Associated thyreoiditis, myasthenia gravis, thymectomy, Chron’s disease, and erythema nodosum: pathogenetic and clinical correlations, immune system involvement, and systemic infectious complications

Chronic lymphatic leukemia is second only to acute leukemia in the frequency of infectious complications. In most cases, severe infectious complications are the cause of death in these patients. Modern chemotherapy makes it possible to preserve the ability to work and the life expectancy of patients for a long time. However, the negative effect of cytostatic drugs on the already altered immune system leads to an even greater suppression of immunity and an increase in the number of infectious complications. The search for new ways to combat infections has shown the advisability of long-term outpatient treatment with antibacterial drugs.

Download Full-text

Abstract 293: Cardiac Arrest and Resuscitation Causes Immunodeficiency That Involves the Hypothalamic-Pituitary-Adrenal Axis

Circulation ◽

10.1161/circ.138.suppl_2.293 ◽

2018 ◽

Vol 138 (Suppl_2) ◽

Author(s):

Yuntian Shen ◽

Qiang Zhao ◽

Jiangbo Wu ◽

Zhuoran Wang ◽

Wei Yang

Keyword(s):

Immune Response ◽

Cardiac Arrest ◽

Immune System ◽

Hpa Axis ◽

Time Course ◽

Immune Cell ◽

Infectious Complications ◽

Hypothalamic Pituitary Adrenal ◽

Immune Organs ◽

High Incidence

Introduction: Cardiac arrest (CA) is associated with high mortality and morbidity, which is in part due to infectious complications developed in CA patients. Infection complications, particularly pneumonia, occur in approximately 60% of CA patients. Given this high incidence, we hypothesized that after CA, the immune system is impaired, which increases the susceptibility of CA patients to potential infections. Therefore, in this study, we systematically examined the immune response in the brain and peripheral immune organs after CA. Methods: Mice were subjected to CA and cardiopulmonary resuscitation (CA/CPR). Flow cytometry, ELISA, immunohistochemistry, and quantitative PCR were used to analyze the immune response in various post-CA organs. Results: First, we characterized the time course of the immune response in the spleen after CA/CPR. CA/CPR induced significant changes in all major immune cell populations. Notably, B cell frequencies decreased, while T cell frequencies increased, in various organs on day 3 post-CA. Further, the levels of pro-inflammatory cytokines, eg IL-6, were markedly increased in the blood and brain after CA. Critically, we found that the lymphocyte counts in the spleen and thymus were dramatically lower in CA mice than in sham mice. Interestingly, CA/CPR caused progressive atrophy of the spleen and thymus. Since it has been shown that CA/CPR alters activity of the hypothalamic-pituitary-adrenal (HPA) axis, we speculated that CA-induced atrophy of lymphoid organs is mediated by the HPA axis. Thus, we treated CA mice with RU486, a glucocorticoid receptor antagonist. Indeed, this treatment reversed CA-induced organ atrophy and mitigated immune cell depletion, both in the thymus and spleen. Conclusions: We provided for the first time evidence that CA/CPR rapidly induced a systemic inflammatory response followed by impairment of the immune system, which eventually led to a massive loss of immune cells in the peripheral immune organs. This CA-induced immunodeficiency appears to be mediated by dysregulation of the HPA axis. Our findings here may be of high clinical significance, considering the high incidence of infectious complications in CA patients and their detrimental effects on CA outcome.

Download Full-text

Primer immunhiány és autoimmun betegségek

Orvosi Hetilap ◽

10.1556/650.2018.31064 ◽

2018 ◽

Vol 159 (23) ◽

pp. 908-918

Author(s):

Györgyi Műzes ◽

Ferenc Sipos

Keyword(s):

Immune System ◽

Autoimmune Diseases ◽

Primary Immunodeficiency ◽

Adaptive Immune System ◽

Infectious Complications ◽

Primary Immunodeficiencies ◽

Cellular Mechanisms ◽

Adaptive Immune ◽

Solid Malignancies ◽

Autoimmune Phenomena

Abstract: Primary immunodeficiencies consist of a group of genetically heterogeneous immune disorders affecting distinct elements of the innate and adaptive immune system. Patients with primary immunodeficiency are more prone to develop not only recurrent infections, but non-infectious complications, like inflammatory or granulomatous conditions, lymphoproliferative and solid malignancies, autoinflammatory disorders, and a broad spectrum of autoimmune diseases. The concomitant appearance of primary immunodeficiency and autoimmunity appears to be rather paradoxical, therefore making the diagnosis of immunodeficiency patients with autoimmune complications challenging. Mutations of one or more genes playing a fundamental role in immunoregulation and/or immune tolerance network are thought to be responsible for primary immunodeficiencies. The diverse immunological abnomalities along with the compensatory and excessive sustained inflammatory response result in tissue damage and finally in manifestation of organ-, cell-specific or systemic autoimmune diseases. Several forms of primary immunodeficiency disorders are characterized by a variety of specific autoimmune phenomena. This overview addresses the spectrum of autoimmune diseases associated with primary immunodeficiencies, and explores the molecular and cellular mechanisms underlying abnormalities of the immune system. The case presented finally highlights that both the recognition of autoimmune diseases in association with immunodeficiencies and the diagnosis of immunodefiency in those phenotypes with predominant autoimmunity could be challenging. Orv Hetil. 2018; 159(23): 908–918.

Download Full-text

Myasthenia gravis exacerbation after melatonin administration: case series from a tertiary referral centre

BMC Neurology ◽

10.1186/s12883-020-01975-y ◽

2020 ◽

Vol 20 (1) ◽

Cited By ~ 2

Author(s):

Velina Nedkova-Hristova ◽

Valentina Vélez-Santamaría ◽

Carlos Casasnovas

Keyword(s):

Immune System ◽

Myasthenia Gravis ◽

Clinical Improvement ◽

Case Series ◽

Adaptive Immune System ◽

Intravenous Immunoglobulins ◽

Postsynaptic Membrane ◽

Referral Centre ◽

Tertiary Referral Centre ◽

Melatonin Administration

Abstract Background Myasthenia gravis is an autoimmune disease mediated by antibodies against proteins associated with the postsynaptic membrane of the neuromuscular junction. Several drugs may trigger an exacerbation of the disease. Melatonin supplements are widely used for the treatment of insomnia as they are well tolerated with few side effects. The role of melatonin in the immune system and its effects in autoimmune disorders remain uncertain. Case presentation We identified three patients in our referral centre from 2014 to 2019 who presented a worsening within days or weeks of starting melatonin. Two of them stopped the treatment without clinical improvement in the next week. Increasing dose of corticosteroids did not lead to clinical improvement in the next month and one of the patients was finally administered intravenous immunoglobulins. Conclusion Melatonin may trigger exacerbations of myasthenia gravis, probably due to an upregulation of the adaptive immune system and an interaction with the corticosteroids and other immunosuppressant treatments. We consider that melatonin should be administered with caution in these patients.

Download Full-text