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The identity and genetic origins of the nonspecific orthophosphate monoesterases with an acid pH optimum--the acid phosphatases--are now becoming clear. They form a family of genetically distinct isoenzymes, many of which show significant posttranslational modification. Four true isoenzymes exist. The erythrocytic and lysosomal forms show widespread distribution and are expressed in most cells; in contrast, the prostatic and macrophagic forms have a more limited expression. The erythrocytic and macrophagic forms are distinguished from the others in resisting inhibition by dextrorotatory tartrate. The prostatic form has long been used as a marker for prostatic cancer and the macrophagic forms have been linked with miscellaneous disorders, notably increased osteolysis, Gaucher's disease of spleen, and hairy cell leukemia, whereas the normal levels of intravesical lysosomal acid phosphatase in I cell disease pointed the way toward the mechanisms underlying its intracellular processing.

SUMMARY Simultaneous 24‐hour intragastric acidity and plasma gastrin concentrations were measured in 12 duodenal ulcer patients before and on the twenty‐eighth day of treatment with either ranitidine 150 mg b.d. or omeprazole 20 mg o.m. Median integrated 24‐hour intragastric acidity was decreased significantly from 1148 to 490 and 36 mmol. hour litre−1 during treatment with ranitidine and omeprazole, respectively, whilst median intragastric 24‐hour plasma gastrin was raised significantly from 328 to 799 and 1519 pmol. hour litre−1 respectively. When the results of all 48 experiments were considered together, there was a significant inverse correlation between the 24‐hour integrated values for intragastric acidity and plasma gastrin concentration. Both drugs caused a significant elevation of plasma gastrin throughout the 24 hours, although ranitidine had no effect on intragastric acidity from 1900 to 2200 hours. When compared with similar profiles of acidity and gastrin in pernicious‐anaemia patients, the modest elevations of plasma gastrin observed in this study suggest that neither drug will be associated with clinically relevant enterochromaffin‐like cell proliferation in duodenal ulcer patients.

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