Faint erythema. Another manifestation of cutaneous sarcoidosis?
Authors: Okano Masaki , Nishimura Hiroshi , Morimoto Yasuhiko , Maeda Hideo 
Published: December 2004

A 44‐year‐old man was seen in the outpatient dermatology clinic with multiple erythematous lesions of 8–12 years' duration. He also had a 23‐year history of chest X‐ray findings of bilateral hilar adenopathy, and had experienced nasal stuffiness for several years. He had no history of dyspnea, chest pain, cough, fatigue, weight loss, or fever. The patient had also suffered from swelling of the fingers and toes, with associated stiff movement of their joints for several years. He had a past history of diabetes mellitus and hypertension. There was no palpable lymphadenopathy or hepatosplenomegaly. A nasal examination disclosed marked thickening of the mucosa, but a biopsy from the inferior turbinates showed no granulomas. An ophthalmologic evaluation revealed neither vitreous opacity nor uveitis. Pulmonary, cardiac, and neurologic evaluations yielded normal results. A chest roentgenogram revealed a bilateral hilar adenopathy and reticulated infiltrates (Fig. 1). A radiograph of the hands and feet disclosed well‐defined phalangeal “punched‐out” areas of transradiancy. Gallium scintiscans showed an increased uptake in the nose and the hilar and mediastinal nodes. Laboratory data included normal complete blood cell count and liver and renal function tests. The levels of serum calcium and phosphate were normal. The serum immunoglobulin G (IgG) revealed an increased level of 2370 mg/dL (normal range, 800‐1800 mg/dL). The serum angiotensin converting enzyme disclosed an elevated value of 32.7 IU/L (normal range, 7–24 IU/L). The serum lysozyme was also increased to a level of 25.5 mg/L (normal range, 4.2–11.5 mg/L). The erythrocyte sedimentation rate was 3 mm/h. An intradermal skin test to purified protein derivative (PPD) was negative. A Kveim test was not performed.

On physical examination, there were widespread multiple erythematous infiltrations at various stages of evolution. The patient had not noticed any prominent change in manifestation of the erythematous lesions over time. Chilblain‐like dusky erythematous lesions had affected the acral regions, including the nose, ears, fingers, and toes, for 8 years. The lesions were purple‐red or purple with a shining surface, swollen, and moderately well demarcated. The nasal skin also presented a papillomatous appearance (Fig. 2). There were multiple oval or round erythematous plaques of various sizes of 12 years' duration, with moderately well‐defined edges, scattered on the back, buttocks, arms, and thighs. They were red or purplish‐red, with fine superficial scaling, and were plainly raised above the surrounding normal skin (Fig. 3). In addition to the nodular plaques of this sort, another form of erythema had been present on the trunk for 10 years. The patient stated that this infiltrate had showed no apparent change. The erythematous infiltrate was rather sparse, and the major part presented a faint appearance. There was partial adhesion among the infiltrates. The lesion was soft, flat, pink or red in hue, and had an irregular and ill‐demarcated margin. No raised infiltrated rim was seen at the periphery. Scaly desquamation was minimal. Apparent telangiectasia was not observed. The erythematous lesion occupied a large part of the abdomen and lateral sides of the chest (Figs 4 and 5).

Skin biopsy specimens from the nasal, toe and abdominal lesions disclosed similar microscopic changes, with islands of granulomatous inflammation. They were composed of numerous epithelioid cells intermingled with Langhans giant cells and chronic inflammatory cell infiltrates. The epithelioid cell granuloma lacked caseation necrosis (Fig. 6).

The cumulative findings were thought to be consistent with a diagnosis of sarcoidosis