• Additive effects of moderate dietary salt reduction and captopril in hypertension

      Kristinsson, A; Hardarson, T; Palsson, K; Petursson, M K; Snorrason, S P; Thorgeirsson, G; Department of Internal Medicine, Landspitalinn-University Hospital, Reykjavik, Iceland. (Distributed by Almqvist and Wiksell, 1988)
      In a randomized, cross-over study 27 patients had diastolic blood pressure of greater than or equal to 96 mmHg during four visits without treatment. Following captopril 25 mg b.i.d. nine patients' blood pressure was less than or equal to 90 mmHg. The remaining 18 were randomized into two treatment modalities, captopril and moderate dietary salt reduction, and captopril and hydrochlorothiazide 25 mg daily. Following a wash-out period the groups crossed over to the alternative treatment. At the end of the control period the average blood pressure was 151/100 +/- 12/6 mmHg recumbent and 140/91 +/- 11/7 standing, following captopril 144/94 +/- 13/5 and 132/92 +/- 12/6, respectively, with low salt diet added to captopril 140/91 +/- 12/6 and 128/89 +/- 11/6 and with hydrochlorothiazide and captopril 133/86 +/- 12/7 and 120/84 +/- 11/7 mmHg supine and erect, respectively. It is concluded that moderate dietary salt reduction, which is easily advised, will significantly potentiate the blood pressure fall following captopril treatment in moderate arterial hypertension.
    • Adenine phosphoribosyltransferase deficiency in Iceland

      Laxdal, T; Jonasson, T A; Department of Paediatrics, St. Joseph's Hospital, Reykjavík, Iceland. (Distributed by Almqvist and Wiksell, 1988-12)
      Two children and two adults of four unrelated families were on regular light microscopic examination found to exhibit identical, spherical urine crystals. Their characteristic appearance led to the diagnosis of 2,8-dihydroxyadenine crystalluria by spectrophotometric or gas-chromatographic/mass-spectrometric analysis. Total deficiency of adenine phosphoribosyltransferase was confirmed by direct measurements of the enzyme activity in lysed red blood cells. Close family members were also examined for the enzyme defect, revealing no additional homozygotes, but 13 heterozygotes among 14 relatives. We suggest that round, brownish urine crystals, even without radiolucent kidney stones, should alert the physician to search for the existence of 2,8-dihydroxyadenine. Proper treatment could then be instituted without delay, preventing eventual kidney damage.