To see the other types of publications on this topic, follow the link: Toxic anemia.
Journal articles on the topic 'Toxic anemia'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 50 journal articles for your research on the topic 'Toxic anemia.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.
1
G.T., Kudeshova, and Kuchkarova L.S. "Activity Of Enteral Lactase And Lactobacilli In Maternal And Hereditary Toxic Anemia." American Journal of Applied sciences 03, no. 06 (2021): 51–57. http://dx.doi.org/10.37547/tajas/volume03issue06-08.
Full textAbstract:
In this paper, the activity of lactobacilli in the small intestine and lactobacilli in the colon, which are involved in the digestion of milk sugar during lactotrophy using phenylhydrazine hydrochloride, studied the effects of toxic anemia on mother and child. Erythrocyte counts, hemoglobin levels, lactase enzyme activity in the small intestine, and lactobacilli activity in the colon were determined in 12- and 24-day-old rats born to mother anemic rats with toxic anemia under the influence of phenylhydrazine hydrochloride, and in growing rats after mother and offspring toxic anemia. Experiments in white rats have shown that in rats growing in experimental toxic anemia of mother and offspring, there is an increase in lactase activity in the small intestine and a decrease in lactobacilli activity depending on the degree of intoxication in the colon.
2
Saidova, F. H., L. M. Ahmedova, Zh B. Aslanova, and N. A. Najafov. "Changes of hematological indices in patients with diffuse toxic goiter." Klinicheskaia khirurgiia 88, no. 3-4 (2021): 76–79. http://dx.doi.org/10.26779/2522-1396.2021.3-4.76.
Full textAbstract:
Objective. To reveal the incidence of various morphological types and degrees of the anemia severity in patients with diffuse toxic goiter.
 Materials and methods. Data of medical histories of 157 patients, operated for diffuse toxic goiter in 2012 yr were analyzed. In accordance to hematological indices estimated there were outlined two Groups of patients: Group I – 98 patients with diffuse toxic goiter and mild anemia, average age (39.4 ± 1.4) yrs old, 57 (58.2%) women and 41 (41.8%) men, and Group II – 59 patients with diffuse toxic goiter and middle degree of the anemia severity, average age (41.1 ± 1.7) yrs old, 48 (81.4%) women and 11 (18.6%) men. Levels of hemoglobin, hematocrit, quantity and average volume of erythrocytes, average content of hemoglobin in one erythrocyte, average concentration of hemoglobin in the erythrocytes were determined in the blood analysis.
 Results. Microcytic type of anemia was noted in 89.8% of patients with anemia of middle degree of severity, while a normocytic one – in 10.2%; in mild anemia – in 87.8 and 12.2% patients, accordingly. Hypochromic and normochromic types of anemia with equal rate were revealed in mild anemia and anemia of middle degree of severity: hypochromic – in 94.9%, normochromic – in 5.1% patients.
 Conclusion. Diffuse toxic goiter is characterized by more frequent development of mild (62.4%), microcytic (88.5%), hyperchromic (94.9%) anemia, caused by iron deficiency.
3
Junaid Ali Thebo, Junaid Ali Thebo, Shaista Khan Shaista Khan, Abdul Aziz Shaikh Abdul Aziz Shaikh, et al. "Role of Trace andamp; Toxic Elements in the Development of Anaemia in School going population of Hyderabad." Journal of the chemical society of pakistan 41, no. 3 (2019): 405. http://dx.doi.org/10.52568/000752/jcsp/41.03.2019.
Full textAbstract:
The aim of this research work was to measure the concentration of essential trace elements, including serum copper, iron and zinc in children suffering from anemia, and also to investigate the effect of heavy metal like lead on causing anemia. The study has been performed on school going children living in Hyderabad, which is a mini industrialized city. The study was carried out in anemic children studying in different schools of Hyderabad having different age groups. 10 ml venous blood samples were obtained after an informed consent form was signed.The samples were used to analyzed the trace elements (Fe,Cu, Zn) and toxic metal Lead (Pb). Trace elements include zinc and copper were found elevated in anemic children than healthy one, Copper is involved in many vital mechanisms in the body, energy production, connective tissue formation, and Fe metabolism, whereas copper found low with relation to the iron in anemic children because copper helps in the absorption of iron. Zinc is an essential micronutrient demanded by living being because of its significant position in-cooperation with structural constituent of proteins and as a cofactor in enzyme catalysis, there is difference between zinc and iron, they have been found to inhibit each other’s absorption due to their competitive absorption pathways. Increased zinc levels found in children with low iron content, whereas control group have normal results of these elements which may be due to their dietary management. The results revealed the environmental pollution and the associated health risks on exposure to lead. Pb concentrations whereas the current research stated a considerable relationship of mild and severe anemia with 10-42.2μg/dl Pb concentrations, the variation in results may be due to a small sample size in the current study, Drinking water from corrosion of plumbing systems through the use of lead sellers and other lead containing materials in connecting household plumbing to public water supplies. Ground and surface water are also contaminated by lead consuming industry and agricultural activities. The concentrations of Pb greater than or equal to (≥)10 μg/dl in children related with an increased threat of mild and severe anemia, diminishing iron absorption . High Lead levels were related with lower concentrations of iron, ferritin and copper, in this study it was found that high levels of lead were found mostly in boys. Lead levels have also found in control group which was below 5 ug/dl, according to WHO ≥ 10 ug/dl is considered as high.
4
G.T., Kudeshova, and Murodova N.B. "Effect of experimental toxic anemia on the pancreas." Partners Universal International Research Journal (PUIRJ) 01, no. 02 (2022): 1–4. https://doi.org/10.5281/zenodo.6726433.
Full textAbstract:
The decrease in hydrolytic capacity relative to polysaccharides observed in the initial hydrolysis phase of carbohydrates was expressed in the small intestinal secretion of α-amylase in the pancreas, a decrease in enzyme activity in the small intestinal chymus. Chronic exposure to toxicants leads to an increase in pancreatic tissue and enzyme activity in the blood due to a decrease in α-amylase activity in the small intestine. Decreased pancreatic secretion and increased secretion are indicative of pancreatic insufficiency. It was shown the regulator treatment of growing rats by hemotoxicants (phenilhydrasine and lead acetate) resulted to increase of incretion and decrease of secretion of pancreas. These changes take place at the histological destroy of pancreas. These data are shown the toxic anemia stimulates the development of pancreatitis in growing rats.
5
Rodriguez-Sevilla, Juan Jose, Xavier Calvo, and Leonor Arenillas. "Causes and Pathophysiology of Acquired Sideroblastic Anemia." Genes 13, no. 9 (2022): 1562. http://dx.doi.org/10.3390/genes13091562.
Full textAbstract:
The sideroblastic anemias are a heterogeneous group of inherited and acquired disorders characterized by anemia and the presence of ring sideroblasts in the bone marrow. Ring sideroblasts are abnormal erythroblasts with iron-loaded mitochondria that are visualized by Prussian blue staining as a perinuclear ring of green-blue granules. The mechanisms that lead to the ring sideroblast formation are heterogeneous, but in all of them, there is an abnormal deposition of iron in the mitochondria of erythroblasts. Congenital sideroblastic anemias include nonsyndromic and syndromic disorders. Acquired sideroblastic anemias include conditions that range from clonal disorders (myeloid neoplasms as myelodysplastic syndromes and myelodysplastic/myeloproliferative neoplasms with ring sideroblasts) to toxic or metabolic reversible sideroblastic anemia. In the last 30 years, due to the advances in genomic techniques, a deep knowledge of the pathophysiological mechanisms has been accomplished and the bases for possible targeted treatments have been established. The distinction between the different forms of sideroblastic anemia is based on the study of the characteristics of the anemia, age of diagnosis, clinical manifestations, and the performance of laboratory analysis involving genetic testing in many cases. This review focuses on the differential diagnosis of acquired disorders associated with ring sideroblasts.
6
Prawej, Ansari. "Comparative Clinical Study of Nabayas Louha: An Ayurvedic Haematinic Preparation and a Conventional Iron Preparation in Female Anemic Patients." Journal of Plant Biochemistry & Physiology 8, no. 5 (2020): 6. https://doi.org/10.5281/zenodo.11931227.
Full textAbstract:
Anemia is common nutritional disorder and it affects one third of population around the globe. Assessing nutritional status of human is an inevitable process to lead a healthy life. Females are affected significantly by anemia compare to male. According to WHO report, developing herbs-based formulation to treat anemic patients is safe and less toxic. In this study a double-blind, cross group comparative clinical trial of Nabayas Louha (NBL) a Ayurvedic haematinic preparation with G-Iron Folic Acid (IFA) was undertaken on 66 female anemic volunteers with age between 20-30 years. It was seen that NBL after being administered at a daily dose of 500 mg for 30 days significantly increased the hemoglobin content of the treated volunteers. It produced an increase in serum iron content and decreases total iron binding capacity. The ESR level was also decreased. These effects of NBL were found to be comparable with IFA. There was a marked decrease in WBC count noticed, however statistically significant increase in the lymphocytes count was seen. Furthermore, the level of toxicity related enzymes SGOT and SGPT was not altered significantly in the NBL treated group which vividly confirm that supplementation of NBL is not toxic. In conclusion, these findings recommend use of NBL as supplement in the treatment of iron deficiency anemia and WBC disorders.
7
Capito, Joseph C., Brianna N. Skaff, Alexandra R. Kinney, and Amie M. Ashcraft. "Methylene blue for hemolytic crisis in patients with met-hemoglobinemia secondary to hemoglobin volga: A case series." Journal of Family Medicine and Primary Care 13, no. 6 (2024): 2499–502. http://dx.doi.org/10.4103/jfmpc.jfmpc_1168_23.
Full textAbstract:
ABSTRACT There is a rare subset of patients with a genetically abnormal hemoglobin structure initially discovered in the Volga region of Europe known as Volga anemia. Key features of this condition include compromised delivery of oxygen to peripheral tissues and altered red blood cells that have a higher likelihood of being broken down or hemolyzed, which can lead to significant hemolytic anemia. Methylene blue is a dye that acts as a reducing agent of oxygen and is commonly used in toxic states that lead to methemoglobin build-up. This paper explores the pathophysiology of this genetic condition and documents three cases across two patients—a father and son—when methylene blue was used during an anemic crisis.
8
Adaobi, Linda Okerulu, and Martins Onwuka Osah. "Macrocytic anemia induced via oral administration of toxic dose of acetaminophen." GSC Biological and Pharmaceutical Sciences 19, no. 1 (2022): 178–84. https://doi.org/10.5281/zenodo.6624407.
Full textAbstract:
The abuse of Acetaminophen (over-the-counter drug) is rapidly increasing globally, thus inducing physiological alterations and toxicity. In this study, it was hypothesized that overdose of acetaminophen may induce certain type of anemia; hence the type of anemia induced by oral exposure to toxic dose of acetaminophen was evaluated. Fifteen (15) Wistar rats weighing approximately 160 g were grouped into three (3) groups; Group 1 (control) received 2ml of distilled water, Group 2 received 200 mg/kg of acetaminophen and Group 3 received 700 mg/kg of acetaminophen for 14 days. After administration, the rats were dissected on anesthesia (chloroform); blood was collected via cardiac puncture. The samples collected were assayed for Red Blood cell (RBC) Count, Hemoglobin concentration (HB), Mean Corpuscular Volume (MCV), Mean Corpuscular Hemoglobin (MCH), Mean Corpuscular Hemoglobin Concentration (MCHC). The data was statistically analyzed using Graph Pad Prism (version 8). Statistical significance was considered at P < 0.05. Results showed that acetaminophen (200 mg/kg and 700 mg/kg) significantly increased MCV, MCH and decreased RBC and HB in a dose dependent manner with no significant effect on MCHC when compared to group 1 (control) (P<0.05). In conclusion, Acetaminophen (700 mg/kg) decreases RBC, HB and increases MCV, MCH and MCHC which suggests that toxic dose of acetaminophen can cause macrocytic anemia in Wistar rats.
9
Lin, Wu, Liao, et al. "In Vitro and In Vivo Evaluations of Mesoporous Iron Particles for Iron Bioavailability." International Journal of Molecular Sciences 20, no. 21 (2019): 5291. http://dx.doi.org/10.3390/ijms20215291.
Full textAbstract:
Chronic renal failure involving hemodialysis results in blood loss during filtration. Iron deficiency and iron deficiency anemia can result. A compensatory increase in iron dosage has many side effects including discomfort. Elemental iron is a highly-pure iron source, which reduces the frequency of dosages; the solubility decreases with increased particle size or pore size. In this study, synthesized mesoporous iron particles (MIPs) were used to relieve iron deficiency anemia. Their bioavailability was measured in vitro by a Caco-2 cell model and in vivo in iron-deficient rats. In vitro bioavailability of MIPs was examined by measuring ferritin content in the Caco-2 cell model. Iron uptake of MIPs was significantly higher than commercial iron particles, which were less porous. In vivo bioavailability of MIPs was examined by measuring body weight gain and red blood cell-related parameters, compared with the bioavailability of standard drug ferrous sulfate in iron-deficient anemic rats. Finally, average hemoglobin content and hemoglobin regeneration efficiency were significantly higher in anemic rats supplemented with commercial iron particles, compared to anemic controls. In the 28-day oral toxicity test, MIPs were not significantly toxic to rat physiology or tissue histopathology. Thus, MIPs may allow effective recovery of hemoglobin in iron deficiency anemia.
10
Lagraoui, Mouna, Brigitte Grouix, Nathalie Julien, et al. "PBI-1402: A Non-Toxic Immunorestorative Small Molecule for the Treatment of Anemia." Blood 108, no. 11 (2006): 4224. http://dx.doi.org/10.1182/blood.v108.11.4224.4224.
Full textAbstract:
Abstract Erythropoiesis is regulated by an intricated network of transcription factors and other molecules that mediate differentiation of stem cell progenitors into erythroid lineage. PBI-1402 is a non-toxic, well-defined chemo- and radio-protective orally active small molecule which stimulates erythropoiesis. In vivo studies demonstrate that PBI-1402 has an immunorestorative effect in anemia induced by phenylhydrazine or lethal irradiation. In phenylhydrazine-induced anemia, PBI-1402 treated mice had an increased number of hematopoietic progenitor cells compared to the control mice. This increase was more pronounced in the erythroid lineage (BFU-E and CFU-E). In myeloablated mice that received a syngeneic bone marrow transplant, oral treatment with PBI-1402 resulted in a significant increase in peripheral erythrocyte count and hemoglobin concentration. In conclusion, these results indicate that PBI-1402 plays an important role in the formation of red blood cells. Therefore, PBI-1402 may be useful for the treatment of anemia associated with chemotherapy, radiotherapy, bone marrow transplantation and cancer.
11
Adaobi Linda Okerulu and Osah Martins Onwuka. "Macrocytic anemia induced via oral administration of toxic dose of acetaminophen." GSC Biological and Pharmaceutical Sciences 19, no. 1 (2022): 178–84. http://dx.doi.org/10.30574/gscbps.2022.19.1.0141.
Full textAbstract:
The abuse of Acetaminophen (over-the-counter drug) is rapidly increasing globally, thus inducing physiological alterations and toxicity. In this study, it was hypothesized that overdose of acetaminophen may induce certain type of anemia; hence the type of anemia induced by oral exposure to toxic dose of acetaminophen was evaluated. Fifteen (15) Wistar rats weighing approximately 160 g were grouped into three (3) groups; Group 1 (control) received 2ml of distilled water, Group 2 received 200 mg/kg of acetaminophen and Group 3 received 700 mg/kg of acetaminophen for 14 days. After administration, the rats were dissected on anesthesia (chloroform); blood was collected via cardiac puncture. The samples collected were assayed for Red Blood cell (RBC) Count, Hemoglobin concentration (HB), Mean Corpuscular Volume (MCV), Mean Corpuscular Hemoglobin (MCH), Mean Corpuscular Hemoglobin Concentration (MCHC). The data was statistically analyzed using Graph Pad Prism (version 8). Statistical significance was considered at P < 0.05. Results showed that acetaminophen (200 mg/kg and 700 mg/kg) significantly increased MCV, MCH and decreased RBC and HB in a dose dependent manner with no significant effect on MCHC when compared to group 1 (control) (P<0.05). In conclusion, Acetaminophen (700 mg/kg) decreases RBC, HB and increases MCV, MCH and MCHC which suggests that toxic dose of acetaminophen can cause macrocytic anemia in Wistar rats.
12
Loukou, Ahou L., Moussa Gbogbo, Raissa S. Assi, Louise Atchibri-Anin, and Kouakou Brou. "Efficacy of the Aqueous Extracts of Justicia Galeopsis Leaves on the Improvement of Hematological Parameters in Anemic Rats." Journal of Food Research 9, no. 5 (2020): 14. http://dx.doi.org/10.5539/jfr.v9n5p14.
Full textAbstract:
Antianemc potential of aqueous of Justicia galeopsis leaves was studied using Wistar Albino rats after induction of anemia by phenylhydrazine hydrochloride. Forty rats (20 male and 20 female) subdivided into five groups of eight rats were used. There was a group as control (not anemic) and four other anemic groups which had received by gavage respectively 1 ml/kg of distilled water, 1 ml/kg of body weight of Vitafer (reference drug commonly used to treat anemia), 100 mg/kg of body weight of extract of J. galeopsis leaves cooked during 30 min and 30 mg/kg of body weight of extract of J. galeopsis leaves cooked during 45 min. Hematological parameters (red blood cells, hemoglobin and hematocrit) were analyzed as indices of anemia and the weights of specific organs (liver, spleen and kidney) were evaluated. The results of this investigation had showed that aqueous extract of J. galeopsis leaves cooked improved red blood cells, hemoglobin and hematocrit levels. These extracts were not toxic for liver, spleen and kidney. The administration of 100 mg/kg/day of extract of leaves cooked leaves during 30 min promotes a better recovery rate of the number of red blood cells (94.80 %), hemoglobin level (159.53 %) and hematocrit (117.72 %) than Vitafer and the extract of leaves cooked for 45 min. This is suggestive that aqueous extracts of Justicia galeopsis leaves cooked during 30 min may be exploited during 2 weeks in the treatment of anemia.
13
Da Costa, Lydie, Thierry Leblanc, and Narla Mohandas. "Diamond-Blackfan anemia." Blood 136, no. 11 (2020): 1262–73. http://dx.doi.org/10.1182/blood.2019000947.
Full textAbstract:
Abstract Diamond-Blackfan anemia (DBA) was the first ribosomopathy described and is a constitutional inherited bone marrow failure syndrome. Erythroblastopenia is the major characteristic of the disease, which is a model for ribosomal diseases, related to a heterozygous allelic variation in 1 of the 20 ribosomal protein genes of either the small or large ribosomal subunit. The salient feature of classical DBA is a defect in ribosomal RNA maturation that generates nucleolar stress, leading to stabilization of p53 and activation of its targets, resulting in cell-cycle arrest and apoptosis. Although activation of p53 may not explain all aspects of DBA erythroid tropism, involvement of GATA1/HSP70 and globin/heme imbalance, with an excess of the toxic free heme leading to reactive oxygen species production, account for defective erythropoiesis in DBA. Despite significant progress in defining the molecular basis of DBA and increased understanding of the mechanistic basis for DBA pathophysiology, progress in developing new therapeutic options has been limited. However, recent advances in gene therapy, better outcomes with stem cell transplantation, and discoveries of putative new drugs through systematic drug screening using large chemical libraries provide hope for improvement.
14
Sasi, Sreethish, and Mohamed A. Yassin. "A Rare Case of Acquired Hemolytic Anemia and Pancytopenia Secondary to Pernicious Anemia." Case Reports in Oncology 13, no. 2 (2020): 783–88. http://dx.doi.org/10.1159/000507981.
Full textAbstract:
The commonest etiologies of new-onset pancytopenia are congenital bone marrow failure syndromes, marrow space-occupying lesions, infections, and peripheral destruction. Nutritional deficiencies, including folate and vitamin B12, can occasionally cause pancytopenia. We report a 48-year-old gentleman who presented with a 1-week history of dizziness and upper gastrointestinal bleeding. Laboratory evaluation revealed pancytopenia, macrocytosis, toxic neutrophils, hemolysis, suppressed reticulocyte count, positive direct anti-globulin test (DAT), severely reduced B12 levels, and positive anti-intrinsic factor and anti-parietal cell antibodies. He was started on weekly intramuscular B12 supplementation and showed improvement in blood cell counts during follow-up. Recognition of B12 deficiency as a cause of pancytopenia and DAT-positive autoimmune hemolytic anemia can help to avoid unwanted investigations and aid in early diagnosis and treatment.
15
Lisette, Del Corso, Balleari Enrico, Arboscello Eleonora, Ghio Riccardo, Mencoboni Manlio, and Racchi Omar. "Mayor Erythropoietic Response after Deferasirox Treatment in a Transfusion-Dependent Anemic Patient with Primary Myelofibrosis." Case Reports in Hematology 2013 (2013): 1–4. http://dx.doi.org/10.1155/2013/520712.
Full textAbstract:
Primary myelofibrosis (PMF) is a myeloproliferative neoplasm frequently complicated by transfusion dependent anemia. Both anemia and transfusion-dependence are associated with a poor outcome, at least in part because of toxic effects of iron overload (IOL). Iron-chelating therapy (ICT) is increasingly used in order to prevent IOL in this setting. Here, we describe the case of a 73-year-old man affected by PMF and severe transfusion-dependent anemia who experienced a dramatic erythroid response after being treated with deferasirox to prevent IOL.
16
Kovalenko, A. N., V. B. Musatov, A. I. Solovev, and V. A. Kapatcyna. "Complexity of the therapy of P. falciparum - malaria in the Russian Federation." Terapevticheskii arkhiv 91, no. 11 (2019): 75–80. http://dx.doi.org/10.26442/00403660.2019.11.000442.
Full textAbstract:
The article presents a clinical case of malaria in a 29-year - old man without immunodeficiency, complicated by the development of infectious - toxic shock, anemia, kidney damage. The brief literature review discusses the complexity of etiotropic therapy, the problem of pathogen resistance to antimalarial drugs, pathogenetic mechanisms that contribute to the formation of shock, anemia and kidney damage in tropical malaria.
17
Sayfutdinova Z.A. "Modern biochemical methods used in the diagnosis of experimental toxic hepatitis." Texas Journal of Medical Science 29 (February 21, 2024): 88–93. http://dx.doi.org/10.62480/tjms.2024.vol29.pp88-93.
Full textAbstract:
Oxygen is required by the cells of most organisms to produce sufficient ATP for metabolic activity. Hypoxia, or oxygen deprivation, occurs in human tissues and cells due to a variety of conditions, including heart and lung diseases, anemia, and circulatory disorders. Depending on the severity, irreversible tissue and cell damage may occur
18
Camaschella, Clara, and Laura Silvestri. "Molecular Mechanisms Regulating Hepcidin Revealed by Hepcidin Disorders." Scientific World JOURNAL 11 (2011): 1357–66. http://dx.doi.org/10.1100/tsw.2011.130.
Full textAbstract:
Iron is essential for human life, but toxic if present in excess. To avoid iron overload and maintain iron homeostasis, all cells are able to regulate their iron content through the post-transcriptional control of iron genes operated by the cytosolic iron regulatory proteins that interact with iron responsive elements on iron gene mRNA. At the systemic level, iron homeostasis is regulated by the liver peptide hepcidin. Disruption of these regulatory loops leads to genetic diseases characterized by iron deficiency (iron-refractory iron-deficiency anemia) or iron overload (hemochromatosis). Alterations of the same systems are also found in acquired disorders, such as iron-loading anemias characterized by ineffective erythropoiesis and anemia of chronic diseases (ACD) associated with common inflammatory conditions. In ACD, iron is present in the body, but maldistributed, being deficient for erythropoiesis, but sequestered in macrophages. Studies of the hepcidin regulation by iron and inflammatory cytokines are revealing new pathways that might become targets of new therapeutic intervention in iron disorders.
19
Hong, C. B., H. V. Ellis, C. C. Lee, H. Sprinz, J. C. Dacre, and J. P. Glennon. "Subchronic and Chronic Toxicity Studies of 2,4-Dinitrotoluene. Part III. CD-1® Mice." Journal of the American College of Toxicology 4, no. 4 (1985): 257–69. http://dx.doi.org/10.3109/10915818509078678.
Full textAbstract:
Subchronic and chronic toxicities of 2,4-dinitrotoluene (2,4-DNT) were evaluated in CD-1® mice. 2,4-DNT was more toxic to males than to females. Male mice fed 47 mg/kg per day or 137 mg/kg per day for 13 weeks gained less weight. However, females fed 52 or 147 mg/kg per day had no adverse effects. Feeding of 413 mg/kg per day for males or 468 mg/kg per day for females lowered feed consumption, depressed body weight, and caused mild anemia and mild hepatocellular dysplasia in both sexes and mild testicular degeneration in males. Both males and females were fed an average of 14 (low dose), 95 (middle dose), or 898 mg/kg per day (high dose) for up to 24 months. In males, there was a high incidence of epithelial renal tumor and hepatocellular dysplasia in all dose groups, Incidence of testicular atrophy was increased in the middle-and high-dose males. In addition, the high dose caused toxic anemia and death. In females, the high dose was associated with toxic anemia, hepatocellular dysplasia, nonfunctional follicle with a lack of corpora lutea, an effect analogous to the testiclar atrophy in males, and death. A generalized pigmentation, probably of 2,4-DNT metabolite origin, was seen in many tissues of especially the high-dose males and females.
20
Fihri, Aicha Fassi, Noori S. Al-Waili, Redouan El-Haskoury, et al. "Protective Effect of Morocco Carob Honey Against Lead-Induced Anemia and Hepato-Renal Toxicity." Cellular Physiology and Biochemistry 39, no. 1 (2016): 115–22. http://dx.doi.org/10.1159/000445610.
Full textAbstract:
Background/Aims: Natural honey has many biological activities including protective effect against toxic materials. The aim of this study was to evaluate the protective effect of carob honey against lead-induced hepato-renal toxicity and lead-induced anemia in rabbits. Methods: Twenty four male rabbits were allocated into four groups six rabbits each; group 1: control group, received distilled water (0.1 ml / kg.b.wt /daily); group 2: received oral lead acetate (2 g/kg.b.wt/daily); group 3: treated with oral honey (1g /kg.b.wt/daily) and oral lead (2 g/kg.b.wt/daily), and group 4: received oral honey (1 g/kg.b.wt/daily). Honey and lead were given daily during 24 days of experimentation. Laboratory tests and histopathological evaluations of kidneys were done. Results: Oral administration of lead induced hepatic and kidney injury and caused anemia during three weeks of the exposure. Treatment with honey prevented hepato-renal lead toxicity and ameliorated lead-induced anemia when honey was given to animals during lead exposure. Conclusion: It might be concluded that honey has a protective effect against lead-induced blood, hepatic and renal toxic effects.
21
Ryzhakova, N. A., T. S. Krivonogova, E. V. Golikova, et al. "Streptococcal toxic shock syndrome in an adolescent." Meditsinskiy sovet = Medical Council, no. 6 (April 27, 2022): 251–55. http://dx.doi.org/10.21518/2079-701x-2022-16-6-251-255.
Full textAbstract:
A special form of streptococcal infection is streptococcal toxic shock syndrome (STS), characterized by rapid development of symptoms and high mortality. Patient O., 14 years old, was taken to the infectious diseases department of OGAUZ DBNo. 1 by the SMP team with complaints of shortness of breath, vomiting, loose stools in a state of moderate severity due to intoxication syndrome. Diagnosis upon admission: Acute infectious gastroenteritis of moderate severity. Acute respiratory infections rhinopharyngitis, acute bronchitis, pneumonia (?), DN1. During examination in the UAC, anemia, leukocytosis, acceleration of ESR, in the biochemical blood analysis – an increase in CRP, in the coagulogram — increased INR, APTT, RFMC, decreased PTI, in urine tests – protein, erythrocytes, on the X–ray — bilateral pleural effusion, in the tank. sputum culture — Streptoccocus oralis 10/3 KOE/ml, PCR SARS-CoV-2: negative, blood test for antistreptolysin-O (ASL-O): 800 IU/ml (norm up to 200 IU/ml), blood for sterility 19.05.20: no bacterial microflora growth was detected. After receiving laboratory data, the diagnosis was made: Acute glomerulonephritis?, Аcute intestinal infection. Double-sided hydrothorax. Internal combustion engine. Anemia of the 1st degree. The final diagnosis: Acute post-streptococcal glomerulonephritis with a debut in the form of streptococcal toxic shock syndrome, a period of extensive clinical and laboratory changes, with a decrease in the debut of kidney function in the form of acute renal failure, recovery period. Against the background of the treatment (2 courses of antibiotic therapy (cefotaxime, amoxicillin), infusion therapy, pulse therapy with metipred (5 pulses), double transfusion of freshly frozen plasma, prednisone, lasix, veroshpiron, enap, curantil, heparin, and other accompanying therapy), pronounced positive clinical and laboratory dynamics was noted. She was hospitalized for 43 days, of which 9 days were in the intensive care unit (5 days on a ventilator). On the 44th day, the child was discharged in a satisfactory condition with recommendations under the supervision of a pediatrician, a pediatric nephrologist at the place of residence
22
Kuneva, Tanja P., Diana B. Apostolova, Zlatka B. Stoyneva, Aneta B. Ivanova, Vladimira V. Boyadzhieva, and Kristina A. Yosifcheva. "Risk Of Lead Intoxication In Exposed Workers." Journal of Biomedical and Clinical Research 7, no. 2 (2014): 123–27. http://dx.doi.org/10.1515/jbcr-2015-0137.
Full textAbstract:
Summary A clinical observation of 15 workers exposed to lead, engaged in recycling of lead accumulators, was carried out. The exposition to lead aerosols varied from 2 months to 14 years. High levels of lead absorption and excretion after application of antidote therapy were found in all workers followed up. There were no manifestclinical signs and symptoms in 7 workers whom we suspected to be lead carriers. Anemia was diagnosed in 8 of the investigated persons. Severe form of intoxication, including paresis of both radial nerves, was established in one worker. Subacute lead poisoning, presenting with lead colic, anemia, toxic hepatitis and toxic polyneuropathy, was diagnosed in three persons with only several months of intensive lead exposure. Association between lead exposure, metal absorption and clinical symptoms in investigated persons were discussed.
23
Smereck, Janet. "Aplastic Anemia: A Possible Toxic Effect of an Herbal “Colon Cleansing” Preparation." Journal of Emergency Medicine 36, no. 2 (2009): 191–93. http://dx.doi.org/10.1016/j.jemermed.2007.11.107.
Full text
24
Rajendran, Durgalakshmi, and Natarajan Chandrasekaran. "Journey of micronanoplastics with blood components." RSC Advances 13, no. 45 (2023): 31435–59. http://dx.doi.org/10.1039/d3ra05620a.
Full textAbstract:
Micronanoplastics (MNPs) interact with blood components, resulting in anemia, cardiovascular diseases, etc. Research gaps include toxic impacts of real-world MNPs, monomers, co-pollutants complex, and so on, emphasizing the need for more research.
25
Christine, Helen, Tenny Setiani Dewi, and Dewi Kania Intan Permatasari. "Tatalaksana lesi oral untuk mendukung asupan nutrisi pasien toxic epidermal necrolysis." Majalah Kedokteran Gigi Klinik 7, no. 1 (2022): 26. http://dx.doi.org/10.22146/mkgk.72005.
Full textAbstract:
Toxic Epidermal Necrolysis (TEN) merupakan reaksi kulit yang berat akibat hipersensitifitas berupa gangguan mukokutaneus akut ditandai epidermolisis lebih dari 30% luas permukaan tubuh disertai gangguan sistemik dan dapat mengancam jiwa. Asupan nutrisi yang adekuat sangat penting untuk pemulihan dari kerusakan jaringan, terutama asupan protein. Keterlibatan mukosa rongga mulut pada TEN berupa lesi erosi pada membran mukosa yang menimbulkan kesulitan makan. Seorang wanita berusia 31 tahun dirujuk dari bagian Ilmu Kesehatan Kulitdan Kelamin dengan keluhan lecet dan gelembung berisi cairan jernih pada hampir seluruh tubuh disertai nyeri menelan sehingga pasien sulit makan sejak 2 hari yang lalu. Pasien didiagnosis TEN ec suspect fenitoin, diazepam dan asam mefenamat. Anemia defisiensi Fe, infeksi saluran kencing, drug induced liver injury, hipoalbuminemia dan hiponatremia. ditemukan dari hasil pemeriksaan laboratorium. Pemeriksaan ekstra oral menunjukan seluruh wajah, leher dan dada terdapat makula kecoklatan disertai daerah erosi pada bagian leher, mata anemis, sklera non ikterik, bibir atas dan bawah bengkak disertai krusta sanguinolenta. Pemeriksaan intra oral ditemukan lesi erosif eritema multipel pada hampir seluruh mukosa rongga mulut. Diagnosis kerja yaitu lesi oral terkait Toksik EpidermalNekrolisis. Terapi yang diberikan berupa kompres bibir larutan dexametason bergantian dengan NaCl 0,9% serta pemberian chlorhexidine gluconate 0,2% mouthwash. Seminggu kemudian pasien mengalami perbaikan dan dapatmakan makanan biasa. Kesimpulan dari penanganan dini yang adekuat terhadap manifestasi oral pasien TEN akan mendukung kondisi sistemik dengan meningkatnya asupan nutrisi sebagai bagian dari perawatan komprehensif.
26
Raghupathy, Radha, and Olga Derman. "Response of Paroxysmal Nocturnal Hemoglobinuria Clone with Aplastic Anemia to Rituximab." Case Reports in Hematology 2012 (2012): 1–5. http://dx.doi.org/10.1155/2012/106182.
Full textAbstract:
Paroxysmal nocturnal hemoglobinuria is caused by expansion of a hematopoietic stem cell clone with an acquired somatic mutation in the PIG-A gene. This mutation aborts the synthesis and expression of the glycosylphosphatidylinositol anchor proteins CD55 and CD59 on the surface of blood cells, thereby making them more susceptible to complement-mediated damage. A spectrum of disorders occurs in PNH ranging from hemolytic anemia and thrombosis to myelodysplasia, aplastic anemia and, myeloid leukemias. Aplastic anemia is one of the most serious and life-threatening complications of PNH, and a PNH clone is found in almost a third of the cases of aplastic anemia. While allogeneic bone marrow transplantation and T cell immune suppression are effective treatments for aplastic anemia in PNH, these therapies have significant limitations. We report here the first case, to our knowledge, of PNH associated with aplastic anemia treated with the anti-CD20 monoclonal antibody rituximab, which was associated with a significant reduction in the size of the PNH clone and recovery of hematopoiesis. We suggest that this less toxic therapy may have a significant role to play in treatment of PNH associated with aplastic anemia.
27
Alrashidi, Sadyah Nedah, Samia Soliman Barghash, Abuzar E. A. E. Albadri, and Sona S. Barghash. "Assessment of Potential Toxic Heavy Metal Levels in Serum of Saudi Patients Under Regular Hemodialysis and Its Association with Parathyroid Hormone, Uremic Pruritus, and Anemia." Toxics 13, no. 4 (2025): 241. https://doi.org/10.3390/toxics13040241.
Full textAbstract:
Worldwide, environmental pollution is a major contributor to illness and mortality, encompassing toxic elements, air pollutants, agricultural pesticides, and contaminated food and water. In patients with end-stage kidney disease, several factors—including impaired renal excretion, the degree of renal impairment, medication use, dialysate contamination, the quality of dialysis water, and metabolic changes—may lead to the accumulation of toxic elements in hemodialysis patients. This study aimed to assess toxic element levels in adults undergoing hemodialysis compared to a control group and to investigate the correlation between parathyroid hormone (PTH) levels, uremic pruritus, anemia and toxic element concentrations. A cross-sectional study was conducted on 60 adult patients undergoing regular hemodialysis for at least three months. Another group of 60 apparently healthy adult voluntaries with matched age and sex with the patient group served as the control. The Inductively Coupled Plasma Mass Spectrometry (ICP-MS) method was used to measure the concentrations of serum levels of aluminum (Al), lead (Pb), cadmium (Cd), chromium (Cr), and arsenic (As) for both groups, as well as in drinking water and dialysate water. The hemodialysis group exhibited significantly higher levels of Al, Pb, Cd, Cr, and As compared to the control group. Serum Pb levels showed a significant negative correlation with PTH, while serum ferritin levels were negatively correlated with Cr. However, no significant correlation was found between toxic element levels and uremic pruritus or anemia. Toxic element concentrations in dialysis and drinking water samples were within acceptable limits and below the detection threshold set by the World Health Organization (WHO) and the Association for the Advancement of Medical Instrumentation/American National Standards Institute (AAMI/ANSI). Therefore, elevated toxic element levels in hemodialysis patients may not be primarily attributable to drinking water or dialysis.
28
Saifutdinov, R. G., and Z. S. Minnullina. "Atypical clinical course of pneumonia in a patient with ummunodeficiency, iron-deficient anemia and dietary supplement intake." Kazan medical journal 93, no. 5 (2012): 840–43. http://dx.doi.org/10.17816/kmj1725.
Full textAbstract:
A clinical case pneumonia and multiple organ dysfunction syndrome in a patient with iron-deficiency anemia and previous intake of a dietary supplement for weight loss is presented, including results of examinations, observation and treatment. A 22 years old female was admitted with complaints on dyspnea, dry cough, malaise, «pulsing» head ache at the back of the head, vertigo while walking, fever up to 39 °С during the previous 3 days. Basing on the results of chest X-ray and laboratory examination the diagnosis of «Community-acquired subtotal right-sided pneumonia of mixed origin, severe clinical course, respiratory failure grade III, complicated by toxic shock syndrome, toxic pulmonary edema, disseminated intravascular coagulopathy stage I. Acute cardiac failure, acute respiratory distress syndrome. Acute iron-deficiency anemia. Acute erosive hemorrhagic gastritis. Obesity, II degree» was set up. In spite of active treatment patient’s condition deteriorated due to intoxication, cardiac failure and respiratory distress progress. Autopsy revealed that the patient has died of severe viral pneumonia, although such an extensive pneumonia is not typical for a 22-year old patient. Severe pneumonia development may be explained by immunodeficiency intensified by acute iron-deficiency anemia, which can be a possible side effect of previous intake of a dietary supplement for weight loss and alimentary factors.
29
Kudeshova, G. T. "Effect of toxic anemia on erythrocyte and hemoglobin levels during gestation and lactation." Asian Journal of Multidimensional Research 10, no. 10 (2021): 1218–22. http://dx.doi.org/10.5958/2278-4853.2021.00910.1.
Full text
30
Bunting, Samuel F., and André Nussenzweig. "Dangerous Liaisons: Fanconi Anemia and Toxic Nonhomologous End Joining in DNA Crosslink Repair." Molecular Cell 39, no. 2 (2010): 164–66. http://dx.doi.org/10.1016/j.molcel.2010.07.016.
Full text
31
Yuliya Sergeevna, Parkhomenko, Vostroilova Galina Anatolyevna, Khokhlova Nina Alekseevna, Zhukov Maksim Sergeevich, Shabanov Dmitriy Igorevich, and Ermakova Tatyana Igorevna. "STUDYING THE EFFECTS OF THE DRUG INTERAMIN IN SIMULATION OF TOXIC HEMOLYTIC ANEMIA." BULLETIN OF VETERINARY PHARMACOLOGY 1, no. 26 (2024): 42–52. http://dx.doi.org/10.17238/issn2541-8203.2024.1.42.
Full text
32
Vercellotti, Gregory M., and John D. Belcher. "Heme and the Vasculature: How the Endothelium Protects Itself Against Toxic Iron." Blood 116, no. 21 (2010): SCI—25—SCI—25. http://dx.doi.org/10.1182/blood.v116.21.sci-25.sci-25.
Full textAbstract:
Abstract Abstract SCI-25 Iron-derived reactive oxygen species (ROS) are involved in the pathogenesis of numerous vascular disorders. Heme-derived iron plays an instrumental role in the pathology of intravascular hemolytic diseases including malaria, sickle cell anemia, transfusion reactions, DIC and PNH. Heme catalyzed oxidative stress promotes a pro-inflammatory/prothrombogenic endothelium, diminution of bio-available nitric oxide (NO) and attraction of leukocytes and platelets. The vasculature is protected against heme-catalyzed injury by plasma proteins including haptoglobin, hemopexin, albumin, alpha-1-microglobulin and by scavenger receptors for heme complexes including CD163 and CD91. Heme and its concomitant oxidative stress induces the cytoprotective and rate-limiting enzyme in heme catabolism, heme oxygenase-1 (HO-1). In the process, HO-1 releases three enzymatic byproducts: carbon monoxide (CO), biliverdin/bilirubin, and iron, which stimulates ferritin synthesis. These HO-1 by-products have established anti-oxidant and anti-inflammatory properties. Human patients and mouse models elevate HO-1 in response to chronic hemolysis. Of all sites in the body, the endothelium may be at greatest risk of exposure to heme. Heme greatly potentiates endothelial cell killing mediated by leukocytes and other sources of ROS. As a defense against heme, endothelial cells upregulate HO-1 and ferritin. If cultured endothelial cells are briefly pulsed with heme and are then incubated for a prolonged period (16 h), the cells become highly resistant to oxidant-mediated injury and to the accumulation of endothelial lipid peroxidation products. This protection is associated with induction of both HO-1 and ferritin. H-ferritin with its ferroxidase activity is especially cytoprotective. In animal models, increased expression of HO-1 has been shown to protect tissues against ischemia-reperfusion injury, oxidative stress, inflammation, transplant rejection, apoptosis, and cell proliferation. Conversely, HO-1 null mice (hmox-1−/−) and human patients deficient in HO-1 are especially prone to oxidative stress and inflammation. Sickle cell anemia is an archetypal example of heme-induced oxidative stress and cytoprotective adaptation. The sickle patient and sickle mouse models defend and adapt to hemolysis by increasing their defenses against heme. HO-1 plays an essential role in the inhibition and resolution of vaso-occlusion in sickle cell anemia. HO-1 and its products, carbon monoxide and biliverdin, modulate vaso-occlusion through multiple mechanisms including reducing oxidative stress, inhibiting NF-kB, down-regulating endothelial cell adhesion molecules, decreasing red blood cell hemolysis and altering vascular tone. However, sickle cell patients often have adaptive increases in HO-1 activity which are insufficient to completely handle the excessive heme burden, particularly during acute bouts of hemolysis. HO-1 gene therapy in sickle mice using Sleeping Beauty-mediated transposition of an HO-1 transgene provides a promising non-viral approach to significantly enhance HO-1 expression in sickle cell anemia. Strategies to minimize heme-iron activation of the vasculature including increasing HO-1 and its products, anti-oxidants, iron chelators, increasing haptoglobin, hemopexin and/or their receptors CD163/CD91 should be explored in hemolytic disease states. Disclosures: Vercellotti: Sangart: Consultancy, Research Funding. Belcher:Sangart: Research Funding.
33
Baj, Jacek, Alicja Forma, Joanna Kobak, et al. "Toxic and Nutritional Optic Neuropathies—An Updated Mini-Review." International Journal of Environmental Research and Public Health 19, no. 5 (2022): 3092. http://dx.doi.org/10.3390/ijerph19053092.
Full textAbstract:
Optic neuropathies constitute a group of conditions with various etiologies and might be caused by different factors; we can distinguish the genetic and acquired causes of optic neuropathies. Even though the symptoms are not highly specific, this condition is primarily characterized by unilateral or bilateral vision loss with worsening color detection. The loss may be acute or gradual depending on the causation. In this article, we included a specification of toxic optic neuropathy (TON) mainly triggered by alcohol abuse and also the usage of other substances, including drugs or methanol, as well as intoxication by metals, organic solvents, or carbon dioxide. Nutritional deficiencies, vitamin absorption disorder, and anemia, which usually appear during excessive alcohol intake, and their effect on the etiology of the optic neuropathy have been likewise discussed.
34
Bredle, D. L., W. E. Bradley, C. K. Chapler, and S. M. Cain. "Muscle perfusion and oxygenation during local hyperoxia." Journal of Applied Physiology 65, no. 5 (1988): 2057–62. http://dx.doi.org/10.1152/jappl.1988.65.5.2057.
Full textAbstract:
Ventilation with O2 was previously shown to decrease whole-body and hindlimb muscle O2 uptake (VO2) in anesthetized dogs, particularly during anemia. To determine whether this was a purely local effect of hyperoxia (HiOx), we pump perfused isolated dog hindlimb muscles with autologous blood made hyperoxic (PO2 greater than 500 Torr) in a membrane oxygenator while the animals were ventilated with room air. Both constant-flow and constant-pressure protocols were used, and half the dogs were made anemic by exchange transfusion of dextran to hematocrit (Hct) approximately 15%. Thus there were four groups of n = 6 dogs each. A 30-min period of HiOx was preceded and followed by similar periods of perfusion with normoxic blood. In HiOx all four groups showed increased leg hindrance, increased leg venous PO2, and no significant changes in leg O2 inflow. Limb blood flow and VO2 decreased approximately 20% in HiOx with constant-pressure perfusion, regardless of Hct. In the constant-flow protocol, leg VO2 in HiOx was maintained by the anemic animals and actually increased in the normocythemic group. We conclude that HiOx directly affected vascular smooth muscle to cause flow restriction and maldistribution. Constant flow offset these effects, but the increased limb VO2 may have been a toxic effect. Anemia appeared to exaggerate the microcirculatory maldistribution caused by HiOx.
35
Flatt, Terrie, Kathleen Neville, Karen Lewing, and Jignesh Dalal. "Successful Treatment of Fanconi Anemia and T-Cell Acute Lymphoblastic Leukemia." Case Reports in Hematology 2012 (2012): 1–4. http://dx.doi.org/10.1155/2012/396395.
Full textAbstract:
Fanconi anemia is associated with an increased risk of malignancy. Patients are sensitive to the toxic effects of chemotherapy. We report the case of a patient with Fanconi anemia who developed T-cell acute lymphoblastic leukemia. He experienced chemotherapy-related complications including prolonged neutropenia, grade IV vincristine neuropathy, and disseminated aspergillosis. He was successfully treated with modified dosing of cytarabine and intrathecal methotrexate followed by allogeneic bone marrow transplant. The aspergillosis was treated with systemic antifungal treatment and surgical resection. Now 30 months after bone marrow transplant the patient is without evidence of aspergillosis or leukemia.
36
Igbokwe, Ikechukwu Onyebuchi, Ephraim Igwenagu, and Nanacha Afifi Igbokwe. "Aluminium toxicosis: a review of toxic actions and effects." Interdisciplinary Toxicology 12, no. 2 (2019): 45–70. http://dx.doi.org/10.2478/intox-2019-0007.
Full textAbstract:
Abstract Aluminium (Al) is frequently accessible to animal and human populations to the extent that intoxications may occur. Intake of Al is by inhalation of aerosols or particles, ingestion of food, water and medicaments, skin contact, vaccination, dialysis and infusions. Toxic actions of Al induce oxidative stress, immunologic alterations, genotoxicity, pro-inflammatory effect, peptide denaturation or transformation, enzymatic dysfunction, metabolic derangement, amyloidogenesis, membrane perturbation, iron dyshomeostasis, apoptosis, necrosis and dysplasia. The pathological conditions associated with Al toxicosis are desquamative interstitial pneumonia, pulmonary alveolar proteinosis, granulomas, granulomatosis and fibrosis, toxic myocarditis, thrombosis and ischemic stroke, granulomatous enteritis, Crohn’s disease, inflammatory bowel diseases, anemia, Alzheimer’s disease, dementia, sclerosis, autism, macrophagic myofasciitis, osteomalacia, oligospermia and infertility, hepatorenal disease, breast cancer and cyst, pancreatitis, pancreatic necrosis and diabetes mellitus. The review provides a broad overview of Al toxicosis as a background for sustained investigations of the toxicology of Al compounds of public health importance.
37
Filippova, O. V. "Specific features of pharmacokinetics and pharmacological advantages of liposomal iron for women’s health." Meditsinskiy sovet = Medical Council, no. 4 (April 26, 2025): 95–103. https://doi.org/10.21518/ms2025-153.
Full textAbstract:
Prevention and management of iron deficiency conditions, including iron deficiency anemia (IDA), in women is an important global health problem. Iron deficiency affects not only the somatic, but also the reproductive health of women, and may lead to decreased fertility. Prevention and management of anemia in pregnant women is essential, as iron deficiency can adversely affect the maternal and fetal well-being. In Russia, anemia is found in 35.5% of pregnant women. The market offers a wide range of iron supplements. Biand trivalent oral iron supplementation is often the first-line prevention and management for iron deficiency conditions, as it is an easy, affordable and effective therapy option. These supplements are not always effective; intestinal disorders and inflammatory diseases may reduce iron absorption. In addition, adverse effects, first of all gastrointestinal (GI) ones, such as abdominal pain, dyspepsia, nausea, vomiting, diarrhea or constipation often limit the use of iron supplements. The causes of GI mucosal injury include the direct toxic effect of iron ions on enterocytes, increased production of intestinal reactive oxygen species, and disruption of the gut microbiota. Intravenous iron therapy can cause iron overload, hypophosphatemia, potential risks of kidney injury and stimulation of atherosclerosis. Liposomal iron is a promising strategy for iron deficiency anemia management. Liposomes ensure absorption of iron from the intestinal lumen by the microfold cells (M cells) of the small intestine, and then by the lymphatic system, thus avoiding hepcidin control over absorption. Liposomal iron is significantly less toxic and is well tolerated by patients. Liposome properties are dependent on the phospholipids that form the lipid bilayer; sunflower lecithin is one of the promising alternatives.
38
Golubeva, M. G. "Role of Haptoglobin in Protecting the Toxic Effects of Hemoglobin in Various Pathologies." Успехи современной биологии 143, no. 2 (2023): 114–22. http://dx.doi.org/10.31857/s0042132423020059.
Full textAbstract:
The review presents modern domestic and foreign literature data on the blood plasma protein haptoglobin, its structure, synthesis, function and interaction with hemoglobin. The ability of haptoglobin in interaction with hemoglobin to reduce the toxic effect of the latter is shown. Clinical studies of such interaction in various pathological conditions such as diabetes mellitus, sickle cell anemia, malaria, sepsis, etc. are described. It is noted that the development of new haptoglobin derivatives can contribute to the prevention of hemoglobin toxicity in hemolytic diseases.
39
., Prihatini, Trisnaningsih ., Muchdor ., and U. N. Rachman. "PENYEBARAN GUMPALAN DALAM PEMBULUH DARAH (DISSEMINATED INTRAVASCULAR COAGULATION) AKIBAT RACUN GIGITAN ULAR." INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY 14, no. 1 (2018): 37. http://dx.doi.org/10.24293/ijcpml.v14i1.923.
Full textAbstract:
Cases of snake bites were seldom happened in town. From the 2500–3000 world-wide distributed species of snakes, 500 are venomous. The snake produce some toxic substance which is dangerous in men , and could cause morbidity or mortality. It’s caused byophitoxaemia, which influence the permeability of capilers with consequence bleeding. There patients must be examined physically, localas well systemic. The laboratoric examinations were based on clinical symptoms, by determination of the snake venom causal and thesequalae in the human body, including coagulopathy, anemia as well as renal failure, etc. The snake venom may cause necrotic tissue offoot and anemia by trombocytopenia.The condition of this victim patient was severre due to his diabetic syndrome. This article presenteda study of snake bite incident on an old man with DIC laboratoric results, following anemia and renal failure which caused his death.
40
Dewi Murniati. "Hubungan Paparan Pestisida Dengan Kejadian Anemia Pada Pada Pekerja Penyemprot Pestisida Di PT. X Tahun 2022." Maeswara : Jurnal Riset Ilmu Manajemen dan Kewirausahaan 1, no. 3 (2023): 152–57. http://dx.doi.org/10.61132/maeswara.v1i3.826.
Full textAbstract:
Pesticides are toxic substances that have a negative impact on human health problems. Anemia is one of the chronic effects of pesticide. The effect of pesticides to the farmer’s health, decreasing production or increasing destruction of red blood cells. The purpose of this study was to analyze the relationship of pesticide exposure with anemia in the blood of pesticide spraying workers at PT. X. The research method used is Cross Sectional at PT. X with a total sample of 61 workers was obtained by Simple Random Sampling. Information was obtained through interviews with questionnaire and examination of hemoglobin levels using a portable hemoglobin meter. Based on the results of the analysis using chi square data, it was found that pesticide exposure were associated with anemia (p = 0.011). It is expected that sprayers pay more attention to the impact of using pesticides with health.
41
Tao, Yiming, Longke Shi, Jie Han, Xiangdong Jian, and Yongsheng Li. "Toxic Encephalopathy and Methemoglobinemia after 5-Amino-2-(trifluoromethyl)pyridine Poisoning." International Journal of Environmental Research and Public Health 19, no. 21 (2022): 14031. http://dx.doi.org/10.3390/ijerph192114031.
Full textAbstract:
The aromatic amino compound 5-amino-2-(trifluoromethyl)pyridine acts as an intermediate in the synthesis of pharmaceutical products. However, the toxicity profile of this compound is sparse and no related poisoning events have been reported. Here, we report the case of a 35-year-old man who inhaled 5-amino-2-(trifluoromethyl)pyridine at work. After inhalation, the patient rapidly developed symptoms such as dizziness, fatigue, nausea, vomiting, chest tightness, and loss of consciousness. After admission, methemoglobinemia, hemolytic anemia, acute renal failure, and toxic encephalopathy occurred. Symptoms improved significantly after intravenous treatment with a low dose of methylene blue. This revealed that 5-amino-2-(trifluoromethyl)pyridine is toxic to the human body and can be absorbed through the respiratory tract, resulting in methemoglobinemia and toxic encephalopathy; thus, caution should be taken in industrial production.
42
Adam, S. E. I. "Effects of Various Levels of Dietary Lepidium Sativum L. Seeds in Rats." American Journal of Chinese Medicine 27, no. 03n04 (1999): 397–405. http://dx.doi.org/10.1142/s0192415x99000458.
Full textAbstract:
A toxicity study was made on Lepidium sativum L. seeds used in Saudi traditional medicine for the treatment of various ailments. Lepidium sativum L. seed fed to Wistar albino rats at 2% (w/w) was non-toxic, Ten percent (w/w) was toxic but not fatal and 50% (w/w) of the diet for 6 weeks was lethal and caused depression in growth rate and entero-hepato-nephrotoxicity. Organ lesions accompanied by anemia and leukopenia were correlated with alterations in serum AST and ALT activities and concentrations of total protein, cholesterol, urea, and other serum constituents.
43
Girard, Sandrine, Franck Genevieve, Emmanuelle Rault, Odile Fenneteau, and Jean-François Lesesve. "When Ring Sideroblasts on Bone Marrow Smears Are Inconsistent with the Diagnosis of Myelodysplastic Neoplasms." Diagnostics 12, no. 7 (2022): 1752. http://dx.doi.org/10.3390/diagnostics12071752.
Full textAbstract:
Ring sideroblasts are commonly seen in myelodysplastic neoplasms and are a key condition for identifying distinct entities of myelodysplastic neoplasms according to the WHO classification. However, the presence of ring sideroblasts is not exclusive to myelodysplastic neoplasms. Ring sideroblasts are as well either encountered in non-clonal secondary acquired disorders, such as exposure to toxic substances, drug/medicine, copper deficiency, zinc overload, lead poison, or hereditary sideroblastic anemias related to X-linked, autosomal, or mitochondrial mutations. This review article will discuss diseases associated with ring sideroblasts outside the context of myelodysplastic neoplasms. Knowledge of the differential diagnoses characterized by the presence of ring sideroblasts in bone marrow is essential to prevent any misdiagnosis, which leads to delayed diagnosis and subsequent management of patients that differ in the different forms of sideroblastic anemia.
44
Dealita Khairani Daulay. "Hubungan Paparan Pestisida Dengan Kejadian Anemia Pada Pada Pekerja Penyemprot Pestisida Di Langkat Nusantara Kepong 2023." Jurnal Ilmiah Kedokteran dan Kesehatan 2, no. 2 (2023): 230–36. http://dx.doi.org/10.55606/klinik.v2i2.2759.
Full textAbstract:
Pesticides are toxic substances that have a negative impact on human health problems. Anemia is one of the chronic effects of pesticide. The effect of pesticides to the farmer’s health, decreasing production or increasing destruction of red blood cells. The purpose of this study was to analyze the relationship of pesticide exposure with anemia in the blood of pesticide spraying workers at PT. Langkat Nusantara Kepong Gohor Lama. The research method used is Cross Sectional at PT. Langkat Nusantara Kepong Gohor Lama with a total sample of 61 workers was obtained by Simple Random Sampling. Information was obtained through interviews with questionnaire and examination of hemoglobin levels using a portable hemoglobin meter. Based on the results of the analysis using chi square data, it was found that pesticide exposure were associated with anemia (p = 0.011). It is expected that sprayers pay more attention to the impact of using pesticides with health.
45
Willingale-Theune, J., M. Schweiger, M. Hirsch-Kauffmann, A. E. Meek, M. Paulin-Levasseur, and P. Traub. "Ultrastructure of Fanconi anemia fibroblasts." Journal of Cell Science 93, no. 4 (1989): 651–65. http://dx.doi.org/10.1242/jcs.93.4.651.
Full textAbstract:
Employing indirect immunofluorescence and conventional electron microscopy, gross nuclear aberrations were observed in cultured interphase fibroblasts derived from a patient suffering from Fanconi's anemia (FA). Such aberrations were predominantly expressed in cells at high passages between 28 and 34. The structure of the nuclei appeared compound in nature, often consisting of two to three nuclear fragments connected to each other by thin nuclear bridges containing chromatin and nuclear lamin material. In other cases, the nuclei appeared lobed or budded but the cells did not contain distinct nuclear fragments. Chromatin was conspicuously absent from some nuclear lobes, revealing empty, cage-like structures comprising nuclear lamin material. Micronuclei were often abundant in the perinuclear cytoplasm but in some instances they appeared to be composed of chromatin lacking a delineating nuclear lamin matrix. Residual cytoskeletons examined by whole-mount electron microscopy revealed a network of intermediate filaments (IFs) within FA fibroblasts forming a bridge between the plasma membrane and the nucleus or its major fragments. In addition, there were thinner, 3–4 nm filaments connecting individual IFs with the surface of the nucleus. Micronuclei that were not connected to the main nuclear body, but which were delineated by a distinct lamina and possessed nuclear pores, did not appear to be anchored to the IF network. Multinuclearity, nuclear fragmentation, irregular chromatin distribution and inter-nuclear chromatin/lamin bridges might result from a failure in the redistribution of chromatin to sister nuclei, incomplete cytokinesis and proliferation of nuclear envelope material. These phenomena point to precocious aging of FA fibroblasts and may occur as a consequence of spontaneous damage to the sister chromatids or through the action of DNA-toxic agents.
46
Krabbe, Simon, Cigdem Gül, Bjarne Andersen, and Niels Tvede. "Toxic Epidermal Necrolysis-Like Lesions and Systemic Lupus Erythematosus Possibly Triggered by Sulfasalazine." Case Reports in Rheumatology 2016 (2016): 1–3. http://dx.doi.org/10.1155/2016/4501937.
Full textAbstract:
This case report describes a patient with arthritis of the large joints, bilateral sacroiliitis, and positive anti-SSA and anti-dsDNA antibody, who received sulfasalazine and shortly thereafter became critically ill. He developed toxic epidermal necrolysis, hemolytic anemia, lymphopenia, markedly elevated ferritin, and muscle wasting. A diagnosis of systemic lupus erythematosus was made, and mycophenolate mofetil and systemic glucocorticoids brought this severe disease under control. Toxic epidermal necrolysis-like lesions and hemophagocytic syndrome have been reported as manifestations of systemic lupus erythematosus. This patient possibly had spondyloarthritis or an undifferentiated connective tissue disease at presentation, and we suggest, based on the timing of events, that sulfasalazine may have acted as a trigger of the severe disease manifestations.
47
Petzer, Verena, Piotr Tymoszuk, Malte Asshoff, et al. "A fully human anti-BMP6 antibody reduces the need for erythropoietin in rodent models of the anemia of chronic disease." Blood 136, no. 9 (2020): 1080–90. http://dx.doi.org/10.1182/blood.2019004653.
Full textAbstract:
Abstract Recombinant erythropoietin (EPO) and iron substitution are a standard of care for treatment of anemias associated with chronic inflammation, including anemia of chronic kidney disease. A black box warning for EPO therapy and concerns about negative side effects related to high-dose iron supplementation as well as the significant proportion of patients becoming EPO resistant over time explains the medical need to define novel strategies to ameliorate anemia of chronic disease (ACD). As hepcidin is central to the iron-restrictive phenotype in ACD, therapeutic approaches targeting hepcidin were recently developed. We herein report the therapeutic effects of a fully human anti-BMP6 antibody (KY1070) either as monotherapy or in combination with Darbepoetin alfa on iron metabolism and anemia resolution in 2 different, well-established, and clinically relevant rodent models of ACD. In addition to counteracting hepcidin-driven iron limitation for erythropoiesis, we found that the combination of KY1070 and recombinant human EPO improved the erythroid response compared with either monotherapy in a qualitative and quantitative manner. Consequently, the combination of KY1070 and Darbepoetin alfa resulted in an EPO-sparing effect. Moreover, we found that suppression of hepcidin via KY1070 modulates ferroportin expression on erythroid precursor cells, thereby lowering potentially toxic-free intracellular iron levels and by accelerating erythroid output as reflected by increased maturation of erythrocyte progenitors. In summary, we conclude that treatment of ACD, as a highly complex disease, becomes more effective by a multifactorial therapeutic approach upon mobilization of endogenous iron deposits and stimulation of erythropoiesis.
48
Lee, C. C., C. B. Hong, H. V. Ellis, J. C. Dacre, and J. P. Glennon. "Subchronic and Chronic Toxicity Studies of 2,4-Dinitrotoluene. Part II. CD® Rats." Journal of the American College of Toxicology 4, no. 4 (1985): 243–56. http://dx.doi.org/10.3109/10915818509078677.
Full textAbstract:
Subchronic and chronic toxicities of 2,4-dinitrotoluene were studied in CD® rats. Feeding of 2,4-dinitrotoluene for 13 weeks at a low dose of 34 mg/kg per day in males and 38 mg/kg per day in females caused depressed weight gain. The middle dose of 93 and 108 mg/kg per day, respectively, was toxic, caused reticulocytosis and splenic hemosiderosis, and decreased spermatogenesis. The high dose of 266 and 145 mg/kg per day, respectively, was more toxic and lethal. Some rats had widespread and stiff-legged gaits and demyelination in the cerebellum and brain stem. After feeding up to 2 years, the low dose (0.57 and 0.71 mg/kg per day, respectively) caused no apparent toxic effects. The middle dose (3.9 and 5.1 mg/kg per day, respectively) was toxic; the high dose (34 and 45 mg/kg per day) was more toxic and shortened the life span. Target organs included the blood (toxic anemia), the liver (hepatocellular carcinoma), the testis (atrophy and depression of spermatogenesis), the connective tissue in males (fibromas), the mammary tissue in females (fibroadenomas), and the neuromuscular system in some rats.
49
Zhu, Bing-Mei, Sara K. McLaughlin, Risu Na, et al. "Hematopoietic-specific Stat5-null mice display microcytic hypochromic anemia associated with reduced transferrin receptor gene expression." Blood 112, no. 5 (2008): 2071–80. http://dx.doi.org/10.1182/blood-2007-12-127480.
Full textAbstract:
Abstract Iron is essential for all cells but is toxic in excess, so iron absorption and distribution are tightly regulated. Serum iron is bound to transferrin and enters erythroid cells primarily via receptor-mediated endocytosis of the transferrin receptor (Tfr1). Tfr1 is essential for developing erythrocytes and reduced Tfr1 expression is associated with anemia. The transcription factors STAT5A/B are activated by many cytokines, including erythropoietin. Stat5a/b−/− mice are severely anemic and die perinatally, but no link has been made to iron homeostasis. To study the function of STAT5A/B in vivo, we deleted the floxed Stat5a/b locus in hematopoietic cells with a Tie2-Cre transgene. These mice exhibited microcytic, hypochromic anemia, as did lethally irradiated mice that received a transplant of Stat5a/b−/− fetal liver cells. Flow cytometry and RNA analyses of erythroid cells from mutant mice revealed a 50% reduction in Tfr1 mRNA and protein. We detected STAT5A/B binding sites in the first intron of the Tfr1 gene and found that expression of constitutively active STAT5A in an erythroid cell line increased Tfr1 levels. Chromatin immunoprecipitation experiments confirmed the binding of STAT5A/B to these sites. We conclude that STAT5A/B is an important regulator of iron update in erythroid progenitor cells via its control of Tfr1 transcription.
50
Raysky, S. M. "On the issue of high blood pressure in chronic lead poisoning." Kazan medical journal 25, no. 11 (2021): 1233. http://dx.doi.org/10.17816/kazmj80515.
Full textAbstract:
Schnitter (Mnch. Med. Wschr. No. 4, 1929) refutes the established belief that chronic lead poisoning usually causes high blood pressure and insists that it is usually normal or even lower than normal if anemia or toxic-endocrine disorders. The increased blood pressure in chronic. lead poisoning, according to the author, speaks of the simultaneous presence of other causes of it.