【摘要】目的：报告1例甲状旁腺机能低下和肾功能衰竭晚期并发弥漫性结膜钙质沉着征患者。方法：病例报告。结果：患者，男，35岁，因为双眼异物感，伴发红、流泪1mo就诊。患者患有甲状旁腺机能低下征和肾功能衰竭晚期，既往做过甲状旁腺次全切除术。查：双眼视力1.0，结膜弥漫性沉着物和充血，结膜组织病理学检查报告，结膜基质层下有较多钙质沉着，血清钙明显高于正常，血清磷正常。通过局部用类固醇激素（倍他米松）和肌肉降钙素后，患者眼部症状明显减轻。结论：弥漫性症状性结膜钙质沉着是一种罕见的眼部钙质沉着征，甲状旁腺机能低下和肾功能衰竭是引发的因素。
【关键词】 结膜钙质沉着征；肾功能衰竭；甲状旁腺机能低下
Correspondence to: Norlaili Mustafa. Department of Ophthalmology, School of Medical Sciences, Universiti Sains Malaysia, 16150 Kubang Kerian, Kelantan,Malaysia. [email protected]
AbstractAIM: To describe a case of diffuse conjunctival calcinosis in hyperpararthyroidism and end stage renal failure patient.METHODS: A case report.RESULTS: A 35yearold gentleman, known case of hyperparathyroidism with subtotal parathyroidectomy done and end stage renal failure, presented with one month history of foreign body sensation of both eyes associated with redness and tearing. On examination, vision was 6/6 OU with diffuse conjunctival deposits and congestion. Conjunctival histopathological examination showed multiple foci of calcium deposits in the subepithelial stroma. Serum calcium was markedly raised and serum phosphorus was normal. His eye symptoms was reduced with topicalsteroid (betamethasone) and intramuscular calcitonin.CONCLUSION: Diffuse and symptomatic conjunctival calcinosis is uncommon condition of ocular calcium deposition. Hyperparathyroidism and renal failure are the contributing factors for the development of it.
KEYWORDS: conjunctival calcinosis; renal failure; hyperparathyroidism
INTRODUCTION
The most common ocular manifestation of calcification occurs in cornea, conjunctiva and limbus. Other ocular structures that can be involved include lens and retina. Various systemic diseases can cause hypercalcemia in a patient, including hyperparathyroidism, chronic renal failure, sarcoidosis and metastatic neoplasia.
Conjunctival calcification usually presented with lesions resembling inflamed pingueculae. The bulbar conjunctiva will become greyish, slightly elevated with areas of focal hyperemia in the interpalpebral fissure[1]. However, another type of presentation of the conjunctival calcinosis which was seldomly reported is multiple conjunctical deposits over the whole conjunctiva. Patient will present with eye redness and foreign body sensation. The deposits produced inflammation, discomfort and irritative feeling to the patient. Herein we would like to report a case of diffuse conjunctival calcinosis in a hyperparathyroidism and end stage renal failure patient.
CASE REPORT
We reported a 35yearold male who is a known case of hyperparathyroidism for 10year duration. He underwent subtotal parathyroidectomy eight years ago. He is also having end stage renal failure for five years and on regular hemodialysis. He presented with symptoms of foreign body sensation in both eyes associated with redness, tearing and discomfort for one month. There was no history of trauma or forein body insertion to the eyes. Otherwise his vision was good. On examination, his vision was 6/6 OU. There were generalized multiple yellowish deposits on the limbal, bulbar and palpebral conjunctiva (Figure 1, 2). However, the cornea was clear. The lens showed no cataractous changes and no calcification signs. There was no retinal changes seen. Other ocular structures and intraocular pressure were normal. The results of tear breakup test and Schirmers test were normal. Conjunctival biopsy was done and histopathological examination showed foci of calcium deposits in the subepithelial stroma (Figure 3). The serum calcium level was more than 400g/L and serum phosphate was normal. He was treated with topical betamethasone every 6 hours to reduce the inflammation. The reactions were further suppressed when the serum calcium was brought down by giving him intramuscular calcitonin 6U twice a day for three days. During the followup, his symptoms were markedly reduced. The calcium deposits on the conjunctiva were also reduced. Currently his calcium remains within the normal range.
DISCUSSION
Deposition of calcium in the eye can be primary or secondary. In primary ocular calcium deposits, it is usually associated with longstanding ocular diseases such as chronic ophthalmitis, previous keratitis, ocular trauma or phthisis bulbi. The secondary causes can be a sign of an underlying systemic condition, for example, hyperparathyroidism andchronic renal failure[1]. In renal failure, the visual system involvement happened as a result of uremia, metabolic imbalances, hypertension or the hemodialysis treatment itself[2,3]. Our patient is a chronic renal failure and has been on hemodialysis for five years. This may impair the calcium metabolism despite the contribution from thesubtotal parathyroidectomy that he had eight years back. However, a study by Emmerich et al[4] in 1986 showed that the deposition of calcium salts in the cornea and conjunctiva of 72 patients were significantly correlated with the duration ofhemodialysis but not the disturbances of the calcium metabolism nor the age.
Corneoconjunctiva at the interpalpebral zone is an exposed area where there is loss of carbon dioxide to the atmosphere. Hence, it provides a favourable environment for the deposition of calcium salts which is relatively alkaline in nature. The presence of an antecedent tissue degeneration acts as more calcifiable matrix and is predisposed to calcium salt deposition[5,6]. Lesions that are located at the limbal conjunctiva resemble the pattern in limbal girdle of Vogt type II and in advanced stage which manifests as band keratopathy[7]. Patients with chronic renopathy treated by long term dialysis may develop inflammatory reactions in the bulbar conjunctiva. Study by KlaassenBroekema et al [8]in 1995 showed that conjunctival hyperemia whether it is diffuse or focal was not associated with serum calcium. Initially Klaassen et al [5]in 1992 thought that the conjunctival congestion was due to the shedding of extra calcium deposits, eroding onto the ocular surface, and causing irritation. Later, they reported that the histopathological examination suggests the hyperemia is the result of a neurogenic inflammatory reaction, in which mast cell degranulation is mediated by the axon reflex[8]. Contradictly, our patient had a marked rise in serum calcium with diffuse conjunctival deposits and hyperemia.
It has been suggested that there is an association between squamous metaplasia and corneoconjunctival calcification. Squamous metaplasia referred to the abnormality of epithelial differentiation in which the normal secretory conjunctival mucosa gradually develops into a nonsecretory keratinized epithelium. The tear film will become unstable due to reduction of the mucin layer[8,9]. However, in study by Dursun et al [10] in 2000, the conjunctival epithelium changes were not related to the presence of calcium deposition. This may explain why our patient had normal tear breakup time (BUT) and Schirmers test. The degree of ocular calcification in dyalisis patient has been shown to be determined by local factor such as minor tissue injury of the limbal conjunctiva epithelium rather than the systemic factors[8].
Previous study have shown that ocular calcifications were usually asymptomatic. Though patients were having red eyes, they did not report any disturbance due to the presence of conjunctival lesion. However, the red eyes were noted to improve after the serum calcium or phosphate product is reduced[11,12]. Our patient experienced the same benefits when his serum calcium was managed to lower down.
In conclusion, though calcium deposits in the conjunctiva remain asymptomatic for most patients, symptomatic patients can present with a very disturbing and irritating lesion. Hyperparathyroidism and renal failure may be the cause of hypercalcemia which contributes to the development of diffuse conjunctival calcinosis.
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