Secondary Hyperparathyroidism in Patients with Endemic Skeletal Fluorosis

Abstract

637tecting deterioration but a separate evaluation by the research team showed that at least 74% of the patients who had been deemed to have relapsed had an increase of florid symptoms. Though one-third of the patients in our sample had florid symptoms when they entered the trial their condition was stabilized at the time. When switched to placebo 83 % of these increased the number of florid symptoms (table VII). The social behaviour of many patients on placebo deteriorated and put additional strain on their relatives (Stevens, 1973), but in most cases it was associated with an exacerbation of schizophrenic symptoms. We therefore conclude that fluphenazine decanoate has a powerful effect in preventing and ameliorating both schizophrenic symptoms and deterioration of behaviour and social functioning.We have stated that we cannot accept the 8% relapse rate of our experimental group at face value. Ninety-five per cent. of our sample had been established on treatment more than three months and most more than a year, so that patients who had been negative responders, relapsed or lapsed from treatment would have been omitted from the sample. Thus the proportion of chronic schizophrenics who relapsed and began treatment with fluphenazine decanoate but were unlikely to remain well-controlled for a year might be expected to be more than 30%, in contrast to patients well established on treatment, of whom only 8% relapsed during nine months in this trial.It is noteworthy that 89% of patients entering our trial received just one 25-mg injection of fluphenazine decanoate monthly. Some centres give much higher doses, but these findings suggest that low doses are effective in most cases.This study has not touched on the problems of the chronic disabilities of these patients. With the greater control of florid symptoms which treatment provides the management of residual disability will become an increasing problem, because of the growing number of chronic patients returning to live in the community. Summary Investigation of 20 patients with skeletal fluorosis showed that five had clear evidence of secondary hyperparathyroidism. The hyperactivity of the parathyroid glands in skeletal fluorosis in the presence of decreased solubility of the bone mineral (fluoroapatite) strongly suggests that it is a compensatory attempt to maintain a normal extraceElular ionized calcium equilibrium. Further study of the parathyroid glands and of bone lesions in skeletal fluorosis is in progress.

Effects of fluoride on bone in Finland: Histomorphometry of cadaver bone from low and high fluoride areas

“…In animal studies, many authors (Faccini & Care 1965, Makhni et al 1979 have shown that excess fluoride stimulates the parathyroid glands. This is thought to be responsible for the many histological findings in human skeletal fluorosis (Teotia et al 1973(Teotia et al , 1976. Nichols et al (1965) assumed that activated parathyroid glands stimulate formation of new bone without any increase in bone resorption.…”

Fluorosis, Osteomalacia and Pseudohyperparathyroidism in a Patient with Renal Failure

“…Since then, its presentation in that country has not been infrequent [4, 7] and has also been reported in other parts around the world (South Africa [4, 8], Tanzania [3, 4], China [4]). In our country, besides the study carried out by Prof. Soriano on the cases of fluorosis caused by wine [6], several cases caused by drinking water [9] have been studied.…”

“…As described in the literature, chronic fluoride poisoning, especially when it is accompanied by a low intake of calcium, produces either direct or indirect stimulation of the parathyroid glands and hyperparathyroidism [3, 4, 7], and an increase in alkaline phosphatase [4, 7] and tubular resistance, shown by the normal phosphoremia values and the low rate of urinary phosphorus excretion [4]. The bone injuries are characterized by a combination of osteosclerosis, osteomalacia and osteoporosis to varying degrees [3, 4], as well as a periosteal inflammation reaction [4, 5, 6, 7]. All of these were found in our patient.…”

Fluoride stimulation of the rat parathyroid gland: An ultrastructural study

“…I t has been suggested that the decreased crystal solubility results in an inhibition of bone resorption and a drop in the serum calcium concentration, thus stimulating parathyroid hormone secretion in order to maintain calcium homeostasis (Rich and Feist, 1970). Although the bulk of evidence suggests that fluoride administration causes hyperactivity of the parathyroid glands in humans (Baylink and Bernstein, 1967;Bernstein and Cohen, 1967;Nichols et al, 1965;Teotia and Teotia, 1973;Teotia et al, 1978) and in some animals (Baylinket al, 1970;Faccini, 1967;Faccini and Care, 1965;Makhni et al, 1979;Nichols et al, 1965;Yates et al, 1964), contradictory findings are common, particulary when the rat is used as the experimental animal. While some studies have shown changes in bone resorption which are consistent with an increase in endogenous parathyroid hormone secretion (Nichols et al, 1965;Yates et al, 1964), others have failed to show any structural or chemical evidence of parathyroid hyperactivity after fluoride administration in the rat (Hac and Freeman, 1967;Kraintz, 1969;Lui and Baylink, 1977;Raisz and Taves, 1967).…”