Tab Application Banner
  • Users Online: 369
  • Home
  • Print this page
  • Email this page
Home About us Editorial board Ahead of print Current issue Search Archives Submit article Instructions Subscribe Contacts Login 


 
 Table of Contents  
IMAGES IN RHEUMATOLOGY
Year : 2016  |  Volume : 11  |  Issue : 4  |  Page : 230-231

Sarcoidosis presenting as proximal myopathy in a patient with unexplained hypercalcemia


Department of Medicine, The Sarvajanik Medical Trust Hospital, Surat, Gujarat, India

Date of Web Publication8-Nov-2016

Correspondence Address:
Dr. Ankur Dalal
70, Sankalp Society, Near Jamana Nagar, Ghod Dod Road, Surat - 395 001, Gujarat
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0973-3698.193592

Rights and Permissions
  Abstract 

Keywords: Hypercalcemia, Magnetic resonance imaging, HRCT, myopathy, sarcoidosis


How to cite this article:
Dalal A. Sarcoidosis presenting as proximal myopathy in a patient with unexplained hypercalcemia. Indian J Rheumatol 2016;11:230-1

How to cite this URL:
Dalal A. Sarcoidosis presenting as proximal myopathy in a patient with unexplained hypercalcemia. Indian J Rheumatol [serial online] 2016 [cited 2019 Jun 20];11:230-1. Available from: http://www.indianjrheumatol.com/text.asp?2016/11/4/230/193592

A 48-year-old female presented with a history of weakness, sense of imbalance, and difficulty in standing up from sitting position for the last 3–4 months. She also gave a history of falls thrice in the same period. Recently, she has had multiple troubles including bilateral knee joint pain with swelling 3 months ago and renal dysfunction 1 month ago. She was under treatment for diabetes, hypertension, and hypothyroidism for the last 5 years. General examination was unremarkable. Systemic examination showed weakness with muscle power of grade 4+/5 around both hip girdles. Musculoskeletal examination was also unremarkable.

The patient had been extensively investigated during the last 3–4 months and was found to have unexplained hypercalcemia. On investigations, her serum calcium was 14.9 mg/dl (8.6–10 mg/dl) and 24 h urine calcium was 312.42 mg/day (100–300 mg/day on average 800 mg/day calcium in normal diet). Her serum phosphorus was 3.7 mg/dl (2.5–4.9 mg/dl) and serum parathyroid hormone 20 pg/ml (9.5–75 pg/ml). Her serum urea, serum creatinine, and serum potassium were 77 mg/dl (10-50 mg/dl), 2.7 mg/dl (0.6-1.4 mg/dl), and 4.1 mEq /L (3.5-5.5 mEq/L) respectively. Serum protein electrophoresis did not show paraproteinemia. A nerve conduction study showed bilateral symmetrical sensory polyneuropathy. Magnetic resonance imaging (MRI) of the brain showed age-related atrophy, and MRI of the spine showed only mild posterior bulging of L3–L4 and L4–L5 discs.

On further investigations, her hemoglobin and platelet count were within normal limits but total count was 13500/cumm (4000-11000/cumm) with 9% (1-6%) eosinophils. Her erythrocyte sedimentation rate (ESR) was elevated at 60 mm/h (3–12 mm/h). Muscle enzyme creatine phosphokinase was normal. Her antinuclear antibody by indirect immunofluorosence was +2 speckled but extractable nuclear antigen profile by immunoblotting was negative. Her serum angiotensin-converting enzyme (ACE) level was grossly elevated at 230 IU/L (20–70 IU/L). A chest X-ray showed minor fissure thickening on the right side. After careful analysis of history and investigation results, the patient was suspected to have myopathy related to sarcoidosis due to the presence of persistent bilateral lower-limb proximal muscle weakness, recent history of bilateral knee joint synovitis, eosinophilia, raised ESR, unexplained hypercalcemia, hypercalciuria, elevated serum ACE, and fissure thickening on chest X-ray. As of these, not a single feature was diagnostic of this condition; a MRI of both thighs was done. It showed diffuse bilateral muscle hyperintensity suggestive of myositis [Figure 1]. High-resolution computed tomography (HRCT) scan of the lungs showed ill-defined randomly distributed peribronchial nodules [Figure 2], suggestive of possible sarcoidosis. Muscle biopsy from the left vastus lateralis muscle showed noncaseating epithelioid granuloma, which was compatible with the clinical diagnosis of sarcoidosis.
Figure 1: Diffuse bilateral muscle hyperintensity suggestive of myositis

Click here to view
Figure 2: Ill-defined randomly distributed peribronchial nodules

Click here to view


The patient was treated with hydroxychloroquine and prednisolone (according to weight) along with treatment to comorbidities. She showed clinical improvement within 1 month, and her calcium level and renal dysfunction were also normalized.

Sarcoidosis is an inflammatory disease characterized by the presence of noncaseating granulomas. Respiratory complaints are the most common presenting symptoms followed by cutaneous and ocular. Hypercalcemia and/or hypercalciuria can occur in about 10% of sarcoidosis patients. The mechanism of abnormal calcium metabolism is increased production of 1,25-dihydroxyvitamin D by the granuloma itself which causes increased intestinal absorption of calcium, leading to hypercalcemia. Direct granulomatous bone and muscle involvement can be seen in only about 10% while direct kidney involvement in <5% of sarcoidosis patients. However, hypercalcemia is the most likely cause of sarcoidosis-associated renal disease in 1–2% of sarcoidosis patients.[1]

Activity of serum ACE was found to be a useful tool in predicting the diagnosis of sarcoidosis. It is recommended that a serum ACE can be useful differential diagnostic marker at levels >100 IU/L or <52 IU/L in the diagnosis of sarcoidosis.[2]

The case is presented due to two reasons:First, because direct muscle involvement is rare in sarcoidosis and presentation of this disease as myopathy is even rarer; second, sarcoidosis should be kept in mind as a differential diagnosis while dealing with unexplained hypercalcemia.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Baughman RP, Lower EE. Sarcoidosis. In: Kasper D, Fauci A, Hauser S, Longo D, Jameson J, Loscalzo J, editors. In: Harrison's Principles of Internal Medicine. 19th ed. United States of America: The McGraw-Hill Companies Inc.; 2015. p. 2205-12.  Back to cited text no. 1
    
2.
Khan AH, Ghani F, Khan A, Khan MA, Khurshid M. Role of serum angiotensin converting enzyme in sarcoidosis. J Pak Med Assoc 1998;48:131-3.  Back to cited text no. 2
    


    Figures

  [Figure 1], [Figure 2]



 

Top
 
 
  Search
 
Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

 
  In this article
Abstract
References
Article Figures

 Article Access Statistics
    Viewed478    
    Printed11    
    Emailed0    
    PDF Downloaded56    
    Comments [Add]    

Recommend this journal


[TAG2]
[TAG3]
[TAG4]