OLIVEIRA, Ciane Martins de , SILVA, Eduane Rhaiza Rodrigues da , VIEIRA, Gleiziane Souza da Silva , BARROS, Samara Cristina Farias , FECURY, Amanda Alves , DIAS, Cláudio Alberto Gellis de Mattos , DENDASCK, Carla Viana , OLIVEIRA, Euzébio de 
OLIVEIRA, Ciane Martins de. Et. al. Systemic Lupus Erythematosus: a failure of the immune system. Scientific Journal Multidisciplinary Nucleus of Knowledge. Year 01, Issue 08, Vol. 06, pp. 52-67. August of 2016. ISSN: 2448-0959
Lupus Erythematosus is an autoimmune inflammatory disease of unknown etiology that can affect several organs. It is known that genetic factors, hormonal, infectious and environmental issues can have important role in its pathogenesis. Its clinical manifestations with period of activity and remission, characterized by high production of autoantibodies, because the organism have a flaw in immunological self-tolerance, passing to attack the body’s own cells and tissues, targeting antibodies against itself, resulting in inflammation and injuries. The most common manifestations are the skin, musculoskeletal, and constitutional symptoms such as fever, fatigue and weight variations are commonly observed in the active phase of the disease. The diagnosis is established using the classification criteria proposed by the American College of Rheumatology. And the treatment must be individualized, depending on the organ or the affected systems and also the severity of these acometimentos; If the aggression is in multiple systems, treatment should be aimed at the most serious commitment. The aim of this article was to identify the immunological and genetic mechanisms in the pathogenesis of the disease; report risk factors associated with and contribute to the planning of nursing care.
Keywords: systemic lupus erythematosus, Autoimmune Disease, Immunological Tolerance.
Living organisms have an immune system, able to mount immune responses in the face of any substance immunogenic, eliminating it with great effectiveness. However, the immune system can sometimes fail, and react in the opposite way, recognizing antigens, which cause the formation of so-called diseases of autoimmune (VIANNA et. Al., 2010).
Among these autoimmune diseases, lupus can be highlight. Lupus Erythematosus (SLE) is an autoimmune inflammatory disease of unknown etiology that can affect several organs. It is known that genetic factors, hormonal, and environmental issues can have important role in its pathogenesis, characterized by increased activity of the immune system and the production of autoantibodies. The clinical course of the disease has periods of exacerbation and remission (CECATTO et al., 2004).
Clinical characteristics of LES may differ from one patient to another, and may present mild symptoms lack of therapeutic interventions, as well as minimum can also present serious facts with damage to vital organs (AIDS “, 2006). The LES can manifest itself in various ways, ranging from chronic illness and the insidious, however, in acute form it can be quick and lethal (FERREIRA et al., 2008).
The most common manifestations are the skin, Musculoskeletal and constitutional symptoms such as fever, fatigue and weight variations are commonly observed in the active phase of the disease. Fever may be permanent, or high and low, at peak and must be differentiated from intercurrent infection. Fatigue is a very common complaint and nonspecific. Already the weight loss most of the time it’s bland, however, in some cases, can be quite severe, leading to cachexia nephritis (SATO, 2008).
The LES is a disease which presents clinical variables and insidious onset, so diagnosis can be difficult, especially in the initial phase (FREIRE et al., 2011).
On the above, the present work had as objective to identify the immunological and genetic mechanisms in the pathogenesis of the disease, describing the risk factors and c contribute to the planning of nursing care in patient care with LES.
MATERIALS AND METHODS
To carry out this study was made a review of the literature, from exploratory, descriptive, qualitative approach of multiple studies on the theme, in the period from February to October 2012. Specific literature were used such as books, scientific articles, dissertations, theses and books published in the last two decades to the present day, using as keywords: lupus, systemic lupus erythematosus, autoimmune disease, Immunological Tolerance.
One of the clinical manifestations typical of the LES is the malar Erythema, also known as “butterfly wings” (CECATTO et al., 2004). (Figure 1).
The organs more compromised by LES are:
- Skin: the skin lesion focuses on an erythematous erupução compromises body extensions chronically exposed to ultraviolet radiation. Typically, the appearance of rash that regresses without leaving any sequel, however, in some cases can result in atrophic scar formation and hypopigmentation or hyperpigmentation. In addition, it is the common appearance of vasculíticas injuries ranging from tangible to purple heart attack. Alopecia can be focal or diffuse limited (SACK; FYE, 2004).
- Joints: Approximately 90% of patients have joint pain, some with non-erosive arthritis committing two or more peripheral joints, distinguished by pain and swelling or joint effusion (VIANA et al., 2010).
- Kidneys: at LES, generally the nephritis is the manifestation more serious patients with proliferative Glomerular lesions dangerous forms present hematuria, abnormal cilindrúria and microscopic proteinuria (> 500 mg/12:00 am); half of the patients manifest lúpicos nephrotic syndrome, and for the most part, hypertension (HAHN, 2006).
- Nervous System: The Lupus is very Pleomorphic the involvement of central and peripheral nervous systems, occurring on 24% to 59% of cases, respectively. The American College of Rheumatology considers the neuro-psychiatric manifestations arising from the LES in:
- Involvement of the central nervous system: headache, acute confusional State, mood disorders, cognitive dysfunction, psychosis, anxiety disorders, cerebrovascular disease, demyelinating syndromes, myelopathy, aseptic meningitis and seizures.
- Involvement of the peripheral nervous system: Polyneuropathy, plexopathy, cranial neuropathy, single or multiple mononeuropathy, Guillain-Barre, autonomic disorder and myasthenia gravis (BANU GRANDSON; BONFÁ, 2006).
- Blood: the most common clinical framework presented by patient with LES is the chronic anemia, which may be caused by the use of certain drugs. During the development of the disease, more than half of patients will present leucopenia and lymphopenia and less than 10% will present severe thrombocytopenia (ASSISI; BAAKLINI, 2009).
- Lung and Heart: In 40% of cases of LES pleural involvement occurs. The patient may present pleural effusion discreetly to moderate, but can also be severe form. The stroke extends for months after the use of steroids, leading to pneumonia, nephritis, which can affect 10% of the patients. It is important to note that the pneumonia nephritis occurs only after deleting an infectious process (AGARWAL, 1992). In the most common cardiac manifestations is the pericarditis, in which the most serious are myocarditis and endocarditis Libman-Sachs fibrinous exudate. Endocardial involvement may result in valve failure, more often the mitral valve or aortic or Embolic episodes. In LES patients have high risk of myocardial infarction, usually resulting from accelerated atherosclerosis (HAHN, 2006).
One of the most striking aspects of the normal immune system is the ability to recognize and respond to a wide variety of microorganisms, but not against the individual’s own antigens. This responsiveness to antigens not own is called autotolerância, induced by prior exposure of the lymphocytes to these antigens. When this meets specific lymphocyte antigens, they can be activated, generating an immune response to antigen or can become inactive or are eliminated, leading to central or peripheral tolerance. In this case, these mechanisms are responsible for a number of important features of the immune system, such as the ability to own antigens of differentiation does not own, but if these immunological mechanisms fail the breakage may occur autotolerância, assaulting the individual cells and tissues, resulting in Autoimmunity, consequently, autoimmune diseases, such as LES (LIPSKY; DIAMOND, 2006).
The presentation of antigens to specific T cells is performed by specialized proteins called major histocompatibility complex (MHC). In humans, the MHC molecules are called human leukocyte antigen (HLA) (LAGES et al., 2007).
MHC genes are divided into MHC Class I, class II and class III. Class I genes encoding HLA-A, HLA-B, HLA-C and recognize the CD8 + T cells; MHC Class II genes encoding HLA-DP, HLA-DQ, HLA-DR and recognize the CD4 + T cells; the genes of the MHC of class III code elements of the complement system C1, C2, C3, C4, C5, C6, C7, C8 and C9, which functions increased phagocytosis, chemotaxis and cellular Lysis (BRODSKY; DPHIL, 2004; LEVY; CHIOCCOLA, 2007).
There is evidence that the genetic components of the haplotypes of the molecules of MHC of class I HLA-B8 and HLA-DR2 class II, HLA-DR3, HLA-DQw2 and HLA-DRw1, have great relevance to the imunopatogenia. In addition to the C2 and C4 complement fractions have been associated with class II HLA DR3 and DR2, respectively, which ratifies the immune genetic influence (BANU GRANDSON; BONFÁ, 2006; SATO et al., 2006).
Thus, by observing the genetic predisposition of the LES, it is evidenced that when identical twins develop an autoimmune disease is more likely that the other twin will develop the same disease than a non-member in the general population (CROW, 2009). The concordance rate in monozygotic twins to LES is approximately 23% against 9% for dizygotic twins twins (ROITT; DELVES, 2004).
For Hahn (2006), the main triggers of autoimmune diseases are susceptibility genes and environmental stimuli. The risk factors are described in table 1.
Table 1-risk factors of the LES.
-Tobacco (GHAUSSY, 2001; HARDY et al .1998).
-Ultraviolet Radiation present in sunlight or in other sources (BIJL; KALLENBERG, 2006).
-Alcohol, stress, cosmetics and vaccines (SIMARD; COSTENBADER, 2007).
|Hormonal factors||–Contraceptives with estrogen or hormone replacement therapy (MOK, 2001; SOUZA et al., 2007).|
|Infectious factors||-Cytomegalovirus, Epstein-Barr virus and Parvovirus B19 (ZANDMAN-GODDARD; SHOENFELD, 2005).|
Source: data compiled by the authors.
In practice, to diagnose the classification criteria of the American College of Rheumatology proposed in 1982 (TAN et al., 1982) and revised in 1997 (HOCHBERG, 1997), which are based on the presence of at least four symptoms among the 11 cited in table 2:
2-Diagnostic framework proposed by the American College of Rheumatology.
|Malar Erythema||Fixed erythematous lesion in malar region, flat or embossed.|
|Discoid lesions||An erythematous lesion, infiltrative, scaly queratóticas attached and follicular plugs, which evolves with atrophic SCAR and discrômica.|
|Photosensitivity||Exposure to ultraviolet light causes skin rash.|
|Oral/nasal ulcers||Oral or nasopharyngeal ulcers, usually painless, observed by the doctor.|
|Arthritis||Non-erosive arthritis involving two or more peripheral joints, characterized by pain and swelling or joint effusion.|
|Serosite||Pleuris or pericarditis documented by ECG or friction or evidence of a stroke.|
|Renal impairment||Persistent proteinuria (> 0.5 g/day or 3 +) or abnormal cilindrúria.|
|Neurological changes||Seizures or psychosis without other causes.|
|Hematologic changes||Hemolytic anemia or leukopenia (<4.000 l)=”” ou=”” linfopenia=””></4.000><1.500 l)=”” ou=”” plaquetopenia=””></1.500><100.000/mL), sem outras causas. l),=”” sem=”” outras=””></100.000/mL), sem outras causas.>|
|Immunological changes||Anti-dsDNA, anti-SM and/or antifosfolipídio.|
|Antinuclear antibodies||Abnormal anti-nuclear antibody titles by indirect immunofluorescence or equivalent test at any time in the absence of drugs known to induce Antinuclear Factor (FAN).|
Source: TAN et al., 1982; HOCHBERG, 1997.
The Table 3 describes the laboratory tests that are used in the diagnosis of SLE.
Table 3 – laboratory tests for diagnosis of LES.
|-Erythrocyte sedimentation rate and C-reactive protein (PRINTO, 2012).|
|-CBC (SACK; FYE, 2004).|
|-Urea, creatinine and 24-hour proteinuria (PRINTO, 2012).|
|-Urine I (SATO et al., 2006).|
|-Determination of serum complement and test to quantitate C3 and C4 (HAUBRICHT; TSCHURTSCHENTHALER, 2009).|
|-Search of antinuclear antibodies Test (VAZ et al., 2007).|
Source: data compiled by the authors.
In LES no cure, it is necessary for the doctor to perform proper planning for the control of disease in severe acute activity and develop a maintenance strategy to re-establish the symptoms to an acceptable level and prevent organs from being injured. Rare cases of patients in a State of continuous complete remission (HAHN, 2006).
The treatment should be individualized for each patient, and will depend on the organ or the affected systems and also the severity of these acometimentos. If this aggression is in multiple systems. Treatment should be aimed at the most serious commitment (CROW, 2009).
The drugs of choice for treatment depend on involvement (table 4).
Table 4-drug Approach in the treatment of SLE.
|Topical corticosteroids (adverse effects): atrophy of the skin, contact dermatitis, Folliculitis, hypopigmentation, infection.||Hidrocortizona (low power), Betamethasone (average power), Clobetasol (high power).|
|NSAIDs (adverse effects): assépica Meningitis, kidney dysfunction, cutaneous vasculitis, transaminite.||The constitutional manifestations, musculoskeletal conditions and light serosites, minimum Treatment lasts 3-4 weeks.|
|Hydroxychloroquine or chloroquine (adverse effects): retinal Lesion, aplásica anemia, ataxia, dizziness, seizures, cardiomyopathy.||The Cutaneous manifestations, associated with the steroids and chronic Constitutional symptoms, 200-400 mg/day.|
|Glucocorticoid (adverse effects): Infection, hypertension, Hyperglycemia, hypokalemia 7, acne, allergic reactions, osteoporosis.||In the hematological, refractory treatment cases.
Oral prednisone -2 0.5 mg/kg/day (according to gravity and the body affected).
|Immunosuppressants (adverse effects): anemia, infections, gastrointestinal intolerance, diarrhea, acute hepatitis, convulsions, malaise.||In severe manifestations.
Methotrexate 15-25 mg/week for 6 months.
Cyclophosphamide 7-25 mg/kg/month EV or -3 1.5 mg/kg/day.
Azathioprine 2 mg/kg/day.
Mycophenolate mofetil 2-3 g/day.
|IV (adverse effects): Infection, hypertension, Hyperglycemia, hypokalemia 7, acne, allergic reactions, aseptic necrosis.||In severe manifestations.
Methylprednisolone 1 g/day for 3 days EV.
Source: HAHN, 2006; SHAI et al., 2007.
The estimated incidence ranges from 1.8 to 20 or more cases per 100,000 inhabitants/year. Between 80% to 90% of patients are female of reproductive age 20 to 40 years, with a ratio of approximately three women to a man (BARROS et al., 2007).
According to Borba Neto and Bonfá (2006), LES afflicts one in every 1000 individuals of the white race, and one in every 250 individuals of black race. It is estimated that there is a case of LES in 2,000 to 10,000 inhabitants, a ratio of nine to ten females to each male.
In Brazil the highest incidence is in the city of Natal (State of Rio Grande do Norte), where in 2000 the population affected was 8.7/100,000 inhabitants/year due to sun exposure, which occurred throughout the year. In the State of para, according to the information system of the Hospital Barros Barreto (DAME, 2012), were made two admissions of drug-induced lupus, and 91 hospitalizations of systemic lupus, totaling 93 admissions in the period from 1/1/2006 to 4/30/2012, where the majority of the affected population is female.
PLANNING OF NURSING CARE
The teaching of self-care the patient with LES is an important aspect for nursing care by generating greater independence to the individual at the time of dealing with changes related to the treatment regimen, the disturbance, the adverse reactions of drugs and their safety at home. Diagnosis and nursing care must be directed to the provision of information about the disease, the daily care and social support (table 5) (SMELTZER et al., 2009).
Table 5-nursing care to the patient lupus.
|NURSING DIAGNOSIS||NURSING INTERVENTION||EXPECTED RESULTS|
|Impaired skin integrity related to cutaneous lesions.||Register the appearance of lesions and rashes; Guide the patient to minimize direct exposure to direct sunlight and fluorescent lights; Guide concerning the use of protection during exposure to the Sun.||Minimize the appearance of lesions;
|Immune system compromised.||Monitor local and systemic signs and symptoms of infection; Monitor the count of white blood cells; Drive the need for a balanced diet; Teach ways to avoid infection as: have a good personal hygiene, washing hands before and after meals and to use the bathroom.||Immune system less committed.|
|Moderate anxiety related to their State of health.
Low self-esteem related to body image disorder caused by injuries.
|Provide information about the disease and treatment; Listen carefully to the patient; Encourage the verbalization of feelings, perceptions and fear.||Reduced anxiety and improved self-esteem.|
|Acute and chronic pain related to inflammation and increased activity of the disease.||Provide comfort measures such as: application of heat or cold, massage, change of position, relaxation techniques and activities of distraction; Administer anti-inflammatory medications, pain relievers and slow-acting antirheumatic agents, according to the prescription.||Improve the comfort level;
Incorporate the techniques of pain management in daily life;
Identify the factors that exacerbate or that influence on pain response.
Source: NANDA, 2008; SMELTZER et al., 2009.
According to Sharma et al. (2007), LES affects more women due to differences in hormonal female standards, because it has been found increased levels of estrogen and testosterone levels decrease in patients with lupus. To Bijl and Kallenberg (2006), exposure to ultraviolet radiation (UVA and UVB), present in sunlight and other sources can induce systemic lupus. However, there are several theories that link the main triggering factors of lupus, such as genetic factors, hormonal, and environmental.
According to Ferreira et al. (2008), Lupus is very heterogênico, depending on each patient’s case it can manifest itself in various ways, ranging from chronic and insidious, and may introduce flashings, however, in acute form can be fast and lethal.
To diagnose Lupus the American College of Rheumatology established eleven criteria, the patient has at least four of these criteria to be considered Lupus (SATO et al., 2002); but for Borba et al. (2008) Although rare, is possible to have patients who have the disease but do not have four of the classification criteria proposed by the American College of Rheumatology. This represents an aggravation in the development of Pathology, making early diagnosis, key factor in the treatment of disease, because of the pleiomorfismo of the manifestations of Lupus (OLIVEIRA, 2011).
Despite the enormous advances in research related to the LES, it is still necessary that further studies be conducted to better understanding of its pathogenesis. Making an early diagnosis of the disease, considering that the majority of patients are diagnosed only when you already have some organic commitment.
Another important aspect refers to treatment, because there is a specific, which apply to all patients in General. This is by the individuality of the clinical manifestations of the disease vary from person to person. What makes impossible the implementation of a clinical Protocol and the lack of standards of customer service hinders the patient’s access to treatment.
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 Biologist. Doctor of biological sciences-Genetics Concentration area. Professor and researcher in CESUPA-Centro Universitário do Pará State.
 Travel nursing academic FAMAZ-Faculdade Metropolitana da Amazônia.
 Travel nursing academic FAMAZ-Faculdade Metropolitana da Amazônia.
 Travel nursing academic FAMAZ-Faculdade Metropolitana da Amazônia.
 Biomedical. Doctorate in Tropical Diseases. Lecturer and researcher at the Federal University of Amapá, AP. Collaborator researcher of the Center for Tropical Medicine UFPA (NMT-UFPA).
 Biologist. Doctor in theory and research. Lecturer and researcher at the Federal Institute of Amapá-IFAP.
 PhD in Clinical Psychoanalysis, researcher for the Center for research and advanced studies. CEPA.
 Biologist. Master in environmental biology. Doctor of medicine/Tropical Diseases. Lecturer and researcher at the Federal University of Pará – UFPA. Collaborator researcher of the Center for Tropical Medicine UFPA (NMT-UFPA).