Zinc gluconate 50mg tablets

ContextThe assessment of zinc status is difficult but essential for the identification of zinc deficiency and evaluation of interventions to improve zinc status.ObjectiveThe purpose of this systematic review (SR) and meta-analysis was to update the previously published SR of biomarkers of zinc status, conducted by the European Micronutrient Recommendations Aligned (EURRECA) network in 2009, to answer the question: Which putative measures (biomarkers) of zinc status appropriately reflect a change in zinc intake of at least 2 weeks?Data sourcesA structured search strategy was used to identify articles published between January 2007 and September 2022 from MEDLINE (Ovid), Embase (Ovid), Cochrane Database of Systematic Reviews, and Cochrane Central Register of Controlled Trials (CENTRAL). Relevant articles were identified using previously defined eligibility criteria.Data extractionData were extracted and combined with data from the previous SR.Data analysisA random-effects model was used to calculate pooled mean differences using STATA (StataCorp). The risk of bias and the certainty of evidence for all outcomes were assessed. Additional data on 7 of the 32 previously reported biomarkers were identified, along with data on an additional 40 putative biomarkers from studies published since 2007. Pooled data analysis confirmed that, in healthy participants, both plasma/serum zinc concentration and urinary zinc excretion responded to changes in zinc intake (plasma/serum: mean effect [95% CI], controlled studies: 2.17 µmol/L [1.73, 2.61]; P ConclusionThe updated analyses support the conclusion that plasma/serum and urinary zinc respond to changes in zinc intake in studies of healthy participants. Several additional putative biomarkers were identified, but more studies are needed to assess the sensitivity and reliability.Systematic review registrationPROSPERO no. CRD42020219843.

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BackgroundType 2 diabetes mellitus (T2DM) remains one of the most significant public health problems, and its incidence rate is steadily increasing worldwide despite scientific and technological progress in the field of medicine. The focus of research in this area is gradually shifting from classic risk factors-such as obesity, sedentary lifestyle and genetic predisposition-toward additional, potentially modifiable contributors such as micronutrient imbalances; among them are disturbances in zinc homeostasis that may influence glucose metabolism and oxidative stress.ObjectiveThis systematic review with narrative synthesis aims to examine the bidirectional relationship between zinc status and T2DM and to evaluate whether zinc screening and personalized nutritional support could contribute to comprehensive metabolic management.MethodsA literature search was conducted in the PubMed database and the Cochrane library for studies published between 2010 and 2024. Studies assessing zinc status or supplementation in relation to the risk, progression, or management of T2DM were included. Data were synthesized narratively, focusing on clinical and mechanistic evidence.ResultsThirty studies met the inclusion criteria. Evidence indicates that zinc imbalance (both deficiency and excess) is associated with T2DM risk and outcomes. Zinc deficiency may impair insulin synthesis and signaling, promote oxidative stress and inflammation, while excessive zinc intake may induce metabolic disturbances. T2DM itself may lead to reduced zinc status via altered absorption and increased excretion. While some studies suggest modest improvements in glycemic or lipid parameters following zinc supplementation, findings remain inconsistent and context-dependent. The prevalence of suboptimal zinc status in certain populations supports the rationale for targeted screening rather than routine supplementation.ConclusionsZinc is mechanistically involved in insulin synthesis, antioxidant defense, and inflammation control, but current clinical evidence does not justify its use as a therapeutic agent in T2DM. Instead, assessment of zinc status and individualized correction of deficiency may represent a component of personalized nutritional support, particularly for patients with long disease duration, poor dietary quality, or genetic predispositions affecting zinc metabolism.

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Radiation-induced oral mucositis (RIOM) frequently causes severe pain and treatment interruptions in patients with head and neck cancer. While earlier guidelines suggested zinc supplementation, updated MASCC/ISOO guidelines downgraded it to 'No Guideline Possible' due to highly conflicting evidence. This study aims to resolve these inconsistencies by evaluating zinc's prophylactic efficacy and investigating whether the route of administration determines its clinical benefit. Following PRISMA guidelines and INPLASY registration (INPLASY202620063), we searched PubMed, Embase, and the Cochrane Library through February 2026. We included randomized controlled trials (RCTs) comparing prophylactic zinc versus placebo or standard care in head and neck cancer patients receiving radiotherapy. Risk of bias was assessed using the Cochrane Risk of Bias 2 (RoB 2) tool. The primary outcome was severe (Grade 3-4) RIOM incidence. Data from five RCTs (332 patients) were pooled using a random-effects model. Overall, zinc significantly reduced severe mucositis risk (RR = 0.35, 95% CI: 0.17-0.73, p = 0.005). Crucially, an exploratory subgroup analysis revealed a striking divergence based on delivery route. Topical zinc mouthwash demonstrated encouraging protection (RR = 0.16, 95% CI: 0.05-0.49, p = 0.001) with zero heterogeneity (I2 = 0%). In contrast, systemic zinc yielded borderline, inconsistent benefits (RR = 0.52, 95% CI: 0.27-1.01, p = 0.055, I2 = 37%). In conclusion, the localized pool of contemporary evidence clearly demonstrates that the systemic oral ingestion of zinc supplements does not provide a reliable prophylactic benefit against severe radiation-induced oral mucositis in head and neck cancer care. Conversely, topical zinc mouthwashes exhibit an encouraging protective trend; however, the severe paucity of available randomized trials and low cumulative patient volume preclude definitive clinical verification. While these exploratory findings suggest that topical administration may provide a more consistent protective trend compared to systemic routes, they should be interpreted as hypothesis-generating rather than definitive. Future large-scale, multi-center RCTs are strictly warranted to validate these promising route-specific benefits before formal guideline integration.

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This systematic review and meta-analysis aimed to comprehensively evaluate the prevalence of zinc deficiency in patients with inflammatory bowel disease (IBD). A systematic literature search was conducted across PubMed/MEDLINE (Medical Literature Analysis and Retrieval System Online), Embase, Scopus, Web of Science, and Cochrane Library from inception to November 2025. Studies reporting zinc deficiency prevalence in IBD patients using validated biomarkers were included. Two independent reviewers performed study selection, data extraction, and quality assessment using the Newcastle-Ottawa Scale. Meta-analysis was performed using a random-effects model, with subgroup analyses conducted by IBD subtype. Seven studies comprising 2,403 IBD patients were included. The pooled prevalence of zinc deficiency was 35% (95% CI: 19-52%), with substantial heterogeneity (I² = 98.5%). Subgroup analysis revealed a higher prevalence in Crohn's disease patients (40%, 95% CI: 21-59%) compared to ulcerative colitis patients (33%, 95% CI: 18-51%). These findings underscore the significant burden of zinc deficiency in IBD populations and highlight the need for routine nutritional screening, particularly in Crohn's disease patients. Clinicians should consider zinc assessment as part of comprehensive IBD management, with targeted supplementation for deficient patients to potentially improve clinical outcomes and quality of life.

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