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  Table of Contents  
LETTER TO EDITOR
Year : 2016  |  Volume : 26  |  Issue : 4  |  Page : 313-314
 

Secret in the eyes - fish eye disease


1 Department of Medicine, All India Institute of Medical Sciences Bhopal, Bhopal, Madhya Pradesh, India
2 Department of Ophthalmology, All India Institute of Medical Sciences Bhopal, Bhopal, Madhya Pradesh, India

Date of Web Publication1-Jul-2016

Correspondence Address:
V K Ingle
Department of Medicine, AIIMS Bhopal, Saket Nagar, Bhopal - 462 024, Madhya Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0971-4065.179304

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How to cite this article:
Ingle V K, Maharana P K, Rajesh P. Secret in the eyes - fish eye disease. Indian J Nephrol 2016;26:313-4

How to cite this URL:
Ingle V K, Maharana P K, Rajesh P. Secret in the eyes - fish eye disease. Indian J Nephrol [serial online] 2016 [cited 2019 Dec 7];26:313-4. Available from: http://www.indianjnephrol.org/text.asp?2016/26/4/313/179304




Sir,

In response to “Co-existence of classic familial lecithin-cholesterol acyltransferase deficiency and fish eye disease in the same family”,[1] we would like to report a case of Fish eye disease.

A 42-year-old male was referred for physician consultation for low high-density lipoprotein (HDL) cholesterol levels. It was found that patient had persistently low HDL cholesterol (<10 mg/dl) and persistently high serum triglycerides (>200 mg/dl) on multiple occasions.

The patient was nonobese, nonsmoker, and had no other addictions. He had no history of premature cardiovascular events or renal failure in the family. Patient's fasting blood sugars, renal function tests, and urine analysis were normal.

This mystery of persistent hypoalphalipoproteinemia was solved when it was noticed that patient had bilateral corneal opacities [Figure 1]. Ophthalmologic evaluation revealed corneal opacities involving all the layers of the cornea with maximum density near the limbus, without any impairment of vision.
Figure 1: Corneal opacities

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Persistent hypoalphalipoproteinemia with characteristic corneal opacities led to the provisional diagnosis of fish eye disease. Plasma lecithin- cholesterol acyltransferase (LCAT) activity performed at Pacific Biomarkers, USA, was normal. Genetic studies could not be performed because of economic non-viability. Family members had no dyslipidemia or corneal opacities.

Fish eye disease is a rare disease with only about thirty case reports.[2] Fish eye disease or partial LCAT deficiency was named after the appearance of cornea similar to that of boiled fish.[3] There is a partial deficiency of alpha-LCAT activity (present in HDL) while beta-LCAT activity is preserved.[4]

In contrast to total LCAT deficiency, fish eye disease patients have no anemia or renal failure. There is no risk for premature coronary artery disease.[5]

The patient was reassured and advised to follow-up with ophthalmologists at regular intervals.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Mahapatra HS, Ramanarayanan S, Gupta A, Bhardwaj M. Co-existence of classic familial lecithin-cholesterol acyl transferase deficiency and fish eye disease in the same family. Indian J Nephrol 2015;25:362-5.  Back to cited text no. 1
  Medknow Journal  
2.
National Library of Medicine (US). Genetics Home Reference [Internet]. Bethesda (MD): The Library; 2013 Sep 16. Fish eye disease; Available from: http://www.ghr.nlm.nih.gov/condition/fish-eye-disease. [reviewed 2013 Aug; Last accessed on 2016 Jan 31].  Back to cited text no. 2
    
3.
Carlson LA, Philipson B. Fish-eye disease. A new familial condition with massive corneal opacities and dyslipoproteinaemia. Lancet 1979;2:922-4.  Back to cited text no. 3
[PUBMED]    
4.
McIntyre N. Familial LCAT deficiency and fish-eye disease. J Inherit Metab Dis 1988;11 Suppl 1:45-56.  Back to cited text no. 4
    
5.
Calabresi L, Baldassarre D, Castelnuovo S, Conca P, Bocchi L, Candini C, et al. Functional lecithin: Cholesterol acyltransferase is not required for efficient atheroprotection in humans. Circulation 2009;120:628-35.  Back to cited text no. 5
    


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