ArtsAutosBooksBusinessEducationEntertainmentFamilyFashionFoodGamesGenderHealthHolidaysHomeHubPagesPersonal FinancePetsPoliticsReligionSportsTechnologyTravel
  • »
  • Health»
  • Diseases, Disorders & Conditions

Systemic Lupus Erythematosus: Clinical Manifestations And Laboratory Investigations Prior To Its Diagnosis

Updated on February 13, 2014

Lupus Picture

Source

A General Overview

Systemic Lupus Erythematosus manifests on the kidney, respiratory system, the heart, the central nervous system, Muscles, the eyes and the blood. This is the continuation of the previous hub which also elaborates on its effects on the skin and joints.

Cardiovascular System:This system is affected in 25- 40% of cases. Cardiac lesiongs include dry pericarditis, pericardial effusion, myocarditis with cardiac failure and valvulitis involving the mitral valve. Libmansack’s endocarditis is a non-bacterial verrucous endocarditis affecting the mitral valve which is occasionally seen. It results in mitral incompetence. Vasculitis leads to Raynaud’s phenomenon, necrotic ulcers of the finger pulp and chronic ulcers.

Respiratory system: This system is affected in 50% of cases. Common lesions are dry pleurisy, pleural effusion, fibrosing alveolitis and lupus pneumonitis.

Kidney: This organ is affected in about 60% of cases. Renal involvement used to be the most important lesion deciding the prognosis. Renal involvement may remain asymptomatic with only proteinuria for long intervals or may manifest as hematuria, acute nephritic syndrome or renal failure. The histological pattern is that of focal glomerulonephritis, diffuse glomerulonephritis or membraneous glomerulonephritis. The wire loop lesions which are produced by thickening of the glomerular walls are characteristic on histology. Treatment instituted early in the disease helps in averting renal involvement.

Central nervous system: This is affected in 50% of the cases. Psychosis, convulsions, rarely peripheral neuropathy, myelopathy, cranial nerve paralysis, chorea and cerebella ataxia constitute the neurological manifestations.

Muscles: Myalgia and rarely polymyositis with wasting and weakness of proximal muscles are seen.

Hematology: Most of the cases show normocytic normochromic anemia. Other abnormalities include Coomb’s positive autoimmune hemolytic anemia, leucopenia and thrombocytopenia. Lupus erythematosus (LE) cells are demonstrable by suitable techniques. These are polymorphonuclear material under the influence of antibodies. Their number increases with the activity of the disease. The liver is enlarged in 60%, spleen in 60% and lymph nodes in 25% of cases. Abdominal emergencies may be produced by the development of acute peritonitis, perisplenitis, or pancreatitis.

Eyes: These may be affected in a few cases. Lesions include dryness of the conjunctiva and retinal abnormalities such as hemorrhage and exudates known as cytoid bodies.

SLE

This 42-year-old woman with systemic lupus erythematosus developed digital infarcts during a flare of disease activity. She had a positive antinuclear antibody titer of 1:1280 on Hep-2 cells by immunofluorescent antibody.
This 42-year-old woman with systemic lupus erythematosus developed digital infarcts during a flare of disease activity. She had a positive antinuclear antibody titer of 1:1280 on Hep-2 cells by immunofluorescent antibody.

Laboratory Investigations

SLE gives rise to an array of abnormalities, some being specific and the others nonspecific. The nonspecific features include, markedly elevated ESR (above 100 mm/1st hour), moderate anemia, leucopenia, proteinuria. The specific tests depend upon the immunological abnormalities and they are indicated below.

Serological abnormalities in SLE: The Antibuclear antibodies (ANA): They occur in over 99% of cases. These are composed of antibodies against DNA single strand, DNA double stand, RNA and several other nuclear components. These antibodies by themselves are not harmful, but they combine with antigens at different sites to form immune complexes and set up inflammatory responses. Though, the ANA are not specific for SLE, presence of three or more components is almost diagnostic of this disease. The titire is high during exacerbation and low during remission. Low levels of ANA occur in rheumatoid arthritis (20%), Sjogren’s syndrome 60%), scleroderma (40%) dermatomyositis (30%) and drug reactions in a variable number.

© 2014 Funom Theophilus Makama

Comments

    0 of 8192 characters used
    Post Comment

    No comments yet.