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Systemic Lupus Erythematosus

Systemic Lupus Erythematosus (SLE) or more commonly known as Lupus, is a systemic autoimmune disease. This disease occurs when the immune system mistakenly attacks healthy tissues of the human body. SLE can cause inflammation in many areas and organs of the human body such as joints, skin, heart, lungs and kidneys. This disease has chronic characteristics and can manifest through periods of flare-ups and remission.

 

Diagnosis of Real Causes & Treatment of Systemic Lupus Erythematosus

  • Gradual restoration of cellular function
  • Personalized therapeutic protocols, without chemical residues and excipients
  • Treating the real causes
  • Therapeutic formulas that work alone or in combination with any other medication
  • Adopting a Molecular / Therapeutic Nutrition Plan

 

Symptoms of Systemic Lupus Erythematosus

The most common symptom of Lupus is a butterfly-shaped rash on the facial area that spreads to the cheeks and nose. Nevertheless, rashes can develop in other areas of the body as well. Other symptoms include fever, chest pain, shortness of breath, eye dryness, hair thinning or loss, anemia, confusion, headaches, joint pain/swelling or fatigue.

 

 

Epidemiology of Systemic Lupus Erythematosus

Lupus is more common in women and usually develops in the ages of 15-45. It is estimated that in USA almost 1.5 million people suffer from SLE. Race and ethnic background affect the frequency of SLE. More specifically, the disease is more frequent in blacks and Hispanics.

Worldwide, the prevalence of SLE varies considerably. Increased prevalence of the disease has been reported in Spain, Italy and the Afro-Caribbean population of the United Kingdom.

 

Lupus Erythematosus

Pathophysiology of Systemic Lupus Erythematosus

Systemic Lupus Erythematosus is a chronic autoimmune disorder. In this disease numerous inflammation sites are reported. Furthermore, autoantibodies are produced and may be present for long periods of time before any symptoms arise.

The real causes of lupus remain largely unknown. However, people with a genetic predisposition (more than 60 genes are reported) for lupus can develop the disease after coming in contact with environmental factors (e.g. sunlight), certain medications (e.g. antibiotics, blood pressure drugs) or during an infection.

A proposed mechanism for the disease, implicates a defective apoptotic procedure (i.e. the programmed cell-death) that not only increases the cell death but also causes immune intolerance.

Antinuclear antibodies (ANAs) are present in almost all individuals suffering from SLE. Antibodies to native double-stranded DNA (dsDNA) is another biomarker used for the diagnosis of SLE.

 

 

Causes for the appearance of Systemic Lupus Erythematosus

Multiple genetic predispositions and environmental factors (exposure to UV radiation, specific drugs, microbial infections) have been identified as possible causes for the disease.

Patients suffering from SLE tend to have higher levels of antibodies against Epstein-Barr virus and higher viral circulating loads. Viral infections are known to stimulate the immune system and more specifically B-cells. Chronic infections have been blamed for the possibility of triggering mistaken responses by the immune system and thus contributing to the onset of autoimmune diseases.

Early-life factors have also been proposed as triggers for the disease. These factors include:

  • Low birth weight (<2500g)
  • Preterm birth (>1 month)
  • Exposure to agricultural pesticides during childhood

Vitamin D deficiency is long known to be implicated in autoimmunity and rheumatic illnesses such as SLE. More specifically, scientific studies have shown that Vitamin D deficiency in individuals with distinct gene polymorphisms increased the risk of developing SLE.

There are also other risk factors that have been identified as possibly contributing to the onset of SLE. These include:

  • Smoking
  • Silica dust
  • Estrogen intake in post-menopausal women
  • Photosensitivity

 

 

Complications

People suffering from SLE present a higher risk of developing:

  • Pregnancy complications (increased risk of miscarriage)
  • Infections
  • Heart inflammation (pericarditis)
  • Kidney failure
  • Impaired memory
  • Behavioral changes
  • Pleuritis

Treatment of Systemic Lupus Erythematosus

A variety of drugs are used for the treatment of SLE depending on the patient’s signs and symptoms. The medications and dosages can also differ considerably as the disease progresses and may manifest through periods of flare-ups and remission.  The most common medications for SLE include the following:

Non-steroidal anti-inflammatory drugs (NSAIDs). Ibuprofen, naproxen sodium and aspirin are among the most commonly used NSAIDs to treat SLE’s symptoms such as pain, swelling and fever. In certain cases more-potent drugs may be used. NSAIDs are known to cause side-effects such as gastrointestinal irritability, increased hepatic enzymes levels and increased risk for cardiovascular medical issues.

Corticosteroids. Steroid medications such as prednisone are used to address the active inflammation sites. Possible side effects include weight gain, high blood pressure, increased risk for infections and mood swings.

Immunosuppressants. These medications suppress the function of the immune system and may be helpful for many patients suffering from SLE. Azathioprine, methotrexate, cyclosporine and leflunomide are included in this category. As their name reveals, these medications can cause an increased risk for infections. Other side effects include dizziness, liver issues and in some cases increased risk for cancer.

Anti-malarial drugs. Medications such as hydroxychloroquine can help address the SLE’s flares. Gastrointestinal irritation is rather common while taking this medication.

 

 

The modern medical approach to Systemic Lupus Erythematosus – Treating the causes of the disease

Functional Medicine provides a causal approach to the disease.  After filling in a thorough Medical history questionnaire, a certified Health Specialist will address a series of targeted questions to you, to assess whether your symptoms could be indicative of Systemic Lupus Erythematosus or evaluate the route of the disease. Then your specialist may recommend a specialized blood or antibodies test, or other molecular-level diagnostic tests to confirm/complement the diagnosis. Your personalized treatment plan will be based upon the diagnostic tests results, the symptoms described and your medical history overall.

This treatment plan may be accompanied by a Molecular Therapeutic Nutrition program that will be compiled after a distinct consultation with a Molecular Nutritionist and will aim towards achieving even higher levels of health and well-being along with alleviating not only the symptoms but the true causes of Systemic Lupus Erythematosus.

 

 

Dr. Nikoleta Koini, M.D.

Doctor of Functional, Preventive and Regenerative Medicine

Diplomate and Board Certified in Anti-aging, Preventive, Functional and Regenerative Medicine from A4M (American Academy in Antiaging Medicine).

Partners
Functional Corporation

References


  • Autoimmune diseases. National Institute of Allergy and Infectious Diseases. Last reviewed May 2, 2017. Accessed June 4, 2020.
  • Hood E. Measuring autoimmunity in America. Environmental Factor. Published April 2018. Accessed June 4, 2020.
  • Autoimmune diseases. National Institute of Environmental Health Sciences. Last Reviewed May 6, 2020. Accessed June 4, 2020.
  • Marker of autoimmunity increases in the U.S. National Institutes of Health. Published April 21, 2020. Accessed August 19, 2020.
  • Roberts MH, Erdei E. Comparative United States autoimmune disease rates for 2010-2016 by sex, geographic region, and race. Autoimmun Rev. 2020;19(1):102423. doi:10.1016/j.autrev.2019.102423
  • The Autoimmune Diseases Coordinating Committee. Progress in Autoimmune Diseases Research: Report to Congress. National Institutes of Health; 2005. Accessed August 31, 2020.
  • Somers EC, Marder W, Cagnoli P, et al. Population-based incidence and prevalence of systemic lupus erythematosus: the Michigan Lupus Epidemiology and Surveillance program. Arthritis Rheumatol. 2014;66(2):369-378. doi:10.1002/art.38238
  • Ramos PS, Shedlock AM, Langefeld CD. Genetics of autoimmune diseases: insights from population genetics. J Hum Genet. 2015;60(11):657-664. doi:10.1038/jhg.2015.94
  • Dinse GE, Parks CG, Weinberg CR, et al. Increasing prevalence of antinuclear antibodies in the United States. Arthritis Rheumatol. 2020;72(6):1026-1035. doi:10.1002/art.41214
  • American College of Rheumatology. Antinuclear antibodies (ANA). Updated March 2019. Accessed August 20, 2020.
  • Aringer M, Costenbader K, Daikh D, et al. 2019 European League Against Rheumatism/American College of Rheumatology classification criteria for systemic lupus erythematosus. Ann Rheum Dis. 2019;78(9):1151-1159. doi:10.1136/annrheumdis-2018-214819
  • Rösken GHJ, van Beek AA, Bakker-Jonges LE, Schreurs MWJ. Antinuclear antibodies in systemic autoimmune disease. Ned Tijdschr Geneeskd. 2020;164:D4066.
  • Pérez D, Gilburd B, Cabrera-Marante Ó, et al. Predictive autoimmunity using autoantibodies: screening for anti-nuclear antibodies. Clin Chem Lab Med. 2018;56(10):1771-1777. doi:10.1515/cclm-2017-0241
  • Bloch DB. Patient education: antinuclear antibodies (ANA) (beyond the basics). UpToDate. Updated December 18, 2019. Accessed August 28, 2020.
  • Tan EM, Feltkamp TE, Smolen JS, et al. Range of antinuclear antibodies in “healthy” individuals. Arthritis Rheum. 1997;40(9):1601-1611. doi:10.1002/art.1780400909
  • Lyons R, Narain S, Nichols C, Satoh M, Reeves WH. Effective use of autoantibody tests in the diagnosis of systemic autoimmune disease. Ann N Y Acad Sci. 2005;1050:217-228. doi:10.1196/annals.1313.023
  • Nancy AL, Yehuda S. Prediction and prevention of autoimmune skin disorders. Arch Dermatol Res. 2009;301(1):57-64. doi:10.1007/s00403-008-0889-3
  • Ramos-Remus C, Castillo-Ortiz JD, Aguilar-Lozano L, et al. Autoantibodies in prediction of the development of rheumatoid arthritis among healthy relatives of patients with the disease. Arthritis Rheumatol. 2015;67(11):2837-2844. doi:10.1002/art.39297
  • Rakieh C, Nam JL, Hunt L, et al. Predicting the development of clinical arthritis in anti-CCP positive individuals with non-specific musculoskeletal symptoms: a prospective observational cohort study. Ann Rheum Dis. 2015;74(9):1659-1666. doi:10.1136/annrheumdis-2014-205227
  • Rose NR. Prediction and prevention of autoimmune disease in the 21st century: a review and preview. Am J Epidemiol. 2016;183(5):403-406. doi:10.1093/aje/kwv292
  • Choi MY, Fritzler MJ. Autoantibodies in SLE: prediction and the pvalue matrix. Lupus. 2019;28(11):1285-1293. doi:10.1177/0961203319868531
  • Mu Q, Kirby J, Reilly CM, Luo XM. Leaky gut as a danger signal for autoimmune diseases. Front Immunol. 2017;8:598. doi:10.3389/fimmu.2017.00598