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CASE REPORT
Year : 2021  |  Volume : 1  |  Issue : 2  |  Page : 259-261

Cataract secondary to iatrogenic iron overload in a severely anemic patient


Department of Ophthalmology, Eskişehir Osmangazi University Medical School, Meşelik Kampüsü, Odunpazarı, Eskişehir, Turkey

Date of Submission09-Sep-2020
Date of Acceptance14-Dec-2020
Date of Web Publication01-Apr-2021

Correspondence Address:
Dr. Eray Atalay
Department of Ophthalmology, Eskişehir Osmangazi University Medical School, Meşelik Kampüsü, Odunpazarı, Eskişehir
Turkey
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijo.IJO_2872_20

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  Abstract 


High levels of iron may be toxic and cause various pathologies in the human body, including the eye. Studies have shown increased iron concentration in certain subtypes of senile cataracts. High serum levels of its non-reactive depot form, ferritin, has also been associated with juvenile cataracts in hereditary hyperferritinemia-cataract syndrome. Whereas this form of hyperferritinemia is inherited, there is no report on cataract formation in iatrogenic hyperferritinemia. Herein, we report a 43-year-old case who was diagnosed with bilateral cataracts a few years after she received intensive intravenous iron replacement therapy for severe iron deficiency anemia.

Keywords: Cataract, hereditary hyperferritinemia cataract syndrome, hyperferritinemia, iron overload


How to cite this article:
Erol MA, Ozalp O, Atalay E. Cataract secondary to iatrogenic iron overload in a severely anemic patient. Indian J Ophthalmol Case Rep 2021;1:259-61

How to cite this URL:
Erol MA, Ozalp O, Atalay E. Cataract secondary to iatrogenic iron overload in a severely anemic patient. Indian J Ophthalmol Case Rep [serial online] 2021 [cited 2021 Aug 3];1:259-61. Available from: https://www.ijoreports.in/text.asp?2021/1/2/259/312399



Iron is an essential element for the human body. Seventy-five percent of it is present in hemoglobin, while 10–20% is stored in the protein ferritin. The remainder 5–15% is found in the iron transport protein transferrin, as well as in myoglobin, cytochromes, and as unbound (free) iron.[1] Excess elemental iron is primarily stored in the form of ferritin and hemosiderin in the liver, spleen, bone marrow, duodenum, and skeletal muscle. Iron had also been detected in ocular tissues both in physiological states and in pathological conditions including intraocular fluids, the lens, retina, and retinal pigment epithelium.[2] Due to its highly oxidizing properties, an increase in iron concentration in the crystalline lens had been unequivocally linked to cataract formation.[3],[4]

Hereditary hyperferritinemia-cataract syndrome (HHCS) is a rare inherited autosomal dominant disorder characterized by early-onset bilateral cataracts and increased serum L-ferritin, in the absence of iron overload.[5] As excess L-ferritin accumulates in the crystalline lens, bilateral cataract ensues, which is the only known organ damage in HHCS.

Whereas this inherited form of hyperferritinemia is essentially associated with early cataract development, there is no report on cataract formation in iatrogenic hyperferritinemia. Herein, we report a 43-year-old case who was diagnosed with bilateral cataracts a few years after she received intensive intravenous iron replacement therapy for severe iron deficiency anemia.


  Case Report Top


A 43-year-old female patient was admitted to our ophthalmology clinic with a complaint of gradually deteriorating vision for about 2 years. The best-corrected visual acuity (BCVA) were 20/50 and 20/80, IOP values were 14 and 15 mmHg right and left eye respectively. Bilateral posterior subcapsular opacities and fine crystals in the yellow-to-red color spectrum were noted within the cataractous lens [Figure 1]. The fundus examination was normal in both eyes.
Figure 1: Fine crystals in the yellow-to-red color spectrum at the cataractous lens

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Her past medical history revealed a severe iron deficiency anemia that was diagnosed in 2016 and was recalcitrant to multiple courses of systemic iron replacement. No other systemic disease was found. Her family history was unremarkable for any eye disease. Upper and lower gastrointestinal system endoscopy findings at the time of iron deficiency anemia diagnosis were suggestive of chronic atrophic gastritis (CAG) which was considered causative for her condition. Although she was initially started on oral iron replacement therapy, her treatment was switched to intravenous iron infusion (Ferinject® (Vifor Pharma, France) 500 mg/10 ml, whose active ingredient is iron carboxymaltose, once a week, 3 times in total) as no improvement was observed in her parameters with the former after 18 months of follow-up. At the first month visit after three courses of weekly intravenous iron infusion, serum ferritin reached 832 ng/ml, a level that is approximately 6 times the upper limit of the normal range [Figure 2]. Serum ferritin levels remained well above the upper limit for another six months after which it dropped to its pre-treatment levels. The serum iron level at the same visit was 164 μg/dL [Figure 3] and remained within the normal range without any other organ involvement finding throughout the follow-up.
Figure 2: Serum ferritin level

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Figure 3: Serum iron level

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The patient reported that her vision complaints began approximately a year after her serum ferritin levels peaked. During phacoemulsification surgery, samples were taken from the lens material with the help of a Simcoe cannula and were sent to energy dispersive spectroscopy (EDS) analysis for chemical characterization. Elemental analysis by weight and the atomic percentage is presented in [Table 1].
Table 1: Elemental analysis by weight and atomic percentage

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  Discussion Top


In this case, other causes of early cataracts such as trauma, diabetes mellitus, uveitis, prolonged topical steroid use, previous intraocular surgery, family history of early cataract, etc., were excluded. Considering that the color of crystals sequestered within the lens material was reminiscent of ferritin accumulation, our initial impression was that the cause of cataracts could be due to iron overload after intravenous iron infusion. To confirm our initial diagnosis, we obtained samples from the lens material during cataract surgery and were able to show the presence of elemental iron using EDS.

The only iron-related cataract has been reported as part of the HHCS.[4],[6] In this disease, serum ferritin levels can increase up to 15 times the normal level and the level of hyperferritinemia correlates with cataract development.[4] The majority (90%) of non-inherited hyperferritinemia is due to diseases such as alcohol-related liver disease, hematological diseases, kidney failure, neoplastic diseases, and metabolic syndrome.[7],[8],[9] It has also been reported in patients receiving oral or intravenous iron supplementation for extended durations.[10] In our case, hyperferritinemia was triggered after intravenous iron infusion because lack of iron absorbsion due to CAG which resulted in extremely high levels of serum ferritin (6 times the upper limit) as observed in the hyperferritinemia cataract syndrome. Interestingly, although serum ferritin peaked after intravenous iron infusion, serum iron levels stayed relatively stable. According to the patient's medical history, symptoms of visually significant cataract was observed approximately 2 years after the serum ferritin peak. Therefore, we think that one of the reasons for causing cataracts in the patient may be the defect in the lens iron metabolism.

Studies on the detection of various elements in cataractous lenses have invariably utilized atomic absorption spectrophotometry which measures dry weights of elements. The method that we employed, namely energy dispersive spectroscopy, measures weight, and atomic percentages of elements and hence is not comparable with the literature. Furthermore, during sample collection, there was inevitable contamination with aqueous and balanced salt solution which possibly could have diluted the concentration of iron as measured by EDS. Nonetheless, the typical color of crystals embedded within the lens material and concurrence of the visual disturbance and cataract with the ferritin peak is highly suggestive that the primary etiology of cataract is due to iron overload.


  Conclusion Top


Bilateral cataract is a rare possibility secondary to iatrogenic iron overload in a severely anemic patient.

Ethics statement

Written informed consent was obtained from the patient.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Adams PC, Barton JC. A diagnostic approach to hyperferritinemia with a non-elevated transferrin saturation. J Hepatol 2011;55:453-8.  Back to cited text no. 1
    
2.
Goralska M, Ferrell J, Harned J, Lall M, Nagar S, Fleisher LN, et al. Iron metabolism in the eye: A review. Exp Eye Res 2009;88:204-15.  Back to cited text no. 2
    
3.
Garland D. Role of site-specific, metal-catalyzed oxidation in lens aging and cataract: A hypothesis. Exp Eye Res 1990;50:677-82.  Back to cited text no. 3
    
4.
Levi S, Girelli D, Perrone F, Pasti M, Beaumont C, Corrocher R, et al. Analysis of ferritins in lymphoblastoid cell lines and in the lens of subjects with hereditary hyperferritinemia-cataract syndrome. Blood 1998;91:4180-7.  Back to cited text no. 4
    
5.
Bonneau D, Winter-Fuseau I, Loiseau MN, Amati P, Berthier M, Oriot D, et al. Bilateral cataract and high serum ferritin: A new dominant genetic disorder? J Med Genet 1995;32:778-9.  Back to cited text no. 5
    
6.
Christiansen G, Mohney BG. Hereditary hyperferritinemia-cataract syndrome. J AAPOS 2007;11:294-6.  Back to cited text no. 6
    
7.
European Association For The Study Of The L. EASL clinical practice guidelines for HFE hemochromatosis. J Hepatol 2010;53:3-22.  Back to cited text no. 7
    
8.
Hearnshaw S, Thompson NP, McGill A. The epidemiology of hyperferritinaemia. World J Gastroenterol 2006;12:5866-9.  Back to cited text no. 8
    
9.
Goot K, Hazeldine S, Bentley P, Olynyk J, Crawford D. Elevated serum ferritin-what should GPs know? Aust Fam Physician 2012;41:945-9.  Back to cited text no. 9
    
10.
Papadatos G, Davies M, Dedman N, Chambers J, Gaulton A, Siddle J, et al. SureChEMBL: A large-scale, chemically annotated patent document database. Nucleic Acids Res 2016;44:D1220-8.  Back to cited text no. 10
    


    Figures

  [Figure 1], [Figure 2], [Figure 3]
 
 
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  [Table 1]



 

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