False negative effect of high triglycerides concentration on vitamin D levels: A big data study

Background: Inaccurate test results may be a reason why vitamin D deficiency is seen as a common problem worldwide. Interferences from the sample matrix during testing are the most important factors in measurement errors. In this study, the relationship between triglycerides and total cholesterol levels and vitamin D levels in Turkey was investigated. Methods: The 25-hydroxyvitamin D test results and lipid test results studied in Turkey in 2021 were compared. Data were obtained from the Ministry of Health National Health Database. Simultaneously, 25-hydroxyvitamin D, triglyceride, and total cholesterol levels were studied, and 1,135,644 test results were taken as the basis. Results: In the group of patients with total cholesterol levels between 0-10.33 mmol/L, the proportion of patients below 20 mg/L ranged from 56.8% to 61.8%. In the patient group with cholesterol between 10.36-259 mmol/L, the rate of patients with less than 20 mg/L was between 70.8-100%, while the rate of patients with cholesterol above 100 mg/L was 0%. The mean 25-hydroxyvitamin D level was 20.1 mg/L in the patient group with a total cholesterol level between 0-10.33 mmol/L, and 16 mg/L in the patient group with a cholesterol level above 10.36 mmol/L. The mean 25-hydroxyvitamin D level was 20.11 mg/L in the patient group with triglycerides 0-10.16 mmol/L, and the 25-hydroxyvitamin D level was 12.28 mg/L in the patient group with triglycerides 10.17-113 mmol/L. The proportion of patients with vitamin D levels above 100 mg/L was found to be 0% in the group of patients with triglycerides above 10.17-113 mmol/L. Conclusions: According to this study, there is a risk of toxicity when administering vitamin D therapy in patients with high cholesterol and triglycerides levels. This study is the first of this size in the literature. High triglycerides and cholesterol levels can cause inaccurate measurement of vitamin D levels, so care should be taken when evaluating these tests

Experimental investigation of immunoglobulin and complement concentrations in exposure to ivig, hbig, rituximab, tocilizumab, and bevacizumab

Background Immunoglobulins (Igs) are produced in plasma cells in response to glycoprotein-like immunogens and they are also used as therapeutics in the pharmaceutical industry. It may be important to know the effects of therapeutic Igs on Ig levels during therapy to eliminate any misconceptions about the immunity of patients. Objective This study aimed to investigate the effects of monoclonal antibody (mAb) derivative drugs and therapeutic antibody (intravenous Ig [IVIG] and hepatitis B immune globulin [HBIG]) treatments on blood IgG, IgA, IgM, IgE, complement component 3 (C3), and complement component 4 (C4) levels. Methods N Protein Control SL / Low (Siemens, Marburg, Germany, Lot: 084654) was used as the control solution. Aliquots of IVIG, HBIG, rituximab, tocilizumab, and bevacizumab (20 & mu;L) were added to 180 & mu;L of the control solution, and the solutions were vortexed (5 s). The samples were studied using a Dade Behring BN II (Siemens, Marburg, Germany) nephelometer. All measurements were repeated three times by performing the same process in which distilled water (20 & mu;L) was added to the control solution to determine the target value, and the average values were taken. The bias formula was used to calculate the amount by which the results deviated from the target value. Results IVIG caused the greatest deviation (45.97%) to IgG levels. HBIG, rituximab, tocilizumab, and bevacizumab caused the IgG level to deviate by 0.81%, 9.68%, 27.42%, and 30.65%, respectively. In the IgA test, tocilizumab increased the reading by 8.66%, while the other therapeutics caused reductions in the reading, with the smallest and largest changes caused by HBIG (-0.93%) and bevacizumab (-4.98%). Tocilizumab increased the IgE level by 0.48%, and rituximab and bevacizumab reduced the IgE level by -0.21% with -8.47%, respectively. Tocilizumab, IVIG, and HBIG caused 1.41%, 2.70%, and 4.32% deviations, respectively, in the C3 levels. Whereas bevacizumab (-1.08%) and rituximab (-5.41%) caused reductions in the C3 levels. Tocilizumab, HBIG, rituximab, IVIG, and bevacizumab caused deviations of 0.87%, -2.31%, -3.76%, -6.36%, -8.38%, respectively, in the C4 levels. Conclusion Deviations in measured IgG levels after therapeutic Ig and mAb infusions may cause errors in clinical decisions. It is recommended that Ig levels be measured before infusion or when the therapeutic drug has been eliminated from the blood

BTD Gene Mutations in Biotinidase Deficiency: Genotype-Phenotype Correlation

Objective: To identify the biotinidase (BTD) gene mutations in patients with biotinidase deficiency in our region; and to determine the phenotype-genotype correlations in the presence of clinical findings

The Protective Effect of Naringenin-Oxime on Cisplatin-Induced Toxicity in Rats

The aim of this study is to examine the protective effect of naringenin-oxime (NOX) on cisplatin-induced major organ toxicity and DNA damage in rats. Thirty-five male Wistar albino rats were equally split into five groups as follows: control (i.p., 0.1 ml of saline), Cis administration (i.p., 7 mg/kg b.w.), NOX treatment (i.p., 20 mg/kg b.w., daily for ten days), Cis + NOX20, and Cis + NOX40 combination (i.p., 20 and 40 mg/kg b.w., daily for ten days). Serum and peripheral blood mononuclear leukocytes (PBMC) were obtained from blood. Malondialdehyde, glutathione, total antioxidant and oxidant status, and catalase were measured in serum, liver, and kidney, and oxidative stress index was calculated. In parallel, paraoxonase and arylesterase activities were tested in liver and serum. We used 8-OHdOG as a marker for DNA damage in serum via ELISA and in PMBC via comet assay. Treatment with Cis elevated the levels of serum biochemical parameters, oxidative stress, and DNA damage. Pretreatments of NOX restored biochemical and oxidative stress parameters in serum, renal, and liver tissues (p<0.01) and reduced 8-OHdG level, a finding further supported by comet assay in PBMC. Observations of the present study support the fact that treatment with NOX prevents Cis-induced hepatotoxicity, nephrotoxicity, and genotoxicity by restoring antioxidant system

Selective inhibition of carbonic anhydrase-IX by sulphonamide derivatives induces pH and reactive oxygen species-mediated apoptosis in cervical cancer HeLa cells

Selective inhibition with sulphonamides of carbonic anhydrase (CA) IX reduces cell proliferation and induces apoptosis in human cancer cells. The effect on CA IX expression of seven previously synthesised sulphonamide inhibitors, with high affinity for CA IX, as well as their effect on the proliferation/apoptosis of cancer/normal cell lines was investigated. Two normal and three human cancer cell lines were used. Treatment resulted in dose- and time-dependent inhibition of the growth of various cancer cell lines. One compound showed remarkably high toxicity towards CA IX-positive HeLa cells. The mechanisms of apoptosis induction were determined with Annexin-V and AO/EB staining, cleaved caspases (caspase-3, caspase-8, caspase-9) and cleaved PARP activation, reactive oxygen species production (ROS), mitochondrial membrane potential (MMP), intracellular pH (pHi), extracellular pH (pHe), lactate level and cell cycle analysis. The autophagy induction mechanisms were also investigated. The modulation of apoptotic and autophagic genes (Bax, Bcl-2, caspase-3, caspase-8, caspase-9, caspase-12, Beclin and LC3) was measured using real time PCR. The positive staining using γ-H2AX and AO/EB dye, showed increased cleaved caspase-3, caspase-8, caspase-9, increased ROS production, MMP and enhanced mRNA expression of apoptotic genes, suggesting that anticancer effects are also exerted through its apoptosis-inducing properties. Our results show that such sulphonamides might have the potential as new leads for detailed investigations against CA IX-positive cervical cancers

Investigation of the effect of vitamin K1 prophylaxis on newborn screenings tests in newborns

Background: Routine screening for hereditary disorders in newborns includes screening for treatable metabolic and endocrine disorders, such as biotidinase deficiency, galactosemia, maple syrup urine disease, hypothyroidism, and cystic fibrosis. Incorrect test results may be encountered due to the use of vitamin K1. To investigate the interference effect of vitamin K1 on neonatal screening tests and to raise awareness of erroneous measurements. Methods: Heel blood samples were taken from 25 newborns born in a neonatal intensive care unit. Dry blood C0, C2, C3, C4, C4DC, C5:1, C5OH, C5DC, C6, C6DC, C8, C8:1, C8DC, C10, C10:1, C10DC, C12, C14, C14:1, C14:2, C16, C16:1, C18, C18:1, C18:2, C18:OH, methylglutaryl, valine, leucine/isoleucine, methionine, phenylalanine, argininosuccinic acid, aspartate, alanine, arginine, citrulline, glycine, ornithine, and glutamate tests were studied using the tandem mass spectrometry (MS) method. The results of the heel blood samples obtained before and after the application of vitamin K1 (Phyto menadione) were compared. Results: In two studies conducted with in vitro and in vivo tests, C0, C2, C3, C4, C4DC, C5, C5OH, C6, C8, C10, C10:1, C14, C16, C16:1, C18, C18:1, methylglutaryl, phenylalanine, argininosuccinic acid, tyrosine, aspartate, arginine, citrulline, glycine, and glutamine were all significantly elevated (p < 0.05). Conclusions: Heel blood samples may yield false results due to vitamin K1 administration. In the case of doubtful results, a new sample should be taken and the measurement should be repeated. © 2023 Sciendo. All rights reserved

Assessment of the antiproliferative and apoptotic roles of sulfonamide carbonic anhydrase IX inhibitors in HeLa cancer cell line

Carbonic anhydrase IX (CA IX) has recently been validated as an antitumor/antimetastatic drug target. In this study, we examined the underlying molecular mechanisms and the anticancer activity of sulfonamide CA IX inhibitors against cervical cancer cell lines. The effects of several sulfonamides on HeLa, MDA-MB-231, HT-29 cancer cell lines, and normal cell lines (HEK-293, PNT-1A) viability were determined. The compounds showed high cytotoxic and apoptotic activities, mainly against HeLa cells overexpressing CA IX. We were also examined for intracellular reactive oxygen species (ROS) production; intra-/extracellular pH changes, for inhibition of cell proliferation, cellular mitochondrial membrane potential change and for the detection of caspase 3, 8, 9, and CA IX protein levels. Of the investigated sulfonamides, one compound was found to possess high cytotoxic and anti-proliferative effects in HeLa cells. The cytotoxic effect occurred via apoptosis, being accompanied by a return of pHe/pHi towards normal values as for other CA IX inhibitors investigated earlier