Neonatal &drug-induced lupus

Presented by : balsam Atheer

Neonatal Lupus Erythematosus (NLE)
A rare disorder caused by the transfer of transplacental autoantibodies (IgG anti-
SSA/Ro

and/or anti-SSB/La) from the mother to the fetus.

➢ This syndrome is characterized by one or more of the following findings:

1. Subacute cutaneous lupus–like annular and polycyclic lesions (50%).

2. Congenital heart block (50%).

3. Cardiomyopathy.

4. Cholestatic hepatitis.

5. Thrombocytopenia.
The skin lesions usually appear within the first month of life and may be initiated by sun
exposure.
➢ Lesions present with plaques of erythema with central atrophy. Crusted lesions
predominate in male infants. Lesions appear on the scalp, arms and legs, trunk, and groin.
➢ The lesions heal without scarring or atrophy within 6 months.
➢ A periorbital “owl-eye” or “eye mask” facial rash is common. The autoantibodies
disappear with the rash.

Fig (6 A&B).
A- an owl
B- owl eye rash
Fig (7).Neonatal lupus lesions in Fig (8).Neonatal lupus lesions in
the face and scalp the trunk with crustations
The congenital heart is a permanent defect that develops in utero during the late
2nd and

the 3rd trimesters of pregnancy. Many babies require pacemakers, and

approximately
10% die of complications related to cardiac disease

Diagnosis:

➢ Two lesional skin biopsies are taken: one for hematoxylin and eosin and the
other for

immunofluorescence.
➢ The finding of anti-Ro/SS-A antibody in the infant and mother confirms the
Drug-induced Lupus Erythematosus (DILE)
An autoimmune phenomenon where the patient develops symptoms similar to
systemic

lupus erythematosus (SLE) after exposure to certain drugs. More than 80 drugs
have

been associated with DILE.

➢ The drugs that have been documented to induce DILE include: hydralazine,

procainamide, isoniazid, methyldopa, chlorpromazine, and quinidine.

Clinical Presentation:
Most commonly the onset of symptoms occurs many months after the drug has
been

initiated.

➢ DILE resembles mild SLE.

➢ It usually occurs in older age groups; SLE commonly occurs in young women.

➢ DILE is characterized by arthralgia and/or arthritis (80% to 90%), myalgia (up to

50%),

serositis (pleurisy and pericarditis), fever, hepatomegaly, splenomegaly, and skin

manifestation. Arthralgia or arthritis is sometimes the only clinical symptom. The
small
Skin Manifestations: Skin manifestations appear in 25% to 50% of patients and
includelesions compatible with the typical lesions of SLE. Butterfly rash, alopecia,
discoid lesions,and mucosal ulcers are usually absent.
Diagnostic criteria:

1. Exposure (3 weeks to 2 years) to a drug suspected to induce DILE.

2. No history for SLE before the use of the drug therapy.

3. Detection of positive ANA with at least one clinical sign of SLE.

4. Rapid improvement and gradual decrease in the ANA and other serologic
findings upon

withdrawal of the drug.

Treatment: DILE does not usually require treatment. Patients with pericarditis,
pleural

effusions, or pulmonary infiltrates often require prednisone. They respond quickly,