PubMed · 16149496
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Fuitoshi Satoh, Katsumi Yoshida. 2005. [Prolactin].. https://pubmed.ncbi.nlm.nih.gov/16149496/
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PURPOSE OF REVIEW: The purpose of this review is to comment on the current findings on Carney complex, a dominantly inherited disease and a unique multiple endocrine neoplasia syndrome. RECENT FINDINGS: Sequencing of the PRKAR1A gene in more than 150 kindreds has revealed a number of pathogenic mutations; in more than 90% of the cases, the sequence change was predicted to lead to a premature stop codon and, thus, mutant mRNAs were subject to nonsense-mediated mRNA decay. In Carney complex syndrome cells carrying these mutations, protein kinase A activity is irregularly stimulated by cAMP. Mutations that did not lead to a premature stop codon have also been described; these were also associated with abnormal protein kinase A activity. Animal models of the disease have been recently developed; they reproduced some of the stigmata of Carney complex syndrome but not all. Genetic testing of patients' family members has been introduced in recent years, leading to early detection and a better overall prognosis. SUMMARY: New treatments have yet to be applied; the elucidation of the molecular pathways regulated by PRKAR1A holds the promise of leading to molecularly designed therapies.
By clinical experience, rhinitis has been suggested as caused by some endocrine disorders, but the evidence for this is vague, and the few descriptions almost anecdotal. Rhinitis of the menstrual cycle has been more described, although a solid picture is still lacking. Pregnancy rhinitis is therefore so far the only clearly defined "hormonal rhinitis." However, the cause of pregnancy rhinitis is not simply estrogen or progesterone, but seems multifactorial, and may possibly be associated with the PGH. Treatment consists mainly of information, physiological measures, and nasal saline washings.
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