Sarcoidosis is a multisystem granulomatous disorder of unknown etiology characterized by non-caseating granulomas. It most commonly affects the lungs presenting as bilateral hilar lymphadenopathy and pulmonary infiltrates. Extrapulmonary involvement can include the skin, eyes, liver and musculoskeletal system. Diagnosis involves clinical features and exclusion of other causes. Treatment involves corticosteroids while prognosis depends on organ involvement with lung fibrosis carrying the worst prognosis.

1. SARCOIDOSIS
PRESENTOR
• Dr PRITI

2. CONTENTS
• HISTORY AND EPIDEMIOLOGY
• RISK FACTORS
• PATHOLOGY
• CLINICAL FEATURES
• DIAGNOSIS
• TREATMENT
• PROGNOSIS AND MORTALITY

3. SYNONYMS
Besnier Boeck Disease
Schaumann's syndrome

4. INTRODUCTION
• Multisystem non-caseous granulomatous disorder
of unknown aetiology
• Characterized by depression of cutaneous delayed
type hypersenstivity and heightened Th1 immune
response in affected organs.
• Most commonly affecting young adults
• Presenting most frequently with bilateral hilar
lymphadenopathy, pulmonary infiltration and skin
or eye lesions.

5. EPIDEMIOLOGY
• Occurs worldwide
• Highest incidence - United States and
Sweden.
• Lower - Asian
• Prevalence - 10 and 40 cases per 100,000
• Mortality - 1 to 5 percent

6. • Environmental exposures - winter and early
spring months
• Geographic variation and time–space clustering
• Occupational association- health care
professionals,firefighters, military personnel.

7. • Age : 20-40 yr
• Sex : female ; bimodal
• 16 times more common in blacks
• Genetic influence
monozygotic : dizygotic twins (13: 1)

8. AETIOLOGY
• Unknown
• Exposure to pine pollen or beryllium
• Infection with Mycobacterium, viruses and
fungi
• protoplast or L form of the tubercle bacillus
may be a cause of sarcoidosis

9. ACCESS STUDY
• A Case Control Etiologic Study of Sarcoidosis
• 706 subjects
• Absence of occupational and environmental
association
• Weak assoc-insecticide;mold;musty odour
• No association-berylium;wood ;rural; smoking
• No single dominant factor
• Gene environmental factors

10. INFECTIONS
Mycobacterium DNA
• DNA studies :0-80%
• Control :0-30%
• Propionibacterium acne
• 80-98%
• Control 0-60%

11. • Borrelia
• Chlamydiae
• Rickettsiae
• Viruses : EBV,CMV,herpes 6
• High titres of these viruses may be reflect
generalised B cell activation in sarcoidosis

12. AUTOIMMUNITY
ANA,RF,hypergammaglobulinaemia
Molecular mimicry

13. BIOCHEMICAL EVIDENCE
• mKatG (mycobacterial catalase peroxidase
protein) -50% of patients

14. GENETICS
• STRONG EVIDENCE
• ACCESS STUDY
• Siblings are higher risk than parents
• More of mother-child than father-child
associations.

15. ROLE OF HLA
• HLAB 8 – most consistently associated.
• HLA-B1,B8, DR3- also associated with abnormal
immune responsiveness.
• DR1, DR 4 – protective.
• HLA-B8, DR3, Cw7 associated with good
prognosis in caucasians.
• Other alleles are associated with chronic disease,
favorable outcomes.

17. Non-HLA genes:
• TNF genes(polymorphisms associated
with 1.5 fold increased risk)
• CC chemokine receptors.
• ACE complement receptor 1.
• German study – Chromosome 6
• SAGA study – Chromosome 5

18. Non-HLA Candidate Genes Evaluated
in Sarcoidosis

19. PATHOGENESIS

21. • IL-12 contributes to proliferation of activated T
cells in early disease.
• Increased levels of IL-12 and IL-18 stimulate
IFN-gamma production.
• TGF-beta inhibits IL-12 and IFN-
gammadownregulation of granulomatous
inflammation in sarcoidosis.
• Elevated levels of IL-6 and IL-8 in BAL in active
sarcoidosis.

22. HISTOPATHOLOGY
• The pathologic hallmark is presence of non
caseating
epitheloid cell granuloma.
• Active sarcoidosis has nodular collections of large
closely packed, pale-staining histiocytes -
epithelioid cells with giant cells.
• Necrosis doesn’t occur.
• Electron microscopy showed that epitheloid cells
tend to be central and macrophages peripheral.
• As lesion ages, reticulin fibres between epitheloid
cells ramify and converted to collagen.

23. The cytoplasm of giant cells have inclusion bodies
1) Schaumann bodies- round or oval and vary in size from
that of a leucocyte to about 100μm in diameter.The larger
of these bodies ( conchoid bodies) seem to be formed of
basophilic concentric lamellae that appear to contain
calcium and iron
2) Doubly refractile crystalline inclusion bodies are 1–20 μm
in diameter and may take up stains for calcium and iron.
3) Asteroid bodies consist of a central mass 2.3–3μm in
diameter with radiating straight or centred spinous
projections, the whole being 5–25μm in diameter
4) Hamazaki wesenberg bodies.

26. DIFFERENCES BETWEEN GRANULOMA
OF TB and SARCOIDOSIS

27. Histological features of sarcoid lesionare
not specific. Can also be seen in
• tuberculosis
• leprosy
• tertiary syphilis
• brucellosis
• primary biliary cirrhosis
• hypogammaglobulinemia
• Brucellosis
• fungal infections.

30. CLINICAL PRESENTATION
Acute Sarcoidosis
• Lofgren's syndrome - acute erythema nodosum
with
bilateral hilar lymphadenopathy, fever, and
polyarthritis, non granulomatous uveitis
• Symptoms are typically abrupt in onset and have a
transient course.
• A vesicular or maculopapular rash, acute iritis,
conjunctivitis, and Bell's palsy may also be features
of acute disease

31. CHRONIC SARCOIDOSIS
• More gradual, insidious onset, is more likely to
develop chronic disease.
• Other risk factors for chronic disease include the
presence of lupus pernio, which is a persistent,
disfiguring, violaceous rash over the nose, cheeks,
and ears, and the presence of multiorgan involvement
at the time of diagnosis.
• Chronic eye involvement includes chronic uveitis,
cataracts, glaucoma, or keratoconjunctivitis sicca,which
can be confused with Sjogren's syndrome

33. Major Clinical Manifestations

35. LUNGS
First site involved
• Begins with alveolitis involving small bronchi
and small blood vessels
• Alveolitis either clears up spontaneously or
leads to granuloma and fibrosis.

36. Around 50% patients asymptomatic.
• Dry cough and dyspnoea
• Chest pain-rare
• Wheezing secondary to endobronchial disease,
extrinsic compression by lymphadenopathy or
bronchial distrortion secondary to fibrosis.
• Productive cough- traction bronchiectasis
• Hemoptysis- bronchiectasis or aspergilloma

39. RADIOGRAPHIC FEATURES
• Chest radiograph abnormal in 90% of sarcoidosis
patients.
• Bilateral hilar lymphadenopathy in 50-85%cases.
• Lymph nodes big and sharply defined with clear line
of transluscency between mediastinum and lymph
nodes- POTATO NODES.
• Unilateral lymphadenopathy- rare
• Pulmonary infiltrates in 25-60% cases

40. SCADDING STAGING SYSTEM
• Stage 0: Absence of radiographic abnormalities
• Stage I: Bilateral hilar and/or mediastinal adenopathy
without pulmonary parenchymal abnormalities
• Stage II: Hilar and/or mediastinal lymphadenopathy
with pulmonary parenchymal abnormalities (generally
a diffuse interstitial pattern)
• Stage III: Diffuse parenchymal disease with out nodal
enlargement
• Stage IV: Pulmonary fibrosis with evidence of volume
loss, cystic or honeycomb changes, bullae, emphysema.

41. • Radiographic staging of intrathoracic
sarcoidosis
• Staging also helps in prognosis.

43. Sarcoidosis stage I: left and right hilar
and paratracheal adenopathy
(1-2-3 sign)

45. STAGE I - Thoracic lymphadenopathy.
Normal lung parenchyma (50%)

46. STAGE II - Hilar and mediastinal
lymphadenopathy.
Abnormal lung parenchyma. ( 30% )

47. STAGE III - Abnormal lung parenchyma.
No lymphadenopathy( 15% )

48. Differential diagnosis of sarcoidosis
with pulmonary infiltrates
• Extrinsic Allergic alveolitis
• Fibrosing alveolitis
• Carcinomatous infiltration
• Pneumoconiosis
• Miliary tuberculosis
• Metastatic malignancy
• Alveolar cell carcinoma
• Honey comb lung.

49. STAGE IV-Extensive pulmonary fibrosis
is typically worst in the upper lobes

50. STAGE IV-Broad bands of fibrosis in the
upper lobes

51. ADENOPATHY AT TIME OF DIAGNOSIS
Marked enlarged hilar and mediastinal
lymph nodes

52. Radiographic abnormalities on chest x ray.
• 1) disseminated miliary lesions
• 2) disseminated nodular lesions
• 3) linear type of infiltration extending fan-wise from the hilum
• 4) diffuse and confluent patchy shadows;
• 5) diffuse fibrosis
• 6) diffuse fibrosis with cavitation
• 7) diffuse ground-glass shadowing
• 8) changes similar to chronic tuberculosis as regards location
and distribution
• 9) bilateral confluent massive opacities resembling areas of
pneumonia
• 10) atelectasis.

53. UNUSUAL
• “Egg shell” calcification of hilar nodes
• Pleural effusions
• Cavitations
• Atelectasis
• Pulmonary hypertension
• Pneumothorax
• Cardiomegaly

54. HRCT findings in Sarcoidosis.
• Common findings:
– Small nodules in a perilymphatic distribution
(i.e. along subpleural surface and fissures, along
interlobular septa and the peribronchovascular
bundle).
– Upper and middle zone predominance.
– Lymphadenopathy in left hilus, right hilus and
paratracheal (1-2-3 sign). Often with
calcifications.

57. SARCOIDOSIS: typical presentation

58. Uncommon findings:
– Conglomerate masses in a perihilar location.
– Larger nodules (> 1cm in diameter, in < 20%)
– Grouped nodules or coalescent nodules
surrounded by multiple satellite nodules (sarcoid
galaxy sign)
• Nodules so small and dense that they appear as
ground glass or even as consolidations (alveolar
sarcoidosis)
• Reverse halo sign

60. SARCOIDOSIS with fibrous tissue

61. GALLIUM 67 SCAN
• Gallium 67 concentrated in metabolically and mitotically
active tissues.
• Intravenous injection of 11X107 Bq of gallium 67 citrate,
simultaneous anterior and posterior scans performed 3 days
later.
• Close correlations between gallium uptake and total number
of lymphocytes recovered in BAL.
• Not specific for sarcoidosis.
• Expensive and radiation exposure.

62. the parotid, salivary and lacrimal gland
region (panda sign) is pathognomic for
sarcoidosis

64. Gallium scan
showing increased
uptake in the
lacrimal and parotid
glands and
pulmonary regions
in a patient with
active sarcoidosis

65. Other Intrathoracic Manifestations
Pleural invovlment in 5-10% cases.
( effusions and pleural thickening)
• Aspergilloma
• Bronchiectasis
• Necrotising sarcoid angitis
• Superior venacaval syndrome
• Mediastinal lymph node calcification
• Mediastinal fibrosis
• Vanishing lung syndrome (giant bulla)

66. Functional abnormalties
• Seen in 20%-40% in patients with normal chest x
ray and 50%-70% when x ray is visibly abnormal.
• Abnormalities in vital capacity, diffusion
capacity, PaO2 at rest, PaO2 at exercise and lung
compliance.
• Usually restrictive defect noted on PFT but
obstructive defect in endobronchial
involvement leading to airflow obstruction, also
from airway distortion secondary to lung fibrosis

67. EXTRAPULMONARY SARCOIDOSIS

68. UPPER RESPIRATORY TRACT
Uncommon but disabling.
• Nasal mucosa- crusting,obstruction, discharge. The
mucosa erythematous and granular with polypoid
hypertrophy.
• Laryngeal and pharyngeal mucosa- hoarseness,cough,
dysphagia,dypsnoea
• Patients with sarcoidosis of upper respiratory tract
have 50% chance of developing lupus pernio
• Nasal septal and palatal perforations in untreated
cases.
• d/d tuberculosis, wegeners granulomatosis, leprosy

69. KRESPI STAGING SYSTEM
• Stage I : mild nasal disease without paranasal sinus
disease. - saline nasal spray, nasal irrigation, and topical
nasal steroids.
• Stage II : moderate disease, with involvement of both
nasal and paranasal sinuses; it is typically treated with
both stage I therapy and intralesional steroids.
• Stage III : severe, often irreversible, nasal and sinus
disease that usually requires the therapeutic
interventions of stages I and II, as well as systemic
therapy.

70. LYMPHATIC SYSTEM
• Hilar and Mediastinal lymph nodes (>90% of
patients)
• Peripheral lymphadenopathy (5%–30%).
• Cervical, axillary, epitrochlear, and inguinal
regions.
• Non tender, mobile
• Of superficial nodes, right scalene group most
common

71. EYES
• Upto 25% of sarcoidosis patients ant uveitis most
common manifestation.
• Anterior uveitis - acutely, with pain, photophobia,
lacrimation, and redness, self limiting
• Posterior uveitis is typically gradual in onset and is
more likely to result in visual morbidity, chronic form of
disease.
• Chronic uveitis leads to glaucoma, cataracts and
blindness ,Keratoconjunctivitis sicca Papilledema
• 10% of patients with sarcoid-associated uveitis
develop blindness in at least one eye

72. CONJUNCTIVITIS

73. PAPILLEDEMA - Often associated with
7th nerve facial palsy

74. Multifocal choroiditis & candle waxy spots

75. Ocular Involvement - KPs as ‘mutton fat’ -
large and greasy facial palsy

76. SKIN
• Most common manifestation- erythema nodosum.
• Erythema nodosum typically presents as raised, tender, red
nodules, 1 to 2 cm in diameter, on the anterior surface of the
lower legs.
• Lupus pernio is a rare lesion,most severe dermatological
manifesation - purplish plaques typically found over the
nose, cheeks, lips, and ears. Associated with poor prognosis
and severe pulmonary disease.
• Skin abnormalities include red-brown to orange macules and
papules, keloids, and hyper- or hypopigmentation.

77. LOFGREN'S SYNDROME; acute triad of
erythema nodosum,polyartropathy, bilateral
hilar adenopathy and non granulomatous
uveitis

78. LUPUS PERNIO

79. LUPUS PERNIO
Indurated and violaceous range from a few
small lesions to large lesions

80. ERYTHEMA NODOSUM
These reddish raised lesions

81. PSORIASIS LIKE LESIONS
These small white lesions closely resemble
psoriasis

82. LIVER
• 33% have hepatomegaly or biochemical
evidence of disease
• Symptoms usually absent
• Cholestasis, fibrosis, cirrhosis, portal
hypertension, and the Budd-Chiari syndrome
have been seen

83. MUSCULOSKELETAL
• Bone involvement most commonly affects terminal
phalanges of hands and feet and proximal bones in
severe cases.
• Three types of bony lesions:
 Lytic
 Permeative
 Destructive
• Bone lesions not affected by corticosteroids

84. PUNCHED OUT LYTIC LESIONS
Focal osteolytic lesions in the fingers are
most common abnormality

85. SCLEROTIC LESIONS,NONSPECIFIC
Focal sclerosis (arrows) of distal phalanges
is unusual

86. • Subcutaneous swellings also noted along with
digit abnormalities but they respond to
corticosteroid therapy.
• Skeletal granulomas commonly affecting
pectoral,shoulder, arm and calf muscles

87. NERVOUS SYSTEM
• Peripheral neuropathy or mononeuritis multiplex
• Cranial nerve palsy- 7th nerve facial palsy is most
common (sarcoidosis is most common cause of
bilateral facial nerve palsy)
 Acute, transient, and can be unilateral or bilateral
 HEERFORDT'S SYNDROME: facial palsy accompanied
by fever, uveitis, and enlargement of the parotid gland
• Lymphocytic meningitis
• Meningoencephalitis
• SOLs
• Epilepsy
• Brain stem and spinal cord syndromes

88. • Hematopoietic system: splenomegaly common
• Genitourinary system: nephrocalcinosis due to
unexplained increase in senstivity to vitamin D
leading to increased absorption of calcium from
gut.
• Rarely glomerulonephritis and sarcoidosis of
epididymis.

89. CARDIAC
• Extensive pulmonary fibrosis leading to cor
pulmonale.
• Involvement of myocardium leading to dysrhythmias,
conduction disorders, heart failure and sudden death.
• PAH may occur due to parenchymal fibrosis distorting
the pulmonary vasculature, granulomatous
inflammation of pulmonary vasculature,hypoxic
pulm arterial vasoconstriction and from elevated left
ventricular diastolic pressure of cardiac involvement

90. ATS criteria diagnosis of
pulmonary sarcoidosis
(1) Presence of a consistent clinical and
radiographic picture
(2) Demonstration of noncaseating granulomas
on biopsy
(3) Exclusion of other conditions that can
produce granulomatous inflammation

91. Recommended Test for all patients :
• Complete blood count with differential count
• Chest radiograph
• PFT-spirometry, diffusion capacity, lung volumes
• Ophthalmologic examination
• Complete metabolic profile
• ECG
• PPD skin test. (<10mm reaction to 5TU has 100%
sensitivity but not specific. About 2/3rd of patients
with active disease fail to react to 100TU and 1/4th
to 100TU and less than 1/10th to 10TU.)
• Serum & Urine Calcium

92. Organ Specific Test :
Cardiac-
• ECG
• Holter monitoring
• Thalium or sestamibi myocardial scan
• Cardiac MRI
• Cardiac PET.
Neurologic-
• Brain or spine MRI with gadolinium enhancement
• CSF examination
• EMG or nerve conduction studies.

93. URT :
Flow-volume loop
ENT evaluation.
X-Ray PNS
CT Scan PNS
Endocrine :
Pituitary function test
Thyroid profile.
Biopsy :
Tissue biopsy is essential.
Biopsy almost always +ve if skin, lymphnodes,
conjunctiva involved accessible sites.

94. • Transbronchial lung biopsy is usually performed
because high yield and relative safe.
• The diagnostic yield of TBLB is ranges 40-90% if
atleast 4 biopsies are taken.
• Higher yield if pulmonary infiltrates an CXR or CT
scan shows.
• TBLB in advanced fibrocystic sarcoidosis has a
low yield.
• TBNA has diagnostic sensitivity of 100%
• Combining EBUS with TBNA increases the
sensitivity

95. BAL Findings
• Increased lymphocytes.
• Raised CD4: CD8 ratio >3.5 to 4.0 supports the diagnosis of
sarcoidosis.
• When FOB is non diagnostic – Mediastionscopy, VATS
• Open lung biopsy establish the diagnosis at >90% diagnostic yield.
• For organs that are difficult to biopsy image techniques such as
gallium 67 scan or more recently 18F – fluoro deoxyglucose position
emmison tomography (FDG-PET) may help.
• F-methyltyrosine-PET uses amino acids that is preferentially taken up
and expressed on tumor cells and is negative in sarcoidosis

96. • Tissues from mediastinoscopy +ve in 95%.
• Scalene lymph node biopsy positive in 80

97. Serum ACE levels (SACE levels) :
Libermann first to report raised ACE in sarcoidosis
• Produced by epitheloid cells.
• Elevated in 30 to 80% of patients.
• Elevated levels are seen in infections , graulomatous
disease, lymphoma, hepatitis, DM, thyroid disease.
Thus SACE is not recommended as a diagnostic test.
• Neither sensitive nor specific to be used as a
diagnostic tool.
• Provides good monitor of disease activity

98. Kveim-stiltzbach test :
Intradermal injection of homogenised tissue of organs
involved with sarcoidosis causes delayed cutaneous
reaction in 4 – 6 weeks.
Method of testing
• The test is performed by injecting intradermally 0.1- 0.2
ml of suspension of human sarcoid tissue , usually
obtained from cervical gland.
• Rarely , splenectomy for splenomegaly due to
sarcoidosis allows the preparation of large quantities of
test substance.

99. Within 2-3 wks positive test shows purplish red
nodule at the site of injection.
• Biopsy at 4- 6 wks reveals sarcoid tissue on
histological examination.
• Value of the test : false positive reactions are rare,
only 1 – 2% .
• Positive test can be regarded as a virtual proof of
active sarcoidosis.
• Positive results are obtained in 75% of patients with
clinical evidence of disease.

100. FDG PET SCAN

101. Assessment of disease activity
Best is by clinical assessment by worsening or
persistence of symptoms, with skin lesions and
changes in chest radiograph and PFTs.
• Serum ACE levels
• Others:
blood( lysozyme, neopterin,soluble IL-2 receptor)
BAL fluid(high lymphocytes, CD4/CD8 ratio, TNFalpha,
collagenase etc.,)

102. Differential Diagnosis

106. Diagnostic criteria for diagnosis of
tuberculous sarcoidosis
• Age: 25-45 years
• Gender: No gender predisposition
• History of previous tuberculosis infection which was
adequately treated with ATT with adequate drug
combinations, dosages and duration.
• H/O close contact with pt’s having tuberculosis
infection or family
• H/O tubeculosis or association with type II DM.
• Onset: Asymtomatic or with mild fever, anorexia
and loss of weight

107. • Important symtoms: Chronic cough, brethlessness
on exertion.
• Important signs: Involvement of multiple nodes, Eg-
Scalene or
• cervical group of lymph nodes, at Multiple
locations.
• B/L bibasilar end inspiratory velcrow crackles.

108. • The Marshall Protocol is a medical treatment
• While other treatments for chronic disease
use palliative medications in an effort to cover
up symptoms, the Marshall Protocol is a
curative treatment, which strives to address
the root cause of the disease process

109. TREATMENT- WHEN TO TREAT ??
• Pulmonary disease:
 Stage 1 disease - Asymptomatic with or without erythema
nodosum without extrapulm disease- NO TREATMENT
 Stage 2 disease without symptoms and mild functional lung
impairment- followed up without treatment
 Stage 2 disease with symptoms- treated
 Stage 2, asymptomatic with severe lung impairment- treated.
 Stage 3 disease with or without symptoms-treated
 Stage 4 disease- respond poorly or not at all to corticosteroids
or immunosuppressive therapy.

110. • Extrapulmonary disease:
 Ocular, cardiac, neurological, upper airway
involvement-treated with higher doses(40-60mg/day)
 Glandular, splenic, parotid, cutaneous lesions
treated with modest doses (20-30mg/day)
 Hepatic no treatment required but regular follow
up required.

111. Choice of drug
Corticosteroids drug of choice.
Act by gene transcription leading to inactivation of
nuclear Factor-kappa B which inhibits synthesis of most
known cytokines.
• Prednisolone 40mg daily maximum dose recommended
for acute pulmonary sarcoidosis which is tapered after
3-6months to maintainance dose of 5-10mg/day in
patients responding to therapy with close monitoring
for relapse and treatment continued for 12months.
• Insufficient data to recommend inhalational
corticosteroids in pulmonary disease

112. Major complication of corticosteroids therapy is
osteoporosis for which calcium and vitamin D
considered after ruling out hypercalcemia and
hypercalciuria.
• Use of bisphosphonates recommended in patients
with >5mg prednisolone for >3 months.
• Others: hypertension, diabetes, increased
susceptibility to infection, mood changes, skin
thinning, cataracts, weight gain etc

113. Alternative drugs
CYTOTOXIC DRUGS:
Rationale use of cytotoxic drugs with low doses of
corticosteroids enhances efficacy and reduces toxicity.
• Methotrexate preferred 2nd line drug. 10-15mg
once a week given often in combination with
steroid therapy.
• Others: azathioprine, chlorambucil,
cyclophosphamide

114. ANTI MALARIAL DRUGS:
• Good response in upper airway, sarcoid related
hypercalcemia and neurosarcoid.
• Chloroquine and hydroxychloroquine
• Hydroxychloroquine 200-400mg daily.
• Side effects of irreversible retinopathy and
blindness. (more with chloroquine)
• Rare side effects- agranulocytosis and myopathy

115. Reports clinical improvement in refractory
neurosarcoidosis, cardiac sarcoid, upper airway
sarcoid and skin lesions.
Drugs: infliximab and adalimumab
Infliximab- 3-5mg/kg intravenous infusion on weeks
0 and 2 with repeat dose every 4-8 weeks thereafter.
Concern is reactivation of latent tuberculosis and
other opportunistic infections. And also lymphomas,
new onset and worsening of congestive cardiac
failure and demyelinating diseases

116. • Other rare drugs include:
• leflunomide, mycophenolate,colchicine,
• pentoxyfylline, cyclosporin A

117. Treat how long??
• Duration individualised based on symptoms, organ
involved and response.
• Mostly for 1 year.
• Some from 6 months to even 10 years.
• If needed for longer periods, alternate day regimen to
minimise side effects.
• Recently showed that in acute exacerbations of
pulmonary sarcoidosis a 20mg prednsiolone for 21days
improved spirometry back to baseline and improved
clinical symptoms.

118. Treatment of complications
• Sarcoidosis associated fatigue - dexmethylphenidate
hydrochloride
• Bronchiectasis - antibiotic therapy, postural drainage,
anti inflammatory therapy
• Extensive lung fibrosis - long term oxygen therapy
• Sarcoid cardiomyopathy - decongestive therapy
• Refractory neurosarcoidosis - whole brain irradiation
• Bronchostenosis following sarcoidosis- bronchoscopic
balloon dilatation with topical mitomycin C
• Pulmonary HTN- sildenafil and bosentan. Candidates
for lung transplantation

119. PROGNOSIS AND MORTALITY
Prognosis related to severity of disease.
• Mortality rates of 1-6%
• Fibrosis in lung and forced vital capacity of less than
1.5litres are predictive of death due to respiratory
failure caused by sarcoidosis.
• In survival analysis, sarcoidosis has better prognosis
at 5 years (91.6% survival) compared to other
diffuse interstitial lung diseases

120. THANK YOU….