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immunoglobulins from the mother to the fetus through the placenta. Affected neonates present with an urticarial erythematous vesicular rash with occasional blisters. Their disease is milder and usually resolves spontaneously within days to weeks, sometimes before the maternal antibodies are removed from the neonate’s blood. The primary goal of treatment is to relieve pruritus and prevent new blister formation. Mild cases of PG respond well to topical steroids and antihistamines. Systemic steroids are the treatment of choice. Prednisone or prednisolone is given at a dose of 0.5 to 1 mg/kg/day and is adjusted depending on response. It is usually tapered preterm, but may need to be increased postterm because of postpartum flares. Other treatment options that have been used in refractory cases include cyclosporine, cyclophosphamide, azathioprine, dapsone, intravenous immunoglobulin, rituximab, plasmapheresis, goserelin, pyridoxine, sulfapyridine, and tetracyclines with nicotinamide for postpartum flares. For this series the recommended choices are: 1, c; 2, e; 3, a; 4, b.

Cohen et al have proposed a comprehensive diagnostic and treatment plan for patients diagnosed with MTS or carrying an MTS-prone sebaceous neoplasm and their family members. This includes a review of the patient’s annual medical records and a comprehensive physical examination, regular monitoring of the serum carcinoembryonic antigen level, upper gastrointestinal endoscopy and colonoscopy, chest radiography, urine cytology, computed tomography scans of the abdomen and pelvis, mammography, cervical smear, and endometrial biopsy. Immunohistochemical staining for MSH2, MSH6, and MLH1 protein expression was found to be useful for identifying the underlying mismatch repair defects in the sebaceous neoplasm and for additional molecular analysis of the disease. For this series, the recommended choices are: 1, a; 2, c; 3, c; 4, d.

Interstitial granulomatous drug reactions are an uncommon entity presenting as asymptomatic, annular, erythematous to violaceous plaques. The incidence of such reactions has been increasing with the use of biologic agents. We report, to the best of our knowledge, the first such reaction to the interleukin (IL)-1 inhibitor anakinra. Our patient presented with pink dermal plaques and nodules in the periaxillary region which resolved with discontinuation of anakinra and recurred upon restarting anakinra. Biopsy revealed a diffuse dermal infiltrate of lymphocytes and histiocytes with interspersed neutrophils and eosinophils. Fragmentation and degeneration of collagen and elastic fibers was also present. Withdrawal of anakinra led to complete resolution of the lesions. Interstitial granulomatous drug reactions are increasing in frequency and we add anakinra to the list of causative agents.

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