| Dr.Hassan sent the following set
of abstracts:-
1: Handchir Mikrochir Plast Chir 1999 Jan;31(1):57-60
[Surgical treatment of Thibierge-Weissenbach syndrome and other calcinoses of the hand.
Case report and review of the literature]. [Article in German]
Kauschke T, Zilch H Klinikum Grosshadern,
Orthopadische Klinik und Poliklinik, Munchen.
Soft-tissue calcifications in the hands may often be a sign of a systemical disease. The
calcification then appears as a secondary manifestation of this disease. In that case,
operative treatment ought to be a part of the overall treatment of the primary disease.
When operating on fingers, the surgeon must pay attention not to compromise blood supply.
Publication Types: Review Review, tutorial PMID: 10080064, UI: 99179800
2: J Eur Acad Dermatol Venereol 1998 Jul;11(1):69-71
Benign nodular calcification and calciphylaxis in a haemodialysed patient.
Strumia R, Lombardi AR, Bedani PL, Perini L Clinica Dermatologica, Universita di Ferrara,
Italy.
Several types of soft tissue calcification can be detected from radiographic evaluation of
patients with end-stage renal failure. The factors that predispose to such calcification
include an increase in CaxP product in serum, the degree of secondary hyperparathyroidism,
the level of blood magnesium, the degree of alkalosis, and the presence of local tissue
injury. Three major varieties include calcification of medium-sized arteries,
periarticular or tumoral calcification and visceral calcification. Calciphylaxis is a
phenomenon consisting of acute ischemic necrosis in presence of calcification of
dermohypodermic arterioles. It occurs mostly in chronic renal failure patients with
secondary or tertiary hyperparathyroidism with a persistently elevated calcium-phosphorus
product. There are few options in treating calciphylaxis and the outcome is generally
poor. The authors report the case of a haemodialised patient with benign nodular
calcification and calciphylaxis. The coexistence of both entities in the same patient has
never been described.
PMID: 9731971, UI: 98400720
3: Handchir Mikrochir Plast Chir 1994 Nov;26(6):330-4
[Hypercalcinosis of the hands in scleroderma. 2 case reports]. [Article in German]
Eckardt J, Towfigh H Malteser-Krankenhaus St. Josef in Hamm.
Hypercalcinosis of the hand in association with scleroderma represents a rare and benign
soft-tissue calcification. Reported are two cases of symmetric affection of soft-tissue
layers of both hands in association with scleroderma. Superinfection and exulcerations
necessitated surgical treatment. Diagnosis, therapy, and progress are described.
PMID: 7867986, UI: 95172441
4: J Hand Surg [Br] 1994 Oct;19(5):642-6
Soft tissue calcification in children with terminal transverse defects of the upper
limb--is it tumoral calcinosis?
Itoga H, Jones JM, Hooper G Princess Margaret Rose Orthopaedic Hospital, Edinburgh, UK.
We report five children with transverse defects of the upper limb who developed calcified
deposits at the distal end of the limb. The lesions were excised from two children and had
the typical histological appearance of tumoral calcinosis but on clinical grounds it is
unlikely that this is the same condition as that previously described as tumoral
calcinosis.
PMID: 7822929, UI: 95123228
5: J Hand Surg [Am] 1994 Sep;19(5):809-12
Uremic tumoral calcinosis: acute hand presentations mimicking infection.
Asuncion GF, Tzarnas CD Mercy Catholic Medical Center, Darby, Pennsylvania.
Tumoral calcinosis is an uncommon condition of the hand characterized by deposition of
calcium salts in the soft tissues of the extremities. The condition may be hereditary or
acquired. Acquired tumoral calcinosis, also called tumoral calcification, is a rare
manifestation of renal osteodystrophy due to derangement in divalent ion metabolism. Two
chronic dialysis patients with tumoral calcification of the hand are presented. These
cases are unusual in their rapid onset of presentation, mimicking acute infection. Prompt
recognition of the condition may allow early nonsurgical intervention to preserve
function.
PMID: 7806807, UI: 95105487
6: Nephrol Dial Transplant 1993;8(6):530-4
Calcium carbonate (CaCO3): an efficient and safe phosphate binder in haemodialysis
patients? A 3-year study.
Sperschneider H, Gunther K, Marzoll I, Kirchner E, Stein G Department of Internal
Medicine, Friedrich-Schiller-University of Jena, Germany.
In an uncontrolled study, 22 dialysis patients (46 +/- 14 years, duration of dialysis 20
+/- 11 months) were treated with CaCO3 over a period of up to 3 years to lower their serum
phosphate. The use of 4.5-9 g CaCO3 daily over a period of 9 months led to a reduction of
mean serum phosphate from 2.51 to 1.51 mmol/l in 77% of patients, with a simultaneous
increase in mean calcium concentration from 2.23 to 2.47 mmol/l, and an improved control
of secondary hyperparathyroidism by reduction in mPTH from 1552 to 1032 pg/ml and in APH
activity from 6.25 to 4.55 mumol/s/l. In long-term CaCO3 treatment of up to 3 years,
however, a constant effective phosphate reduction could not be achieved. There was a
progression (77%) of pre-existing microcalcification and a new appearance (42%) of
microcalcification in vessels and soft-tissue areas of the hand. The percentage of
patients with soft-tissue calcification increased from 43 to 67% during a treatment period
of 3 years. We conclude that CaCO3 alone is not suitable on a long-term basis for
phosphate reduction in dialysis patients.
Comments: Comment in: Nephrol Dial Transplant 1994;9(3):335-6
PMID: 8394534, UI: 93354644
7: Orthop Rev 1989 Apr;18(4):440-2
Tumoral calcinosis. Case presentation and review.
Buschmann WR, Myers W, Sager G Division of Orthopaedics, Bronx-Lebanon Hospital Center,
New York.
Tumoral calcinosis is a disease of unknown etiology with a greater prevalence among
blacks, in which subcutaneous calcifications are found around the extensor surface of the
hip, shoulder, hand and occasionally the knee. They must be differentiated from other more
common causes of calcification.
Publication Types: Review Review of reported cases
PMID: 2654827, UI: 89239636
8: J Hand Surg [Am] 1984 Mar;9(2):243-5
A case report of calcinosis universalis.
Haher TR, Devlin VJ, Haher JN, Freeman B, Smith AG
Calcium deposits in soft tissues without previous trauma may represent calcinosis
universalis, a condition without systemic manifestations and with laboratory values of
blood and urine that are consistently normal. Radiographs reveal areas of calcification
with homogenous density, and microscopic examination of these deposits shows foreign body
giant cell reaction without capsule formation. In this case of calcinosis universalis,
wide excision and lavage of the calcium deposits were temporarily beneficial, but the
deposits recurred in this patient.
PMID: 6715834, UI: 84186747
9: ROFO Fortschr Geb Rontgenstr Nuklearmed 1983
Aug;139(2):150-7
[Soft tissue calcifications of distal phalangeal tuberosities of the fingers]. [Article in
German]
Fischer E
Soft tissue calcification at the margin of the tuberosity of the distal phalanges of the
fingers occurs in 7% of normal adults, varying between 0 and 14.5%, depending on age and
sex. This type of calcification is least common in the little finger. The fingers on the
right are more frequently affected than those on the left. Presumably this calcification
results from mechanical injury ot the collagen fibres close to their insertion into the
margin of the tuberosity.
PMID: 6409749, UI: 83263473
10: Am J Kidney Dis 1991 Dec;18(6):706-10
Uremic tumoral calcinosis: preliminary observations suggesting an association with
aberrant vitamin D homeostasis.
Quarles LD, Murphy G, Econs MJ, Martinez S, Lobaugh B, Lyles KW
Department of Medicine, Duke University Medical Center, Durham, NC.
Periarticular tumoral calcification is a unique form of soft tissue calcification that
occurs infrequently in patients with end-stage renal disease. The mechanism underlying
such massive periarticular calcifications is unknown. The radiographic similarity between
uremic tumoral calcifications and those found in hereditary tumoral calcinosis, a disorder
of calcitriol and phosphorus homeostasis, caused us to examine whether abnormalities in
vitamin D metabolism were associated with uremic calcinosis as well. We examined two
uremic subjects with massive periarticular tumoral calcifications and found that they had
inappropriately high serum calcitriol levels for the degree of renal function,
hyperparathyroidism, and hyperphosphatemia. The source of calcitriol could not be
identified in one subject, but likely was derived from granulomatous tissue in the other.
In the subject with marrow granulomas, we found that calcitonin administration further
stimulated calcitriol production. Although epidemiological studies are needed to confirm
this preliminary association between calcitriol and uremic tumoral calcinosis, our
observations suggest that normal serum calcitriol levels in association with
hyperphosphatemia may be a contributing factor in the development of this rare disorder.
PMID: 1962658, UI: 92074502
11: Clin Exp Dermatol 1996 Mar;21(2):163-6
Tumoral calcinosis: an unusual cause of cutaneous calcification.
Harwood CA, Cook MG, Mortimer PS
Department of Dermatology, St. George's Hospital, London, UK.
Tumoral calcinosis is an uncommon ectopic calcification syndrome characterized clinically
by the presence of irregular, painless, periarticular soft tissue calcifying masses, and
pathologically by fibrous-walled cystic spaces containing structureless calcific debris
and associated with a variable inflammatory reaction. The pathogenesis remains obscure but
the condition probably represents a disordered tissue reparative process. Of the previous
literature reports, almost all have been in patients of African origin. We report a case
in a white English woman.
PMID: 8759210, UI: 96336860
12: Int Orthop 1993 Nov;17(5):279-81
Tumoral calcinosis of the fingers. A report of two cases.
Malik M, Acharya S
Central Institute of Orthopaedics, Safdarjang Hospital, New Delhi, India.
Tumoral calcinosis is an uncommon condition which usually appears in the region of large
joints. It is rare in the hand. We present two cases affecting the fingers. No causative
abnormality was found.
PMID: 8125661, UI: 94171424
13: Nephrol Dial Transplant 1996;11 Suppl 3:37-42
A clinical approach to the uraemic patient with extraskeletal calcifications.
Drueke TB
INSERM Unit 90, Necker Hospital, Paris, France.
Soft tissue calcifications are a frequent complication in patients with chronic renal
failure. In most instances they remain clinically silent. However, in a minority of
patients they are responsible for complications and may even become life-threatening.
Various locations and types of calcium deposits have been characterized. Numerous
underlying factors are thought to favour their formation, in particular increased calcium
x phosphate product and advanced age. In most cases, local factors probably are involved
as well. Tumoral calcinosis is a rarely observed form of extraskeletal calcification which
is often invalidating. Since treatment is generally difficult, prevention should be the
preferred goal.
Publication Types:
Review
Review, tutorial
PMID: 8840310, UI: 96437701
14: J Nucl Med 1990 Jun;31(6):1099-103
Periarticular tumoral calcinosis and hypercalcemia in a hemodialysis patient without
hyperparathyroidism: a case report.
Eisenberg B, Tzamaloukas AH, Hartshorne MF, Listrom MB, Arrington ER, Sherrard DJ
Service of Nuclear Medicine, VA Medical Center, Albuquerque, New Mexico 87108.
We present a case of a 58-yr-old male to illustrate the scintigraphic, roentgenographic,
clinical, and pathologic features of periarticular tumoral calcinosis that occurred in a
hemodialysis patient. Soft-tissue calcifications developed 3 yr after onset of
hemodialysis, became progressively larger during the ensuing five years, and culminated in
voluntary withdrawal from dialysis because of the extreme discomfort and lack of mobility
that resulted from the calcinosis. Histologically, an aplastic disorder was present with
very low bone formation. On bone scintigraphy, intense calcium uptake in soft tissues
implied that it was metabolically active. We hypothesize that this high metabolic activity
contributed to the persistent hypercalcemia observed during the patient's last year of
life.
PMID: 2348239, UI: 90270939
15: J Rheumatol 1992 Oct;19(10):1640-2
Massive soft tissue calcification causing complete loss of extensor tendon function in
renal failure.
Schenkier SL, Gertner E
Section of Rheumatology, St. Paul-Ramsey Medical Center, MN 55101.
Extraskeletal soft tissue calcifications occur commonly in patients with uremia receiving
dialysis. Rarely, a large tumoral calcinosis-like mass may develop. A patient receiving
chronic ambulatory peritoneal dialysis for only 7 months developed a tumoral
calcinosis-like mass that encased the extensor tendons of his wrist with loss of extensor
tendon function, initially suggesting extensor tendon rupture. Surgical debridement
restored tendon function. Tumoral calcinosis-like lesions are uncommon, but may cause
limitation of joint movement, pain or ulceration through the skin. Measures aimed at
controlling factors contributing to soft tissue calcification should be undertaken in any
event whether surgery is required or not.
PMID: 1464882, UI: 93100713
16: Skeletal Radiol 1996 May;25(4):388-90
Idiopathic tumoral calcinosis involving the cervical spine.
Ohashi K, Yamada T, Ishikawa T, Yamaguchi S, Nakajima H, Takagi M
Department of Radiology, St. Marianna University Hospital, Kanagawa, Japan.
We report a case of a 12-year-old girl with idiopathic tumoral calcinosis of the neck.
There are calcium deposits in the paraspinal soft tissue with bony involvement in the
cervical spine. CT and MR images are presented along with
clinical and pathological features. Bony involvement in this disease has not been
recognized before.
PMID: 8738007, UI: 96347341
17: Postgrad Med J 1977 Sep;53(623):570-3
Tumoral calcinosis: a manifestation of extreme metastatic calcification occurring with 1,
alpha-hydroxycholecalciferol therapy.
Walker GS, Davison AM, Peacock M, McLachlan MS
Two cases are reviewed, both of which developed tumoral calcinosis whilst receiving 1,
alpha-hydroxy-cholecalciferol therapy. Tumoral calcinosis is an extreme form of
peri-articular calcification, and its occurrence in patients
with chronic renal failure is unusual. These peri-articular masses developed around the
shoulders in both patients, and the action of 1,alpha-hydroxycholecalciferol as a possible
factor promoting this form of metastatic calcification is discussed.
PMID: 928257, UI: 78052668
18: Orthop Rev 1993 Mar;22(3):365-9
Combined modality treatment for tumoral calcinosis.
Calloway DM, Saldana MJ
Eastern Virginia Medical School, Norfolk.
Tumoral calcinosis is a rare syndrome marked by periarticular and intramuscular
calcifications. We present the case of a 13-year-old black girl who has received treatment
since age 2 for tumoral calcinosis with bilateral shoulder
involvement.
PMID: 8474774, UI: 93234119
19: Kidney Int 1990 Nov;38(5):931-6
Soft tissue calcification in pediatric patients with end-stage renal disease.
Milliner DS, Zinsmeister AR, Lieberman E, Landing B
Department of Pediatrics, Mayo Clinic, Rochester, Minnesota.
Soft tissue calcification is a recognized complication of uremia in adult patients and has
been implicated as a cause of ischemic necrosis, cardiac arrhythmias, and respiratory
failure. However, soft tissue calcification has been regarded as rare in pediatric renal
patients. Following a sudden death due to pulmonary calcinosis in an adolescent after
renal transplantation, we retrospectively reviewed clinical, biochemical and autopsy data
of 120 patients with uremia, on dialysis, or following renal transplantation cared for at
Childrens Hospital of Los Angeles from 1960 to 1983. Soft tissue calcification was found
in 72 of 120 patients (60 percent). Forty-three patients (36 percent) had systemic
calcinosis (Group A): the most frequent sites of mineral deposition were blood vessels,
lung, kidney, myocardium, coronary artery, central nervous system, and gastric mucosa.
Vascular calcification was uniformly accompanied by deposits in other organs. Twenty-nine
patients had small amounts of focal calcification (Group B) and 48 patients had no soft
tissue calcification (Group C). By multiple logistic regression analysis, the use of
vitamin D or its analogues, the form of vitamin D medication prescribed, the peak calcium
x phosphorus product, the age at onset of renal failure, and male sex were jointly
associated with calcinosis (Group A). Vitamin D therapy showed the strongest independent
association with calcinosis and the probability of calcinosis was greater in patients
receiving calcitriol when compared with dihydrotachysterol and vitamin D2 or D3. The
duration of renal failure, peak serum calcium, serum calcium at death, serum phosphorus at
death, and primary renal diagnosis, were not statistically associated with
calcinosis.(ABSTRACT TRUNCATED AT 250 WORDS)
PMID: 2266678, UI: 91094234
20: J Rheumatol 1999 Feb;26(2):379-85
Uremic tumoral calcinosis in patients receiving longterm hemodialysis therapy.
Cofan F, Garcia S, Combalia A, Campistol JM, Oppenheimer F, Ramon R
Orthopedic Department, Hospital Clinic, University of Barcelona, Spain.
OBJECTIVE: To analyze a series of uremic tumoral calcinosis (UTC) in patients receiving
longterm dialysis therapy. METHODS: Twelve patients receiving longterm hemodialysis
affected by tumoral calcinosis were analyzed. Clinical,
radiological, and pathological features were evaluated and pathogenic factors were
reviewed. RESULTS: The most common sites for UTC were the elbow, hip, hand, and wrist. The
lesions were multiple (67%, n = 8), of large size, and symptomatic with joint mobility
impairment (75%, n = 9) as well as nerve compression (33%, n = 4). High serum calcium and
phosphate concentrations were detected in 50% (n = 6) and 100% of the patients,
respectively. An increased calcium-phosphorus product (Ca x P) was observed in all
patients, either due to overt secondary hyperparathyroidism (42%, n = 5), or secondary to
iatrogenic hypercalcemia and/or severe hyperphosphoremia of multifactorial etiology (i.e.,
prolonged and excessive administration of calcitriol and calcium carbonate, insufficient
dialysis and inadequate phosphorus chelating therapy, etc.) (58%, n= 7). Several treatment
strategies were followed (surgical excision, parathyroidectomy, renal transplant) in
combination with aggressive medical therapy to decrease Ca x P product, achieving complete
remission in 83% of the patients. CONCLUSION: UTC lesions show clinical and pathogenic
features that differ from those of idiopathic tumoral calcinosis. The most important
pathogenic factor involved in UTC is an increase in Ca x P, not necessarily related to
hyperparathyroidism. Combined treatment strategies allow complete remission in a high
proportion of patients. A low Ca x P is necessary to prevent development of UTC.
PMID: 9972973, UI: 99137258
21: Rev Chir Orthop Reparatrice Appar Mot 1994;80(3):261-6
[Tumoral calcinosis: a clinical and pathological study of 8 cases reported in Tunisia].
[Article in French]
Ammar A, Ben Romdhane K, Khattech R, Ben Othman M, Ben Ghachem M
Service d'Anatomie et Cytologie Pathologiques Institut Salah Azaiz, Tunis.
Tumoral calcinosis is a distinct clinicopathological entity characterized by periarticular
soft-tissue calcium deposits. It is a rare condition in Tunisia (8 cases during 23 years).
Six patients were aged 14 years or younger. There was male predominance (SR: 7/1). Lesions
were located about the hip in five patients and the elbow in three patients. Multiple
localisations occurred in two patients. Histologically, all cases exhibited active phase
of the disease. In our patients lesions were only surgically excised.
PMID: 7899646, UI: 95207544
22: J Dermatol 1996 Aug;23(8):545-50
Tumoral calcinosis: report of a case and brief review of the literature.
Abraham Z, Rozner I, Rozenbaum M
Department of Dermatology, Reish Policlinic, Haifa, Israel.
A patient with a 32-year history of tumoral calcinosis is described. The calcified lesions
involved the soft tissues in the hips, shoulders, and ankles.Periodically, a chalky
semifluid material extruded through several cutaneous sinuses. Laboratory tests including
serum calcium concentration were normal, except for slight elevation of serum phosphorous
levels. Ophthalmologic examination revealed the interesting finding of subretinal angioid
streaks. The dental radiograms disclosed pathognomonic short bulbous roots and partial
obliteration of pulp cavities, while the radiological evaluation of the tumoral masses
revealed typical features of tumoral calcinosis.
Publication Types:
Review
Review of reported cases
PMID: 8854587, UI: 97007312
23: Acta Orthop Belg 1993;59(3):249-54
Tumoral calcinosis, a clinical report of eleven cases.
Noyez JF, Murphree SM, Chen K
Department of Surgery, H. Hartziekenhuis, Roeselare, Belgium.
Clinical observations of 11 new cases of tumoral calcinosis are reported. The condition is
characterized by calcified masses of varying size in the region of major joints. Surgical
excision is recommended in selected cases determined by the size of the lesion, the
deformity present and functional complaints. In this series surgical excision was done in
6 patients, and the diagnosis was confirmed histopathologically. After a complete excision
of the tumor, no recurrences were seen in 5 cases with a mean follow-up time of 25 months.
Incomplete excision led to multiple recurrences in one patient.
PMID: 8237339, UI: 94055670
24: Rev Chir Orthop Reparatrice Appar Mot 1989;75(5):340-4
[Tumor calcinosis. Review of the literature: apropos of a case]. [Article in French]
Haddad SN, Ghossain MA, Jebara VA, Roucos S, Kharrat K, Boustany FN
Service de Radiologie, Hotel-Dieu de France, Beyrouth, Liban.
Tumoral calcinosis is an uncommon disease of unknown etiology characterized by the
presence of single or multiple lobulated, para-articular, cystic soft tissue productions.
Hyperphosphatemia is the only biological abnormality which can be detected. The honeycomb
roentgenographic pattern is characteristic. CT scan and ultrasound are useful in showing
the extra-articular location of the mass. The treatment is surgical and the prognosis is
good.
Publication Types:
Review
Review of reported cases
PMID: 2682818, UI: 90047896
25: Arch Surg 1993 Jul;128(7):737-44; discussion 744-5
Tumoral calcinosis. Controversies in the etiology and alternatives in the treatment.
Tezelman S, Siperstein AE, Duh QY, Clark OH
Surgical Services, Mount Zion Medical Center, San Francisco.
OBJECTIVE: To examine our experience and review the literature concerning the diagnosis,
origin, and treatment of tumoral calcinosis (TC). DESIGN/SETTING: Case series based on
patients with TC treated in University of California-San Francisco hospitals from 1981 to
1992 and the review of the patients described in the English-language literature.
PATIENTS: The study included a total of 17 patients: 10 women and seven men. MAIN OUTCOME
MEASURES: Sex, age, origin, symptoms, localization, treatment, and morbidity.
RESULTS: Seven men and six women, from 32 to 62 years of age, had known disorders of
calcium metabolism, and four women, from 37 to 84 years of age, did not. The main causes
of the calcium metabolic disorder were secondary hyperparathyroidism in 11 patients (85%)
and primary hyperparathyroidism in two patients. In three patients there
was a history of trauma at the involved site and in one patient the origin was unknown.
Swelling and pain are the most common presenting complaints. Generalized pruritus was
observed in 54% of the patients with metabolic
disorders (P < .001) but not in patients without metabolic disorders. Among our
patients with metabolic disorders, TC occurred most frequently at the shoulder (46%) and
elbow (31%). Eleven patients with secondary hyperparathyroidism had received calcium
carbonate to bind phosphate, a high level of calcium in the dialysate, and calcitriol
(1,25-vitamin D) either orally, intravenously, or both, and three received epoetin alfa
(Epogen). Following parathyroidectomy, the patients with hyperparathyroidism improved
symptomatically, although calcifications did not change in size. One patient had the
calcifications resected and did well, whereas another was treated by subtotal resection
and had a recurrence 3 years later. All four of our patients without a metabolic disorder
had complete resection of TC with no recurrence. CONCLUSION: We believe TC is becoming
more common in uremic patients with secondary hyperparathyroidism because of recent
changes in the medical treatment of these patients. The
increased use of calcium carbonate to bind phosphate as well as calcitriol and calcium to
suppress parathyroid function and possibly epoetin alfa are causing more patients to
develop TC.
PMID: 8317954, UI: 93304999
26: Clin Exp Dermatol 1993 Jul;18(4):370-2
Cutaneous calcinosis--an unusual complication of intravenous phosphate administration.
Mills CM, Knight AG
Department of Dermatology, University Hospital of Wales, Cardiff, UK.
The case of an 80-year-old woman who developed extensive cutaneous calcification following
intravenous phosphate administration is presented. Also the circumstances under which
cutaneous calcification may occur are discussed.
PMID: 8403480, UI: 94007256
27: Am Surg 1994 Feb;60(2):81-6
Calciphylaxis: early recognition and management.
Roe SM, Graham LD, Brock WB, Barker DE
Department of Surgery, University of Tennessee, College of Medicine-Chattanooga
Unit 37403.
Calciphylaxis, a syndrome of disseminated calcification found in chronic renal failure
patients with secondary hyperparathyroidism, results in soft tissue calcification and
vascular medial calcinosis leading to subsequent ischemic tissue necrosis. It is a rarely
occurring condition in which patients present with painful, violaceous, mottled lesions of
the extremities and/or trunk that progress to skin and subcutaneous tissue necrosis,
non-healing ulcers, and gangrene. We reviewed the clinical course of seven patients (aged
24-69) with calciphylaxis treated at our institution over a 4-year period (October
1988-June 1992). All seven patients underwent parathyroidectomy, with a mean time of 8
weeks (range 3-20 weeks) between the onset of calciphylactic symptoms and
parathyroidectomy. Four patients died, three secondary to wound-related sepsis. Of the
three survivors, two healed soft tissue lesions primarily. The other required extremity
amputation and wound excision before healing. Neither anatomical location of the soft
tissue lesions nor post-parathyroidectomy serum calcium and phosphorus levels had any
bearing on wound healing or mortality. Lesion severity at the time of parathyroidectomy
appeared to best correlate with clinical course. Although treatment with phosphate-binding
antacids, total or subtotal parathyroidectomy, and avoidance of challengers such as
Vitamin D or local tissue trauma remain the mainstays of therapy, the uniform cure for
calciphylaxis remains elusive. Prognosis for patients with calciphylaxis is dismal, even
following late surgical intervention. Earlier recognition of the signs and symptoms of
calciphylaxis should lead to timely parathyroidectomy in the hopes of ameliorating the
symptoms and preventing or retarding its progressive sequelae.
PMID: 8304650, UI: 94136837
28: J Formos Med Assoc 1993 Jun;92(6):569-76
Differential diagnosis between fibrodysplasia ossificans progressiva and childhood
dermatomyositis with calcinosis.
Wu T, Chen SS
Department of Neurology, Chang Gung Medical College and Memorial Hospital, Taipei, Taiwan,
R.O.C.
Both fibrodysplasia ossificans progressiva (FOP) and childhood dermatomyositis with
calcinosis are rare diseases, and present with ossifying or calcifying processes. Six
cases of FOP and one case of childhood dermatomyositis with calcinosis are studied. All
six FOP patients had the typical digital anomalies and the characteristic ectopic bone
formation starting from the trunk. Calcification in the case of childhood dermatomyositis
occurred in the limbs. A carefully differentiated diagnosis between these two diseases is
needed, because they share common clinical and radiologic features, but require different
management. Delay in the diagnosis of FOP is common, although early recognition of FOP
prevents a child from accidental or iatrogenic injury, which can precipitate ectopic
ossification. Surgical removal of the ectopic bone or release of the contracture in three
FOP patients was followed by rapid
recurrence. Entrapment neuropathy and a mild myopathic pattern in two FOP patients, who
underwent nerve conduction and electromyographic studies, were secondary to ectopic bone
formation. One FOP patient received a computed tomography examination which showed basal
ganglia calcification. No coexistence of FOP and childhood dermatomyositis with calcinosis
was found.
PMID: 8106047, UI: 94034472
29: J Clin Invest 1976 Mar;57(3):700-5
Bone pyrophosphate in uremia and its association with extraosseous calcification.
Alfrey AC, Solomons CC
The mean bone pyrophosphate was 0.360 +/- 0.15 mg/g in 8 controls and 1.22 +/- 1.39 mg/g
bone in 27 uremic patients (P less than 0.0025). 13 of the 27 uremic patients had bone
pyrophosphate levels greater than 2 SD above control values. The ash content of uremic
bones with increased pyrophosphate levels (group II) was 56 +/- 9% as compared to 64 +/-
2% in control bones (P less than 0.01) and 60 +/- 7% in uremic bones having normal
pyrophosphate levels (P less than 0.1) (group I). The magnesium content of bones in group
II was 338 +/- 47 as compared to 211 +/- 13 (P less than 0.0005) in the controls and 294
+/- 73 mmol/kg ash (P less than 0.05) in group I. In group II, but not group I, there was
a significant inverse correlation between duration of dialysis and percent bone
ash (r = -0.59) (P less than 0.05). A definite relationship existed between elevated bone
pyrophosphate levels and soft tissue calcification. In group II the mean pulmonary calcium
content was 530 +/- 459 as compared to 32 +/- 26 mmol/kg/ash in group I (P less than
0.0025). All patients with a bone pyrophosphate level greater than 1.4 mg/g bone had
extensive pulmonary calcification. It is concluded that the excess bone pyrophosphate
present in some uremic patients is either deposited in the apatite crystal in the
transphosphorylated form or else as the magnesium salt since the pyrophosphate is
resistant to pyrophosphatase and surface adsorption of pyrophosphate is not
altered by the increased bone pyrophosphate levels. The excess bone pyrophosphate could
disturb bone calcification mechanisms in uremic patients. The association between
increased bone pyrophosphate and soft tissue calcification suggests that the disordered
pyrophosphate metabolism may be important in the pathogenesis of extraosseous
calcification.
PMID: 175092, UI: 76120832
30: Chir Narzadow Ruchu Ortop Pol 1989;54(2):159-63
[Calcinosis tumoralis. Pharmacological alternatives to surgical treatment and its
etiological justification]. [Article in Polish]
Gregosiewicz A, Warda E, Stolecka D, Kandzierski G
A detailed case history of a 6 years old child, including biochemical and radiological
examinations, has been presented. The disease started with a commonplace contusion of the
patella and rapidly progressed after arthrotomy. Dihydroxy-aluminium-natrium carbonicum
was applied as well as the low calcium and phosphorus diet. After 4 weeks of treatment,
the joint recovered its correct contours; and after further 7 months, only vestigial
calcification was observed.
PMID: 2625052, UI: 90168496
The following additional papers are selected from a
PubMed Search for "Calcinosis[MeSH] and tumoral" Focusing on large series, hand
cases and cases in the orthopaedic literature. The papers above are not included, although
most of them turned up in the list of citations.
Idiopathic tumoral calcinosis associated with congenital malformation of the hand. Case
report.
Ann Chir Main Memb Super. 1998;17(1):59-62.
Tumoral calcinosis: a case report.
Turk J Pediatr. 1999 Jul-Sep;41(3):375-9.
Hyperphosphatemic tumoral calcinosis.
Plast Reconstr Surg. 2000 Jan;105(1):162-5. Review.
Tumoral calcinosis of the lumbar spine. Case illustration.
J Neurosurg. 1999 Jul;91(1 Suppl):137. No abstract available.
Tumoral calcinosis and atypical juvenile dermatomyositis: case report.
Eur J Pediatr Surg. 1998 Dec;8(6):382-4.
Tumoral calcinosis-like lesion of the foot. A case report.
J Am Podiatr Med Assoc. 1998 Feb;88(2):87-91.
Tumoral calcinosis: a clinicopathological study of 111 cases with emphasis on the
earliest changes.
Histopathology. 1997 Jul;31(1):18-24.
Tumoral calcinosis in an infant.
J South Orthop Assoc. 1997 Summer;6(2):101-5. No abstract available.
Tumoral calcinosis of the triangular fibrocartilage complex: a case report.
J Hand Surg [Am]. 1997 Mar;22(2):350-3.
Proposal for a pathogenesis-based classification of tumoral calcinosis.
Int J Dermatol. 1996 Apr;35(4):265-71. Review.
Tumoral calcinosis of the plantar forefoot: a case study.
J Am Podiatr Med Assoc. 1996 Feb;86(2):99-103. No abstract available.
[Tumoral calcinosis--an independent disease]?
Zentralbl Chir. 1996;121(6):496-502. Review. German.
Tumoral calcinosis: radiologic-pathologic correlation.
Skeletal Radiol. 1995 Nov;24(8):573-8.
[Tumoral calcinosis--a rare benign calcification of soft tissue].
Orv Hetil. 1995 Jun 25;136(26):1393-5. Hungarian.
Tumoral calcinosis after thumb tip injury: case report.
J Trauma. 1995 Jun;38(6):952-4.
Hyperphosphataemic tumoral calcinosis in Bedouin Arabs--clinical and radiological
features.
Clin Radiol. 1995 Apr;50(4):259-64.
Tumoral calcinosis associated with congenital malformations of the hand.
J Hand Surg [Br]. 1994 Oct;19(5):647-52.
Tumoral calcinosis associated with congenital malformations of the hand.
J Hand Surg [Br]. 1994 Oct;19(5):647-52.
PMID: 7822930; UI: 95123229
Chronic recurrent multifocal osteomyelitis associated with tumoral calcinosis.
J Bone Joint Surg Br. 1994 Mar;76(2):325-7. No abstract available.
Tumoral calcinosis.
Acta Orthop Belg. 1992;58(2):243. No abstract available.
Tumoral calcinosis of the ischium.
Arch Orthop Trauma Surg. 1992;111(5):284-6.
Tumoral calcinosis causing carpal tunnel syndrome (a case report).
Indian J Cancer. 1991 Dec;28(4):228-30. No abstract available.
[Tumoral calcinosis. A case report].
Minerva Chir. 1991 Jan;46(1-2):61-3. Italian.
Tumoral calcinosis: a study of cases from Papua New Guinea.
J Trop Med Hyg. 1990 Dec;93(6):403-7.
Arthritis mutilans, tumoral calcinosis, Raynaud's phenomenon and Sjogren's syndrome.
Br J Rheumatol. 1990 Aug;29(4):303-5.
Tumoral calcinosis with extensive pedal involvement.
J Foot Surg. 1990 Jul-Aug;29(4):388-91.
Tumoral calcinosis of the foot: case report and literature review.
J Foot Surg. 1990 May-Jun;29(3):278-83. Review.
Tumoral calcinosis simulating osteomyelitis.
J Foot Surg. 1989 Nov-Dec;28(6):547-8.
Tumoral calcinosis in Somalia and Ethiopia: a report of twenty one cases and brief
review of literature.
East Afr Med J. 1989 Jul;66(7):476-80. Review.
Tumoral calcinosis. Case report with treatment failure.
Orthop Rev. 1989 Jun;18(6):687-90. Review.
Tumoral calcinosis in two infants.
Clin Orthop. 1989 May;(242):272-6.
Tumoral calcinosis in scleroderma.
J Dermatol. 1989 Feb;16(1):82-5.
Tumoral calcinosis in a child.
J Pediatr Orthop. 1988 Jul-Aug;8(4):474-7.
Tumoral calcinosis: a case report and review of the literature.
J Hand Surg [Am]. 1985 Sep;10(5):744-8.
Tumoral calcinosis in multiple digits: a case report.
J Hand Surg [Am]. 1985 Sep;10(5):739-43.
Tumoral calcinosis.
Ital J Orthop Traumatol. 1984 Sep;10(3):399-404.
Tumoral calcinosis in the foot and hand. A case report.
J Am Podiatry Assoc. 1983 Mar;73(3):153-5. No abstract available.
Tumoral calcinosis in an infant. A case report.
Bull Hosp Jt Dis Orthop Inst. 1983 Spring;43(1):78-83.
Tumoral calcinosis: a surgical problem.
J Pediatr Orthop. 1982 Oct;2(4):409-15. No abstract available.
Tumoral calcinosis. Report of a case with successful medical management.
J Bone Joint Surg Am. 1981 Sep;63(7):1167-9. No abstract available.
Tumoral calcinosis in a patient undergoing hemodialysis.
Acta Orthop Scand. 1979 Feb;50(1):27-31.
Tumoral calcinosis. A clinical and pathological study of eleven unreported cases in
Turkey.
J Bone Joint Surg Am. 1978 Dec;60(8):1131-5.
Tumoral calcinosis with hyperphosphatemia. A report of a family with incidence in four
siblings.
J Bone Joint Surg Am. 1969 Jul;51(5):913-25. No abstract available.
Tumoral calcinosis. A report of six cases.
J Bone Joint Surg Am. 1967 Jun;49(4):721-31. No abstract available.
Tumoral calcinosis.
J Bone Joint Surg Br. 1967 Nov;49(4):698-703. No abstract available.
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