{'fraction_non_alphanumeric': 0.020899591094956836, 'fraction_numerical': 0.002271694684234439, 'mean_word_length': 5.838509316770186, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Epidemiology of pregnancy-induced hypertension.

Mounting evidence clearly indicates an immunologic basis for PIH, parity being the most convincing factor. Genetic susceptibility, physiologic change, and environmental influence may also modulate an individual's risk of developing PIH. Pathologic and follow-up studies further suggests further suggest that currently diagnosed PIH may actually be a heterogeneous entity comprising several disorders of different etiologies (150), such as chronic renal disease, borderline chronic hypertension, genetic susceptibility to hypertension, and genuine PIH. For many diseases, etiologic research and clinical management often go hand in hand. Unfortunately, in the case of PIH, etiologic research may have followed clinical steps too closely and have been misled. For clinical management, genuine preeclampsia and preeclampsia superimposed on chronic hypertension are treated as virtually the same: The ultimate goal is to prevent eclampsia. Because a sizable portion of PIH is probably due to chronic renal disease or latent chronic hypertension (33), and late-onset gestational hypertension is of less concern than preeclampsia, one could argue that it may not be clinically important to separate the subtypes of PIH. In etiologic research, however, by focusing on a heterogeneous outcome we have confused ourselves and hampered our progress. On the other hand, one should also realize that currently available techniques are unlikely to substantially improve our proficiency in differential diagnosis. Besides renal biopsy, which is impractical, especially in epidemiologic research, there are virtually no measures available that can distinguish genuine PIH from hypertension due to latent renal disorder, chronic hypertension, or genetic susceptibility. Until noninvasive measures with acceptable-sensitivity and specificity are available for differential diagnosis, frustration in etiologic research on PIH is likely to continue. One clue that may potentially advance our knowledge of the pathogenesis and future prevention of PIH is the finding that smoking reduces risk of PIH. Epidemiologists should transfer this knowledge to laboratory scientists.