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Autoimmune Disease: Sarcoidosis

Introduction

Sarcoidosis is a disease that is characterized by abnormal development and the gathering of chronic inflammatory cells. These cells develop into nodules that collect in a variety of organs. The syndrome is also referred to as sarcoid or Basnier-Boeck-Schaumann. The disease is common in various parts of the world. However, it mainly affects young people between the age of 20 and 29.

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The syndrome is also very prevalent in women above the age of 50. The disease has been spotted in various places across the world with a 16.5 average prevalence in every 100,000 men. It is also in the record that, in every 100,000 women in the world, 19 women have the syndrome. However, the prevalence of the disease is higher in Northern Europe, which has a rating of 60 patients in every 100,000, for example in Iceland and Sweden. Out of all the diagnosed patients, only 50% have relapses while 10% of them are likely to have disabilities. Baughman, Culver, and Judson (2011, p.573) assert that the syndrome may cause serious scars on the lungs, which may eventually lead to death that results from a failure of the respiratory system. Although the symptoms of sarcoidosis may vary over the years, the disease has been attributed to the immune reaction of the body, especially after an infection.

Signs and symptoms of the disease and its occurrence

Sarcoidosis disease is mainly characterized by inflammation of various parts of the body. Askari (2009, p. 567) affirms that the major symptoms of the diseases include fatigue that is not even relieved by sleeping, arthritis, swollen knees, loss of weight, skin lesion, blurred vision, and dry cough. All these symptoms are likely to be vague. The most visible symptoms are those that affect the cuticle such as rashes, nodules, erythema nodosum, lupus pernio, and granuloma annulare. Sometimes, it becomes difficult to diagnose cancer and Sarcoids since the two diseases may have almost similar symptoms. Doughan and Williams (2006, p.282) reveal how the symptoms may be manifested through the infection of the liver, heart, or brain. In some incidences, the patient may develop Lofgren syndrome, which results from a combination of various symptoms such as hilar lymphadenopathy, erythema nodosum, and arthralgia. Infection of the lungs is characterized by localization of the pulmonary tissues with 50% of the patients having permanent damage of the tissues while 5-15 % of them develop lung fibrosis. The infection is physically manifested by dry rales. Askari (2009, p. 567) affirms that liver infection has been associated with sarcoids at a 60-90% rate. Patients develop hepatomegaly due to liver infection. The patients also indicate increased alkaline phosphates. The skin of the patient is also affected in about 25% of the cases. Skin infection is manifested through erythema nodosum, maculopapular eruptions, lupus pernio, and plaques. However, Rossman and Kreider (2007, p.453) observe that skin lesions last for a few weeks and that they may not necessarily require treatment. Infection of the eyes is indicated by uveoparotitis, swelling of the retina, and uveitis. The patient experiences blurred vision in acute cases. He or she may lose sight. Sarcoids also affect the blood of the patient. There is an abnormal diagnosis of the blood such as anemia, which occurs in 4-20%, leukopenia in about 40%, and hypercalcemia in less than 10% of the patients. Infection of the lymph nodes is prevalent in sarcoids. The disease is manifested on the head and neck through cervical lymphadenopathy. Sarcoids can affect all parts of the nervous system. Rossman and Kreider (2007, p.453) assert that, when the brain nerves are affected, the condition is regarded as neurosarcoidosis. It occurs in about 5% of cases. The patient may also show hearing loss and optic nerve dysfunction. In serious cases, the infection results in meningitis. Sarcoids can also be manifested in the exocrine glands. This condition is manifested through enlargement of the parotid gland in 10% of the patients. Sarcoidosis also affects the scalp. The symptoms are manifested on the scalp through loss of hair.

There is no known precise cause of sarcoidosis disease. However, the most followed hypothesis is that sarcoidosis is caused by an alteration in the immune system especially after there has been exposure to pathogens.

Moreover, there is no clear genetic predisposition to sarcoidosis disease. However, although no genetic marker has been confirmed, various genes have been associated with sarcoids. For example, BTNL2 and HLA-DR alleles are associated with sarcoids. In addition, when sarcoid is very persistent, there is a likelihood that HLA and B7-DR15 work together. On the other hand, if the disease is not persistent, HLADR3-DQ2 is in control. The siblings of sarcoidosis patients have a 5-6 danger ratio of inheriting the disease. It is therefore argued that the role of genes in spreading the sarcoids is very low. Heredity of the syndrome can be linked to the fact that members of the same family are likely to be brought up in the same environment.

Relationship of sarcoidosis with the immune system and the components of the immune system

Sarcoidosis is mainly manifested through inflammation or granulomatous. The infection invades the body’s defense mechanism making the body unable to defend itself. Inflammation of various body parts results from the gathering of monocytes, active T-lymphocytes, and macrophages. These cells have very high inflammatory mediators. The IFN-gamma, IL-12, and TNF-alpha cells are also affected. Sarcoidosis suppresses the immunity of the body against tuberculin and suchlike infections. Contrary to the norm of many infections, sarcoidosis does not negatively affect defense cells but rather increases their production rate. Baughman, Culver, and Judson (2011, p.573) assert that sarcoidosis increases the number of macrophages and activation of CD4 aiding T-cell. This increase results in increased inflammation of various organs of the body. The infection develops a condition where the body is in dire need of energy since there is both hyper-reactivity and hypo-reactivity of the body. Perhaps these increased energy levels result in body infections and cancer. The body experiences challenges in regulating the antigens. The secretion of IL-2 is suppressed by the T-lymphocytes, which regulate the secretion along with the granulomas of sarcoid. The suppressed IL-2 cells are responsible for controlling and regulating the memory of antigens in ensuring that it is very specific. The granuloma contains Langhans cells that contain calcium and proteins. In-patients of sarcoid glanulomas are mainly found in schaumann bodies. The TNF-alpha cells aid the creation of granulomas. Lymphocytes and leucocytes are therefore affected. The production of these defense cells, therefore, becomes uncontrolled. The cells are produced in very huge quantities, thus making the body unable to control them. Out of the increased and uncontrolled production of these cells, body inflammations are witnessed.

Treatments and vaccines available for the disease

Diagnosis of sarcoidosis is made through the exclusion method. Doughan and Williams (2006, p.282) observe that medics use X-ray, PET scan, CT scan, lung biopsy, endobronchial ultrasound, mediastinoscopy, and endoscopic ultrasound in diagnosing sarcoidosis using exclusion. The collected tissue from the lymph nodes is screened for cancer, fungi, and other strains of microorganisms. Physicians also use angiotensin enzymes converters. These enzymes control the blood levels in sarcoidosis patients. Angiotensin-converters are also used in monitoring the progress of sarcoidosis patients. The process of diagnosis may involve all body organs since doctors carry out the elimination method to arrive at the symptoms of the disease. The doctor has to differentiate sarcoidosis from lymphoma, rheumatoid nodules, varicella infection, metastatic, and other related infections. For instance, Grunewald, Eklund, and Olerup (2004, p.696) observe that sarcoidosis can easily be confused with diseases such as lymphoma among others, which have almost similar characteristics. Such characteristics include a single-nucleated cell that causes inflammation of the granulomatous. It is also recommended that doctors closely examine the thyroid gland in female patients because sarcoidosis in female patients manifests itself in thyroid diseases such as hyperthyroidism and hypothyroidism. The infundibulum is also enveloped in sarcoid patients. It is also advisable to check whether the disease wraps the small lobes on the front parts. Rossman and Kreider (2007, p.457) assert that sarcoidosis is also manifested by clear lesions from vermin and from the ventricles.

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In treating sarcoidosis, not every patient will need therapy. For example, about 30-70% of patients with this disease do not require immediate therapy. Treatment becomes very necessary and urgent in cases where patients’ lungs are impaired. It is only when symptoms refuse to decrease in severity that the patient is put on therapy. Sarcoidosis is normally treated using corticosteroids. In modern-day medicine, doctors prefer prednisolone corticosteroids in the treatment of sarcoidosis. Treatment of sarcoidosis has been very effective with the use of corticosteroids. However, Grunewald, Eklund, and Olerup (2004, p.696) argue that some sarcoidosis patients are resistant to any steroids and steroid medicine. It may be difficult to use corticosteroids in sarcoidosis patients with mild symptoms since the disease is manifested spontaneously. Medics also recommend that corticosteroids be used only in cases where the case is very progressive to the level of threatening the existence of an organ. Steroids have many side effects that can negatively influence the patient’s health.

In case the disease has reached a severe point, physicians treat it with azathioprine and/or methotrexate. However, some doctors also use cyclophosphamide in treating the disease. Various immunosuppressants have been used in treating sarcoidosis. This kind of treatment is informed by the fact that the granulomas that result in the gathering of various cells of the immunity system, for example, the T-cells, have been associated with causing the disease. Such immunosuppressants include antitumor necrosis factor-alpha and interleukin-2. However, the use of immunosuppressants has not proved to be effective in treating sarcoids. On the contrary, its side effects can be devastating since it can result in the reactivation of tuberculosis. The impact of latent tuberculosis in sarcoidosis patients may be fatal. According to Antonelli et al. (2006, p 526), since sarcoidosis affects various body organs, patient follow-up should be done using an electrocardiogram, liver tests, eye examinations, and blood tests. There is also the constant need for serum calcium tests and urine calcium tests. Such tests will act as indicators of whether these organs are functioning properly. If the organs have been affected by the infection, the physician should treat the specific organ as the patient continues with therapy.

Reference List

Antonelli, A., Fazzi, P., Fallahi, P., Ferrari, M., & Ferrannini, E. (2006). Prevalence of hypothyroidism and Graves disease in sarcoidosis. Chest, 130(2), 526–32.

Askari, A. (2009). A middle-aged man with progressive fatigue. Cleveland Clinic journal of medicine, 76(10): 564–574.

Baughman, P., Culver, A., & Judson, A. (2011). A concise review of pulmonary sarcoidosis. American journal of respiratory and critical care medicine, 183(5), 573–81.

Doughan, A., & Williams, B. (2006). Cardiac sarcoidosis. Heart British Cardiac Society, 92(2), 282–288.

Grunewald, J., Eklund, A., & Olerup, O. (2004). Human leukocyte antigen class I alleles and the disease course in sarcoidosis patients. Am. J. Respir. Crit. Care Med., 169(6), 696–702.

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Rossman, D., & Kreider, E. (2007). Lesson learned from ACCESS (A Case Controlled Etiologic Study of Sarcoidosis). Proc Am Thorac Soc, 4(5), 453–60303.

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