The authors describe 13 cases of elastofibroma seen by them and review 23 cases from the literature. With the exception of one tumor on the trochanter major, all of the tumors were subscapular. Microscopic and electron‐microscopic studies showed that hypertrophy and degeneration of the elastic fibers and lamellae were essential for the formation of the tumor. Histo‐ and biochemical studies suggested that the fibers were composed of elastin. The fibers were resistant to collagenase but treatment with elastase resulted in a marked decrease in stainability of the fiber substance with elastic stains. Tests for sulphydryl groups were positive. Chemical analysis of one tumor showed 8% elastic and 75–80% collagenous tissue. This investigation indicates that elastofibroma is not a real neoplasm but rather a degenerative pseudotumor of the elastic tissue.

In a series of 235 autopsies, changes in the subcapsular thoracic fascia similar to elastofibroma dorsi (Järvi & Saxén 1959, ‐et al. 1969) were found in 39 cases, all at least 58 years old. In people over 55 years, the frequency was 24.4 per cent in females and 11.2 per cent in males. In addition to hypertrophy and secondary degeneration of elastic fibres, necrosis of collagenous‐, adipose‐, muscular‐, and nervous tissue, as well as formation of clefts, cysts and bursae was found in 85 per cent of cases presenting elastic changes—both in connection with them and outside the degenerated areas—as well as in 39 per cent of cases where no elastic degeneration occurred. Other changes included extensive scarring of the tissue, followed by reduction of fat and, more seldom, oedema and inflammatory infiltration. Breaks in the elastic cage, necrosis and fibrosis of arterial walls were found in 44 per cent of cases of elastic degeneration and in 14 per cent of cases without degeneration. In veins, more extensive wall fibrosis occurred, leading to necrosis; in cases of elastic degeneration the adventitial elastic network was also involved. Venous changes were found in 90 per cent of the cases of elastic degeneration and in 30 per cent of cases without degeneration. Direct mechanical stress on elastic tissue may be an important cause of hypertrophy and secondary degeneration of elastic fibres, and also of diffuse increase of collagenous tissue. On the other hand, nutritional deficiency due to failing resistance of the vascular system against friction of the scapula and streching movements of the upper extremities may play a main part in necrotic tissue changes.

In view of uncertainty regarding the criteria and significance of gastric dysplasia as a precancerous lesion, members of the Pathology Panel of the International Study Group on Gastric Cancer (ISGGC) reviewed microslides of 93 gastric lesions showing varying degrees of mucosal abnormality, and reached the following consensus: (1) immature and proliferating gastric epithelium can be divided into two categories: hyperplastic and dysplastic; (2) the term dysplasia, especially of high‐grade type, should be restricted to precancerous lesions, and hyperplasia is applied to regenerative changes; (3) regenerative hyperplasia may be simple or atypical, but dysplasia includes both moderate and severe abnormalities, since they often coexist and can not be sharply separated; and (4) occasionally the possibility of malignancy can not be excluded in a severely dysplastic epithelium; in such a case rebiopsy and diligent follow‐up are necessary to establish the diagnosis. Criteria for diagnosing dysplasia and hyperplasia are presented and discussed. The opinions are offered as guidelines for establishing the diagnosis of gastric dysplasia and for prospective studies.

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