			Home About us Contact

Dystrophic Calcification (dystrophic + calcification)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Dystrophic calcification as a cause for non healing leg ulcers

INTERNATIONAL WOUND JOURNAL, Issue 2 2005
Article first published online: 28 JUN 200
Calcifications dystrophiques comme cause de non cicatrisations d'ulcères de jambe Malgré les avancées en biologie moléculaire et un répertoire d'autres optiosn thérapeutiques, les ulcères de jambe chroniques restent un problème significatif dans notre société.Il y a un certain nombre de raisons variées, locales et systémiques, qui contribuent à l'état de non cicatrisation de ces plaies. Parmi elles, les calcifications dystrophiques ( CD) ou les dépôts calciques dans le lit de l'ulcère, bien que rares, est un problème récurrent rare très décrit. En présence de CD, la cicatrisation ne peut se faire selon un processus chronologique ordonné et il en résulte un ulcère de jambe;Dans ce papier, nous discutons l'étiologie, la physiopathologie et les options de prise en charge de ces conditions rarement rapportées; Nous rapportons également leur pronostic clinique par une série de pateints porteurs d'ulcères de jambe chroniques compliqués de CD antraînant des difficultés de cicatrisation Dystrophe Kalzifikation als Ursache nichtheilender Fußulzerationen Obwohl die Molekularbiologie Fortschritte erzielt hat und ein größeres Spektrum an therapeutischen Möglichkeiten zur Verfügung steht, gehören chronisch venöse Fußulcera zu den bedeutensten Problemen unserer Gesellschaft. Es gibt verschiedene Gründe, sowohl lokaler als auch systemischer Genese, die zu einer ausbleibenden Heilung beitragen. Mögliche Ursachen sind dystrophe Kalzifikationen (DC) oder Kalkablagerungen im Wundbett. Obgleich deren Vorkommen gering ist, werden diese oft übersehen und finden in der Literatur nur selten Beachtung. Bei Vorliegen einer DC kann keine zeitgerechte oder adäquate Wundheilung stattfinden und es resultiert ein nicht abheilendes Ulkus. In dieser Abhandlung wird die Äthiologie, Pathophysiologie sowie therapeutische Möglichkeiten dieser selten berichteten Ursache diskutiert. Darüber hinaus wird die klinische Prognose von Patienten mit venösen Ulzera und komplizierter Wundheilung aufgrund einer DC erläutert Calcificazione distrofica come causa di ulcere delle gambe che non guariscono Nonostante il progresso della biologia molecolare ed il repertorio di altre opzioni terapeutiche, le ulcere venose croniche degli arti inferiori rimangono un problema significativo della nostra società. Esistono varie cause, sia locali che sistemiche, che contribuiscono alla propensione verso la mancata guarigione di queste ulcere. Tra queste la calcificazione distrofica (DC) o il deposito di calcificazioni all'interno del fondo di ferita, sebbene raro, è un reperto sottostimato e spesso all'origine delle lesioni. In presenza di DC, la riparazione tessutale non può procedere verso un percorso ordinato e temporale. In questo lavoro, abbiamo discusso l'eziologia, la patofisiologia e le opzioni di gestione di questa condizione raramente segnalata. Riportiamo inoltre la prognosi clinica utilizzando una serie di pazienti con ulcere venose complicate da DC verso una guarigione ritardata. La calcificación distrófica como causa del retraso de la cicatrización en úlceras vasculares A pesar de avances en biología molecular y un conjunto de otras opciones terapéuticas, las úlceras vasculares venosas crónicas siguen siendo un problema significativo en nuestra sociedad. Existen varios motivos, tanto locales como sistémicos, que contribuyen al retraso en el proceso de cicatrización de tales heridas. Entre ellos, la calcificación distrófica (CD), o depósitos calcificados dentro del lecho ulceroso, es una causa rara descrita en contadas ocasiones. En presencia de una CD, la curación de la herida no puede evolucionar favorablemente, con el resultado de la no cicatrización de la úlcera. En este trabajo discutimos la etiología, la fisiopatología y las opciones terapéuticas de este proceso que se describe en raras ocasiones. También informamos de su pronóstico clínico utilizando una serie de pacientes con úlceras venosas complicadas por CD, que conlleva dificultades para su cicatrización. Dystrofisk kalcifiering som orsak till icke-läkande bensår Trots framsteg i molekylärbiologi och en repertoire av andra terapeutiska möjligheter kvarstår kroniska bensår som ett betydande problem i vårt samhälle. Orsakerna som bidrar till den icke-läkande karaktären av dylika sår är varierande, de är både lokala och systemiska. Bland annat är dystrofisk kalcifiering (DC) eller kalcifierade depositioner i sårbädden, även om sällsynt, en förbisedd och sällan rapporterad orsak. Sårläkning kan inte framskrida i tidsenlig ordning i närvaro av DC och resulterar i ett icke-läkande sår. I detta paper, diskuterar vi etiologi, patofysiologi och behandlingsmöjligheter av detta sällan rapporterade tillstånd. Vi redogör också för den kliniska prognosen med hjälp av en serie patientfall av venösa ulcera med DC komplikation som lett till läkningssvårigheter. [source]

Dystrophic calcification and amyloidosis in old subcutaneous injection sites

ANZ JOURNAL OF SURGERY, Issue 7 2003
Benjamin P. C. Wei
No abstract is available for this article. [source]

Dystrophic calcification following neonatal heel-prick testing

AUSTRALASIAN JOURNAL OF DERMATOLOGY, Issue 3 2010
Ann-Maree Kurzydlo
ABSTRACT A 7-year-old boy presented with a 5-year history of dystrophic calcification manifesting as solitary nodules on the plantar aspect of both heels. Microscopic examination showed hyperkeratosis and psoriasiform hyperplasia overlying an area of dystrophic calcification. Multiple heel-prick tests carried out during the neonatal period to monitor blood glucose levels are the likely causative mechanism. [source]

Multiple nodules of the scrotum: histopathological findings and surgical procedure.

JOURNAL OF THE EUROPEAN ACADEMY OF DERMATOLOGY & VENEREOLOGY, Issue 6 2006
A study of five cases
Abstract Background, Multiple nodules of the scrotum are uncommonly reported. Their origin is controversial. Treatment is always surgical but the best procedure is still to be determined. Materials and methods, Five new cases are reported with description of the histopathological findings and surgical procedure. Results, Nodules of the scrotum were more frequent in patients with dark skin suggesting an ethnic susceptibility. No other predisposing factors were noted. Screening for disturbances of phosphate or calcium balance was negative. The following histopathological findings were observed: non-calcified epidermoid cysts (3 patients), calcified epidermoid cysts (1 patient) and nodular calcifications without epithelial or glandular structures (1 patient). Subtotal excisions of the scrotum wall using tumescent anaesthesia were performed in all patients without any significant complications. Cosmetic results were excellent. No new lesions were observed during the 1-year follow-up period. Conclusions, Most cases of multiple nodules of the scrotum are due to non-calcified epidermoid cysts. The term scrotal calcinosis is therefore probably abusively used by many authors. Some cases of nodular calcifications may be due to dystrophic calcification of epidermoid cysts, but calcifications may also occur without any visible epithelial or glandular structure. Subtotal excision of the scrotum wall is a safe and effective surgical procedure to treat multiple nodules of the scrotum. Cosmetic results are excellent and recurrences are rare. [source]

Dystrophic calcification following neonatal heel-prick testing

Pseudotumoral encapsulated fat necrosis with diffuse pseudomembranous degeneration

JOURNAL OF CUTANEOUS PATHOLOGY, Issue 8 2004
F. Felipo
An extraordinary case of encapsulated fat necrosis characterized by its large size, diffuse formation of pseudomembranes, and tendency to recur after excision is reported. A 67-year-old Caucasian woman suffering from morbid obesity was admitted for diagnosis and surgical treatment of a soft tissue mass showing a longest diameter of 14 cm and lying adjacently to the scar from previous appendicectomy. Histopathologic features were consistent with a nodular-cystic encapsulated fat necrosis with diffuse pseudomembranous transformation. Eight months after surgery, a new larger mass (longest diameter of 18 cm) sharing identical histopathologic features appeared in the same location. Encapsulated fat necrosis is a well-defined entity even though several names have been proposed for this condition, including mobile encapsulated lipoma, encapsulated necrosis, or nodular-cystic fat necrosis. Its pathogenesis seems to be related to ischemic changes secondary to previous trauma. It may occasionally show degenerative changes, including dystrophic calcifications and presence of pseudomembranes. To our knowledge, these are the first reported cases of encapsulated fat necrosis presenting as lesions of such size and showing diffuse formation of pseudomembranes; these particular features made diagnosis difficult and led to consideration of a wide range of potential diagnostic possibilities. This case expands the clinico-pathologic spectrum of membranocystic fat necrosis, including the potential ability of this subcutaneous fatty tissue abnormality to recur after surgical excision. [source]

Study of a myo -inositol hexaphosphate-based cream to prevent dystrophic calcinosis cutis

BRITISH JOURNAL OF DERMATOLOGY, Issue 5 2005
F. Grases
Summary Background, Calcinosis cutis is a disorder caused by abnormal deposits of calcium phosphate in the skin and is observed in diverse disorders. Myo -inositol hexaphosphate (InsP6) is a diet-dependent molecule found in all mammalian fluids and tissues, which exhibits an extraordinary capacity as a crystallization inhibitor of calcium salts. Objectives, To establish the effects of topically administered InsP6 cream on artificially provoked dystrophic calcifications in soft tissues. Methods, Fourteen male Wistar rats were randomly assigned into two groups: control and treated groups. Rats were fed with an InsP6 -free or phytate diet. Plaque formation was induced by subcutaneous injection of 0·1% KMnO4 solution. From 4 days before plaque induction to the end of the experiment, control rats were treated topically with a standard cream, whereas treated rats were treated with the same cream with 2% InsP6 or phytate (as sodium salt). Calcification of plaques was allowed to proceed for 10 days. InsP6 in urine was determined. The plaques were excised and weighed. Results, It was found that when InsP6 was administered topically through a moisturizing cream (2% InsP6 -rich), the plaque size and weight were notably and significantly reduced compared with the control group (1·6 ± 1·1 mg InsP6 -treated, 26·7 ± 3·0 mg control). The InsP6 urinary levels for animals treated with the InsP6 -enriched cream were considerably and significantly higher than those found in animals treated topically with the cream without InsP6 (16·96 ± 4·32 mg L,1 InsP6 -treated, 0·06 ± 0·03 mg L,1 control). Conclusions, This demonstrates the important capacity of InsP6 as a crystallization inhibitor and also demonstrates that it is possible to propose topical use as a new InsP6 administration route. [source]