2013, Number 2
<< Back Next >>
Acta Pediatr Mex 2013; 34 (2)
Lupus and autoimmune shock: Use of intravenous gammaglobulin. Case report and proposal for a new designation
Hernández-Bautista VM, Stamatelos-Albarrán D, Vázquez-García RE, Martínez-Borja LM, Rodríguez-Lozano AL
Language: English
References: 19
Page: 81-84
PDF size: 222.03 Kb.
ABSTRACT
Shock is a state of hypotension and hypoperfusion which in turn leads to cellular dysfunction, neuroendocrine responses, inflammatory mediator release, and alterations of the microcirculation. There are various ways of classifying tissue perfusion failure. A simple method is dividing them into a distributive category, such as septic or anaphylactic shock, and a non-distributive category such as hypovolemic shock. There is extensive knowledge on septic shock; the interaction between bacteria and the antigen presenting cell receptor (TRL-2, TRL-4) releases a proinflammatory cytokine storm, favoring the production of nitric oxide, thus perpetuating the hypotensive state. The imbalance between proinflammatory and anti-inflammatory cytokines creates an immunologic dysfunction, which favors the systemic inflammatory response syndrome and unleashes a shock state, a situation named
immunologic dissonance by Dr. Roger Bone in 1996. From our perspective, this term explains the alterations presented in one particular case, where the cornerstone is the dysfunction of the patient’s immune system and its culmination in a distributive form of shock, which from our hypothetical perspective is of autoimmune origin. We consider autoimmunity to be the platform leading to the state of immunologic dissonance responsible for autoimmune shock, which we believe merits a non-traditional approach. For this reason in a case in which we suspect shock based on autoimmunity, intravenous gammaglobulin was used in conjunction with a bolus of methylprednisolone in an attempt to counteract the immunologic dissonance; satisfactory results were obtained.
REFERENCES
Bone RC. Immunologic Dissonance: A Continuing Evolution in Our Understanding of the Systemic Inflammatory Response Syndrome (SIRS) and the Multiple Organ Dysfunction Syndromes (MODS). Ann Intern Med 1996;125:680-7.
Russell JA. Management of sepsis. N Engl J Med 2006;355:1699-713.
Hotchkiss RS, Karl IE. The pathophysiology and treatment of sepsis, N Engl J Med 2003;348(2):138-50.
Medzhitov R, Janeway C. Innate immunity. N Engl J Med 2000;343:338-44.
Shakoor N, Michalska M, Harris CA, et al. Drug-induced systemic lupus erythematosus associated with etanercept therapy. Lancet 2002;359:579-80.
Medzhitov R. Toll-like receptors and innate immunity. Nat Rev Immunology 2001;1:135-44.
Remick DG. Pathophysiology of sepsis. Am J Pathol 2007;170:1435-44.
van Amersfoort ES, van Berkel TJC †, Kuiper J. Receptors, mediators, and mechanisms involved in bacterial sepsis and septic shock. Clin Microbiol Rev 2003;379–414.
Salinas J, Fica A. Inmunoglobulinas en sepsis y shock séptico. Rev Chil Infect 2005;22:21-31.
Ronda N, Kaveri SV, Kazatchkine MD. Treatment of autoimmune diseases with normal immunoglobulin through manipulation of the idiotypic network. Clin Exp Immunol 1993;1:14-15.
Kirou KA, Lee C, Crow MK. Measurement of cytokines in autoimmune disease. Methods Mol Med 2004;102:129-54.
Semenzato G, Bambara LM, Biasi D, et al. Increased serum levels of soluble interleukin-2 receptor in patients with systemic lupus erythematosus and rheumatoid arthritis. J Clin Immunol 1988;8:447-52.
Lit L, Wong C, Tam L, et al. Plasma concentration and ex vivo production of inflammatory chemokines in patients with systemic lupus erythematosus. Ann Rheum Dis 2005;65:209-15.
Wallace D, Hahn B. Dubois´ Lupus Erythematosus Ed Lippincott Williams and Wilkins; 2007. p. 161-75, 255-72, 370-407, 1175-97.
Wong CK, Ho CY, Li EK, Lam CWK. Elevation of proinflammatory cytokine (IL-18, IL-17, IL-12) and Th2 cytokine (IL-4) concentrations in patients with systemic lupus erythematosus. Lupus 2000;9:589–93.
Smolen JS, Steiner G, Aringer M. Anti-cytokine therapy in systemic lupus erythematosus. Lupus 2005;14:189–91.
Svenungsson E, Andersson M, Brundin L. Levels of proinflammatory cytokines and nitric oxide metabolites in neuropsychiatric lupus erythematosus. Ann Rheum Dis 2001;60:372–9.
Anolik JH. B cell biology and dysfunction in SLE. Bull NYU Hosp Jt Dis 2007;65:182-6.
Selye H. The evolution of the stress concept. Am Scien 1973;61:629-39.