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Calcification of the skin occurs in three main forms: dystrophic; metastatic; and idiopathic. Idiopathic calcinosis cutis of the penis is a rare event and only 4 cases have been reported. Herein we present another case in a 19-year-old man and discuss its probable pathogenic origin.
Two patients with limited elbow motion due to tumoral calcinosis underwent resection of calcified masses around the elbow joints. This necessilated removal of the distal two thirds and three fourths of the biceps muscles. The resulting defects were reconstructed with homologous Achilles tendon grafts. Both patients regained M4 muscle power and no recurrences were observed.
A case of calcinosis cutis caused by calcium extravasation around the wrist is presented. During excision, the lesion was seen to be surrounding the dorsal branch of the ulnar nerve. The possibility of peripheral nerve involvement in extravasation injuries is emphasized.
Calcinosis cutis is the cutaneous deposition of calcium phosphate. We present the first reported case of symmetrical calcium deposits being present in both hands at birth.
A case of tumoral calcinosis presenting as a supraclavicular mass in an infant is reported. After confirmation by incisional biopsy, the lesion spontaneously resolved without further surgical or medical treatment. This phenomenon has not been described previously in a child with this condition.
An excised specimen from a 39-year-old man with idiopathic calcinosis of the scrotum was examined by electron microscopy. Mineral deposits were located in the dermis in which collagen fibers were numerous. These collagen fibers appeared mineralized to varying degrees. Mineral crystals frequently were present in the cytoplasm of fibroblasts near large deposits. The mineral portion was identified as a compound consisting of calcium and phosphorus, and the elementary mapping of calcium and phosphorus in the skin tissue was analyzed by an energy dispersive x-ray spectrometer. No calcification was observed in dartos muscle cells or in mast cells.
Two black patients from Africa presented idiopathic tumoral calcinosis. This rare disease, defined by the presence of calcified deposits in peri-articular tissues remains poorly elucidated. Pathogenesis is still hypothetical. The diagnosis can be established with careful physical examination and appropriate complementary exams, allowing early complete surgical resection without biopsy. Pathology examination is required for formal differential diagnosis. The present tumors were particularly large, but did not produce signs of compression. In the first patient, the tumor developed after pregnancy in the zone of antibiotic injections. The second patient presented multiple bilateral symmetrical localizations with bone invasion. Histology confirmed the nature of the lesions and revealed bony metaplasie in the first patient, an element rarely described. Prognosis is excellent with early treatment. Recurrence is the rule in the event of incomplete resection. We discuss the appropriate diagnostic and therapeutic management.
A 47-year-old man complained of a constellation of prostatitis-like symptoms for 4 years. Physical examination revealed a firm nodule within the scrotum. Surgical excision was performed under local anesthesia and microscopic examination confirmed scrotal calcinosis. The patient remained symptom free for at least 12 months after excision. Although the real mechanism of prostatitis-like symptoms is unknown, this rare disease may be considered in the differential diagnosis or etiologies of chronic prostatitis, and meticulous physical examination of the scrotum is necessary for patients presenting with chronic prostatitis syndrome.
Cutaneous calcinosis following extravasation of calcium gluconate in a 6-day-old neonate is reported. After extravasation of a 10% calcium gluconate infusion, rapid and marked swelling, erythema, and signs of soft tissue necrosis developed over the dorsum of the right hand and wrist. Small eschars were soon formed on the skin surface and began to slough, the underlying base appearing necrotic. Through the small channels of the destroyed epidermis, tiny white pieces of calcific masses were eliminated spontaneously. Histologically, the dermal collagen was massively degenerated and the calcium deposits were found as amorphous masses throughout the dermis and subcutaneous adipose tissue, surrounded by mild lymphohistiocytic cell infiltration. This is a case which again warns of the danger of using 10% calcium gluconate intravenously in the neonate or young infant.
A case of calcinosis cutis is presented in a patient with hypercalcemia of unknown etiology. The axillae and inguinal areas were involved and the clinical and histologic picture is compared with pseudoxanthoma elasticum. We propose that the similarities between the two diseases stem from a common origin in damaged elastic fibers.
A case of localized calcinosis cutis of the hands and fingers is described in an oil field worker with normal serum calcium and phosphorus levels. The proposed mechanism consists of percutaneous penetration and subsequent deposition of calcium from the daily exposure to industrial drilling fluids containing calcium salts.
Hyperphosphatemic tumoral calcinosis (HTC) is a rare inherited metabolic disorder manifested by pararticular calcification and hyperphosphatemia, caused by an elevated renal phosphate reabsorption threshold and elevated serum 1,25-dihydroxyvitamin D levels. The disorder usually affects African-American subjects, but has also been described in Caucasians and Hispanics. Vascular calcifications and angioid streaks have been reported to be associated with the disorder; however, dementia has not been previously reported. Our medical center has followed two African-American siblings, with HTC for over 30 years, who have developed dementia at 56 years and 67 years of age. Neither man has been hypertensive, however, magnetic resonance imaging (MRI) scans in both cases revealed multiple periventricular infarcts, suggestive of infarcts caused by vascular calcification in the central nervous system. These two brothers with HTC suggest that periventricular infarcts with dementia may be a long term complication of this disorder.
The case of a young female child with dermatomyositis and flexion contracture in the dominant hand secondary to calcinosis is presented. Function was improved by flexor tenosynovectomy and removal of calcium deposits.
Tumoral calcinosis usually appears in the vicinity of large joints, and its appearance in the fingers must be quite rare since no reports of such an occurrence have been found. A case report of the presence of tumoral masses of hydroxyapatite in multiple digits is presented. No causative or related metabolic or collagen-vascular disease was identified, and the patient remains in good health.
The authors describe a case of tumoral calcinosis of the hand in a three-year-old child, involving the digits and carpus, and associated with ectrodactyly. The clinical features, diagnostic imaging procedures, particularly radiography and MRI, and therapeutic approach, in most cases radical excision, of this rare soft tissue tumour are discussed.
A case of tumoral calcinosis, occurring in the periarticular region of the temporomandibular joint of a 66-year-old Japanese man, is presented. The relevant literature is discussed.
Hyperphosphatemic tumoral calcinosis (HTC) is an inherited metabolic disorder characterized by calcified soft tissue masses and hyperphosphatemia. Besides these typical features, a number of less common manifestations have been reported, all of them related to pathologic calcification of various tissues. We have investigated the case of a woman with hyperphosphatemia, recurrent episodes of lumbar pain, and a positive familial history of HTC. A bone scan showed markedly increased uptake in the lower lumbar spine. Magnetic resonance imaging showed pathological changes in L5 compatible with an inflammatory reaction and not suggestive of neoplastic process. There was no evidence of infection, trauma, malignancy, or other disease that could cause the lesion. We treated the patient with analgesics and NSAIDs and the pain remitted over a period of 1 week. In a follow-up magnetic resonance imaging 7 months later, the L5 lesion had disappeared completely. A computed tomography scan analysis with a bone window showed a sclerotic area at the L5 vertebral body. We believe that this patient was affected by the syndrome of HTC and that the inflammatory phenomena found in L5 are a manifestation of this disease.
Familial tumoral calcinosis (FTC; OMIM 211900) is a severe autosomal recessive metabolic disorder that manifests with hyperphosphatemia and massive calcium deposits in the skin and subcutaneous tissues. Using linkage analysis, we mapped the gene underlying FTC to 2q24-q31. This region includes the gene GALNT3, which encodes a glycosyltransferase responsible for initiating mucin-type O-glycosylation. Sequence analysis of GALNT3 identified biallelic deleterious mutations in all individuals with FTC, suggesting that defective post-translational modification underlies the disease.