: Subjects with untreated dymenorrhea lasting more than five years had a significantly high level (p < 0.05) of ALT (39.47 ± 15.74 IU/L) and AST (44.37 ± 13.74 IU/L). Transaminases levels were significantly associate (p < 0.01) and positively correlate (0.251 for ALT and 0. 223 for AST) with the disease duration. Dysmenorrheic individuals on medication for more than 9 years had significantly higher ALT (25.14 ± 7.85 IU/L) and AST (35.26 ± 0.70 IU/L) levels (p < 0.05) compared to those under treatment for less than 5 years (19.37 ± 8.27 UI/L and 27.68 ± 8.56 UI/L). The use of analgesics, regardless of the duration of treatment, had normal creatinine clearance (107.44 ± 30.86 ml/min), compared to those treated with either anti-inflammatory drugs (71.56 ± 26.44 ml/min), or a combination of analgesics and anti-inflammatory drugs (81.34 ± 31.97 ml/min), which was significantly reduced (p < 0.05). Conclusion: Dysmenorrhea duration, type and duration of treatment potentially expose participants to liver and kidney disorders.
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Chlorhexidine and oral cancer: A short review

Published on: 18th February, 2020

OCLC Number/Unique Identifier: 8535180883

Owing to the ever westernizing lifestyles in developing countries like India, the escalation of oral cancer patients are in need of urgent plan of action. With tobacco being the commonest cause for causation of oral cancer, Global Adult Tobacco Survey, 2016-17 revealed that almost 28% of whole population of India is consuming tobacco in either smoking or smokeless form. With these increasing numbers, the expected death toll to be expected to touch 1-2 million mark by the year 2035 [1]. Although, the current Onco-medicine fraternity excels in rendering care to oral cancer patients in the form of surgeries, chemotherapy and radiation-therapy. Often, these treatment modalities impart some unwanted adverse effects like, docetaxel (DCT) is known for its hepatotoxicity [2,3] whereas, one of the commonly used cisplatin (CIS) presents with nephrotoxicity, neurotoxicity, bone marrow suppression and vomiting [4,5]. Literature suggests of many non conventional medicaments being tested in past for their anti onco-genic effect, where few being effective and others being questionable ones. Chlorhexidine being one among them showing some how promising anti onco-genic activity with feeble amount of studies being conducted in past. Chlorhexidine, one of the most commonly prescribed mouthrinse in the field of dentistry, with varying concentrations of 0.12% and 0.2% concentrations. Although, apart from being broad spectrum antibiotic, its capability to dismantle the protein – protein bond between anti – apoptotic Bcl-2 family protein Bcl-xL and its pro – apoptotic binding partners [6]. The current study was conducted on three cell lines of squamous cell carcinoma (SCC-4, SCC-9, SCC -15) and two pharynx carcinoma cell lines (FaDu and Detroit 562). The compounds induced apoptosis through mitochondria dependent apoptotic pathway in oral tumour cell lines. Another study conducted to assess the similar anti – oncogenic activites of chlorhexidine mouthrinse along with cranberry [7]. It was evident from results that, with increasing concentrations of chlorhexidine mouthrinse, there was increase in mean percent growth inhibition. The authors concluded saying, chlorhexidine has showed both anti cancerous as well as anti bacterial activity required to tackle common oral infections, part of common anti cancer therapy. Fernando Martínez-Pérez et al (2019) conducted study, where antitumor activity of Lipophilic Bismuth Nanoparticles (BisBAL NPs) and chlorhexidine on human squamous cell carcinoma was assessed using energy dispersive X – ray spectroscopy in conjunction with scanning electron microscopy (EDS-SEM). Study revealed, BisBAL NPs and chlorhexidine both showed cell growth inhibition on both cancer cell line (CAL-27) and human gingival fibroblasts (HGFs). Although, chlorhexidine showed non specific cytotoxicity for both tumoral and non tumoral control cells. The suggestive mechanism of action might be loss of cell membrane integrity [8]. Although Eliot MN (2013) conducted study, to assess the risk of head and neck squamous cell carcinoma secondary to use of alcohol containing and non alcoholic mouthwashes including chlorhexidine. The study was concluded with an assumption based on chlorhexidine mouthwash alters the oral flora [9], thus resulting in increasing risk exponentially through diverse change in oral bacteria and altered immune response with contribution towards genesis or promotion of cancer [10]. On the contrary, alcohol consumption and smoking are predisposing factors towards upper digestive tract cancer. The main causative factor being the first metabolite of alcohol, acetaldehyde. And much higher levels are derived from oral bacteria and thus, same can be altered in favour through usage of chlorhexidine mouthwash, to avoid excessive production of acetaldehyde intra orally. In conclusion, chlorhexidine mouthwash has been into dental practice since long and the role it plays in either ways has to be assessed by a multi dimensional study with cell lines including that of control to derive better compared conclusions.
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Renal function effects of FDS, a saponin isolated from Filicium decipiens seeds: Biochemical and Histopathological studies

Published on: 31st October, 2019

OCLC Number/Unique Identifier: 8312821337

Physicochemical and pharmacological studies indicated that Filicium decipiens seeds contained various specialized metabolites, including saponins. The aim of this work is to reveal the nephrotoxicity of FDS, a saponin isolated from Filicium decipiens seeds on male Wistar rats histopathological and biochemical parameters. Rats were submitted to oral ingestion of FDS (6.0 mg/kg) and crude extract (120.0 mg/kg) and were observed high levels of urea and creatinine in blood analyses of all animals followed by an acute renal failure by glomerular retraction. In the present study, FDS and crude extract when administered in Wistar rats induced an increase of serum levels of Urea and Creatinine, biochemical markers of kidney function. Table 1 shows Urea concentration at Test group with FDS (54.3 ± 1.80 mg/ml) and Test group with crude extract (49.7 ± 2.00 mg/ml), were 47% and 34.7% higher, respectively, when compared to control group (36.9 ± 2.00 mg/ml), and Creatinine at the test group with FDS (2.1 ± 0.03 mg/ml) and test group with crude extract (1.6 ± 0.09 mg/ml) presented a value 3.5 and 2.8 times higher, respectively, than control (0.6 ± 0.08 mg/ml). Based on these results, our data demonstrate a significant effect in renal function of rats treated with F. decipiens saponin.
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Ceftriaxone in pediatrics: Indication, adverse drug reaction, contraindication and drug interaction

Published on: 5th April, 2022

OCLC Number/Unique Identifier: 9470678055

Ceftriaxone is having many uses and useful “third-generation” cephalosporin that necessitates being given every day. Ceftriaxone acts as binds to one or many of the penicillin-binding proteins which inhibit the final transpeptidoglycan step of peptidoglycan synthesis in the bacterial cell wall, thus inhibiting biosynthesis and arresting cell wall assembly resulting in bacterial cell death.Ceftriaxone-associated biliary adverse events in children less than eighteen years cause biliary pseudolithiasis and scarcely nephrolithiasis often happen in children less than eighteen years after receiving overdoses of ceftriaxone. Ceftriaxone perhaps binds with calcium and figure insoluble chelation leading to biliary pseudolithiasis. Cholelithiasis, increased biliary thickness, and pseudolithiasis rarely happen in a period of being a child, but there are two modes of distribu¬tion described by two peaks, the first being at an early stage of development and the second is a period of life when a child develops into an adult. Hyperbilirubinemia is significantly contraindicated for neonates administrated ceftriaxone, particularly premature neonates, because of the displacement of bilirubin from albumin-binding sites and increase in blood concentrations of free bilirubin. A child than one month old and a child less than twelve-month old in special are at great risk of poor results because of bilirubin encephalopathy. Coincident administrations of ceftriaxone with aminoglycosides such as gentamycin and loop diuretics (furosemide) perhaps increase the risk of nephrotoxicity (rapid degeneration in the kidney function to the toxic outcome of double or triple medications). Coincident administrations of ceftriaxone with anticoagulant medications such as warfarin are associated with bleeding due to increased prothrombin times, which is reversible with vitamin K.
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