The human MxA protein can be detected in the cytoplasm of IFN-alpha/beta-treated cells, whereas other cytokines, including IFN-gamma, are poor inducers. Because IFN-alpha/beta is predominantly synthesized in response to viral infections, MxA protein should be detectable in virally infected tissue. Biopsy specimens (n = 64) of 12 different dermatoses were therefore screened with an MxA-specific monoclonal antibody on formalin-fixed, paraffin-embedded and microwave-treated tissue sections. As expected, high amounts of MxA protein were found in acute viral skin lesions (chickenpox, Herpes zoster, and Herpes labialis). In addition, MxA protein was also detected in some inflammatory skin lesions of unknown etiology (lupus erythematosus, lichen planus, Schoenlein-Hennoch's anaphylactoid purpura and psoriasis). MxA protein was not found in non-viral infections (bacterial, mycotic, and parasitic) and was also not detectable in various other dermatoses (eczema, scleroderma, urticaria, granulomatous and bullous disorders). MxA staining proved a reliable, sensitive histochemical viral marker for infectious dermatoses. The positive results in non-infectious inflammatory dermatoses might implicate viral involvement or activation of the IFN system by thus far unknown mechanisms.

We report on 3 patients who developed a generalized eczematous skin rash under treatment with simvastatin and pravastatin for hypercholesterolemia. These drugs are 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors and suppress cholesterol synthesis in the liver. Based on experimental data from the literature that showed eczematous changes in mice treated topically with the HMG-CoA reductase inhibitor lovastatin, we suspect that the rash observed in our patients may be a consequence of skin barrier dysfunction following inhibition of cholesterol biosynthesis.

We describe a 34‐year‐old woman with periarteritis nodosa (PAN) presenting as a breast lesion. Localized involvement of the breast is an unusual manifestation of PAN. To date, 10 cases have been reported: all were in women with an age range of 45–78 years (mean 63). In most cases, breast lesions were an isolated finding, and the prognosis was favourable, setting them apart from the more common form of systemic PAN. The case presented is unusual in that vasculitis developed in the postpartum period, and was associated with cutaneous PAN‐like lesions elsewhere on the body, and digital artery occlusion. The most important differential diagnoses of PAN of the breast are infectious mastitis, mammary malignancy and other forms of idiopathic vasculitides of the breast, e.g. giant cell arteritis and Wegener granulomatosis.

We describe a case of necrotizing granulomatosis of Wegener's type involving the breasts of a 40-year-old man. There were no signs of generalized disease. Involvement of the breast is rare in Wegener's granulomatosis (WG). To date, 17 cases have been reported, and all were women. They predominantly presented with a unilateral breast mass, and mammary malignancy was the principal concern. In the majority of cases, breast lesions of WG have been a presenting sign of, or preceded, disseminated disease. Our patient is unusual in that the necrotizing granulomas developed as an isolated finding in a site remote from those usually affected by WG, and, as far as we are aware, represents the first case of Wegener's type granulomatosis involving the male breast.

A 23-year-old woman presented with subcutaneous ossification, which together with short stature, stocky physique, round face and brachydactyly suggested Albright’s hereditary osteodystrophy (AHO). Serum calcium and phosphorus levels were normal. AHO refers to the phenotype of the syndromes of pseudohypoparathyroidism (PHP) type la and pseudopseudohypoparathyroidism (PPHP), both considered genetically related variants with a defect of the α sub-unit of the stimulatory G protein of adenylate cyclase necessary for the action of parathyroid and other hormones using cyclic AMP as an intracellular second messenger. PPHP differs from PHP in that it lacks parathyroid hormone resistance manifesting itself as hypocalcemia. Other endocrine end organ unresponsiveness, e.g. hypothyroidism and hypogonadism, may also be found with PHP. Both PHP and PPHP usually exhibit characteristic phenotypic abnormalities, of which subcutaneous ossification may be a presenting feature. The differential diagnosis of cutaneous calcification and ossification is outlined.