Abnormal Phosphorus Research Articles

Rickets Associated With Long-Term Anticonvulsant Therapy

The study presented by Crosley et al. in the July 1975 issue of Pediatrics (page 52) is the first dealing with noninstitutionalized children. A significantly higher value of serum alkaline phosphatase was observed in treated children than in the control population, while calcium and phosphorus abnormalities were minimal in both groups. We concluded a study on the serum alkaline phosphatase, calcium, and phosphorus levels in noninstitutionalized children, including 50 who were from 3 to 14 years old and who were receiving long-term anticonvulsant therapy (either diphenylhydantoin, phenobarbital, or both for more than 12 months) and 57 age-matched controls, all living at home.

OCCULT OSTEOMALACIA AMONGST HEALTHY AND PREGNANT WOMEN IN PAKISTAN

A survey has been carried out on 206 healthy Pakistani women attending with their sick children at the pædiatric outpatients department and 252 pregnant Pakistani women near term attending the antenatal clinic of the Karachi Postgraduate Medical Centre. 12·6% of healthy women and 33% of pregnant women had biochemical abnormalities in serum calcium, phosphorus, and alkaline phosphatase which were corrected with subsequent administration of vitamin D. The absence of clinical disease has been ascribed to the supplementation received through the ultraviolet irradiation of the skin.

Rickets Associated With Long-Term Anticonvulsant Therapy in a Pediatric Outpatient Population

Over a 12-month period, an ambulatory pediatric population receiving long-term anticonvulsants was surveyed for the presence of biochemical and radiologic rickets. There were 74 treated children and 95 matched controls. Elevations of serum alkaline phosphatase activity occurred in 31 of the 74 (42%) treated children (23 of 47 children between 2 and 10 years and 8 of 21 children between 10 and 16 years). This frequency of abnormal values was significantly greater than that which occurred in our control population. Calcium and phosphorus abnormalities were minimal in both treated and control populations. Radiologic rickets occurred in 6 of the 74 (8%) of the treated children and in none of the control population. Neither the severity of the rickets nor the degree of hyperalkaline phosphatasemia were correlated with age of the patient, duration, and/or dose of anticonvulsant therapy.

Hypophosphataemia and hyperphosphataemia in a hospital population

During a 4-mth-period 100 cases of hypophosphataemia and 84 of hyperphosphataemia occurring in a hospital population were studied in order to determine the cause of the abnormality. Intravenous administration of carbohydrate, usually glucose, was the commonest cause of a low serum phosphorus, and accounted for 40% of cases. Next in order were vomiting and gastric aspiration, followed by cirrhosis of the liver. Administration of insulin for diabetic coma or aluminium hydroside containing antacids accounted for 9%. There were 2 cases of familial hypophosphataeniia, 1 case of probable hyperparathyroidism, and 1 example of Gram-negative septicaemia. In many instances there was more than one aetiological factor present. No diagnosis could be made in 26% of cases. The causes of hyperphosphataemia were more varied and more evenly distributed. They were adolescence, a high phosphorus intake, vitamin D therapy, diabetic coma, bone tuniours, hyperthyroidism, hvpoparathyroidism, heparin administration, leukaemia, haemolysis and healing fracture. In both groups the undiagnosed cases were examined for the presence of factors whlch have been incriminated in the production of abnormalities in serum phosphorus or have been serum to have an effect on phosphorus metabolism. During a 4-mth-period 100 cases of hypophosphataemia and 84 of hyperphosphataemia occurring in a hospital population were studied in order to determine the cause of the abnormality. Intravenous administration of carbohydrate, usually glucose, was the commonest cause of a low serum phosphorus, and accounted for 40% of cases. Next in order were vomiting and gastric aspiration, followed by cirrhosis of the liver. Administration of insulin for diabetic coma or aluminium hydroside containing antacids accounted for 9%. There were 2 cases of familial hypophosphataeniia, 1 case of probable hyperparathyroidism, and 1 example of Gram-negative septicaemia. In many instances there was more than one aetiological factor present. No diagnosis could be made in 26% of cases. The causes of hyperphosphataemia were more varied and more evenly distributed. They were adolescence, a high phosphorus intake, vitamin D therapy, diabetic coma, bone tuniours, hyperthyroidism, hvpoparathyroidism, heparin administration, leukaemia, haemolysis and healing fracture. In both groups the undiagnosed cases were examined for the presence of factors whlch have been incriminated in the production of abnormalities in serum phosphorus or have been serum to have an effect on phosphorus metabolism.

Abnormal phosphorus metabolism in a potassium transport mutant of Escherichia coli

Abstract : Studies with K transport mutant, strain RD-2, reveal that the mutant does not take up inorganic phosphorus normally. The abnormality in phosphorus uptake is reflected in a reduced rate of 32P sub i incorporation into phospholipid. The 32P sub i uptake reaction of the mutant is superstimulated by potassium and inhibited by sodium, characteristics which resemble the behavior of the potassium-stimulated enzymes that are most commonly found catalyzing reactions in intermediate metabolism that involve the transfer of a phosphate group. (Author)

Serum calcium and phosphorus abnormalities in leukemia

The records of all cases of leukemia at the University of California Medical Center during the five year period from January 1960 to December 1964 were reviewed for data on serum calcium, phosphorus and alkaline phosphatase determinations and roentgenologic examination of the skeleton. A total of 260 cases were found, 123 of which included a calcium and phosphorus determination. Three patients (2.5 per cent) had hypercalcemia, and twenty-two (18 per cent) in whom renal function was not impaired had hyperphosphatemia. Increased alkaline phosphatase activity was found in 34 per cent of the patients tested. Hyperphosphatemia and increased alkaline phosphatase activity could not be correlated with other clinical or laboratory findings. Roentgenologic evidence of bone disease was found in eleven of twenty children examined, but in only ten of fifty-three adult patients.Seven cases of leukemia with hypercalcemia are reported. Six of the patients had acute leukemia; in the seventh case, however, the hypercalcemia was not related to the coexisting chronic lymphocytic leukemia. Symptoms of hypercalcemia preceded other evidence of acute leukemia in one case and in two reported previously. Early recognition of these cases is important since the hypercalcemia and its symptoms were reversed by corticosteroid therapy in all three instances. Roentgenologic evidence of bone disease was not always present at the time the hypercalcemia was discovered but usually appeared later. Serum phosphorus levels are usually normal or elevated in association with the hypercalcemia of leukemia, suggesting an osteolytic action other than that of parathyroid hormone. In one case of chronic lymphatic leukemia, hypercalcemia, hypophosphatemia and low tubular resorption of phosphate were corrected by removal of a parathyroid adenoma. In the first case, and in one reported previously, with hypercalcemia and hypophosphatemia, there was no evidence of parathyroid abnormality.

BRONCHOGENIC CARCINOMA SIMULATING HYPERPARATHYROIDISM.

METASTATIC malignant disease to bone is known to cause hypercalcemia. 1-5 In nonmetastatic cases, the occasional findings of associated serum and urinary phosphorus abnormalities and the disappearance of the hypercalcemia with the removal of the tumor suggest a relationship to a hyperparathyroid state. 3-27 The following case report of nonmetastatic bronchogenic carcinoma demonstrates the typical features of hyperparathyroidism and their reversal by surgical removal of the tumor. Report of Case A 66-year-old Caucasian man was hospitalized for evaluation of an intrapulmonary mass on June 18, 1963. He had been in excellent health all his life until three months prior to admission when he noted the onset of cough, anorexia, dysphagia and a 20 lb (9.1 kg) weight loss. There were no other pulmonary, cardiac, renal, or metabolic symptoms. The patient's past history revealed that he had smoked 1½ packs of cigarettes a day for 40 years. Physical examination revealed a

Idiopathic hypoparathyroidism: unusual response to vitamin D.

ABSTRACT A balance study of a patient with idiopathic hypoparathyroidism demonstrated an abnormal response to vitamin D2. Dosages up to 1 million units daily did not correct the abnormal calcium and phosphorus metabolism, but dihydrotachysterol in a dosage of 3 cc. daily reversed the metabolic effects. Six years before this study, the patient had first experienced convulsive seizures. At that time, and five years later when lenticular cataracts developed, the serum calcium concentration was normal. The diagnosis of hypoparathyroidism was made at the time the patient entered the hospital for eye surgery, when hypocalcemia and hyperphosphatemia were present. The patient also exhibited trophic changes in the fingernails and episodes of psychotic behavior. In addition to the abnormal serum calcium and phosphorus levels, there were low serum levels of citric acid, increased renal reabsorption of phosphate, and a normal response to intravenous parathyroid hormone.