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1. ADAMA HOSPITAL MEDICAL COLLEGE
1
GRAND ROUND
PRESENTED BY: Dr. Kebede M.(Med R2)
Dr. Melaku Y.(Med R1)
Dr. Mengistayehu T.(Intern)
MODERATOR: Dr. Shoba Ibrahim(MD internist, Assist.prof)
2. OUTLINE
2
Summary of the History, Physical Examination and Investigation.
Discussion of differential diagnosis and mgt.
Final diagnosis.
References.
6. HISTORY OF PRESENT ILLNESS
6
She is an 18 years old female patient presented with gradual onset
of the above complaint for the past two months with no aggravating
and relieving factors noticed by the pt and the family.
7. Associated to it:
7
She has dry cough of 5 months for which she visited near by hospital
one month back and was given unspecified injectable medication for
two wks, but no improvement
She has LGIF, night sweat, chest pain of three wks, dysphagia and
SOB of one wk duration
She has multiple joint pain, hand and feet swelling of 5 months
She has tinnitus, vertigo, head ache, decreased appetite of three wks
8. CONT…
8
She has also progressive type of skin lesion over the right leg
and foot which initially was fluid filled and later progressed to
pus filled for the past three months for which she visited the
near by health institution and was given un specified oral
medication ,but no improvement apart from slight improvement
from pain and decreased purulent discharge.
9. Otherwise:
9
No orthopnea, PND, palpitation
No abdominal distension, pain or bowel habit change
No yellowish discoloration of eyes or use of herbal medication
No hx of urine color change or decreased UOP
No hx of TB tx or contact with chronic cougher
No hx of ABM or LOC
10. CONT…D
10
No hx of trauma to the leg
No heat or cold intolerance or anterior neck swelling
No self or family hx of DM, HTN or cardiac illness
13. 13
H.E.E.N.T
Pale conjunctiva and non icteric sclera
LGS: No LAP
RESPIRATORY SYSTEM
Decreased air entry over the posterior lower third chest
bilaterally
Coarse crepitation over the lt lower lung field
14. 14
CARDIOVASCULAR EXAMINATION
JVP is flat
S1 and S2 well heard, no M/G
ABDOMINAL EXAMINATION
Flat and moves with respiration
- No tenderness
- No Organomegally or SFC
- Normo-active bowel sound (16/min)
15. 15
GENITOURINARY SYSTEM
No CVAT
INTUGEMENTARY AND MUSCLOSKELETAL SYSTEM
There are two well demarcated and discoid skin lesions over the medial and
dorsal aspect of the rt foot each measuring 3*4cm and 3*3 cm respectively with
hyper pigmented base and punched out center and inverted edges, no discharge.
24. In favor:
Constitutional symptoms
Anemia, increased ESR
Abnormal Urinalysis
Multiple organ involvement
Ulcer
Improvement with steroid
management
Against:
Age
No palpable purpura
No Reynaud's phenomenon
No rhinitis, sinusitis or asthma
ANA Positive
No nasal or oral involvement
5.Vasculitis
25.
26.
27.
28. Mixed connective tissue disease (MCTD) is defined as a
generalized connective tissue disorder
characterized by the presence of high titer anti-U1
ribonucleoprotein (RNP) antibodies in combination with clinical
features
commonly seen in systemic lupus erythematosus (SLE), systemic
sclerosis (SSc), and polymyositis (PM)
4.Mixed connective tissue disorders(MCTD)
29.
30. In favor:
All non specific constitutional symptoms
Bilateral joint pain
Dysphagia
Heartburn
ANA –Positive
Increased LDH
Remission after steroid
Against:
No proximal muscle weakness
No Reynaud's phenomenon
No localized muscle pain
Markedly increased ESR
Age
Renal and lung involvement
4.Mixed connective disorders
31. Describes those patients having overlapping features of SLE and
Rheumatoid arthritis
In these cases sever joint deformities, nodules and erosions may
occur
3.Rhupus
32. In favor:
Joint swelling
Constitutional symptoms
Duration of symptoms(>6
weeks
Increased ESR
ANA-Positive
Failed antibiotic treatment
Improvement with steroid
Against:
No morning stiffness
Large joint involvement
Decreased platelets
3.Rhupus
33. In favor:
TB symptom Complex
Epidemiology
Lung, Pleura and skin
Increased ESR
Marked Improvement after anti-
TB treatment
Against:
No TB contact history
Sputum gene X-pert-negative
Chest x-ray finding
Pleural fluid analysis
Relapsing and remitting course
Kidney involvement
2.Disseminated Tuberculosis( Lung, Pleura,Skin)
34. In favor:
Fulfills diagnostic
criteria(EULAR 2019)
Marked Improvement after
treatment for SLE
Against:
Pleural fluid analysis
Skin lesions are not on photo-
Sensitive areas
1.Systemic Lupus Erythematosus
35.
36.
37.
38. CASE SUMMARY
This is an 18-yr old F patient admitted to MW 3 weeks back
complaining of worsening of cough of 3 months and SOB of 2
months.
She also has multiple joint pain, swelling of hands and feet,and
fatigue of 5 months.
In addition,she has night sweating, pleuritic chest pain, skin
color change with ulceration and LGIF.
After admission,she also abnormal behaviour,lack of
sleep,headache and tingling sensation.
Her past medical history was Rx with antibiotics twice with no
improvement.
39. Her lab Ixs from CBC:wbc-3700,L-6%;hgb-6.6;plt-
916000;ESR-100;
Cr-3.99;Urea-154;AST-84,ALT-48;
U/A-albumin +4;RBC +3;
CXR-symmetric mid lung bilateral opacity ;
ANA +ve;Hbsag and HCV ab –ve;PIHCT –ve;
Abd,U/S-normal.
Pleural fluid analysis-gluc-46,alb-1.5g/dl,RBC-1500,WBC-
7500:N-77%;sputum gene xpert –ve;
40. Final Dx
Life-threatening SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)
(hematologic,renal,cns,pulmonary,skin)+?Diss.
TB(lung,pleura,skin)+NCPE 2ry to AKI 2ry to
Lupus Nephritis+?CAP+Mod. Anemia 2ry ACD
+Ecthyma
43. Introduction
SLE is a chronic inflammatory multisystem disease of
unknown cause.
Ninety percent of patients are women of child-bearing years;
people of all genders, ages, and ethnic groups are
susceptible.
Sixty-five percent of patients with SLE have disease onset
between the ages of 16 and 55
44. Etiology and pathogenesis
Interactions between susceptibility genes and
environmental factors result in abnormal immune
responses:
lowered activation thresholds and abnormal activation
pathways in adaptive immunity cells
ineffective regulatory CD4+ and CD8+ T cells and
reduced clearance of immune complexes and of
apoptotic cells
45.
46. Clinical Manifestations
SLE is a multisystem disease with diverse organ involvement
and multiple different manifestations within an organ system.
The system most commonly involved is the musculoskeletal
system, with 95% of patients having involvement, usually as
arthralgias or myalgias.
Arthritis is also common and is one of the diagnostic criteria for
SLE.
53. The goals of therapy for SLE are :
to ensure long-term survival,
achieve the lowest possible disease activity,
prevent organ damage,
minimize drug toxicity,
improve quality of life, and
educate patients about their role in disease management
55. PHARMACOLOGIC:
Renal disease
Treatment of LN includes an initial induction phase, followed
by a more prolonged maintenance phase.
MMF and CYC are the IS agents of choice for induction
treatment;
MMF or AZA may be used as maintenance therapy
56. Induction
0.5 –1g of methylprednisolone IV daily for 3d then prednisone 0.5–
1mg/kg/d for 4–6wks thereafter, doses are tapered or
Prednisone 0.5–1mg/kg/day PO 4–6wks then taper
+
Cyclophosphamide 3 g every 2 wks over 3mo or
Mycophenolate mofetil 3 g/d for 6 months or
Azathioprine (Less effective) 2 mg/kg body weight/day
58. Haematological disease
GC in combination with IS agent (AZA, MMF or cyclosporine)
Initial therapy with pulses of intravenous MP (1–3 days) is
encouraged.
In patients with no response to GC or relapses, RTX should
be considered, considering also its efficacy in ITP
59. Thrombopoietin agonists or splenectomy should be reserved
as last options.
Autoimmune leucopaenia is common in SLE but rarely needs
treatment
60. In refractory or relapsing disease, RTX may be considered.
CNIs may be considered as second-line agents for induction
or maintenance therapy mainly in membranous LN,
podocytopathy, or in proliferative disease with refractory
nephrotic syndrome
61. Neuropsychiatric disease (NPSLE
Treatment of NPSLE depends on whether the underlying
pathophysiological mechanism is inflammatory or
embolic/thrombotic/ischaemic
GC and/or IS agents should be considered in the former, while
anticoagulant/antithrombotic treatment is favoured when aPL
antibodies are present
62. Skin:
Protection from ultraviolet exposure with broad-spectrum sunscreens and
smoking cessation
topical agents (GC and/or CNIs) and antimalarials, with or without
systemic GC
MTX can be added.
Others retinoids, dapsone and MMF or EC-mycophenolic acid
63. Lung
mild, may respond to treatment with nonsteroidal anti-
inflammatory drugs (NSAIDs);
when more severe, patients require a brief course of
glucocorticoid therapy.
Life-threatening pulmonary manifestations probably require
early aggressive immunosuppressive therapy as well as
supportive care.
64. Infections
Risk of infection in SLE is associated with both disease-related
and treatment-related factors
Protection against infections should be proactive, focusing
both on primary prevention, as well as timely recognition and
treatment.
Vaccination is preferable during stable disease
65. Abstract
infection one of the leading causes of morbidity and mortality
The reasons for the high incidence of infection are immunosuppressive
therapy and immune disturbances of lupus itself.
Bacterial infections are most frequent, followed by viral and fungal infections
Vaccination is the most important tool in the prevention of infections.
Prophylaxis of tuberculosis and pneumocystosis are also recommended to
prevent those deadly infections.
66. TB and SLE:(From Journal of Clinical and Diagnostic Research)
SLE and TB are intricately related with an increase in the risk of TB in SLE.
There were case series of five female patients of SLE with TB who presented
between January 2015 and December 2015 in a tertiary care teaching
hospital in North Eastern India.
All the patients were young to middle aged females having SLE with or
without lupus nephritis who were on immunosuppressive therapy with
corticosteroids, mycophenolate mofetil or cyclophosphamide.
67. Two of the cases had sputum positive pulmonary tuberculosis
while rest had Extra-Pulmonary TB (EPTB).
The response to anti-tubercular therapy led to clinical
improvement in all the cases except one who had an adverse
outcome.
The series further substantiates the increased risk of TB in
SLE thus, prompting further research towards better
management of these two disease entities in conjunction.
68. SLE are prone to develop intercurrent infections because of:
(i) compliment deficiency;
(ii) mannose binding lectin (MBL) deficiency;
(iii) chronic inflammation and tissue damage; and
(iv) use of immunosuppressive therapy
69. TB is a common infection in SLE patients and the prevalence
of TB in patients with SLE ranges from 5% - 11.6% in studies
reported from India.
The incidence of TB in SLE patients is considered to be 15-
fold higher;
extra-pulmonary involvement and disseminated TB are more
common
70. differentiating disease flare from active TB disease in patients with
SLE based remains a challenge.
Evidence is available suggesting that monoclonal antibodies raised
against TB can cross react with DNA,
features of autoimmunity are evident in mycobacterium induced
arthritis in experimental models,and
detection of antibodies in patients with TB similar to that found in
SLE
71. In a study from Taiwan among 2721 patients with SLE
antecedent TB was present in 44 (1.8%) of patients;
TB patients were found to have an odds ratio of 2.09 for
subsequent development of SLE after controlling for other
potential risk factors.
Some even advocated isoniazid prophylaxis in patients with
SLE receiving long term corticosteroid treatment.
72. Follow up
At least quarterly visits recommended
CBC,sCr,U/A
Complement levels and anti-dsDNA as adjuncts to detect lupus
flares
Opportunistic infection detection
Contraception and Family planning
74. TAKEHOME MESSAGE
TB and SLE share several similar clinical manifestations
So, differentiating disease flare from active TB disease in
patients with SLE based on clinical manifestations alone
remains a challenge.
high index of suspicion and focussed evaluation in the
diagnosis of intercurrent infections, particularly, TB in patients
with SLE is crucial.
75. REFERENCES
HARRISON 20th Edition
EULAR 2019 Management of SLE
ACR and EULAR 2019 Classification criteria
UPTODATE 2018
Journals