Case Study On The Patients With Sle And Its Diagnosis

What might have caused the lack of energy in patient, and what type of tests might be ordered to support this conclusion

Lack of energy and fatigue is a constitutional manifestation of SLE, but it can also possibly indicate a hematologic manifestation (Medscape, 2017-e). It is the autoantibodies that cause disease in SLE-hemolytic anemia, lymphopenia and thrombocytopenia are also seen in SLE due to specific autoantibodies that target RBCs and lymphocytes (Lupus Foundation of Minnesota, 2013).

Fatigue is consistent with anemia because with anemia the red blood cell’s capacity to carry oxygen throughout the body is reduced and poor, causing hypoxemia (McCance & Huether, 2014). In this case acquired hemolytic anemia should be considered because these anemias are immunologic, characterized by erythrocyte destruction by autoantibodies against erythrocyte antigens (McCance & Huether, 2014).

Labs to differentiate between anemias include complete blood count (CBC), plasma iron, total iron-binding capacity, ferritin, serum B12, folate, bilirubin, free erythrocyte protoporphyrin and transferrin (McCance & Huether, 2014). In hemolytic anemia the H&H is typically low (low circulating RBCs due to autoantibody destruction), reticulocyte count may be high (bone marrow is working hard to replace the destroyed RBCs), and bilirubin may be high (much hemoglobin being broken down) (NIH, 2014). Mean cell volume (MCV) may be normal to high (consistent with normocytic anemia), plasma iron may be normal to high (inefficient erythropoiesis) (McCance & Huether, 2014). A Coombs test can determine if antibodies are being made to destroy RBCs (NIH, 2014). The remainder of the above labs should be normal in hemolytic anemia (McCance & Huether, 2014).

The patient should have a thorough workup to rule out other causes. This is especially true with SLE which can present so differently from person to person. A complete metabolic panel (CMP) can be done to assess renal function and assess for a wide variety of other underlying causes. Serum albumin, alkaline phosphatase and creatinine can be checked to evaluate for malnutrition due to anorexia/weight loss. Thyroid function can be assessed per TSH, T4 and T3 levels.

What is the pathophysiology that underlies lymph node enlargement in this patient

Lymph node enlargement, or lymphadenopathy, can be defined as the excessive production of a lymphocyte (lymphoproliferation) and the autoimmune destruction of blood cells. It is categorized by changes in the characteristics, number, and size of the lymph nodes. They are typically soft, nontender, and vary in size. They are commonly occurring and noted in about 50% of those diagnosed with SLE.

Lymphadenopathy in autoimmune diseases reflect involvement of the reticuloendothelial system, secondary to an increase in normal lymphocytes and macrophages in lymph tissue/nodes (Medscape, 2017-c). In SLE, lymphadenopathy can be caused by an infection or lymphoma. The risk of infection and lymphadenopathy occur more often in patients with SLE because of their deficiencies in their immune system.

Which of the three blood tests results directly above would be of most concern? Give a likely cause for the abnormality

A low white blood cell count (leukopenia) is a decrease in immune cells (leukocytes) which is related to a decrease in neutrophils. The low WBC count is of most concern due to the already immunosuppressed state that patients with SLE have. The low WBC is consistent with the suppressed immune system in a patient with SLE. SLE is an autoimmune disorder that results in the body’s immune system attacking itself which can cause a decrease in WBCs. Additionally, the prednisone prescribed by her PCP that she was placed on for two months could be a cause of the low WBC count since it suppresses the immune system (McCance and Huether, 2018).

Why patients with SLE should receive an influenza vaccination every year and a pneumococcal vaccination every 5 years

Patients with SLE have an immunosuppressed condition at baseline, and may be functionally asplenic (Medscape, 2017-b). In addition, immunosuppressants and steroids that are typically within a patient’s medication regime further make one vulnerable to contagious infectious disease. Therefore, yearly (every season) influenza vaccination is essential (CDC, 2017-b). Immunocompromised persons are more likely to get flu complications, such as pneumonia, bronchitis, sinus infections and ear infections that can result in hospitalization and sometimes death (CDC, 2017-c).

Pneumococcal vaccination is important for the same reason. The pneumococcal polysaccharide vaccines for immunocompromised persons greater than or equal to 2 years of age who are at risk for infection should be given the vaccine (CDC, 2017-e). This is the PPSV23 or Pnuemovax® (CDC, 2017-d).

Levels of antibodies to most pneumococcal vaccine agents remain elevated for at least 5 years per the CDC (2017-e). Therefore, this vaccine should be administered every 5 years. Both the flu and pneumococcal vaccines can be given at the same time (separate injections) without an increase in side effects or a decrease in efficacy. (CDC, 2017-e). Of note, respiratory infections, regardless of bacterial or viral can rapidly lead to serious systems decline.

Why is hypocomplementemia consistent with a diagnosis of SLE

Hypocomplementemia is consistent with a diagnosis of SLE due to C3 and C4 (complement proteins) level depression in patients with active SLE as a result of their consumption by immune complex - induced inflammation (Medscape, 2017-b). Measurement of C3 and C4 is useful in diagnosis because some patients may also have a congenital complement deficiency that predisposes them to SLE (Medscape, 2017-b).