Survival in spinal muscular atrophy type 1 patients has increased in recent years, in relation to the growing trend toward more proactive clinical care.

Significant hyperkalaemia occurred in 406 out of 29 063 patients admitted to a major Scottish teaching hospital in one year (1 4%). Mortality was higher in these patients than in control patients and was strongly correlated with the severity of the hyperkalaemia. Overall seven deaths were directly due to hyperkalaemia (out of 58 deaths among patients with hyperkalaemia). Factors contributing to a poor prognosis were severity and speed of onset of hyperkalaemia and the presence of appreciable renal impairment. Patients with hyperkalaemia were older and more likely to be male; this trend was present in all diagnostic subcategories. Genitourinary disease, gastrointestinal disease, and cancer were significantly more common among the patients with hyperkalaemia than the controls. Hyperkalaemia due to drug treatment was invariably mild and non-fatal, whereas genitourinary disease was often associated with moderate to severe hyperkalaemia, which in two cases proved fatal. Use of electrocardiographic monitoring was rare, and although the treatment of hyperkalaemia was effective, it was often used when not required. Hyperkalaemia is a potential hazard in diabetic ketoacidosis, and use of potassium supplements should be carefully monitored during correction of the acidosis.

Summary:Retrospective analysis of biochemical data from 58,167 hospital inpatients revealed that 21% developed hypokalaemia during hospitalization -in 5.2% the serum potassium was less than 3.0 mmol/l. Subsequent evaluation showed a positive correlation between hypokalaemia and both female sex and hospital mortality. Patients with leukaemia and lymphoid tumours, especially when receiving antibiotic or cytotoxic therapy, and patients with gastrointestinal malignancy were amongst those most frequently experiencing hypokalaemia. There was no significant association with cardiovascular disease. Drug and intravenous fluid administration accounted for the hypokalaemia in 56% of patients. While drug-related hypokalaemia was most commonly seen with diuretics, it was also apparent following use of steroids, insulin and haematinics.

The antihypertensive effect of the angiotensin-converting enzyme inhibitor trandolapril administered in doses of 1, 2, and 4 mg/d was compared in 207 white patients and 91 black patients with mild to moderate hypertension following a double-blind, randomized, placebo-controlled, parallel study design. Trandolapril is a prodrug that is rapidly hydrolyzed to its active diacid metabolite, trandolaprilat. After 6 weeks of double-blind treatment, trandolapril lowered baseline sitting diastolic pressure in both white and black patients. A comparison of the antihypertensive response of the two populations revealed that the black patients required between two and four times the dose of trandolapril to obtain a response similar to that observed in the white patients. A dose of 1 mg/d trandolapril resulted in a 6.1 mm Hg mean decrease in baseline sitting diastolic pressure for white patients; a similar response (-6.5 mm Hg) was observed in the black patients at 4 mg/d. In contrast to the population differences in blood pressure, the decreases in angiotensin-converting enzyme activity were similar for both populations. An evaluation of trandolaprilat levels revealed that there were no racial differences in the trandolaprilat concentrations required to achieve a given degree of angiotensin-converting enzyme inhibition. Therefore, it appears that the antihypertensive response of black patients is not completely explained by a reduction in angiotensin-converting enzyme activity. The lack of response at a lower dose but increasing response at a higher dose could reflect another vasodepressor activity of trandolapril or just be evidence of reduced sensitivity of high blood pressure in blacks to angiotensin-converting enzyme inhibition.

Using a battery of simple tests, psychomotor performance was assessed in 11 healthy subjects, 14 untreated epileptic patients and 66 epileptics on chronic anticonvulsant medication. Significant differences were found between controls and untreated patients for choice reaction time, card sorting and Simple Simon memory game. Treated patients performed less well than both untreated epileptics and controls in choice reaction time (p less than 0.05; p less than 0.001), card sorting (p less than 0.01; p less than 0.001), Simple Simon (p less than 0.05; p less than 0.001) and finger tapping (p less than 0.05; p less than 0.001). Patients with centrencephalic epilepsy were slower than those with discrete focal EEG abnormalities in reaction time and card sorting. Patients receiving treatment with carbamazepine, phenytoin or sodium valproate alone all performed similarly to each other and to those patients taking anticonvulsant polypharmacy. Monotherapy patients with potentially "toxic" plasma anticonvulsant concentrations did no worse than those within or below the "therapeutic" range. Both the disease and its treatment reduce psychomotor performance. All major anticonvulsants appear to cause a similar degree of impairment across a wide range of concentrations. The effect of chronic anticonvulsant medication on "quality of life" should not be neglected in the pursuit of perfect seizure control.

No abstract

No abstract

Serum sex hormone binding globulin, thyroxine binding globulin, cortisol binding globulin and vitamin D binding globulin, together with total levels of the appropriate bound hormones, were determined in 21 epileptic subjects who had been stabilised by long-term anticonvulsant therapy. Serum sex hormone binding globulin capacity was higher in these patients than in appropriate control groups (men p less than 0.05; women p less than 0.01), and values correlated with serum phenytoin levels in the female subjects (p less than 0.01). Thyroxine binding globulin levels were unaffected by anticonvulsants, but significant reductions in serum thyroxine (men p less than 0.05; women p less than 0.001) and triiodothyronine (men p less than 0.05; women p less than 0.01) were observed. Cortisol binding globulin capacity was appreciably elevated in patients of either sex (p less than 0.001), and in the women this was accompanied by a reduction in serum cortisol (p less than 0.001) and a significant correlation with the serum phenytoin concentration (p less than 0.01). Neither vitamin D binding globulin capacity nor serum 25-hydroxycholecalciferol levels were influenced by anticonvulsants in this study. It is concluded that anticonvulsant drug therapy causes widespread alterations in the normal homeostasis between hormones and their serum binding globulins. Such alterations may well have clinical significance.