OBJECTIVE: To provide an overview of thyroid abnormalities that can occur after delivery. METHODS: We review the diagnosis and management of various types of postpartum thyroid dysfunction. RESULTS: A common problem during the postpartum period, thyroid dysfunction is found in approximately 5% of new mothers in the general population. Such thyroid dysfunction can manifest in various forms (hyperthyroid or hypothyroid, transient or persistent), each of which necessitates different treatment. The most common type of thyroid dysfunction is destructive thyrotoxicosis, which is due to the aggravation of autoimmune thyroiditis. It occurs at 1 to 3 months after delivery as sudden thyrotoxicosis and lasts for 1 to 3 months, after which transient hypothyroidism may ensue in some cases. Simply symptomatic treatment may be sufficient for such transient thyroid dysfunctions. Postpartum Graves' disease is found in approximately 11% of the cases of postpartum thyroid dysfunction. Graves' hyperthyroidism usually occurs at 3 to 6 months after parturition. In the treatment of postpartum Graves' disease, one may choose radioactive iodine, antithyroid drugs, or surgical therapy; however, transient Graves' hyperthyroidism, which often occurs in patients with postpartum Graves' disease, may require neither radioactive iodine therapy nor thyroidectomy. Mothers at high risk for development of postpartum thyroid dysfunction can be screened by testing for antimicrosomal antibodies. Although a strong correlation exists between the presence of antimicrosomal antibodies and postpartum thyroid dysfunction, the cost-effectiveness of screening for postpartum autoimmune thyroid syndrome remains controversial. CONCLUSION: For optimal management of the postpartum conditions of Graves' disease, destructive thyrotoxicosis, and hypothyroidism, the clinician should be aware of diagnostic techniques that will facilitate early intervention or will prompt careful surveillance.

Journal Article↗

PubMedDate not supplied

A newly synthesized pyridine derivative, (Z)-5-methyl-2-[2-(1-naphthyl)ethenyl]-4-piperidinopyridine hydrochloride (AU-1421), as a reversible gastric proton pump inhibitor.

A newly synthesized pyridine derivative, (Z)-5-methyl-2-[2-(1-naphthyl)ethenyl]-4-piperidinopyridine hydrochloride (AU-1421), was found to inhibit the gastric proton pump in vitro and in vivo. In the leaky membrane vesicles of hog gastric mucosa, AU-1421 inhibited the K(+)-stimulated H, K-ATPase activity competitively with respect to K+, with a Ki value of 0.18 microM at pH 7.4 and 0.10 microM at pH 6.4. This inhibition was not affected by the length of the preincubation time of the enzyme with AU-1421, and activity was restored by dialysis. In the intact hog gastric membrane vesicles, which developed a pH gradient in the presence of valinomycin, AU-1421 also inhibited the gastric proton pump activity as measured by the quench of acridine orange fluorescence. In the isolated rabbit gastric glands, AU-1421 inhibited the histamine-, dibutyryl cAMP- and K(+)-stimulated uptake of [14C]aminopyrine into gastric glands with similar IC50 values of about 1 microM. Furthermore, AU-1421 suppressed gastric acid secretion in acute fistula rats and Heidenhain-pouch dogs with the same potency as cimetidine. These results suggest that AU-1421 is an antisecretory agent which reversibly inhibits the H,K-ATPase.

Adenosine Triphosphatases↗