Abdomen agudo durante la gestación y el puerperio / Acute abdomen during pregnancy and the puerperium

El abdomen agudo en la gestación y el puerperio constituye un diagnóstico complejo y un reto terapéutico. Nuestro objetivo es realizar una revisión bibliográfica de esta patología a propósito de un caso de peritonitis secundaria a absceso tubárico con apendicitis por helmintos concomitante. Principalmente, su sintomatología se resume en el dolor y la distensión abdominal, las náuseas y/o los vómitos. Estos síntomas se encuentran presentes en el embarazo normal, dificultando el diagnóstico diferencial. El abdomen agudo es relativamente infrecuente durante la gestación y el puerperio, siendo la apendicitis aguda la principal causa de origen no obstétrico. Asocia una elevada morbimortalidad materno-fetal, que aumenta a medida que la gestación avanza, requiriendo un manejo multidisciplinar para alcanzar un diagnóstico precoz y un tratamiento efectivo. Fundamentalmente, el abordaje terapéutico es quirúrgico debido, en gran medida, al diagnóstico tardío con frecuente asociación de complicaciones. Un manejo temprano será primordial para minimizar riesgos para la madre y el feto

Acute abdomen in pregnancy and the postpartum period is a complex diagnostic and therapeutic challenge. We review the literature on this topic and report a case of peritonitis secondary to tubal abscess with concomitant helminth appendicitis. The main symptoms of this entity are pain and bloating, nausea and/or vomiting. These symptoms are present in normal pregnancy, which hampers the differential diagnosis. Acute abdomen is relatively uncommon during pregnancy and the postpartum, and the main obstetric cause is acute appendicitis. Maternal and fetal morbidity and mortality are high and increase as the pregnancy progresses, requiring multidisciplinary management to achieve early diagnosis and effective treatment. The therapeutic approach is mainly surgical, largely due to late diagnosis and associated complications. Early management is essential to minimize the risks to the mother and fetus

Studying the antiemetic effect of vitamin B6 for morning sickness: pyridoxine and pyridoxal are prodrugs.

Vitamin B6 has been known to possess antiemetic effects since 1942. This water soluble compound has several forms in the circulation including pyridoxine, pyridoxal, and pyridoxal phosphate. The active antiemetic form of vitamin B6 is unknown. This was a pre-specified substudy of a randomized, placebo-controlled trial comparing the antiemetic effect of the doxylamine-vitamin B6 combination (Diclectin®) (n = 131) to placebo (n = 126) in women with nausea and vomiting of pregnancy. Serum concentrations of pyridoxine, pyridoxal, and pyridoxal 5' phosphate (PLP) and doxylamine were measured on Days 4, 8, and 15. With Diclectin® exhibiting a significant antiemetic effect in pregnancy, serum concentrations of pyridoxine were unmeasurable in almost all patients and those of pyridoxal were undetectable in half of patients. In contrast, PLP was measurable at sustained, stable steady-state levels in all patients. Our data suggest that there is a correlation between PLP levels and PUQE score of morning sickness symptoms when pyridoxine and pyridoxal levels are undetectable, and hence they might be prodrugs of PLP, which may be the active antiemetic form of vitamin B6.

Pregnancy sickness and parent-offspring conflict over thyroid function.

Pregnancy sickness is widespread in human mothers but its etiology, somewhat surprisingly, remains unclear. Human chorionic gonadotropin (hCG) has long been considered a prime hormonal suspect, but the correlation between pregnancy sickness and hCG levels is imperfect resulting in uncertainty about its causal role. As others have noted part of this uncertainty likely stems from the structural and functional diversity of hCG. One enigmatic role of hCG is its action as a thyroid stimulator during early gestation. Native hCG is weakly thyrotropic but is produced in prodigious quantities and suppresses the production of thyroid stimulating hormone (TSH) but not curiously when TSH levels are in the higher deciles. Higher levels of hCG induce higher maternal production of thyroxine (T4). hCG thus appears to augment and sometimes even supplant TSH in the regulation of thyroid hormone in early gestation. This has lead to the suggestion that hCG serves as a backup system, albeit incomplete, for the production of essential thyroid hormone during pregnancy. Another interpretation, however, is that hCG, produced by the embryo, serves as a second control circuit for the thyroid during pregnancy. If so, it serves embryonic interests that are at odds with maternal interests (maternal-embryo conflict) under conditions of iodine deficiency. Iodine is an essential micronutrient for neurodevelopment and thyroid function, and has been in short supply for most humans over most of our evolutionary history. Iodine deficiency during gestation has severe impacts on embryo neuromotor development, but also induces thyroid disease in mothers, impairing her future reproductive prospects. Under this view, embryos use hCG to push mothers to release more thyroid hormone. hCG, however, is produced outside the normal maternal thyroid control circuit and thus is not subject to a normal negative feedback. hCG also serves multiple functions simultaneously therefore its production is likely not fine-tuned for thyroid function per se. hCG levels may remain high even when thyroid hormone production is more than sufficient to meet the needs of mother and embryo. Instead, the system appears to be regulated at the back end by clearing surplus hormone using placental Type II (D2) and Type III (D3) deiodinases. As maternal thyroid hormone levels rise, placental D3 is upregulated, shunting more T4 and T3 into a deactivating pathway. The metabolites that result, particularly the inert metabolite of T4, reverse T3, are correlates of surplus thyroid hormone production and thus are strong candidates for the proximate triggers of pregnancy sickness. Nausea and vomiting of early pregnancy thus arises as a by-product of an antagonistic pleiotropy between mother and embryo over the allocation of iodine: when dietary iodine is scarce, a benefit accrues to the embryo at a cost to mother; when iodine is plentiful, pregnancy sickness ranging from frequently mild to occasionally severe, is a sequelae of undiminished embryonic demands. If pregnancy sickness serves as a marker of thyroid function, an absence of first trimester nausea and vomiting sickness may indicate a higher priority for testing of thyroid function to avert the inimical effects of hypothyroidism during gestation.

Morning sickness: adaptive cause or nonadaptive consequence of embryo viability?

"Morning sickness" is the common term for nausea and vomiting in early human pregnancy (NVP). Recent interest in why NVP occurs-that is, in the evolutionary costs and benefits of NVP-has spurred the development of two alternative hypotheses. The "prophylaxis," or "maternal and embryonic protection," hypothesis suggests that NVP serves a beneficial function by expelling foods that may contain harmful toxins and microorganisms and triggering aversions to such foods throughout pregnancy. The alternative "by-product" hypothesis suggests that NVP is a nonfunctional by-product of conflict--over resource allocation--between the pregnant woman and the embryo. The critical predictions of the prophylaxis hypothesis have been developed and tested, whereas the by-product hypothesis has not been subjected to similar scrutiny. To address this gap, we developed a graphical model and used it to derive predictions from the by-product hypothesis under two different assumptions, namely, that NVP is either (i) a by-product of current conflict between a pregnant woman and an embryo or (ii) a by-product of honest signals of viability produced by the embryo. Neither version of the by-product hypothesis is fully consistent with available data. By contrast, the timing of NVP, its variation among societies, and associated patterns of food cravings and aversions are consistent with the prophylaxis hypothesis.

Nitrogen balance and delta15N: why you're not what you eat during nutritional stress.

While past experiments on animals, birds, fish, and insects have shown changes in stable isotope ratios due to nutritional stress, there has been little research on this topic in humans. To address this issue, a small pilot study was conducted. Hair samples from eight pregnant women who experienced nutritional stress associated with the nausea and vomiting of morning sickness (hyperemesis gravidarum) were measured for carbon (delta13C) and nitrogen (delta15N) stable isotope ratios. The delta13C results showed no change during morning sickness or pregnancy when compared with pre-pregnancy values. In contrast, the delta15N values generally increased during periods of weight loss and/or restricted weight gain associated with morning sickness. With weight gain and recovery from nutritional stress, the hair delta15N values displayed a decreasing trend over the course of gestation towards birth. This study illustrates how delta15N values are not only affected by diet, but also by the nitrogen balance of an individual. Potential applications of this research include the development of diagnostic techniques for tracking eating disorders, disease states, and nitrogen balance in archaeological, medical, and forensic cases.