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Band keratopathy with bilateral deafness as a presenting sign of hyperparathyroidism
342
CURRRNTOPHTHALMOLOGY
Surv Ophtholmol 23 (5) March-April 1979
evaluate the patient and to monitor the patient’s condition more carefully, thus aiding greatly in the approach to therapy. Ultrasonography and CT scanning can both be of great assistance to the physician in attempting to pinpoint the cause of the patient’s abnormality. These diagnostic techniques can quite conclusively distinguish between “thyroid exophthalmos” and the exophthalmos produced by neoplastic disease, orbital inflammation, pseudotumor, mucocele, etc. (Enzmann D et al: Radiology 118:615-620, 1976; Enzmann D et al: Radiology 120:597-601,1976; Grove AS Jr: N Engl JMed292:1005-1013,1975; Kriss JP et al: Recenf Prog Harm Res 32:533-566, 1975; Werner SC et al: N Engl J Med 290: 1447-1450, 1974). GEORGE L. SPAETH
Band Keratopathy with Bilateral Deafness as a Presenting Sign of Hyperparathyroidism, by M. Petrohelos, D. Tricoulis, and P. Diamantacos. Br J Ophthalmol61.494-495, 1977 An unusual case of hyperparathyroidism is reported in which calcification of the cornea was the presenting clinical and diagnostic sign. The patient was a 24-year-old housewife who developed bilateral deafness with marked decrease of vision, pronounced weakness, anorexia, vomiting and weight loss. Physical examination showed a chronically ill woman who was deaf bilaterally and had lost 61 pounds. Examination of the eyes revealed bilateral band-shaped cornea1 opacities, symmetrical in both eyes. The cornea1 changes consisted of a subepithelial diffuse collection of whitish material located in Bowman’s membrane. The bulbar conjunctiva also showed glass-like subepithelial crystals temporally and nasally in the limbus. The vision was 6/30 in the right eye and 6/9 in the left. A biopsy of cornea1 and conjunctival tissues was done. Pathologically, there was a heavy deposit of crystalline material in the supporting tissue and beneath the epithelium. The substance took a pale blue stain with hemalum and eosin, indicating a probable calcium content. Laboratory analysis showed serum calcium 16.2 mg, inorganic phosporus 4.1 mg, alkaline phosphatase 10.5 units, and cerebrospinal fluid calcium 6.8 mg. The tympanic membranes were covered with thick whitish plaques bilaterally resulting in a severe perceptive deafness. With a presumptive diagnosis of parathyroid adenoma, an exploratory examination of the neck was done which disclosed a large parathyroid adenoma. This was totally removed. The postoperative course was uneventful and when she was reexamined a month later her vision was 6/6 in each eye, and her hearing had returned to normal. (Abstract by M. Petrohelos)
Comment Clinical manifestations of hyperparathyroidism are multiple and by no means pathognomonic. Furthermore, there is a difference between the symptoms that result from acute hypercalcemia and those
TABLE 1 Clinical Manifestations of Hyperparathyroidism A. Acute hypercalcemia
1. Anorexia, nausea, and vomiting 2. Dehydration and azotemia 3. Somnolence and confusion 4. Electrocardiographic changes B. Chronic hypercalcemia and hypercalciuria I. Weakness and hypotonia 2. Failure, depression, and psychosis 3. Recurrent renal stones, polyuria and polydipsia, renal failure 4. Dyspepsia, constipation 5. Calcification of cornea and conjunctiva 6. Pseudogout 7. Neonatal hypocalcemia of offspring
TABLE 2 Differential Diagnosis of Band Keratopathy 1. Chronic ocular infection 2. Ocular trauma 3. Hypercalcemia Hyperparathyroid disease Neoplastic disease Sarcoidosis Milk-alkali syndrome Acute osteoporosis of disuse Thyrotoxicosis Vitamin D intoxication Idiopathic hypercalcemia of infancy Hypophosphatasia Chronic renal failure 4. Idiopathic
CURRENTOPWTHALMOLOGY
343
that follow chronic hypercalcemia. The patient described in this interesting article by Petrohelos showed some manifestations of acute and chronic hypercalcemia (Table 1). The authors have done us a service to recall to mind that individuals with hyperparathyroidism can have as their presenting symptom band keratopathy. In fact any condition causing hypercalcemia may produce band keratopathy. Since hypercalcemia is a serious biochemical abnormality, its recognition is important. Furthermore, in many cases, such as that of the patient described with hyperparathyroidism, appropriate treatment is highly effective. The ophthalmologist caring for a patient with band keratopathy must keep in mind the full differential diagnosis of this clinical manifestation (Table 2). GEORGE L. SPAETH
CURRRNTOPHTHALMOLOGY
Surv Ophtholmol 23 (5) March-April 1979
evaluate the patient and to monitor the patient’s condition more carefully, thus aiding greatly in the approach to therapy. Ultrasonography and CT scanning can both be of great assistance to the physician in attempting to pinpoint the cause of the patient’s abnormality. These diagnostic techniques can quite conclusively distinguish between “thyroid exophthalmos” and the exophthalmos produced by neoplastic disease, orbital inflammation, pseudotumor, mucocele, etc. (Enzmann D et al: Radiology 118:615-620, 1976; Enzmann D et al: Radiology 120:597-601,1976; Grove AS Jr: N Engl JMed292:1005-1013,1975; Kriss JP et al: Recenf Prog Harm Res 32:533-566, 1975; Werner SC et al: N Engl J Med 290: 1447-1450, 1974). GEORGE L. SPAETH
Band Keratopathy with Bilateral Deafness as a Presenting Sign of Hyperparathyroidism, by M. Petrohelos, D. Tricoulis, and P. Diamantacos. Br J Ophthalmol61.494-495, 1977 An unusual case of hyperparathyroidism is reported in which calcification of the cornea was the presenting clinical and diagnostic sign. The patient was a 24-year-old housewife who developed bilateral deafness with marked decrease of vision, pronounced weakness, anorexia, vomiting and weight loss. Physical examination showed a chronically ill woman who was deaf bilaterally and had lost 61 pounds. Examination of the eyes revealed bilateral band-shaped cornea1 opacities, symmetrical in both eyes. The cornea1 changes consisted of a subepithelial diffuse collection of whitish material located in Bowman’s membrane. The bulbar conjunctiva also showed glass-like subepithelial crystals temporally and nasally in the limbus. The vision was 6/30 in the right eye and 6/9 in the left. A biopsy of cornea1 and conjunctival tissues was done. Pathologically, there was a heavy deposit of crystalline material in the supporting tissue and beneath the epithelium. The substance took a pale blue stain with hemalum and eosin, indicating a probable calcium content. Laboratory analysis showed serum calcium 16.2 mg, inorganic phosporus 4.1 mg, alkaline phosphatase 10.5 units, and cerebrospinal fluid calcium 6.8 mg. The tympanic membranes were covered with thick whitish plaques bilaterally resulting in a severe perceptive deafness. With a presumptive diagnosis of parathyroid adenoma, an exploratory examination of the neck was done which disclosed a large parathyroid adenoma. This was totally removed. The postoperative course was uneventful and when she was reexamined a month later her vision was 6/6 in each eye, and her hearing had returned to normal. (Abstract by M. Petrohelos)
Comment Clinical manifestations of hyperparathyroidism are multiple and by no means pathognomonic. Furthermore, there is a difference between the symptoms that result from acute hypercalcemia and those
TABLE 1 Clinical Manifestations of Hyperparathyroidism A. Acute hypercalcemia
1. Anorexia, nausea, and vomiting 2. Dehydration and azotemia 3. Somnolence and confusion 4. Electrocardiographic changes B. Chronic hypercalcemia and hypercalciuria I. Weakness and hypotonia 2. Failure, depression, and psychosis 3. Recurrent renal stones, polyuria and polydipsia, renal failure 4. Dyspepsia, constipation 5. Calcification of cornea and conjunctiva 6. Pseudogout 7. Neonatal hypocalcemia of offspring
TABLE 2 Differential Diagnosis of Band Keratopathy 1. Chronic ocular infection 2. Ocular trauma 3. Hypercalcemia Hyperparathyroid disease Neoplastic disease Sarcoidosis Milk-alkali syndrome Acute osteoporosis of disuse Thyrotoxicosis Vitamin D intoxication Idiopathic hypercalcemia of infancy Hypophosphatasia Chronic renal failure 4. Idiopathic
CURRENTOPWTHALMOLOGY
343
that follow chronic hypercalcemia. The patient described in this interesting article by Petrohelos showed some manifestations of acute and chronic hypercalcemia (Table 1). The authors have done us a service to recall to mind that individuals with hyperparathyroidism can have as their presenting symptom band keratopathy. In fact any condition causing hypercalcemia may produce band keratopathy. Since hypercalcemia is a serious biochemical abnormality, its recognition is important. Furthermore, in many cases, such as that of the patient described with hyperparathyroidism, appropriate treatment is highly effective. The ophthalmologist caring for a patient with band keratopathy must keep in mind the full differential diagnosis of this clinical manifestation (Table 2). GEORGE L. SPAETH