Subject(s)
Stomach Ulcer/diagnosis , Adolescent , Child , Child, Preschool , Female , Gastroscopy , Humans , Infant , Infant, Newborn , MaleABSTRACT
The study comprised 31 ambulatory epileptic children aged 1,5-14 years (mean: 7.37), receiving treatment with anticonvulsant drugs. Authors found that renal threshold for bicarbonate was inferior when compared to control group (mean = 21.3 mEq/l., SD = 1.75; mean = 25.34 mEq/l., SD = 1.29; p less than 0.0001), low calcemia (mean = 9.12 mg./dl., SD = 0.51; mean = 9.43, SD = 0.45; p less than 0.01) and elevated alkaline phosphatase (mean = 212.6 mU/ml., SD = 75.9; mean = 127.4, SD = 50.2; p less than 0.01). No significant difference in urinary excretion of cyclic AMP, phosphate or calcium was observed. Nineteen patients who had subnormal threshold (inferior to -2 SD in the control group) when compared with control group, had: low calcemia (p less than 0.01), high alkaline phosphatase (p less than 0.0001) and a similar urinary cyclic AMP, calciuria and phosphaturia. A negative correlation between renal threshold to bicarbonate and serum phosphate (r = -0.49, p less than 0.01) and a negative correlation between the urinary cyclic AMP and the duration of treatment (r = -0.42, p less than 0.05) was found. It is commented that although in deficiency rickets, proximal tubular acidosis is due to secondary hyperparathyroidism, in their patients despite they had biochemical characteristics of rickets, low calcemia and elevated alkaline phosphatase, the descent of renal threshold to bicarbonate is a nonparathoromone mediated phenomenon.
Subject(s)
Acidosis, Renal Tubular/chemically induced , Anticonvulsants/adverse effects , Bicarbonates/metabolism , Epilepsy/metabolism , Adolescent , Child , Child, Preschool , Cyclic AMP/metabolism , Epilepsy/complications , Epilepsy/drug therapy , Female , Humans , Hyperparathyroidism, Secondary/etiology , Infant , Kidney Tubules, Proximal/drug effects , MaleABSTRACT
The subjects of this study were 18 patients with essential or secondary epilepsy under treatment with anticonvulsant drugs (hydantoins and phenobarbital) for periods of time varying between 8 months and 22 years. In all of them the serum levels of calcium, phosphorus, alkaline phosphatase, and the renal tubular capacity to acidify the urine were measured. Mean serum calcium and phosphorus levels were normal, while alkaline phosphatase was significantly elevated (p less than 0.0005). The renal threshold for bicarbonate was lowered to a mean of 23.01 +/- 2.86 (p less than 0.01). Distal tubular function was normal in all cases. When the patients are divided into two groups according to the duration of treatment (more or less than 100 months), the group with longest therapy shows an elevation of alkaline phosphatase (p less than 0.0005), a lowering of serum calcium (p less than 0.025) and a reduction of the renal threshold for bicarbonate (p less than 0.005) when compared to the group with shortest therapy.
Subject(s)
Anticonvulsants/pharmacology , Kidney Tubules/drug effects , Adolescent , Adult , Alkaline Phosphatase/blood , Anticonvulsants/therapeutic use , Bicarbonates/blood , Calcium/blood , Epilepsy/drug therapy , Female , Humans , Hydrogen-Ion Concentration , Kidney Tubules/metabolism , Male , Middle Aged , Phosphorus/blood , Time FactorsABSTRACT
The renal capacity of acidification of urine was studied in 21 patients with hypergammaglobulinemia (polyclonal gammapathies) secondary to several conditions. The reabsorption threshold of bicarbonate was determined by Rodriguez-Soriano's technique; the acid and ammonium production was measured using Wrong and Davies' technique. Values for the bicarbonate threshold ranged from 18.5 to 29 mmol/liter of plasma bicarbonate with a mean value of 25 +/- 2.29; they were not significantly different from the control values. Urinary pH ranged from 4.6 to 5.8; ammonium excretion ranged from 18.4 to 114.5 microEq/min (mean value 63.01 +/- 25.36). Acidity values ranged from 13 to 65.05 microEq/min (mean value 33.61 +/- 19.36). Thhre was no statistical difference between these values and those obtained from the controls. We found no evidence that the acidification function of urine was limited in patients with hypergammaglobulinemia secondary to several conditions as compared with normal subjects. In the two cases in which this function was altered there was no reason why it should be attributed to hypergammaglobulinemia.
