Background The dynamics of essential metals such as Copper (Cu) and Zinc (Zn) may be associated with the novel coronavirus disease 2019 (COVID-19) that has spread across the globe. Objectives The aim of this study is to investigate the relationship between serum levels of Cu and Zn, as well as the Cu:Zn ratio in the acute phase of COVID-19 along with the assessment of their connection to other laboratory parameters (hematological, biochemical, hemostatic). Methods Serum levels of Cu and Zn were measured by atomic absorption spectrometry in 75 patients in the acute COVID-19 phase and were compared with those of 22 COVID-19 patients evaluated three months after the acute phase of the disease (‘non-acute’ group) and with those of 68 healthy individuals . Results In comparison with both the non-acute patients and the healthy controls, the acute patients had lower levels of hemoglobulin and albumin, and higher levels of glucose, creatinine, liver transaminases, C-reactive protein (CRP), and higher values of the neutrophils to lymphocytes ratio (NLR) at the hospital admission. They also exhibited increased levels of Cu and decreased of Zn, well represented by the Cu:Zn ratio which was higher in the acute patients than in both non-acute patients (p = 0.001) and healthy controls (p <0.001), with no statistical difference between the last two groups. The Cu:Zn ratio (log scale) positively correlated with CRP (log scale; r = 0.581, p <0.001) and NLR (r = 0.436, p = 0.003). Conclusion Current results demonstrate that abnormal dynamics of Cu and Zn levels in serum occur early during the course of COVID-19 disease, and are mainly associated with the inflammation response.

Ascorbate has long been thought to play an important role in intestinal iron absorption. The recent identification of a possible ascorbate-dependent duodenal ferric reductase suggests a role for intracellular ascorbate in the control of iron absorption. We set out to determine whether duodenal ascorbate concentrations are altered by treatments known to alter the rate of iron absorption and whether ascorbate levels affect duodenal reductase activity. Duodenal ascorbate was extracted and assayed by HPLC and/or a chemical assay. Ferric reductase was assayed in vitro with ferric nitrilotriacetate or nitroblue tetrazolium as substrates. Duodenal ascorbate concentrations were increased by iron deficiency, genetic hypotransferrinemia, and hypoxia. Parenteral iron overload increased iron stores but did not affect duodenal ascorbate concentrations. Hemolytic anemia induced in mice by phenylhydrazine injection also did not affect duodenal ascorbate concentrations. In vitro studies with incubated duodenum showed that decreased tissue ascorbate was associated with decreased mucosal ferric reductase activity, whereas incubation with dehydroascorbate prevented both the decrease in ascorbate concentration and reductase activity. Mouse duodenum ascorbate concentrations changed in response to treatments that altered iron absorption rates; in particular, ascorbate levels generally increased when iron absorption was increased by iron deficiency, hypoxia, or genetic hypotransferrinemia. We conclude that changes in ascorbate levels are associated with changes in ferric reductase activity. These findings are consistent with the proposal that duodenal ascorbate plays a role in intestinal iron absorption.

Iron deficiency in humans is associated with increased duodenal ascorbate concentrations. This finding suggests that increased reductase activity is partly due to an increase in this substrate for duodenal cytochrome b reductase 1.

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Summary Anemia is an important public health problem worldwide. Although iron (Fe) deficiency is considered the main factor in the pathogenesis of anemia, only 40-60% of anemia cases are responsive to Fe supplementation. Considerable data exist that other micronutrient deficiencies, such as selenium (Se), could be possible causes of anemia. The issue of Se deficiency as a risk factor for the development of anemia is of particular interest to our country since the Balkan region is known by a low Se content of soils. The aim of the study was to examine the contemporary conception of the influence of Se deficiency on the development of anemia by a review of the scientific literature. Most animal studies have shown a significant relation between Se deficiency and anemia, but one study indicates that there is no impact of Se deficiency on the hematological parameters. Associations of low serum Se with anemia have been found in a number of human studies including subjects of various age groups and pathological conditions. Three possible biological mechanisms have been suggested for the involvement of Se deficiency in the development of anemia: increased oxidative stress, modulation of inflammation through induction of interleukin-6, and increased expression of heme oxygenase-1. A more categorical clarification of the relationships between Se deficiency and development of anemia is needed with respect to appropriate trace element supplementation in cases of anemia with insufficient or absent therapeutic response to Fe treatment.

The aim of the present study was to assess -cell function using homeostasis model (HOMA-B) and disposition index (DI) in pregnant women with/without gestational diabetes, and after delivery. A total of 102 pregnant women between 24-28 gestational weeks (53 with gestational diabetes mellitus (GDM) and 49 with normal glucose tolerance (NGT) and 22 GDM postpartum women (8-12 weeks after delivery) were included in the study. All postpartum women had a history of GDM. HOMA indexes (insulin resistance -HOMA-IR and HOMA-B for assessing -cell function) were calculated from fasting glucose and insulin concentrations. To estimate insulin secretion independent of insulin sensitivity, DI was calculated using glucose and insulin levels at 0 and 60 min during the course of a 2 h 75g oral glucose tolerance test (OGTT). In GDM pregnant women HOMA-B was signifi cantly lower compared to NGT women (p = 0.017), but there was no signifi cant difference compared to women after birth (NS). There was difference between NGT and postpartum women (p < 0.05). DI was signifi cantly lower for GDM pregnant women in comparison to NGT and postpartum women (p < 0.0001; p = 0.011), between NGT and women after birth (p < 0.04). In our study, comparison of НОМА-В in NGT and GDM pregnant women demonstrated that the OR of developing GDM was 0.989 (95% CI, 0.980-0.998, P = 0.013), and comparison of DI in healthy pregnant and GDM showed that the OR of developing GDM was 0.967 (95% CI, 0.947-0.988, P = 0.002). Therefore, HOMA-B and DI appear to be protective factors in the risk of developing GDM. According to our results, assessment of -cell function, using HOMA-B and DI, showed that they are lower in GDM than NGT group and postpartum women. It is important to note that HOMA-B did not show signifi cant difference between GDM pregnant and women after delivery with a history for GDM. We assume that pregnant women with GDM have a pancreatic -cell defect that remains after birth. These women are at increased risk for developing diabetes mellitus, the most frequent type 2 diabetes, in the future after birth.

Gestational diabetes mellitus (GDM), one of the most common pregnancy complications, is defined as glucose intolerance with onset or first recognition during pregnancy. Its prevalence varies worldwide in dependence on characteristics of the underlying population and applied diagnostic criteria. The etiology is multifactorial and not sufficiently elucidated. Available evidence suggests that the base of pathogenesis is relatively diminished insulin secretion coupled with pregnancy-induced insulin resistance. Modifiable and non-modifiable risk factors for development have been identified. Trace elements and vitamin D could be contributed to modifiable factors for prediction the risk in a large population. Essential trace elements in pregnancy are necessary to overcome systemic oxidative, metabolic and inflammatory stress. Evidence, still inconclusive, has been accumulated about the relation between higher incidence of vitamin D failure/deficiency during pregnancy and GDM. The lower level of 25-OH vitamin D could be associated with increased risk for anemia development, also including pregnant women. This review intends to provide an overview of the possible link between both vitamin D and trace elements as risk factors for GDM development.

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