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Author: admin, 20.05.2015. Category: Organic Food Delivery

Original Editors - Alli Christian from Bellarmine University's Pathophysiology of Complex Patient Problems project.
Systemic lupus erythematosus (SLE) is a chronic, rheumatic, inflammatory disease that can affect a person’s skin, joints, kidneys, lungs, heart, nervous system, blood, and mucous membranes.
Non-Steroidal Anti-inflammatory Drugs (NSAIDS): These medications help to decrease tissue inflammation, and therefore decrease the patient’s joint and muscle pain. Corticosteroids[2]: These drugs are only prescribed to patients with severe SLE who experience signs and symptoms that are not improving with any other drug therapy. Stress- It has been determined that stress can provoke changes in the neuroendocrine system causing changes in the function of immune system cells. Learn about the shoulder in this month's Physiopedia Plus learn topic with 5 chapters from textbooks such as Magee's Orthopedic Physical Assessment, 2014 & Donatelli's Physical therapy of the shoulder 2012.
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Glucocorticoid Therapy in Systemic Lupus Erythematosus – Clinical Analysis of 1,125 Patients with SLEHiroshi Hashimoto[1] Professor Emeritus, Aiwakai Medical Corporation, Bajikouen Clinic, Rheumatology, Tokyo, Japan1.
H Hashimoto, S Hirose, S Kano, et al1992Studies on clinical subsets and severity of systemic lupus erythematosus based on a 1987 questionnaire conducted in Japan-Clinical analysis of the outcome and treatments in clinical subsets.
M Seki, C Ushiyama, N Seta, et al1998Apoptosis of lymphocytes induced glucocorticoids and relationship to therapeutic efficacy in patients with systemic lupus erythematosus.
S Hirohata, Y Kanai, A Mitsuo, et al2009Accuracy of cerebrospinal fluid IL-6 testing for diagnosis of lupus psychosis. L Sinigaglia, M Varenna, L Binelli, et al1999Determinations of bone mass in systemic lupus erythematosus: a cross sectional study on premenopausal women.
We did not include subjects with a history of organic brain diseases, head injury with loss of consciousness, metabolic or systemic diseases, or drug or alcohol dependence.
Objective Solutions for Medicolegal Assessment E Objective identification and differentiation of psychological and organic factors.
Delirium ? Delirium is a transient, potential y reversible dysfunction in cerebral metabolism, that has an acute or subacute onset and is typical y manifested by alterations of levels of consciousness and change in cognition.
The diagnostic features of delirium in the current DSM (DSM-IV) ? Disturbance of consciousness? Change in cognition? The disturbance that develops over a short period of time (usual y hours to days) and tends to fluctuate during the course of the day. Prevention ? Good general medical and nursing care ? Recognition and effective treatment? Screening for alcohol dependence is important ? Elderly patients unwel physical y or having a major procedure, who have pre-existing cognitive problems.
The following list includes common signs and symptoms of SLE in order of the most to least prevalent.
Corticosteroids can give the patient relief from constitutional symptoms, arthritis, and cutaneous problems caused from SLE. Low white blood cell or platelet counts can be indicative of SLE, whereas low red blood cell counts can be indicate of anemia which commonly occurs in conjunction with SLE. Clinical trials in systemic lupus erythematosus (SLE): lessons from the past as we proceed to the future- the EULAR recommendations for the management of SLE and the use of end-points in clinical trials.
Physiopedia is not a substitute for professional advice or expert medical services from a qualified healthcare provider.
Remission rate of lupus nephritis according the WHO classification type and degree of proteinuria3.2. The clinical course of SLE patient (46 years old, female) with organic brain syndrome (OBS)3.3.
IntroductionSystemic lupus erythematosus (SLE), which is an inflammatory disease of unknown cause, is a representative autoimmune disease. If you interesting in "Organic Mental Disorders" powerpoint themes, you can download to use this powerpoint template for your own presentation template. All of the below symptoms might not be present at the initial diagnosis of SLE, but as the disease progresses more of a person’s organ systems become involved. L Dubois, 1987Prognostic subsets, natural course, and causes of death in systemic lupus erythematosus, In: Wallace DJ, Dubois EL editors.
C Roberts, 1975The heart in systemic lupus erythematosus and the changes induced in it by corticosteroid therapyA study of 36 necropsy patients. For viewing only, you can play with our flash based presentation viewer instead of downloading the ppt file.
E Gallacher, et al2011Efficacy and safety of belimumab in patients with active systemic lupus eryhematosus: a randomized, placebo-controlled, phase 3 trial.
Glucocorticosteroids (steroids) have anti-inflammatory and immunosuppressive effects, although the biological effects of steroids are multiple.
Nothing contained in this site is or should be considered or used as a substitute for professional medical or mental health advice, diagnosis, or treatment. The anti-inflammatory effect of steroids is powerful and acts rapidly, and the immunosuppressive effect after administration of large doses of steroids is also strong.
Never disregard medical advice from your doctor or delay seeking it because of something you have read on the Internet. Therefore, steroids play a major and essential role in the treatment and management of SLE patients, especially those having severe and active SLE. However, the effectiveness and usefulness of steroids are limited because of their severe side effects, unresponsiveness and resistance to steroids. In these situations, additional therapies such as immunosuppressive agents or plasmapheresis, etc.
Clinical findings One thousand one hundred and twenty-five SLE patients fulfilling four or more of the revised ACR (American College of Rheumatology) criteria [2] were examined and treated at the Department of Internal Medicine and Rheumatology in Juntendo University School of Medicine between 1955 and 2002.
In all patients, the diagnosis and treatment procedures were conducted during a period when the use of steroids and immunosuppressive agents was common. In children and adults over the age of 50, the incidence of SLE demonstrated only a slight female predominance, however, for those in their twenties, thirties and forties, close to 90% of patients were women. The frequencies of major clinical manifestations and laboratory findings from observations together with the data from other investigators [3-6] are shown in Table 1. Treatment according to disease severity Clinical subsets of SLE were divided into three groups according to disease severity that related to prognosis [7]. Moderate disease: lupus nephritis without renal failure, pleuritis, pericarditis, meningitis, hemolytic anemia, thrombocytopenic purpura, etc. Although there are several kinds of steroids, prednisolone (PSL) is commonly used to treat SLE. The initial dose of steroids was usually determined according to the severity and activity of the disease.
Furthermore, steroids characteristically have a high risk of serious side effects such as infection, gastric ulcer, diabetes mellitus, osteoporosis, etc.
Therefore, the effectiveness and usefulness of steroids were limited because of severe side effects, unresponsiveness and resistance to steroids.
Recently, belimumab (anti-BLyS antibody), the first targeted biological drug, was approved for treatment of SLE by the FDA [10].

Prognosis and causes of deathIn this paper, the survival rate was 93% at 5years, 89% at 10years and 69% at 20years after diagnosis. The causes of death were renal failure (30%), cerebrovascular diseases (23%), infection (19%), and others. In the last 2 or 3 decades it has been noted that the prognosis of SLE has improved [11-13]. Changes in the mortality rate in accordance with the cause of death in SLE patients were also observed, showing a significant reduction in death due to renal failure. The clinical pictures of LN and the types of the World Health Organization (WHO) classification according to histopathological findings [14] in this study are shown in Table 3. Abnormal urinary sediments including erythrocytes, leukocytes and casts were observed frequently. Diffuse proliferative glomerulonephritis (DPGN) of Type IV, which has a poor prognosis, could be seen in 55 of 216 cases (25%), which underwent renal biopsy.
Membranous glomerulonephritis (MGN) of Type V characteristic of nephrotic syndrome, was observed in 18% of cases.
Types I and II, which are thought to have better prognosis, were observed in 23% and 16% of cases, respectively. Treatment of LNThe available therapeutic procedures include steroids, immunosuppressive agents, plasmapheresis, anticoagulants and hemodialysis, etc. However, doses of steroids were determined according to urinary findings, renal function and renal histopathological findings evaluating the activity and severity of LN. It led to more rapid recovery which might be result of a rapid nongenomic physicochemical effect.
After PSL administration for 3-6 weeks, the dosage of PSL was then reduced by nearly 10% every 2–3 weeks according to the improvement in proteinuria, urinary sediments, abnormal renal function, low serum complement levels and high titers of anti-dsDNA antibodies. If PSL had no or incomplete response, the dosage was increased by 20% or steroid pulse therapy was conducted again. In the patients with DPGN or RPGN, intravenous pulse therapy of cyclophosphamide (IVCY) (500-750mg, monthly for 3 to 6 months), as immunosuppressive agent, was used. Alternative induction therapies included combined therapies with steroids and immunosuppressive agents such as daily oral cyclophosphamide, azathioprine, tacrorimus, mizoribine, and cyclosporine, etc. If an incomplete response after 2 months treatment with PSL alone was also observed, immunosuppressant agents were administered in addition to PSL. Outcome and prognosis of LNDuring the past half century, the prognosis of SLE has significantly improved.
This is assumed to be partially due to early diagnosis and early treatment with the development of diagnostic procedures, as well as the development of treatments including the implementation of hemodialysis [1,11-13].
Figure 1.Remission rate of lupus nephritis according the WHO classification type and degree of proteinuriaFigure 1 shows the remission rate after onset according to the WHO classification type and degree of proteinuria.
The remission rates of patients with Type IV (DPGN) and profuse peroteiniria or nephrotic syndrome tended to decrease during the course of the disease, while the remission rates of patients with Type II and persistent proteinuria tended to increase. Patients with Type V (MGN) had a low remission rate through out the course of the disease, but no decrease in the remission rate was observed until later on. This fact suggests that the underlying disease types had a greater influence on the remission rate than the treatment method. Clinical analysis of NPLEThe frequencies of various neuropsychiatric manifestations of SLE (NPLE) have been reported to vary from 28 to 59%. Table 4.Frequencies of neuropsychiatric manifestations (NPLE) in 1125 lupus patientsThe American College of Rheumatology (ACR) proposed new criteria for the classification of neuropsychiatric syndrome of systemic lupus erythematosus (NPSLE) in 1999 [16]. The frequency of psychiatric manifestations was higher than that of neurological manifestations.
Many NPLE cases were considered to be caused by lupus itself, excluding obvious causes such as antiphospholipid antibody syndrome (APS), necrotizing angiitis, and complications.NPLE is one of the diseases that influence the prognosis of SLE as well as LN. Especially, patients with acute confusional state or organ brain syndrome (OBS), cognitive dysfunction, recurrent seizure, and cerebrovascular disease, etc., had poor prognosis. Acute OBS showed an 85% correlation with SLE activity and exacerbation, which was greater than that of the psychiatric illness group (57%) and the psychosyndrome group (23%) [17].Although acute OBS was correlated with active SLE lesions, correlations with high titers of anti-dsDNA antibodies and low complement levels, which were seen in active LN, were not necessarily observed. Steroid-induced psychosis appears half a month to one month after administration of steroids.
In addition, patients with both focal and diffuse syndromes should have various examinations including CSF, electroencephalogram (EEG), and an imaging studies (such as computed tomography (CT) and magnetic resonance imaging (MRI)), cerebral blood flow by angiography or single photon emission computerized tomography (SPECT), etc. Treatment of NPLEIf NPLE was active and there was severe major organ involvement, steroid therapy was indicated.
However, when improvement could not be seen within 48 hours after treatment, 250 to 500mg of hydrocortone was administered every 12 hours.
When the patients showed panic or marked agitation and their hallucinations and delusions were threatening, several antipsychotic drugs in conjunction with steroids were also used. Figure 2.The clinical course of SLE patient (46 years old, female) with organic brain syndrome (OBS)Figure 2 shows the clinical course of an SLE patient with OBS who was a 46-year old female. She was diagnosed as SLE with malar rash, eruption, leucopenia, thrombocytopenia, proteinuria and positive anti-nuclear antibodies, etc.
In April 1997, she had recurrent unconsciousness with delirium, disturbance of articulation with high fever and a worsening malar rash.
PleuritisPleuritis is by far the most common pulmonary manifestation, occurring at some time in the course in 40 to 50% of lupus patients.
However, the frequency of pleuritis in Japanese SLE patiens was lower than that in European countries and the United States. On chest X-rays, slight to moderate pleural effusion caused by pleural inflammation could be observed bilaterally in approximately half of cases. As clinical symptoms, fever, chest pain, dry cough, severe dyspnea, and occasional hemoptysis were noted.
The majority of patients were hypoxic, requiring supplemental oxygen or intubation for assisted ventilation. All patients with alveolar hemorrhage were treated with steroid pulse therapy following large doses of PSL, but it was also necessary to concomitantly use other immunosuppressive tharapies such as cyclophosphamide including IVCY, and plasmapheresis. PericarditisThe most common cardiac abnormality was pericarditis, which occured in 8-25% [27], but it was relatively rare in Japan, with a frequency of 7% (47 out of 1,125cases) in this study. In cases with myocarditis, positive CRP, elevated CK, IgG class anti-dsDNA antibodies, hematuria, etc., in conjunction with tachycardia, cardiac enlargement, congestive heart failure could often be observed. Myocardial infarction and coronary artery diseaseCoronary artery disease due to arteriosclerotic changes is more common in SLE patients. Death from myocardial infarction late in the course of the disease is one of the most frequent causes of death after 10 to 30 years of SLE [28]. The average age at diagnosis of SLE was 37 years old (26–63 years old), and the average age at development of myocardial infarction was 51 years old (41–66 years old) in these patients. There were two death cases, including one case of death from cardiac rupture.Several risk factors that cause myocardial infarction due to atherosclerosis in SLE are considered.

They are renal involvement, hypertension, hyperlipidemia, long-term administration of steroids, diabetes mellitus, anti-phospholipid syndrome, smoking, etc.
In this study, 4 patients had hypertension, hyperlipemia and diabetes mellitus as risk factors.
Death from myocardial infarction due to inflammation of the coronary arteries has been reported in SLE patients dying early in the course of their disease, but this is a rare event [28]. Regarding the treatment in this study, conservative medical management without large doses of steroids was used in most cases. Vasculitis was observed in 9 of 11 cases with abdominal surgery, and intestinal perforation was observed in 6 cases.
When a rapid improvement was not obtained, intermittent IVCY therapy was simultaneously used. In cases associated with bowel infarction or perforation, treatment for infection was also needed.
Hematologic manifestationsHematologic manifestations in SLE include normochromic-normocytic anemia caused by chronic inflammation, autoimmune hemolytic anemia (AIHA), iron-deficiency anemia, leukocytopenia, lymphocytopenia, thrombocytopenia, thrombocytopenic purpura (TP), thrombotic thrombocytopenic purpura (TTP), and antiphosphlipid syndrome (APS), etc. AIHA is rare in Japanese SLE patients in comparison to those in Europe and the United States.
Steroids were the mainstay of the treatment for AIHA and a response was achieved in about 75% of patients. The reticlocyte count was a reliable indicator of both responsiveness to treatment and relapse.
However, thrombocytopenia lower than 50,000 was relatively rare, and it occured in approximately 10% of cases. After an increase in platelet count occurred in response to steroids, the dose was gradually reduced after 4 weeks. If thrombocytopenia did not respond to steroids with bleeding from the major organs such as gastrointestinal tract, kidney, bladder, other mucosal surface, steroid pulse therapy was used. TTPTTP usually consists of a pentad of TP, microangiopathic hemolytic anemia, fever, renal failure, and neurologic manifestations. TTP has been reported in association with various other diseases, including SLE, most of which are characterized by some degree of vasculitis of the small vessels and circulating immune complexes [30].
The main cause of acquired TTP including SLE is assumed to be an autoantibody that is an inhibitor (IgG inhibitor) of von Willebrand factor cleaving protease [31]. It has been clarified that congenital TTP is caused by a mutation in the ADAMTS-13 gene of cleaving protease.
TTP must be differentiated from DIC or catastrophic antiphospholipid syndrome, but coexistence of both are often observed. Regarding treatment, plasmapheresis using fresh frozen plasma, and transfusion therapy of normal plasma are used. In addition, large-doses of steroids including steroid pulse therapy, immunosuppressive drugs, IVIg therapy, and anti-platelet drugs, etc.
Pregnancy and birthWhen an SLE patient wished to conceive and give birth, a medical determination as to whether pregnancy would be possible was considered.
Basically, there were presumed to be almost no problems in pregnancy when the patient was in remission with a maintenance dosage of steroids, and when serious organ failure was not observed. Moreover, even if the patient had active disease, pregnancy was allowed after the disease improved with treatment. Treatment and management during pregnancy It was important for the physician and the gynecologist to be in close communication for the treatment and management during pregnancy. Usually, it was unnecessary to change the maintenance dose of the steroid during pregnancy.
When mild deterioration was observed in the early stage of pregnancy, an increased steroid dosage was attempted according to the clinical manifestations. If the clinical manifestations required administration of a large-dose of steroids, considering the risks to the mother and the effect of the steroids on the fetus, an artificial abortion was performed at an early stage. Although the level of serum cortisol in the fetus decreases during the steroid administration, cortisol secretion and response to ACTH are believed to remain normal [32]. If a mother is treated with prednisolone or hydrocortisone, these steroids are assumed to have a minimal effect on the fetus because they are inactivated by 11-?-dehydrogenase in the placenta. Prevention of exacerbationThe mother was hospitalized prior to the expected delivery date for management of the mother and fetus. If pregnancy remained steady, and SLE activity was not observed, the dose of steroids was increased immediately after delivery to prevent any exacerbation of SLE. The dose was reduced by 10% every 4 to 7 days while confirming no exacerbation, and continually observed until eventually reducing it to the dosage at the time of delivery. Adverse effects and complications due to steroid treatmentSide effects of prolonged treatment with oral steroids are well known.
Although reversible with a discontinuation or reduction in dose, hypertension, peptic ulcer, diabetes mellitus, pancreatitis, osteoporosis, psychosis, etc. Thinning of the skin, cataracts, glaucoma, osteoporosis, and osteonecrosis could be observed as irreversible side effects. Susceptibility to infection, particularly bacterial infection, was increased with steroid use. However, it is unclear whether this reflects pro-atherogenic effects of the underlying disease process or adverse metabolic effects associated with steroid use [36]. Table 5 shows the frequencies of these complications at the time of occurence in 97 SLE patients who had been observed for over 20 years.
Most of the above complications were thought to be due to treatment including steroids, as well as aging.
Steroid–induced osteoporosis leading to fracture, particularly vertebral collapse, was a major problem.
Aseptic osteonecrosis (AON) was observed in approximately 10% of SLE, with the femoral head being a common site. It also appeared in the femoral condyle, caput humeri, proximal end and distal end of the tibia, etc..
It has been suggested that increased doses of steroids (especially in the first year of treatment) and the duration of steroid therapy are correlated with a grater risk of AON in SLE patients [40]. ConclusionIn this paper, steroid therapy for SLE based on the clinical analysis of 1,125 cases, especially for principal organ involvement that required large doses of steroids, was evaluated.
Although there is no doubt that steroids contribute to a significant improvement in the prognosis in SLE, the effectiveness and usefulness of steroids are limited because of severe side effects, unresponsiveness and resistance to steroids.Now, new biological agents that target B cells, T-B cell interaction, co-stimulatory pathways, intracellular molecules, etc.

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