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CHAPTER V
DISCUSSION

RN, a 14 years old girl, with 36 kg of body weight and 155 cm of body
height, came to RSUP Haji Adam Malik Medan on 10thDecember. His main
complaint is to continue the chemotherapy. Patient was registered as allergic
and immunologic division’s patient in Adam Malik Hospital diagnosed with
Systemic Lupus Erythematosus. She was primarily diagnosed with Systemic
Lupus Erythematosus on April 2015.
Pain on joints was not complain by the patient. History of joint pain has
been complained since September 2015. This is the main complaint of patients
before being diagnosed with SLE this is consistent with the theory that states
arthralgia is the a most complaint felt by patients with SLE.3 . The complaint
was detected especially on feet joints and getting worse during patient on
walking. This is also consistent with theory that states arthritis in usually
primarily affecting the small joints of the hands, wrists, and knees.3
Another Clinical Manifestations in this patient which has been
identified are classic lupus butterfly rash in malar distribution and precipitated
by unlight exposure and alopecia. This is also consistent with theory that states
The classic lupus ‘butterfly’ rash is common presents acutely as an
erythematous, elevated lesion, pruritic or painful, in a malar distribution,
commonly recipitated by exposure to sunlight in SLE patient. Alopecia
defined as exaggerated hair loss occurs in most SLE patients. It may involve
the scalp, eyebrows, eyelashes, beard, and body hair. 3

According epidemiology SLE affects women more frequently than men


and is more common among Afro-Caribbean and Asian compared to Caucasian
subjects. Incidence rates in Europe vary, but generally fall between 2 and 4.7 x
105 per year. While SLE is generally thought to affect primarily women in the
third and fourth decade of life, the peak incidence seems to be later among
patients of European descent. In about 15%-20% of cases, disease onset occurs
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during childhood and tends to be more severe with faster and more severe
damage accrual.4 In this case patient is a 14 years old girl.

Several risk factors for SLE are genetic factor, hormonal factor and
environmental factor. There is no family history of SLE in this case. There is
no history of consuming oral contraceptive drug and hormonal replacement
theraphy. Environmental triggers of SLE include ultraviolet light,
demethylating drugs, and infectious or endogenous viruses or viral-like
elements. Sunlight is the most obvious environmental factors that may
exacerbate SLE. It is well established that induced Certain drugs
autoantibodies in a significant number of Patients. Over 100 drugs have been
Reported to cause drug-induced lupus (DIL), Including a number of the newer
biologics and antiviral agents. In this case, Patients has history of consuming
anti-tuberculosis drugs in which one of the components of the drug, isoniazid
can induce SLE. However, the possibility of isoniazid causing SLE reported is
very low. Anti histones can be used as a guide if SLE occurs due to drug
induction or not.3

We diagnose this patien with SLE by finding 4 from 11 American


College of Rheumatology (ACR) criteria. They are malar rash, discoid rash,
photosensitivity, arthritis, and abnormality antinuclear antibodies. The
diagnosis of systemic lupus erythematosus is based on clinical and laboratory
criteria. The criteria set developed by the American College of Rheumatology
(ACR) is most widely used. The criterias are malar rash, discoid rash,
photosensitivity, oral ulcers, arthritis, serositis, renal disorder, neurologic
disorder, hematologic disorder and antinuclear antibodies8. In this case renal
function test within normal limits (Ureum=15,5 and creatinine=0,43). Serositis
is also not found. There is no sign and symptom for pleuritis, peritonitis, and
pericarditis from physical examination.

SLE is classified into 3 namely mild (kaegori I), moderate (category II)
and severe (category III). Category I (Mild SLE) is Characterized by arthritis,
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arthralgia, myalgia, fatigue, mild mucocutaneous involvement, low-grade


fever, mild as rositis, lupus headache. Musculoskeletal complaints are the
commonest features of SLE. For mild symptoms, NSAIDs and analgesics
suffice. Patients who are not responding to NSAIDs maybe treated with low-
dose steroid therapy (prednisolone 0.3-0.5 mg / kg / day) for 4-6 weeks
Followed by slow tapering. For lupus dermatitis, there is Also a role of local
steroids, includeing topical creams and ointments and injections into
unresponsive skin lesions. However, the steroid cream application for facial
rash is not recommended. Adequate protection against sun is essential.7

Category II (Moderate SLE) characterised by high-grade fever,


toxaemia, severe mucocutaneous manifestations, marked photosensitivity,
moderate to severe serositis, lupus pneumonitis, mild to moderate myocarditis,
mesangioproliferative or minimal change lupus nephritis, haemolytic anaemia
and thrombocytopenia.For moderate and severe manifestations, prednisolone 1
mg/kg orally per day is the drug of choice. Antimalarials may be administered
concomitantly. High dose of steroid must be continued till disease activity is
well controlled that usually takes up to 6 weeks when it should be tapered off
slowly over 6 to12 months. In a toxic appearing patient, the administration of
intravenous pulse methylprednisolone (15 mg/kg,max. 1 g) over an hour for 3
or 5 consecutive days may achieve rapid control of lupus activity.
Dexamethasone 100 mg is a good, cheap and equally effective alternative
steroid for pulse therapy. Although rare, arrhythmias, accelerated hypertension,
psychosis, seizures and sudden death have been reported with pulse therapy.
The pulses should be followed by oral prednisolone. Calcium supplements (1
gm/day) and vitamin D (800 units/day) prescribed along with steroids retard
osteoporosis. Alendronate 10 mg daily or 70 mg once a week is a good
antiresorptive drug for prevention of osteoporosis in patients starting on
longterm steroid therapy.7
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Category III (Severe SLE) characterised by organ/life-threatening


features such as focal/diffuse proliferative glomerulonephritis with or without
azotaemia/hypertension, lupus cerebritis with recurrent seizures, acute
confusional state, coma; systemic necrotizing vasculitis such as one causing
peripheral gangrene, GI bleeding or mononeuritis multiplex. A combination
therapy consisting of high-dose daily oral prednisolone (40-60 mg/day) and
intravenous cyclophosphamide pulses (0.75 gm/m2, maximum of 1 g, over 1
hour) is recommended for severe SLE. The cyclophosphamide pulses are given
once a month for 6 months by which time usually remission is achieved and
then a maintenance pulse is administered every 3 months for a total of 2 years
of cytotoxic therapy. Prednisolone is tapered off or reduced to a very low dose
i.e. 5-7.5 mg per day by 6 months.7

In this case SLE already involve CNS disorders (lupus cerebritis). RN


several times is found unconscious. Cerebral involvement is cathegorized as
severe SLE (Category III). Theraphy for this patient Inj. Methylprednisolone
1000 mg in 100cc NaCl 0.9% finish in 1 hour, Inj. CPA 840mg (700/m3 mix
with Mesna 500mg, Methyl prednisolone tab 3-3-3. This also consistent with
the teory.