Sarcoidosis


Article Author:
Syed Rizwan Bokhari
Hassam Zulfiqar


Article Editor:
Abeera Mansur


Editors In Chief:
Juan Batlle
Jitendra Sisodia
Jeffrey Miller


Managing Editors:
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Frank Smeeks
Kristina Soman-Faulkner
Benjamin Eovaldi
Radia Jamil
Sobhan Daneshfar
Saad Nazir
William Gossman
Pritesh Sheth
Hassam Zulfiqar
Navid Mahabadi
Steve Bhimji
John Shell
Matthew Varacallo
Ahmad Malik
Mark Pellegrini
James Hughes
Beata Beatty
Hajira Basit
Phillip Hynes


Updated:
6/6/2019 2:07:51 PM

Introduction

Sarcoidosis is a multisystem disorder of unknown etiology that mostly affect young adults worldwide and presents with noncaseating granulomas in various organs. Characteristically it presents with bilateral hilar lymphadenopathy and reticular opacities in lungs. Other major involved sites include skin, eyes, and joints, although it can express to a variable degree in the musculoskeletal system, reticuloendothelial system, exocrine glands, heart, kidney, and central nervous system.[1][2][3]

Etiology

It is an inflammatory disease of unknown etiology that manifests as noncaseating granulomas in multiple systems. Various associations have been described, including occupational and environmental exposures to beryllium, dust, and other agents causing asthma. Various microorganisms like mycobacteria and propionibacteria have been associated. Possible infective etiology has been described in few studies where sarcoidosis developed in a previously negative individual after cardiac or bone marrow transplantation.[4][5]

Genetic component and disease in more than one family member are usually related with antigens of the major histocompatibility complex (MHC), especially DR alleles. Few studies have described other less common genomes and angiotensin converting enzyme genotypes in few patients.

Cytokines including Th1, IL-2, IL6, IL 8, IL12, IL 18, IL 27, and interferon (IFN) gamma, and tumor necrosis factor (TNF) alpha are closely associated with sarcoidosis. Few of these are implicated in granuloma formation with macrophage and epithelioid accumulation, activation, and aggregation. Some of these Interleukins are believed to act as disease modifiers.

Epidemiology

The incidence is 11 cases per 100,000 population in whites but 34 cases per 100,000 population in African Americans with a lifetime risk of 2.4 percent in the USA. Extrapulmonary sarcoid is seen in up to 25 to 30 percent of patients. Cardiac involvement is seen more commonly in males while skin and eye features are more prominent in women. Extrapulmonary features can be different in terms of age of presentation, gender, and ethnicity.[6][7]

Pathophysiology

Pathogenesis of cutaneous sarcoidosis is poorly understood and attributable to both genetic and environmental factors. Key role in the development of sarcoidosis is played by T cells as they promote cellular immune reaction and usually associated with an inverted CD4/CD8 ratio. It is well characterized by noncaseating granuloma typically containing macrophages, multinucleated giant cells and epithelioid cells, in addition to lymphocytes, monocytes, mast cells, and fibroblasts  There is a role of tumor necrosis factor (TNF) and TNF receptors, both are increased in this disease.  This has been explained by the role of anti-TNF agents, such as pentoxifylline and infliximab. In addition to T cells role, B cell hyperreactivity with immunoglobulin production is implicated as well. Active sarcoidosis has also been associated with plasmatic hypergammaglobulinemia. Angiotensin-converting enzyme (ACE) levels correlated with elevated Soluble HLA class I antigens levels in serum.[8]

Histopathology

Biopsy of lymph nodes will reveal non-caseating granulomas.

History and Physical

Symptoms are variable; typically patients present with persistent dry cough, fatigue, and shortness of breath. Other symptoms include painful red lumps on the skin, uveitis with the blurring of vision, hoarseness of voice, palpable lymph nodes at multiple sites including armpit, neck, painful swollen joints, hearing loss, seizures, or psychiatric disorders could be observed as part of neurological manifestations. Cardiomyopathy, conduction defects, renal calculi and enlarged liver are observed in few cases.

A wide range of cutaneous manifestations can be classified as papular, maculopapular, nodular, subcutaneous, hypopigmented and plaque sarcoidosis. Most common lesions in cutaneous sarcoidosis are Papular sarcoidosis involving the upper half of face, back of neck and previous trauma /scar sites and tattoos A variant of cutaneous sarcoidosis that presents with violaceous or erythematous papules, plaques, or nodules mainly involving the central facial skin is called lupus pernio. Other well-described skin manifestations of sarcoidosis include nodular sarcoidosis. Plaque-like lesions and subcutaneous nontender nodules are also commonly seen.

Erythema nodosum (EN) is seen in a variety of other conditions including sarcoidosis and usually presents with painful nodules on shins. It is characterized as panniculitis and is a part of Lofgren syndrome. Skin lesions can appear up to 10 or more years after the initial injury or tattoo.

Evaluation

Lab tests:

  • Complete blood count and differential looking for anemia, leukopenia nd thrombocytopenia, liver function tests, blood urea nitrogen, creatinine, glucose, electrolytes, serum calcium looking for hypercalcemia. ESR and c-reactive protein are nonspecific tests, often elevated.
  • Elevated serum alkaline phosphatase concentration suggests diffuse granulomatous hepatic involvement.
  • Serologic tests including serum angiotensin converting enzyme (ACE), adenosine deaminase, serum amyloid A, and soluble interleukin-2 receptor can be considered.
  • Kveim test is similar to tuberculin skin test and evokes a sarcoid granulomatous response. It is of limited significance.

Radiographic tests:

  • Lungs are the main site of involvement; imaging tests include chest radiograph, CT Chest, fluorine-18-fluorodeoxyglucose-positron emission tomography (FDG-PET), gallium-67, thallium-201, technetium sestamibi (MIBI-Tc) and single photon emission computed tomography (SPECT).
  • Cardiac or CNS affected sarcoidosis is better diagnosed with the help of MRI or PET scan.

Radiographic stages are as follows:

  • Stage I: Presence of bilateral hilar adenopathy
  • Stage II: Bilateral hilar adenopathy and reticular opacities
  • Stage III: Reticular opacities with shrinking hilar nodes ( mainly infiltrates)
  • Stage IV: Reticular opacities with Fibrosis

In the case of clear chest X-ray in a patient with unexplained dyspnea or a cough, (HRCT) of the chest should be considered.

Histopathology: characteristically noncaseating granulomas, with aggregates of epithelioid histiocytes, giant cells, and mature macrophages are seen.

In order to rule out systemic disease, pulmonary function test, electrocardiogram, echocardiography, urinalysis and tuberculin skin testing should be considered.

Follow-up of pulmonary disease can be done with pulmonary function tests and a carbon monoxide diffusion capacity test of the lungs for carbon monoxide (DLCO).[9][10][11]

Treatment / Management

Pulmonary sarcoidosis is often asymptomatic, non-progressive disease and requires no treatment, as a majority of patients undergo spontaneous remission. Close monitoring of symptoms, chest radiograph, and pulmonary function is continued at three to six-month intervals should be considered in asymptomatic patients. Patients with pulmonary sarcoidosis causing worsening symptoms, stage II-III radiographic findings should be considered for oral glucocorticoids at 0.3 to 0.6 mg/kg for 4 to 6 weeks.  If there is no improvement in symptoms, radiographic abnormalities, and pulmonary function tests, steroids may be continued for additional four to six weeks. Maintainance steroids are not needed, steroid tapering to a dose of 0.25 to 0.5mg/kg (usually 10 to 20 mg) per day, should be considered over a period of at least six to eight months. Methotrexate, azathioprine, infliximab, leflunomide, and antimalarial agents may be considered as steroid-sparing agents in patients who are unable to tolerate steroids.[12][13]

Differential Diagnosis

  • Tuberculosis
  • Cat scratch disease
  • Lung cancer
  • Lymphoma
  • Occupational lung disease
  • Fungal infection

Enhancing Healthcare Team Outcomes

Sarcoidosis has no obvious cause and hence prevention is not possible. The disorder also resolves spontaneously and hence treatment is not always required. However, severe cases do need to follow up. The management of patients with sarcoidosis is best done in a multidisciplinary fashion with a team of healthcare workers that includes a cardiologist, neurologist, radiologist, pulmonologist, cardiac nurse, respiratory therapist and a pharmacist. The patient needs regular chest x-rays since it is a marker for disease progression. Some patients may benefit from pulmonary rehabilitation and use of bronchodilators. If the disease is advanced, a regular eye exam is important. In addition, the nurse should ensure that the patient gets a regular 12-lead ECG because heart block is not uncommon. The pharmacist should educate the patient on the importance of discontinuing smoking and abstaining from alcohol. Finally, patients who are managed with steroids should be educated about the side effects of these drugs. [14][15](Level V)

Outcomes

In many patients with sarcoidosis. No treatment is required and the disorder spontaneously resolves. However, in a certain number of people, the disease may take a fulminant course with severe symptoms. Factors that indicate a poor prognosis include significant chest imaging findings, extrapulmonary involvement and presence of pulmonary hypertension. Many studies indicate that the chest x-ray is an excellent marker for disease prognosis. In severe cases, patients may require oxygen, experience heart block and respiratory failure. Data regarding mortality are not available because in many cases long-term follow up is missing. Overall, it appears that about one-fifth of patients develop functional impairment and there is a mortality rate of 3-5% in patients who are not treated. The highest mortality rates are in African American females past the fifth decade of life. [16][17](Level V)


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Sarcoidosis - Questions

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A 33-year-old African American female presents with a dry cough of 3 months duration. X-rays reveal bilateral mediastinal adenopathy. Biopsy reveals non-caseating granulomas in the lymph nodes. What is the most probable diagnosis?



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An african american female with a chronic cough presents with symmetrical bilateral hilar adenopathy. What is the likely diagnosis?



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A young black female has been referred to you because of bilateral hilar adenopathy due to a suspected granulomatous disease. Which of the following is not true of this disorder?



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What is the most common cause of death in sarcoid patients?



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Which of the following is a classic finding in a patient with sarcoidosis?

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How is sarcoidosis diagnosed?



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A patient with symptomatic pulmonary sarcoidosis is referred to discuss treatment options. Which of the following is the most appropriate initial option to prevent pulmonary fibrosis?



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What is the most important marker for prognosis in patients with sarcoidosis?



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What causes the hypercalcemia in a patient with sarcoidosis?



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A 17-year-old African American female is found to have bilateral hilar adenopathy, chronic dry cough, and uveitis. What is the likely diagnosis?



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What peptide is elevated in sarcoidosis?



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A 17-year-old African-American female presents with a dry cough, mild shortness of breath, and hilar adenopathy. She denies recent travel or illicit drug use. Biopsy of the mediastinal nodes reveals non-caseating granulomas that are negative for acid-fast bacteria, and there are no Reed-Sternberg cells. She most likely has which condition?



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A young African-American female is sent for evaluation to rule out sarcoid. Her chest x-ray reveals bilateral hilar adenopathy with upper-lobe predominant parenchymal disease. What is the diagnostic procedure that has the highest diagnostic yield for this condition?



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In a young black female with suspected sarcoidosis, which of the following tests should be used first?



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A 33-year-old African American female is found to have bilateral hilar adenopathy, dry cough, and uveitis. What is the most likely diagnosis?



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An African-American woman has recently been diagnosed with sarcoidosis. Which of the following is true regarding her disease process?



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A 36-year-old African American man presents to an otolaryngologist with the chief complaint of daily epistaxis and nasal congestion. He has an external nasal deformity and a large anterior nasal septal perforation. He has no history of surgery or trauma. A preoperative chest x-ray film reveals perihilar adenopathy. What is the best course of action?



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What test should be ordered to diagnose a young African American male who presents complaining of joint pain and cough who is found to have a violet rash on his cheeks and nose and hilar adenopathy on chest x-ray?



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In a patient with sarcoid, the hallmark histological finding of the biopsy specimen will reveal?



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What percentage of patients with sarcoidosis will at some point show adenopathy on chest radiography?



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A muscle and node biopsy is done on a 45-year-old female who has been experiencing progressive weakness. The biopsy reveals non-caseating granulomas and inflammation. What is the most likely diagnosis?



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What test should be ordered to diagnose an African American male who presents complaining of joint pain and cough who is found to have a violet rash on his cheeks and nose and hilar adenopathy on chest x-ray?



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Which organ system is frequently affected by sarcoidosis?



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Which is true of sarcoidosis?



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A 32 year old black female has bilateral hilar lymphadenopathy and lung parenchymal abnormalities. Non-caseating granulomas are found on biopsy. Silver, acid fast, and PAS stains are all negative. Select the most probable diagnosis.



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Which of the following is the least common complication of sarcoidosis?



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Which of the following is not seen in patients with sarcoidosis?



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A 35 year old African American female with a history of sarcoidosis is brought to the emergency department with nausea and confusion. Her family reports that she has been drinking and urinating much more than usual. Physical exam shows dry mucous membranes and orthostasis. Glucose is 85 mg/dL. ECG shows bradycardia and shortened QT interval. What is the most likely explanation of the patient's findings?



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A patient with sarcoidosis develops mental status changes and is found to have serum calcium of 12.2 mg/dL. Which of the following would not be an appropriate intervention?



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A 32-year-old African-American female is found to have bilateral hilar lymphadenopathy incidentally on a chest x-ray. She has no symptoms. Past medical history, physical exam, and labs are normal. CT of the chest shows no further abnormalities. Mediastinoscopy biopsy shows noncaseating granulomas. Select appropriate treatment.



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Which of the following is true regarding sarcoidosis?



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Which of the following is correct regarding the clinical staging of sarcoidosis?



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A 30-year-old female is diagnosed with myopathy based on clinical findings and elevated creatine phosphokinase. Muscle biopsy shows noncaseating granulomas. What is the most likely cause of the myositis?



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Which of the following features is characteristic of sarcoidosis?



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Which of the following electrolyte abnormalities is common in patients with sarcoidosis?



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Which of the following best defines Stage II sarcoidosis?



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Which of the following is the most commonly involved organ in sarcoidosis?



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Which condition causes non-caseating granulomas?



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A patient is suspected of having sarcoidosis. What is the next step for a definitive diagnosis?



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A 32-year-old black female with sarcoidosis reports polyuria which is found to be secondary to the sarcoidosis. Which of the following is most likely true?



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An African American female comes to the emergency room with facial weakness. The right side started yesterday and the left side today. She has had no constitutional symptoms or rashes. She lives in Chicago and has no pets. She is employed in an office and has no hobbies with exposures to chemicals. She has hypertension and is on hydrochlorothiazide. Blood pressure is 130/85 mm Hg, pulse is 85, respirations 16, and she is afebrile. The right side of the face is paralyzed, but she can raise her eyebrow on the left. Chest radiograph has bilateral hilar lymphadenopathy. MRI with gadolinium show enhancement of the seventh cranial nerve and meninges bilaterally. Lumbar puncture yields CSF with an opening pressure of 12 cm H2O, with no red cells, 21 white cells with 82% lymphocytes and 28 percent neutrophils, protein 72 mg/dL, and glucose 62 mg/dL. Gram stain is negative. Select the most likely diagnosis.



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Which of the following tests would be the most definitive in making a sarcoidosis diagnosis?



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Which of the following statements is true regarding the association of sarcoidosis and the spinal cord?



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What disease process can cause bilateral calcified mediastinal lymphadenopathy?



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What percent of sarcoidosis is associated with bilateral hilar adenopathy?



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What happens to the lungs in patients with sarcoidosis?



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Sarcoidosis can involve the abdomen, and can be seen in the following organs except which of the following?



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A 33-year-old woman presented with complaints of bilateral, painful red eyes, joint pains, myalgia, and renal dysfunction. She was referred with the following labs: hemoglobin 10.3 mg/dl (11.5-16.5), white cell count 8 (4.0-11.0), eosinophil count 0.70 (0.04-0.40), serum urea 76 mg/dl, serum creatinine 1.8 mg/dl, ANA negative, anti DsDNA negative, 24-hour urinary total protein 0.9 g (<0.2), urinalysis showed 2+ protein, renal biopsy showed normal looking glomeruli along with interstitial lymphocytic infiltrate, occasional granuloma, and eosinophils. What is the most likely diagnosis?



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A 40-year-old black engineer presents with enlarged hilar lymph nodes, hepatosplenomegaly and hypercalcemia. The most probable diagnosis is:



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A 40-year old presents with complaints of fever, muscle pain, dyspnea, and a cough that has been going on for a few months. The patient denies any recent travel, use of drugs, smoking, or any other illness. The patient had a negative tuberculin skin test a few days ago. The patient has erythema nodosum on both extremities and crackles on auscultation; the rest of the exam is normal. A chest x-ray reveals bilateral hilar adenopathy. Urine analysis reveals hypercalciuria. Which of the following may also be elevated?



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Sarcoidosis - References

References

Ma Y,Gal A,Koss M, Reprint of: The pathology of pulmonary sarcoidosis: update. Seminars in diagnostic pathology. 2018 Sep 24     [PubMed]
Landi C,Carleo A,Cillis G,Rottoli P, Sarcoidosis: proteomics and new perspectives for improving personalized medicine. Expert review of proteomics. 2018 Sep 25     [PubMed]
Petek BJ,Rosenthal DG,Patton KK,Behnia S,Keller JM,Collins BF,Cheng RK,Ho LA,Bravo PE,Mikacenic C,Raghu G, Cardiac sarcoidosis: Diagnosis confirmation by bronchoalveolar lavage and lung biopsy. Respiratory medicine. 2018 Sep 16     [PubMed]
Møller J,Hellmund V,Hilberg O,Løkke A, [Sarcoidosis]. Ugeskrift for laeger. 2018 Aug 20     [PubMed]
Sohn DW,Park JB,Lee SP,Kim HK,Kim YJ, Viewpoints in the Diagnosis and Treatment of Cardiac Sarcoidosis: Proposed Modification of Current Guidelines. Clinical cardiology. 2018 Aug 24     [PubMed]
Wills AB,Adjemian JA,Fontana JR,Steiner CA,Daniel-Wayman S,Olivier KN,Prevots DR, Sarcoidosis-Associated Hospitalizations in the United States, 2002-2012. Annals of the American Thoracic Society. 2018 Sep 10     [PubMed]
Yoon HY,Kim HM,Kim YJ,Song JW, Prevalence and incidence of sarcoidosis in Korea: a nationwide population-based study. Respiratory research. 2018 Aug 28     [PubMed]
Celada LJ,Kropski JA,Herazo-Maya JD,Luo W,Creecy A,Abad AT,Chioma OS,Lee G,Hassell NE,Shaginurova GI,Wang Y,Johnson JE,Kerrigan A,Mason WR,Baughman RP,Ayers GD,Bernard GR,Culver DA,Montgomery CG,Maher TM,Molyneaux PL,Noth I,Mutsaers SE,Prele CM,Stokes Peebles R Jr,Newcomb DC,Kaminski N,Blackwell TS,Van Kaer L,Drake WP, PD-1 up-regulation on CD4{sup} {/sup} T cells promotes pulmonary fibrosis through STAT3-mediated IL-17A and TGF-β1 production. Science translational medicine. 2018 Sep 26     [PubMed]
Shimada S,Furusawa H,Ishikawa T,Kamakura E,Suzuki T,Watanabe Y,Fujiwara T,Tominaga S,Komatsuzaki KM,Natsume I, Development of mediastinal adenitis six weeks after endobronchial ultrasound-guided transbronchial needle aspiration. Respiratory medicine case reports. 2018     [PubMed]
Kobak S,Yildiz F,Semiz H,Orman M, Elderly-onset Sarcoidosis: A Single Center Comparative Study. Reumatologia clinica. 2018 Jul 24     [PubMed]
Niederer RL,Al-Janabi A,Lightman SL,Tomkins-Netzer O, Serum Angiotensin-Converting Enzyme Has a High Negative Predictive Value in the Investigation for Systemic Sarcoidosis. American journal of ophthalmology. 2018 Oct     [PubMed]
Płusa T, [Advances in differential diagnosis and treatment of patients with sarcoidosis]. Polski merkuriusz lekarski : organ Polskiego Towarzystwa Lekarskiego. 2018 Mar 27     [PubMed]
West SG, Current management of sarcoidosis I: pulmonary, cardiac, and neurologic manifestations. Current opinion in rheumatology. 2018 May     [PubMed]
Dubaniewicz A, [The diagnostic algorithm of practice in pulmonary and extrapulmonary sarcoidosis]. Polski merkuriusz lekarski : organ Polskiego Towarzystwa Lekarskiego. 2018 Mar 27     [PubMed]
Matsou A,Tsaousis KT, Management of chronic ocular sarcoidosis: challenges and solutions. Clinical ophthalmology (Auckland, N.Z.). 2018     [PubMed]
Salama A,Abdullah A,Wahab A,Eigbire G,Hoefen R,Alweis R, Cardiac sarcoidosis and ventricular arrhythmias. A rare association of a rare disease. A retrospective cohort study from the National Inpatient Sample and current evidence for management. Cardiology journal. 2018 Sep 20     [PubMed]
Jachiet V,Lhote R,Rufat P,Pha M,Haroche J,Crozier S,Dupel-Potier C,Psimaras D,Amoura Z,Cohen Aubart F, Clinical, imaging, and histological presentations and outcomes of stroke related to sarcoidosis. Journal of neurology. 2018 Oct     [PubMed]

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