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Selected Heritable Skin Diseases of Domesticated Animals
Published in John P. Sundberg, Handbook of Mouse Mutations with Skin and Hair Abnormalities, 2020
Robert W. Dunstan, Robert A. Kennis
Comments — On comparison of canine dermatomyositis with the human disease with which it is most similar, Type 2 juvenile dermatomyositis, there are a fascinating array of similarities and differences.55 A heliotrope rash (periorbital edema with reddish-blue discoloration) is not observed and although Gottron’s sign (erythematous papules over the metacarpophalangeal and interphalangeal joints) is not associated with the canine disease, this may simply be because the anatomy of canine distal extremities is so different than in humans, and analogous sites in dogs would not be as exposed to trauma. Thus, the clinical differences in the cutaneous lesions may be more anatomic than due to a different pathogenesis.28 A key and unexplained difference is the distribution of the myositis. In the dog, the muscles of mastication are most severely involved; in humans, the proximal limb girdle musculature is most severely involved. In addition, tumoral calcinosis, an occasional finding in the juvenile form of the disease, has not been described in affected dogs.28,53–55
Test Paper 2
Published in Teck Yew Chin, Susan Cheng Shelmerdine, Akash Ganguly, Chinedum Anosike, Get Through, 2017
Teck Yew Chin, Susan Cheng Shelmerdine, Akash Ganguly, Chinedum Anosike
Tumoural calcinosis is a rare familial disease, typically presenting in young men of African origin, with progressive large nodular juxta-articular calcified soft-tissue masses. Patients have normal serum calcium and phosphorus and do not have any evidence of renal, metabolic or collagen–vascular disease. The hips are the most frequently affected, followed by the elbows, shoulders and feet, and the disease is usually along the extensor surface of the joints. The knees are almost never affected. Occasionally, fluid–fluid levels are seen with the calcium lying inferiorly, termed the sedimentation sign. The joints themselves are normal.
Metabolic and endocrine bone disorders
Published in Ashley W. Blom, David Warwick, Michael R. Whitehouse, Apley and Solomon’s System of Orthopaedics and Trauma, 2017
For example, in autosomal dominant hypophosphataemic rickets (ADHR), FGF23 levels are elevated due to a gain of function mutation causing resistance to enzymatic cleavage. Similarly, sex-linked hypophosphataemic rickets (XLH), autosomal recessive hypophosphataemic rickets type I (ARHR1) and autosomal recessive hypophosphataemic rickets type 2 (ARHR2) are associated with overproduction of FGF23 in osteocytes due to loss of function mutations in other genes, namely PHEX, DMP1 and ENPP1 respectively (Ruppe and Jan de Beur, 2013). Conversely, a number of mutations have been identified leading to decreased FGF23 levels, resulting in familial tumoural calcinosis in which hyperphosphataemia occurs, leading to soft-tissue calcification.
An unusual case of idiopathic calcinosis of the eyelid
Published in Orbit, 2019
Ashlie A. Bernhisel, Brian E. Zaugg, Nick Mamalis, Jonathan J. Dutton, Bhupendra C. K. Patel
This brings into question which subcategory these cases should be placed into. Subepidermal calcinosis, as its name implies, is calcinosis that is deep to the epidermis but is still within the superficial dermis, which these cases clearly violate. Tumoral calcinosis would not be appropriate either, as these cases are hallmarked by the involvement of calcification within large joints. There are limited reports of calcification outside of the ocular adnexa that also demonstrate idiopathic calcinosis in tissue not only deep within the dermis, but also deep to the dermis. Examples include calcification along the iliac crest, scattered calcinosis through deeper layers of the dermis, as well as in muscular and facial plains.5,9 Perhaps the subcategories of idiopathic calcinosis are arbitrary or maybe they should be categorized further. We recommend that the medical community continue to report cases of idiopathic calcification that occurs deep within or deep to the dermis. This will help determine if these cases are truly idiopathic or whether they share an underlying pathology.
Intradural tumoral calcinosis of the foramen magnum region: A case report
Published in British Journal of Neurosurgery, 2018
Hao Wang, Yuanli Zhao, Jun Yang
Tumoral calcinosis is frequently associated with hereditary disorders of calcium metabolism or renal dialysis but can also occur in degenerated tissues in the absence of systemic disorders.1,2 To our knowledge, our report is the first to document intradural tumoral calcinosis of the foramen magnum region; therefore, the mechanism behind its development is unknown. In our case, we speculate that there may be an association between the patient’s previous neck injury and the development of tumoral calcinosis. Accordingly, some authors1 had suggested that local hemorrhage might lead to deposition of calcium salts, ultimately resulting in post-traumatic tumoral calcinosis.
A case of tumoral calcinosis in anterior vaginal wall
Published in Journal of Obstetrics and Gynaecology, 2022
Batuhan Aslan, Bulut Varlı, Çağatayhan Öztürk, Uğur Fırat Ortaç
Tumoral calcinosis (TC) is a rare disease that is usually localised in the periarticular region. Calcium deposits are observed on histopathological examination, and the lesion is usually observed in the hips, shoulders, elbows, and less frequently in the hands and feet (Bittmann et al. 2003). It is mostly idiopathic or associated with other diseases, particularly end-stage renal disease. In the present case, tumoral calcinosis in the anterior vaginal wall has been described, and surgical treatment was defined. This study was arranged according to the Declaration of Helsinki and the subject gave informed consent and the patient’s anonymity has been preserved.