scholarly journals Prevention and Correction of Immunodeficiency States of Animals, Chemical Etiology

2019 ◽  
Vol 2 (2) ◽  
Author(s):  
Salimov Yu
Keyword(s):  
Immunodeficiency States

Modern approach to the diagnosis and treatment of thrombocytopenia

2021 ◽  
pp. 28-34
Author(s):  
Marina Leonidovna Kochieva
Keyword(s):  
Blood Test ◽  
Healthy Adult ◽  
Clinical Manifestations ◽  
Antithyroid Drugs ◽  
Modern Approach ◽  
Somatic Diseases ◽  
Immunodeficiency States ◽  
Test Treatment ◽  
Main Clinical Manifestation ◽  
Platelet Formation

Normally, the number of platelets in a healthy adult is in the range of 150-320 x 10⁹. A condition in which their number falls below 150x10⁹ is called thrombocytopenia. It can be both associated with a violation of the process of platelet formation in the bone marrow (in particular, with aplastic anemia, hemoblastosis, thrombocytopenic purpura), and be a concomitant pathology, for example, be a consequence of drug treatment of a number of somatic diseases. In the pathogenesis of thrombocytopenia, three main directions are distinguished: a decrease in platelet production, an acceleration of their decay and a violation of the distribution of the platelet pool with their sequestration in the spleen. Most often, drug thrombocytopenia develops against the background of the use of cytostatics, chloramphenicol, antithyroid drugs, NSAIDs. The decrease in the number of platelets can also be influenced by the regular use of alcohol, some infectious diseases, and immunodeficiency states. The main clinical manifestation of thrombocytopenia is hemorrhagic syndrome, proceeding as petechial rashes or ecchymosis, however, in some cases, clinical manifestations may be absent, and then the diagnosis is made on the basis of a clinical blood test. Treatment of thrombocytopenia is carried out taking into account the etiological factor that caused it.

Clostridioides (Clostridium) difficile infection. Review of current clinical guidelines

2020 ◽  
Vol 18 (6) ◽  
pp. 106-112
Author(s):  
I. V. NIKOLAEVA ◽  
◽  
S. V. KHALIULLINA ◽  
G. Kh. MURTAZINA ◽  
V. A. ANOKHIN ◽  
...  
Keyword(s):  
Causative Agent ◽  
Dynamic Assessment ◽  
Tube Feeding ◽  
Laboratory Research ◽  
Surgical Interventions ◽  
First Line Therapy ◽  
Clostridioides Difficile ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
Immunodeficiency States

Clostridioides difficile (CDI) infection is a disease associated with a disruption of the gut microbiome with over-colonization of C. difficile, the toxins of which cause inflammation and damage to the colon. A dynamic assessment of the CDI prevalence indicates a significant increase in laboratory-confirmed cases of infection and a high mortality associated with it. C. difficile is recognized as the main causative agent of nosocomial infections in Europe, USA, Canada and Australia, which develops 48 hours after hospitalization in a medical facility and within 12 weeks after discharge. The severity of CDI is determined by the severity of infectious-toxic, diarrheal and abdominal syndromes. Severe CDI is characterized by manifestations of colitis, accompanied by severe leukocytosis, a decrease in albumin levels and an increase in serum creatinine levels. Development of fulminant forms, pseudomembranous colitis, toxic megacolon, intestinal perforation, sepsis is possible. The risk factors include in-hospital stay; recent use of antibiotics (within the previous 12 weeks, especially the use of fluoroquinolones, cephalosporins of III–IV generations, carbapenems and clindamycin), PPI and H2-histamine blockers; presence of inflammatory bowel diseases (ulcerative colitis, Crohn’s disease), immunodeficiency states, including iatrogenic; recent endoscopic examinations, surgical interventions on the gastrointestinal tract, tube feeding, enemas; possible contact with a family member who recently had a C..difficile infection. The «gold standard» for confirming the CDI diagnosis is the identification of the causative agent and/or toxins of C. difficile in the stool using specific laboratory research methods. Vancomycin or metronidazole are recommended as first-line therapy.

IgE deficiency may indicate underlying hypogammaglobulinaemia?

2014 ◽  
Vol 67 (9) ◽  
pp. 832-833 ◽  
Author(s):  
Shireen McVicker ◽  
M Yousuf Karim
Keyword(s):  
Early Diagnosis ◽  
Common Variable Immunodeficiency ◽  
Immunoglobulin E ◽  
Lung Damage ◽  
Serum Immunoglobulin ◽  
Serum Ige ◽  
New Diagnosis ◽  
Immunodeficiency States ◽  
Common Variable ◽  
Low Serum

Low serum immunoglobulin E (IgE) (<2 kU/L) found during allergy investigations may be a marker for other immunodeficiency states, in particular common variable immunodeficiency. The latter is characterised by recurrent infections, mainly respiratory, resulting in structural lung damage making early diagnosis important. We looked through 4013 samples retrospectively over a 12-month period to identify samples with IgE <2 kU/L. We identified 74/4013 (1.84%) with serum IgE levels <2 kU/L. Only 20 samples had serum immunoglobulin quantification and serum electrophoresis requested. Three of these samples were from the same patient, 10/18 (56%) had one or more classes of immunoglobulin above/below reference range for age and two of these had new diagnosis of immunodeficiency. Serum IgE <2 kU/L can be a marker for hypogammaglobulinaemia or common variable immunodeficiency. As early diagnosis is important to reduce morbidity and mortality, very low serum IgE should trigger further investigation—that is, serum protein electrophoresis and immunoglobulin quantification.

Studies on levamisole--induced agranulocytosis

Blood ◽  
1980 ◽  
Vol 56 (3) ◽  
pp. 388-396 ◽  
Author(s):  
JS Thompson ◽  
JM Herbick ◽  
LW Klassen ◽  
CD Severson ◽  
VL Overlin ◽  
...  
Keyword(s):  
Clinical Evidence ◽  
Myeloid Cell ◽  
Metastatic Carcinoma ◽  
Drug Mechanism ◽  
Myeloid Cell Line ◽  
Neutropenic Patients ◽  
Alternative Choice ◽  
Antigen Antibody ◽  
Immunodeficiency States

Widespread clinical trials of leavo-tetramisole (levamisole) as an immunopotentiating agent in rheumatoid arthritis, metastatic carcinoma, and immunodeficiency states have been complicated by agranulocytosis (AGC) in 2.5%–13% of patients. Other than a relationship with prolonged high dosage, very little is known regarding the pathogenesis of levamisole-induced AGC. Whereas leukoagglutination was negative, fluorochromatic microgranulocytotoxicity (GCY) tests were positive with serum from 10 of 10 acutely neutropenic patients. The antibody was IgM, reacted with 100% of unrelated granulocytes, but not with T or B lymphocytes. Some sera also reacted with monocytes and the myeloid cell line, K-562. Tests for antigen-antibody complexes or cold autoantibodies were negative. Although clinical evidence strongly suggests a haptene (drug) mechanism, in vitro mixing experiments were also negative. An alternative choice parallels the model of aldomet- induced Coombs'-positive hemolytic anemia. Finally, GCY first became positive 2–3 mo prior to the onset of AGC on two patients, suggesting the possibility of identifying those at risk well before the onset of neutropenia.

Sign in / Sign up

Export Citation Format

Share Document