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|Year : 1993 | Volume
| Issue : 2 | Page : 89-90
Thyrotoxicosis with osteomalacia and proximal myopathy.
R Goswami, P Shah, AC Ammini
Dept of Endocrinology and Metabolism, All India Institute of Medical Sciences, Ansari Nagar, New Delhi., India
Dept of Endocrinology and Metabolism, All India Institute of Medical Sciences, Ansari Nagar, New Delhi.
Source of Support: None, Conflict of Interest: None
A 36 year old lady, presented with symptoms of proximal myopathy was found to have a history of thyrotoxicosis for which she had taken carbimazole irregularly for 1-1/2 years. On admission, clinical signs of thyrotoxicosis were detected and confirmed by estimating serum T3 and T4. Neurological examination revealed generalised wasting, loss of power in the proximal muscles with a myopathy confirmed on EMG. Serum calcium, phosphorous levels, and a 24 hour urine calcium excretion were low. Alkaline phosphatase levels were high. A diagnosis of thyrotoxicosis with osteomalacia was made. The patient improved within 3 weeks of starting carbimazole and vitamin D.
Keywords: Adult, Case Report, Female, Human, Muscular Diseases, etiology,Osteomalacia, complications,Thyrotoxicosis, complications,
|How to cite this article:|
Goswami R, Shah P, Ammini A C. Thyrotoxicosis with osteomalacia and proximal myopathy. J Postgrad Med 1993;39:89-90
Clinically detectable chronic muscle weakness is described in upto 50% cases of thyrotoxicosis. The degree of weakness varies. Only a few have a disability severe enough to restrict them to bed. The cause of such severe weakness has to be elicited for judicious therapy. Among the known causes of such myopathy, are myasthenia gravis [1% of Graves disease (GD)], hypokalemic periodic paralysis (up to 24% of GID), and, chronic thyrotoxic myopathy (50% of GID). A century ago von Recklinghausen described a case of osteomalacia in thyrotoxic patient. Since then, 37 cases of thyrotoxicosis occurring in association with osteomalacia have been described,. Here, we describe a case of thyrotoxicosis with severe proximal myopathy. Identification of an associated metabolic disorder helped in effective treatment of the patient.
A 36-year-old lady [Figure:1] presented to the neurology clinic for gradually progressive muscle weakness and bone pains in the lower limbs of eighteen months duration. She had been bed-ridden for the previous three months. Apparently well three years back, she developed nervousness, weight loss, palpitations and tremulousness of the extremities. She was diagnosed as a case of hyperthyroidism and was prescribed carbimazole (30 mg/day); she took this treatment irregularly for the initial one and a half years. She had had four children and three abortions; breast feeding continued for one year for each child. Her estimated daily dietary intake of calcium and vitamin D was about 400 mg and 50 IU respectively. On admission to the Endocrinology ward, examination revealed a grade 2 soft and diffuse thyromegaly. Wayne's clinical score was clearly diagnostic of thyrotoxicosis. Trousseau's sign was elicitable (grade 3). Chvostek's sign was absent. Neurological examination revealed normal higher functions, cranial nerves and sensory system. Muscular system examination revealed generalised wasting, with a power of 3/5 and 2/5 in the shoulder and pelvic girdle respectively. No fasciculations were seen. Tendon jerks were unremarkable.
Hemogram and routine biochemical tests were normal. Other investigations revealed low serum calcium (6.8 mg/dl; Normal: 8.5-11.5), phosphorus (1.5 mg/dl; Normal: 2.54.5) and high alkaline phosphtase (50 K.A. units; Normal: 8-11), low 24 hour urine calcium (78 mg/day; Normal: 200), high serum T3 (350 ng/dl; Normal: 80-160) and T4 (25 ug/dl; Normal: 4-12). Radiological investigations revealed diffuse osteopenia; Looser's zone was present on right scapular border [Figure:2]. Malabsorption studies including barium meal follow-through and 24 hour fecal fat (5.5g/24 hr) were normal. Electromyography revealed a myopathic pattern. A final diagnosis of thyrotoxicosis with osteomalacia was made and the patient was put on carbimazole 60 mg/day along with therapeutic doses of oral vitamin D. Over the ensuing 3 weeks the patient's weakness improved and she was able to walk with support.
Weakness as a symptom of thyrotoxycosis was reported by both Graves and von Basedow. Osteomalacia is associated with thyrotoxycosis,,. In the recent past, no such case with osteomalacia has been reported. This may be attributed to the improvement in nutrition in general. Osteomalacia however is still prevalent in native and emigrant Asians,. In hyperthyroidism, subclinical vitamin D deficiency may get precipitated into an overt form. Various mechanisms of disturbed calcium metabolism in hyperthyroidism are postulated; these include increased urinary, fecal, and, sweat loss of calcium, and decreased production of 1,25 dihydroxy vitamin D and calcium binding protein. All these factors ultimately give rise to a negative calcium balance and later a reduction in 24 hour urinary calcium.
Thyrotoxicosis and osteomalacia can independently give rise to proximal muscle weakness in 61% and 50% cases respectively,. Muscle enzymes, electromyography and ultrastructural study do not differentiate between osteomalacic and thyrotoxic myopathy. Osteomalacia may co-exist with thyrotoxicosis, but may remain undiagnosed, unless clinically suspected and biochemically confirmed. Since the metabolic disorder can be effectively treated as exemplified in the present case, we conclude that features of vitamin D deficiency should be looked for in patients of thyrotoxicosis presenting with unusually severe myopathy, especially in individuals originating from areas in the world where osteomalacia is still prevalent,.
We wish to thank Dr Ish Anand for getting the electromyography study for the patient.
| :: References|| |
Harward CW, Campbell ED, Ross HB. Electromyography and histological findings in the muscles of the patients of thyrotoxicosis. Quart J Med 1963; 32:145-163. |
|2.||Von Recklinghausen F. Die fibroseoder deformenede ostitis, die osteomalacic undie osteoplastiche carcinose, in ihren gegenseitizen. Be-ropes M. Studies on calcium and phosphorus metabolism III. Effect Zeihungen. Festschr. F Rudolf Virchow. Berlin: George Reimer; 1891, pp 1-89. |
|3.||Darin P, Harold TG, McCormick EK, Herdle E. The rationale of calcium phosphorus and vitamin D therapy in clinical hyperthyroidism. Surg Gynecol Obstet 1945; 81:243-265. |
|4.||Eugene PC, Henry GH, Daniel HM, Robert CM, John C. Osteomalacia in thyrotoxicosis. Metabolism 1964; 13:161-171. |
|5.||Graves RJ. Clinical lectures. Lond Med Surg J 1837; 7:516-529. |
|6.||Von Basedow CA. Exophthalmos Durch hypertrophic des Zellgewebes in der augenhole. Wochenschr 1840; 6:197-220 |
|7.||Renuka D, Rao SD, Murthy KSR. A profile of nutritional osteomalacia in Hyderabad city. J Assoc Physicians India 1982; 30:215-217. |
|8.||Nisbet JA, Eastwood JB, Colston KW. Detection of osteomalacia in British Asians, a comparison of clinical score with biochemical measurements. Clin Sci 1990; 78:383-390. |
|9.||Leif M, Erick FE, Peder C. Effect of thyroid on bone and mineral metabolism. Endocrinol Metab Clin North Am 1990; 19:35-63. |
|10.||Schott GD, Wills MR. Muscle in osteomalacia. Lancet 1976; 1:626-628.
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