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Dictionary The Lymphatic System

Systemic Lupus Erythematosus (SLE)

Clinical features, Diagnosis, Management, Prognosis, Nutrition, Herbs,

This is a multisystem connective tissue disease characterised by the presence of numerous autoantibodies, circulating immune complexes, activation of complement and widespread immunologically mediated tissue damage. SLE affects individuals throughout the world but occurs more frequently in the United States (especially Blacks) and the Far East. The onset is most commonly in the 2nd and 3rd decades, with a female to male ratio of 9:1, the prevalence of SLE is around 1:2,500. 

Although the cause of SLE remains obscure, several factors may be involved. 

1.       It appears that genetic factors are important in the aetiology of the disease because of frequent occurrence in identical twins, and higher than expected prevalence of SLE, other autoimmune connective tissue diseases, antinuclear antibodies and immune complexes in related family members. 

2.       Certain environmental factors have been also implicated in pathogenesis of SLE because it has been reported that exposure to sunlight can exacerbate the disease (but probably not cause it), as well as several drugs (especially anti-epileptic diphenylhydantoin, anti-arrhythmic procainamide, vasodilator hydralazine and anti-tuberculotic isoniazid). Exacerbations of SLE commonly occur in pregnancy and after delivery, and become infrequent in menopause; also prevalence is increased in women who have several children and those using oral contraceptives, suggesting the possible role of oestrogens. 

3.       All available evidence suggests that SLE in an autoimmune condition, as many immunological abnormalities are detectable in the blood of patients with SLE:

       Antinuclear and other autoantibodies such as anti-DNA; anti-RNA; anti-Sm, anti-Ro, anti-La (against nucleolar ribonucleoprotein antigens); anti-MA (anti-mitochondrial antibodies)

       Antibodies against erythrocytes, leukocytes and platelets

       Anti-thyroid antibodies and other organ specific autoantibodies

       Rheumatoid factors

       Circulating immune complexes which are frequently deposited in many tissues initiating inflammatory reactions 

Immunologically-mediated tissue damage results from at least two different mechanisms:

       Direct Type II antibody-mediated cytotoxicity with activation of complement may be responsible for brain damage and miscarriage (cytotoxic effect of antibodies which cross-react with fetal tissues and neurons) as well as haemolytic anaemia, leukopenia and thrombocytopenia.

       Immune complex mediated Type III hypersensitivity also known as immune complex disease can explain the mechanism of renal and vascular lesions, which appear to be a consequence of deposition of circulating DNA-anti-DNA and other complexes in tissues with subsequent acute inflammation; vasculitis is thought to underlie probably most of the tissue/organ damage.

Clinical features:  < BACK TO TOP >

           Arthritis, arthralgia and fever

    These are the commonest presenting features and occur in more than 90% of 

    patients and the joints commonly involved are the proximal interphalangeal,  metacarpophalangeal, wrist and knees (differential diagnosis with rheumatoid arthritis is essential).

    Symptoms may begin during pregnancy and there may be a past history of

    spontaneous miscarriages.

    The arthritis can be transient and migratory or a more persistent polyarthritis.

    In contrast to rheumatoid arthritis lupus polyarthritis is usually non-destructive and non-deforming (no actual damage of the joint cartilage).

           Skin/mucosal lesions

    They are seen in more than two-thirds of patients, usually in form of erythematous ‘butterfly?/i> rash across the face  (involving the bridge of the nose and malar areas of the face) and macular reddish-purple lesions on the palms, fingers, arms and trunk.

    Other skin lesions such as widespread rash due to minute skin bleeding (purpura),

    may appear secondary to thrombocytopenia or vasculitis (inflammation in the blood vessel wall with subsequent vessel rupture).

    Alopecia (hair loss) is seen in more than 50% of patients during active phases of SLE but it is generally reversible.

    Painful oral ulcers.

           Cardiopulmonary features

    These include pericarditis with retrosternal chest pain, myocarditis and endocarditis (may produce increased heart rate and fatigue or heart murmurs), pleurisy with pleuritic pain, fibrosing alveolitis with thickening and hardening of alveolar walls.

    ‘Shrinking lung syndrome?/i> (restrictive lung disorder) due to pulmonary fibrosis 

    secondary to immunologically mediated inflammation in the lungs is responsible for 

    decreased lung compliance and breathlessness, especially on exertion.

    Lung function tests reveal impairment of ventilation and gas diffusion in these and many patients without overt clinical or radiological evidence of pulmonary involvement.

           Renal involvement

    Renal lesions follow secondary glomerulonephritis pattern due to deposition of immune complexes in the glomeruli and secondary inflammation.

    Renal involvement may be benign and asymptomatic or serious and relentlessly progressive.

    The most common manifestation is persistent mild proteinuria, but in more severe cases there can be nephrotic syndrome developing eventually into chronic renal failure.

           Central nervous system involvement

    It occurs in up to half the patients in form of migraine-like headaches, mild psychiatric disturbance (personality and mood disorders) or partial organic epilepsy.

    In a few patients there may be severe depression, dementia, organic psychosis,

    cranial nerve lesions, hemiparesis (weakness on one side of the body), ataxia (incoordination, clumsiness) or peripheral neuropathy (sensory and motor).

           Other manifestations

    Abdominal pain is sometimes reported and it can be due to peritonitis, pancreatitis or intraabdominal vasculitis.

    Lymphadenopathy is found in half the patients and a moderately enlarged spleen in 20-30% of patients. 

Diagnosis:  < BACK TO TOP >

           SLE diagnosis is largely clinical and according to American Rheumatism Association at least four of the following eight symptoms must occur, either serially or at the same time before a diagnosis can be made:

    1. abnormal finding in urine

    2. arthritis

    3. butterfly rash on the cheeks

    4. sun sensitivity

    5. mouth sores

    6. seizures or psychosis

    7. low white blood cells count, low platelet count, or haemolytic anaemia

    8. autoantibodies in blood

           The ESR is usually raised in active disease (interestingly C reactive protein can be very low), while haematological findings may include normocytic normochromic anaemia of chronic disease, sometimes autoimmune haemolytic anaemia, leukopenia, thrombocytopenia.

           Immunological findings are essential for diagnosis and include

    Antinuclear antibodies (ANA) can be detected by indirect immuno-fluorescence in the serum of more than 90% of patients but positive tests are found in many other autoimmune conditions.

    Anti-DNA antibodies detected by ELISA (enzyme-linked immunosorbent assay) technique have much greater specificity, but are present in the serum in only half the patients. Other autoantibodies mentioned earlier can also be identified in some but not all patients.

    An evidence for circulating immune complexes may be obtained by using special techniques.

    Tissue evidence for immune complex deposition comes from detection of immunoglobulins by direct immunofluorescence in skin or organ biopsies.

Management  < BACK TO TOP >

           The condition generally runs unpredictable exacerbation-remission course.

           Main treatment is with corticosteroids (e.g., prednisolone [Delta-Cortef, Panafcortelone, Solone]) which can be given initially in large doses.

           With remission of disease careful attempts are made to withdraw steroids or maintain patients on very low doses.

           NSAIDs may be used for symptomatic relief of articular symptoms.

           Immunosuppressive drugs (e.g., azathioprine [Imuran, Thioprine] or cyclophosphamide [Cycloblastin, Endoxan]) are reserved for patients with severe diffuse progressive glomerulonephritis who are not responding adequately to corticosteroids.

           Plasma exchange can be attempted when, using the equipment similar to haemodialysis machine, patient’s plasma can be separated and replaced by fresh plasma (patient’s plasma is then discarded together with autoantibodies and immune complexes).

           In patients who develop chronic renal failure dialysis or kidney transplantation are necessary; kidney transplantation in SLE patients has proven remarkably successful.

           Due to early diagnosis and efficient treatment the prognosis has improved markedly, and 10-year survival today is more than 95%.

Prognosis  < BACK TO TOP >

  • - - 

Nutrition < BACK TO TOP >

Nutrition that alleviate or prevent Systemic Lupus Erythematosus (SLE) :-

Herbs < BACK TO TOP >

Herbs that alleviate or prevent Systemic Lupus Erythematosus (SLE) :-

Discoid Lupus Erythematosus

This condition is more common than SLE and it primarily effects the skin. The main feature is sharply circumscribed round macules and plaques showing erythema, scaling, telangiectasis (visible dilated blood vessels) and in time atrophy. These skin lesions are characteristically sensitive to sunlight, and therefore they tend to appear more frequently on light-exposed areas of the skin (face, ears, upper trunk and extensor surfaces of the extremities). Involvement of the scalp may lead to hair loss (alopecia) that can be permanent. Some patients develop mild systemic features, and a few them may end up later with SLE.
It is advised that patients avoid unnecessary exposure to sun and wear sunscreens whenever going outside. Skin lesions are treated with topical corticosteroid creams, but avoiding their excessive use.

(source : Dr Zoran Pletikosa)

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