Calcium apatite deposition disease: Difference between revisions
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===Imaging Findings=== | ===Imaging Findings=== | ||
* | *MRI is the imaging modality of choice for calcium apatite deposition disease. | ||
*On [imaging study 1], [disease name] is characterized by [finding 1], [finding 2], and [finding 3]. | *On [imaging study 1], [disease name] is characterized by [finding 1], [finding 2], and [finding 3]. | ||
*[Imaging study 2] may demonstrate [finding 1], [finding 2], and [finding 3]. | *[Imaging study 2] may demonstrate [finding 1], [finding 2], and [finding 3]. | ||
=== Other Diagnostic Studies === | === Other Diagnostic Studies === | ||
*[Disease name] may also be diagnosed using [diagnostic study name]. | *[Disease name] may also be diagnosed using [diagnostic study name]. | ||
Revision as of 16:09, 17 April 2018
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Manpreet Kaur, MD [2]
Synonyms: Calcific periarthritis, calcific bursitis, periarthritis calcarea, periarthritis calcarea, and hydroxyapatite rheumatism.
Overview
Historical Perspective
- [Disease name] was first discovered by [scientist name], a [nationality + occupation], in [year] during/following [event].
- In [year], [gene] mutations were first identified in the pathogenesis of [disease name].
- In [year], the first [discovery] was developed by [scientist] to treat/diagnose [disease name].
Classification
There is no classification system of calcium apatite deposition disease.
Pathophysiology
- The pathogenesis of calcium apatite deposition disease is not clear. Various authors have formulated the different hypothesis about the pathophysiology of calcium apatite deposition disease.
- Uhthoff and Loebr described the pathogenesis in four phases: precalcific, formative, resorptive, and postcalcific.[1]
- Precalcific phase: In this stage, collagen fibers of the tendon is undergoing metaplasia into fibrocartilage tissue.
- Formative phase: Chondrocytes start depositing within the areas of fibrocartilage formation which further leads to the formation of calcified apatite crystals.
- After the formative phase sometimes it will go into the resting phase for long period of time.
- Resorptive phase: Calcification will further undergo to an inflammatory resorptive phase, which is characterized by the appearance of leukocytes, lymphocytes, and giant cells leading to the formation of a calcium granuloma.
- Postcalcific phase: Reparative process allows new capillary and collagen fiber formation that is when calcification enters the postcalcific phase.
- The HLA-A1 gene has been associated with the development of calcium apatite deposition disease.[2]
- On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
- On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Differentiating [disease name] from other Diseases
- Calcium apatite deposition disease must be differentiated from the following disease:
- Calcium pyrophosphate dihydrate deposition disease (CPPD)
- Dystrophic calcification
- Renal osteodystrophy
- Hyperparathyroidism
- Hypoparathyroidism
- Collagen vascular disease
- Milk-alkali syndrome
- Hypervitaminosis D
Epidemiology and Demographics
- The prevalence of calcium apatite deposition disease is approximately 7.8% in asymptomatic patients and 42.5% in patients with subacromial pain syndrome.[3]
Age
- Calcium apatite deposition disease is more commonly observed among patients aged of 30–60 years old.[4]
- Calcium apatite deposition disease is also observed among 3 years old.[5]
Gender
- Women are more commonly affected with calcium apatite deposition disease than men.[4]
Race
- There is no racial predilection for calcium apatite deposition disease.
Risk Factors
- Common risk factors in the development of calcium apatite deposition disease are:
- There is a genetic predisposition to the HLA-A1 gene and calcific tendinitis.[2]
- Adult-onset diabetes has the high risk of developing calcium apatite deposition disease.[6]
- Thyroid hormone and estrogen hormone disorder is associated increased risk of developing of calcium apatite deposition disease.[7]
Natural History, Complications and Prognosis
- The majority of patients with calcium apatite deposition disease remain asymptomatic for an indefinite period of time.
- Early clinical features include acute pain or chronic mild pain.
- If left untreated, intraarticular calcification may progress to develop joint destruction.
- Common complications of calcium apatite deposition disease
- Intraarticular calcification leads to joint destruction.
- Milwaukee shoulder syndrome if the shoulder joint is involved.
Diagnosis
Diagnostic Criteria
According to the American association of rheumatology, there is no diagnostic criteria of calcium apatite deposition disease.
Symptoms
- Patients with calcium apatite deposition disease are usually asymptomatic.
- Patients usually experience acute episodes of pain to chronic mild pain.
- Acute episodes of pain usually resolve spontaneously but there are recurrent episodes after an initial episode.[8]
- Acute episodes are usually associated with warmth and swelling.
- Some patients also present with the symptoms of neuropathy.[9]
Physical Examination
- Patients with calcium apatite deposition disease usually appear fatigue and usually in pain.
- Physical examination of the involved joint is remarkable for:
- Redness
- Swelling
- The restricted range of movement
- Some patients show signs of neuropathy such as reduced power, decreased sensation and reflexes.
Laboratory Findings
- There are no specific laboratory findings associated with calcium apatite deposition disease.
Imaging Findings
- MRI is the imaging modality of choice for calcium apatite deposition disease.
- On [imaging study 1], [disease name] is characterized by [finding 1], [finding 2], and [finding 3].
- [Imaging study 2] may demonstrate [finding 1], [finding 2], and [finding 3].
Other Diagnostic Studies
- [Disease name] may also be diagnosed using [diagnostic study name].
- Findings on [diagnostic study name] include [finding 1], [finding 2], and [finding 3].
Treatment
Medical Therapy
- There is no treatment for [disease name]; the mainstay of therapy is supportive care.
- The mainstay of therapy for [disease name] is [medical therapy 1] and [medical therapy 2].
- [Medical therapy 1] acts by [mechanism of action 1].
- Response to [medical therapy 1] can be monitored with [test/physical finding/imaging] every [frequency/duration].
Surgery
- Surgery is the mainstay of therapy for [disease name].
- [Surgical procedure] in conjunction with [chemotherapy/radiation] is the most common approach to the treatment of [disease name].
- [Surgical procedure] can only be performed for patients with [disease stage] [disease name].
Prevention
- There are no primary preventive measures available for [disease name].
- Effective measures for the primary prevention of [disease name] include [measure1], [measure2], and [measure3].
- Once diagnosed and successfully treated, patients with [disease name] are followed-up every [duration]. Follow-up testing includes [test 1], [test 2], and [test 3].
References
- ↑ Uhthoff HK, Loehr JW (July 1997). "Calcific Tendinopathy of the Rotator Cuff: Pathogenesis, Diagnosis, and Management". J Am Acad Orthop Surg. 5 (4): 183–191. PMID 10797220.
- ↑ 2.0 2.1 Sengar DP, McKendry RJ, Uhthoff HK (March 1987). "Increased frequency of HLA-A1 in calcifying tendinitis". Tissue Antigens. 29 (3): 173–4. PMID 3496685.
- ↑ Beckmann NM (2016). "Calcium Apatite Deposition Disease: Diagnosis and Treatment". Radiol Res Pract. 2016: 4801474. doi:10.1155/2016/4801474. PMC 5155096. PMID 28042481.
- ↑ 4.0 4.1 Louwerens JK, Sierevelt IN, van Hove RP, van den Bekerom MP, van Noort A (October 2015). "Prevalence of calcific deposits within the rotator cuff tendons in adults with and without subacromial pain syndrome: clinical and radiologic analysis of 1219 patients". J Shoulder Elbow Surg. 24 (10): 1588–93. doi:10.1016/j.jse.2015.02.024. PMID 25870115.
- ↑ Sakamoto K, Kozuki K (2002). "Calcific tendinitis at the biceps brachii insertion of a child: a case report". J Shoulder Elbow Surg. 11 (1): 88–91. doi:10.1067/mse.2002.119854. PMID 11845156.
- ↑ Mavrikakis ME, Drimis S, Kontoyannis DA, Rasidakis A, Moulopoulou ES, Kontoyannis S (March 1989). "Calcific shoulder periarthritis (tendinitis) in adult onset diabetes mellitus: a controlled study". Ann. Rheum. Dis. 48 (3): 211–4. PMC 1003723. PMID 2930276.
- ↑ Harvie P, Pollard TC, Carr AJ (2007). "Calcific tendinitis: natural history and association with endocrine disorders". J Shoulder Elbow Surg. 16 (2): 169–73. doi:10.1016/j.jse.2006.06.007. PMID 17188907.
- ↑ Kim JK, Park ES (May 2014). "Acute calcium deposits in the hand and wrist; comparison of acute calcium peritendinitis and acute calcium periarthritis". J Hand Surg Eur Vol. 39 (4): 436–9. doi:10.1177/1753193413478393. PMID 23422589.
- ↑ Garayoa SA, Romero-Muñoz LM, Pons-Villanueva J (December 2010). "Acute compartment syndrome of the forearm caused by calcific tendinitis of the distal biceps". Musculoskelet Surg. 94 (3): 137–9. doi:10.1007/s12306-010-0079-2. PMID 20936391.