MECHANISMS OF HEMOSTASIS DISTURBANCES AT VARIOUS PATHOGENETIC TYPES OF ANEMIAS

Author(s):  
В. Желобов ◽  
А. Туев ◽  
А. Агафонов

Введение. Нарушения со стороны системы гемостаза при заболеваниях кроветворных органов чрезвычайно разнообразны как по механизмам развития, так и по клиническим проявлениям. Цель исследования. Изучение причин гемостазиологических расстройств при различных патогенетических вариантах анемических состояний. Материалы и методы. Показатели коагуляционного гемостаза, липидной пероксидации и эндотелий-зависимая вазодилатация исследованы у 30 больных железодефицитной анемией, 22 больных витамин В12-дефицитной анемией и 18 больных апластической анемией. Результаты. Гемическая гипоксия, присущая анемии, сопровождается активацией свободно-радикального окисления липидов — увеличением концентрации малонового диальдегида плазмы и уменьшением антиокислительного потенциала крови. Оксидативный стресс приводит к системному поражению эндотелия, проявляющегося снижением релаксирующих свойств эндотелия сосудов и активацией системы гемостаза, представленной гипокоагуляцией по внутреннему механизму, угнетением плазминовой системы и увеличением концентрации растворимых фибрин-мономерных комплексов. Заключение. Развитие анемии, независимо от ее патогенетического механизма, сопровождается развитием метаболического дисбаланса, дисфункцией эндотелия, что в конечном итоге приводит к нарушениям со стороны коагуляционного гемостаза. Introduction. Hemostasis disturbances in diseases of hematopoietic organs are considerably varied both in mechanisms of development, and in clinical manifestations. The aim: to study the causes of hemostatic disorders at various pathogenetic types of anemias. Materials and methods. In 30 patients with iron defi ciency anemia, in 22 patients with vitamin B12-deficiency anemia and in 18 patients with aplastic anemia parameters of coagulative hemostasis, lipid peroxidation, and endothelium-dependent vasodilation were studied. Results. Attributable to anemia hemic hypoxia is accompanied by activation of free-radical lipids oxidation — increasing concentration of plasma malone dialdehyde and decreasing of blood antioxidant potential. Oxidative stress leads to systemic damage of endothelium that manifested by decreasing of vascular endothelial relaxing properties and hemostasis activation: internal mechanism of hypocoagulation, inhibition of plasmin system and increasing concentration of soluble fibrin monomer complexes. Conclusion. Anemia progression regardless of its pathogenic mechanism is associated with the development of metabolic disbalance, endothelial dysfunction that fi nally leads to disturbances of coagulative hemostasis.

Nutrients ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 2557 ◽  
Author(s):  
Martín-Masot ◽  
Nestares ◽  
Diaz-Castro ◽  
López-Aliaga ◽  
Alférez ◽  
...  

Celiac disease (CD) is a multisystemic disorder with different clinical expressions, from malabsorption with diarrhea, anemia, and nutritional compromise to extraintestinal manifestations. Anemia might be the only clinical expression of the disease, and iron deficiency anemia is considered one of the most frequent extraintestinal clinical manifestations of CD. Therefore, CD should be suspected in the presence of anemia without a known etiology. Assessment of tissue anti-transglutaminase and anti-endomysial antibodies are indicated in these cases and, if positive, digestive endoscopy and intestinal biopsy should be performed. Anemia in CD has a multifactorial pathogenesis and, although it is frequently a consequence of iron deficiency, it can be caused by deficiencies of folate or vitamin B12, or by blood loss or by its association with inflammatory bowel disease (IBD) or other associated diseases. The association between CD and IBD should be considered during anemia treatment in patients with IBD, because the similarity of symptoms could delay the diagnosis. Vitamin B12 deficiency is common in CD and may be responsible for anemia and peripheral myeloneuropathy. Folate deficiency is a well-known cause of anemia in adults, but there is little information in children with CD; it is still unknown if anemia is a symptom of the most typical CD in adult patients either by predisposition due to the fact of age or because biochemical and clinical manifestations take longer to appear.


2020 ◽  
Vol 15 (6) ◽  
pp. 18-26
Author(s):  
S.O. Falaleeva ◽  
◽  
A.V. Morgun ◽  
M.V. Borisova ◽  
E.V. Borisova ◽  
...  

Vitamin B12 deficiency affects not only the bone marrow, but also the nervous system. Usually, B12 hypovitaminosis develops slowly during several years, although infants may also have this disorder. Patients and methods. We performed a retrospective analysis of clinical symptoms and results of routine laboratory testing in patients with vitamin B12 deficiency anemia. Our sample included 19 children of 3–24 month age (Group 1) and 9 adolescents (Group 2). All patients were treated in Krasnoyarsk Regional Clinical Center for Maternal and Child Health in 2012–2019. All participants had serum levels of vitamin B12 below 83 pg/mL. Results. All patients from Group 1 were found to have nervous system disorders, including muscular hypotonia (100%), hypo- or adynamia and retardation of motor skills (63%), and hyporeflexia (42%). More than two-thirds of adolescents (67%) had pancytopenia. One-third of children of 3–24 month age (32%) developed involuntary movements during treatment with cyanocobalamin. Conclusion. Vitamin B12 deficiency in infants may manifest itself with neurological disorders that do not correlate with the severity of anemia. Children with muscular hypotonia and delayed psychomotor development should be tested for their serum level of vitamin B12 if all other potential causes of these disorders have been excluded. It is also important to perform differential diagnosis with paroxysmal conditions, including those induced by cobalamin therapy. Key words: anemia, vitamin B12, involuntary movements, hypodynamia, hyporeflexia, hypotonia, pancytopenia, cyanocobalamin


2018 ◽  
Vol 7 (10) ◽  
pp. 304 ◽  
Author(s):  
Emmanuel Andrès ◽  
Abrar-Ahmad Zulfiqar ◽  
Khalid Serraj ◽  
Thomas Vogel ◽  
Georges Kaltenbach

The objective of this review is to provide an update on the effectiveness of oral and nasal vitamin B12 (cobalamin) treatment in gastrointestinal (GI) disorders. Relevant articles were identified by PubMed and Google Scholar systematic search, from January 2010 and June 2018, and through hand search of relevant reference articles. Additional studies were obtained from references of identified studies, the Cochrane Library and the ISI Web of Knowledge. Data gleaned from reference textbooks and international meetings were also used, as was information gleaned from commercial sites on the web and data from CARE B12 research group. For oral vitamin B12 treatment, 4 randomized controlled trials (vs. intramuscular), 4 narrative and 4 systematic reviews, and 13 prospective studies fulfilled our inclusion criteria. These studies concerned patients with vitamin B12 deficiency related to: food-cobalamin malabsorption (n = 6), Biermer’s disease (n = 3), veganism or vegetarianism (n = 1), total gastrectomy after Roux-en-Y gastric bypass (n = 2) and Crohn’s disease (n = 1). Four prospective studies include patients with vitamin B12 deficiency related to the aforementioned etiologies, except veganism or vegetarianism. The systematic present review documents that oral vitamin B12 replacement, at a daily dose of 1000 μg (1 mg), was adequate to normalize serum vitamin B12 levels and cure main clinical manifestations related to vitamin B12 deficiency, in GI disorders, and thus, with safety profile. For nasal vitamin B12 treatment, only one preliminary study was available. We conclude that oral vitamin B12 is an effective alternative to intramuscular vitamin B12 (except in patients presenting with severe neurological manifestations). Oral vitamin B12 treatment avoids the discomfort, contraindication (in patients with anticoagulation), and cost of monthly injections.


Cureus ◽  
2021 ◽  
Author(s):  
Fadi Busaleh ◽  
Omkolthoom A Alasmakh ◽  
Fatimah Almohammedsaleh ◽  
Maram F Almutairi ◽  
Juwdaa S Al Najjar ◽  
...  

2021 ◽  
Vol 8 (4) ◽  
pp. 546
Author(s):  
Umamaheshwari S. ◽  
Varun Venkat Raghavan ◽  
Ramamurthy P. ◽  
Krishna Kumar Naik T.

Background: HIV/AIDS is a global pandemic. As of 2014, approximately 37 million people have HIV worldwide with the number of new infections that year being about 2 million. This is down from 3.1 million new infections in 2001. The objective of the study was to study the immunological status as indicated by the CD4 count and aetiology of anemia in HIV positive individuals.Methods: This study was carried out on 100 consecutive HIV patients in the Department of Medicine, Vijayanagara Institute of Medical Sciences Bellary, Karnataka during the period from October 2014 to May 2016.Results: In this study, 100 patients with HIV infection and anemia were studied to find the etiology of anemia in HIV positive patients Only patients with Hb less than 10 g/dl (moderate to severe grade) were included in this study. 42% patient had moderate grade anemia and 58% had severe grade anemia patient mild grade anemia was excluded. 13 patient had their MCV <76 fl. 60 patient had their MCV between 76-96 fl and 27% had their MCV of >96 fl. 54% of patient had anemia due to chronic disease.Conclusions: 54% of patient had anemia due to chronic disease, 12% had iron deficiency anemia, 11% had anemia due to vitamin B12 deficiency, 22 % had anemia due to zidovudine induced anemia and 1 patient had anemia due hemolysis. 


2021 ◽  
Vol 12 (2) ◽  
pp. 54-58
Author(s):  
Vinay Krishnamurthy ◽  
Akhila Rao Kerekoppa

Background: Diabetes is one of the largest global health emergencies of the 21st century. Prevalence of anemia in diabetic patients is two to three times higher than for patients with comparable renal impairment and iron stores in the general population. Aims and Objective: This study was done to analyse the prevalence of anemia and its profile in patients with preserved renal function. Materials and Methods: One-hundred diabetic patients with anemia with normal renal functions were selected. Complete blood count, peripheral blood smear, iron studies, vitamin B12 levels were assessed. Diabetic control was monitored by HbA1c. Patients were identified to have specific type of anemia, based on iron profile and vitamin B12 levels. Severity of anemia was also assessed. Appropriate statistical tests were applied to analyse the results. Results: Mean age of subjects in the study group was 53.4±13.6 years. The mean haemoglobin level was 9.41±2.18 g/dl. Out of the 100 cases, 43 patients had iron deficiency anemia, 40 patients had anemia of inflammation, and 8 patients had vitamin B12 deficiency, 8 patients had combined iron and vitamin B12 deficiency, and 1 patient had pancytopenia. Mean HbA1c was higher in iron deficient individuals with a significant p value and mean HbA1c was lower in Vitamin B12 deficient individuals. Among the cases, 16% had mild anemia, 61% had moderate anemia, and 23% had severe anemia. Severe anemia had a significantly lower HbA1c, which was statistically significant. Conclusion: According to our study, iron deficiency anemia was the commonest, followed by anemia of inflammation in diabetic patients with preserved renal function. Diabetes being a pro-inflammatory state had a higher incidence of anemia of inflammation compared to general population. We have to identify and acknowledge the higher prevalence of Anemia of Inflammation in diabetic patients in the absence of renal dysfunction.


Blood ◽  
1951 ◽  
Vol 6 (10) ◽  
pp. 867-891 ◽  
Author(s):  
G. E. CARTWRIGHT ◽  
BETTY TATTING ◽  
JEAN ROBINSON ◽  
N. M. FELLOWS ◽  
F. D. GUNN ◽  
...  

Abstract In an effort to produce a deficiency of vitamin B12 a total of 70 pigs were fed a purified diet containing soybean alpha protein in place of casein. One group of animals was started on the diet at 2 to 7 days of age. A second group began at 21 to 28 days of age. Methionine, iodinate casein, desiccated thyroid and pteroylglutamic acid were added to the diet of certain animals and! omitted from the diet of other pigs. In addition, 9 pigs were gastrectomized. Forty-three of the animals survived for a sufficiently long period of time for adequate evaluation of the results of the experiment. Severe liver damage was observed in 24 of the 25 animals autopsied. The only animal not showing liver damage received vitamin B12 from the beginning of the experiment. Necrosis of the liver cells, fatty infiltration, or both, occurred in the presence of a high fat diet containing apparently adequate amounts of protein, choline, vitamin E and methionine. These pathologic changes were apparently prevented but not reversed by the administration of vitamin B12. Growth of the animals on the above diets without added vitamin B12 was retarded as compared with the growth of animals on the same diet supplemented with this vitamin. The administration of vitamin B12 to the deficient animals resulted in rapid growth. Of the 39 animals not receiving vitamin B12 13 failed to develop anemia, 16 developed a mild anemia and in 10 a moderately severe anemia was present. When present the anemia was normocytic and in 24 pigs was accompanied by a moderately severe neutropenia. Differential cell counts on the sternal marrow were normal except for a slight increase in the proportion of normoblasts. These hematologic alterations were neither consistently or completely corrected by the administration of vitamin B12 in spite of the fact that definite and sometimes marked reticulocyte increases followed. When methionine deficiency was associated with vitamin B12 deficiency, anemia appeared to be more severe. The administration of aureomycin, an "animal protein factor," did not stimulate growth and failed to induce a hemopoietic response. There was no macrocytic anemia, the bone marrow was not megaloblastic, and neurologic disturbances or morphologic alterations in the neutrophils were not observed. These results are in contrast to those obtained in pigs with an experimentally produced deficiency of pteroylglutamic acid. Such animals develop macrocytic anemia, leukopenia and a macronormoblastic type of bone marrow. It is not possible to give with any assurance the reason why megaloblastic anemia was not produced in the "B12-deficient" animals. This may have been due to the fact that (1) the deficiency was not sufficiently severe to result in such a change in the hemopoietic system; or (2) because pteroylglutamic acid prevents the development of megaloblastic anemia even in the absence of vitamin B12.


2020 ◽  
Vol 59 (6) ◽  
pp. 859-861
Author(s):  
Hiroyuki Fukuda ◽  
Munetaka Takekuma ◽  
Yasuyuki Hirashima

2019 ◽  
Vol 60 (5) ◽  
pp. 579-580 ◽  
Author(s):  
Akihiro Tamura ◽  
Nanako Nino ◽  
Nobuyuki Yamamoto ◽  
Akiyoshi Naito ◽  
Kousaku Matsubara ◽  
...  

2017 ◽  
Vol 55 (1) ◽  
pp. 3-7 ◽  
Author(s):  
Mahmoud Arshad ◽  
Sara Jaberian ◽  
Abdolreza Pazouki ◽  
Sajedeh Riazi ◽  
Maryam Aghababa Rangraz ◽  
...  

Abstract Background. The association between obesity and different types of anemia remained uncertain. The present study aimed to assess the relation between obesity parameters and the occurrence of iron deficiency anemia and also megaloblastic anemia among Iranian population. Methods and Materials. This cross-sectional study was performed on 1252 patients with morbid obesity that randomly selected from all patients referred to Clinic of obesity at Rasoul-e-Akram Hospital in 2014. The morbid obesity was defined according to the guideline as body mass index (BMI) equal to or higher than 40 kg/m2. Various laboratory parameters including serum levels of hemoglobin, iron, ferritin, folic acid, and vitamin B12 were assessed using the standard laboratory techniques. Results. BMI was adversely associated with serum vitamin B12, but not associated with other hematologic parameters. The overall prevalence of iron deficiency anemia was 9.8%. The prevalence of iron deficiency anemia was independent to patients’ age and also to body mass index. The prevalence of vitamin B12 deficiency was totally 20.9%. According to the multivariable logistic regression model, no association was revealed between BMI and the occurrence of iron deficiency anemia adjusting gender and age. A similar regression model showed that higher BMI could predict occurrence of vitamin B12 deficiency in morbid obese patients. Conclusion. Although iron deficiency is a common finding among obese patients, vitamin B12 deficiency is more frequent so about one-fifth of these patients suffer vitamin B12 deficiency. In fact, the exacerbation of obesity can result in exacerbation of vitamin B12 deficiency.


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