PubMed Health⌕ Search

PubMed · 11895224

Postpartum thyroid dysfunction and postpartum depression: are they two linked disorders?

Abstract

OBJECTIVE: Postpartum has been considered as a period of risk for developing postpartum depression (PD) by some but not all authors, and this PD has been linked with postpartum thyroid dysfunction (PPTD). The major aim of this study was to evaluate the relation between the presence of PPTD and PD. DESIGN AND PATIENTS: Six hundred and forty-one healthy Caucasian women recruited between their 36th week of pregnancy and fourth day postpartum underwent clinical and laboratory evaluation and were checked again at 1 (n = 605), 3 (n = 552), 6 (n = 574), 9 (n = 431), and 12 (n = 444) months postpartum. MEASUREMENTS: At baseline and at each clinical evaluation, Beck Depression Inventory (BDI) was administered to screen PD. The definitive diagnoses of PD was performed by a psychiatrist according to the DSM-III-R criteria. At each visit, we determined serum free T4 and TSH concentrations. Thyroperoxidase and thyroglobulin antibodies were determined only in patients with abnormal hormone concentrations. Postpartum thyroiditis (PPT) was considered to be present in women with overt or subclinical transient hyperthyroidism between 1 and 3 months postpartum and/or overt or subclinical hypothyroidism between 3 and 6 months postpartum. RESULTS: Fifty-six women developed postpartum thyroid dysfunction (PPTD), corresponding to an incidence rate of 11%: 45 with PPT [incidence rate 7.8%; confidence interval (CI) 5.6-10%], eight with Graves' disease (incidence rate 1.5%; CI 0.5-2.5%) and three with nonpalpable toxic thyroid adenoma (incidence rate 0.5%; CI 0-1.5%). Five hundred and eighty of the evaluated women (incidence rate 90.5%; CI 95% 88.2-92.8) presented BDI scores below 21 and therefore the PD diagnoses was excluded. In 50 cases (incidence rate 7.8%; Cl 95% 5.7-9.8), we detected a BDI score over 21 in some evaluations, but the PD diagnosis was not confirmed. Another 11 (incidence rate 1.7%; CI 95% 0.7-2.7) were diagnosed as having PD and required psychiatric treatment. None of the PPTD was diagnosed as having PD. The BDI scores frequency over 21 was similar between healthy women and those with PPTD. Patients with a previous history of depression developed PD more often (P < 0.0001). One hundred and ninety women breast fed their babies for more than 2 months, without observing a higher PD rate or BDI scores over 21 (P = 0.5). CONCLUSIONS: We found a general PD incidence rate of 1.7% in our group of patients. This figure is not higher in women with hormone abnormalities caused by PPTD. Women with a past history of depression present a higher risk of PD while those who breast fed did not have an increased risk.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

A Lucas, E Pizarro, M L Granada, I Salinas, A Sanmartí. 2001. Postpartum thyroid dysfunction and postpartum depression: are they two linked disorders?. https://doi.org/10.1046/j.1365-2265.2001.01421.x

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

HMGA proteins up-regulate CCNB2 gene in mouse and human pituitary adenomas.

The high mobility group As (HMGAs) belong to a family of nonhistone nuclear proteins that orchestrate the assembly of nucleoprotein complexes. Through a complex network of protein-DNA and protein-protein interaction, they play important roles in gene transcription, recombination, and chromatin structure. This protein family is involved, through different mechanisms, in both benign and malignant neoplasias. We have recently reported that transgenic mice carrying the Hmga1 or Hmga2 genes under transcriptional control of the cytomegalovirus promoter develop pituitary adenomas secreting prolactin and growth hormone. We have shown that the mechanism of the HMGA2-induced pituitary adenoma is based on the increased E2F1 activity. The expression profile of mouse normal pituitary glands and adenomas induced in HMGA transgenic mice revealed an increased expression of the ccnb2 gene, coding for the cyclin B2 protein, in the neoplastic tissues compared with the normal pituitary gland. Here, we show, by electrophoretic mobility shift assay and chromatin immunoprecipitation, a direct binding of HMGA proteins to the promoter of ccnb2 gene, whereas luciferase assays showed that HMGAs are able to up-regulate ccnb2 promoter activity. Finally, we report an increased CCNB2 expression in human pituitary adenomas of different histotypes that is directly correlated with HMGA1 and HMGA2 expression. Because cyclin B2 is involved in the regulation of the cell cycle, these results taken together indicate that HMGA-induced cyclin B2 overexpression gives an important contribution to experimental and human pituitary tumorigenesis.

Adenoma↗

Inhibition of lung carcinogenesis by 1alpha,25-dihydroxyvitamin D3 and 9-cis retinoic acid in the A/J mouse model: evidence of retinoid mitigation of vitamin D toxicity.

9-cis-Retinoic acid (9cRA) and 1alpha,25-dihydroxyvitamin D3 (1,25D) show promise as potential chemopreventive agents. We examined 9cRA and 1,25D, alone and in combination, for their potential to inhibit carcinogen (NNK)-induced lung carcinogenesis in A/J mice. A/J mice (n=14/group) were treated with 9cRA (7.5, 15, or 30 mg/kg diet), 1,25D (2.5 or 5.0 microg/kg diet), or a combination of 9cRA (15 mg/kg diet) plus 1,25D (2.5 microg/kg diet) for 3 weeks before and 17 weeks after carcinogen injection. Lung tumor incidence, tumor multiplicity, plasma 1,25D levels and kidney expression of vitamin D 24-hydroxylase (CYP24) were determined. Compared to carcinogen-injected controls, mice receiving 9cRA supplementation had significantly lower tumor multiplicity at all doses (decreased 68-85%), with body weight loss at the higher doses of 9cRA. Mice receiving 1,25D supplementation had significantly lower tumor incidence (decreased 36 and 82%) and tumor multiplicity (decreased 85 and 98%), but experienced significant body weight loss, kidney calcium deposition, elevated kidney CYP24 expression and decreased fasting plasma 1,25D levels. Although, there was no apparent influence on chemopreventive efficacy, addition of 9cRA to 1,25D treatment effectively prevented the weight loss and kidney calcification associated with 1,25D treatment alone. These data demonstrate that 9cRA and 1,25D, alone or combined, can inhibit lung tumor promotion in the A/J mouse model. Combining 1,25D with 9cRA has the potential to mitigate the toxicity of 1,25D, while preserving the significant effect of 1,25D treatment against lung carcinogenesis. The underlying mechanism behind this effect does not appear to be related to retinoid modulation of vitamin D catabolism.

Adenoma↗

A weighted logistic regression model for estimation of recurrence of adenomas.

In a colorectal polyp prevention trial, some participants might have their follow-up colonoscopy conducted before the scheduled time (i.e. at the end of the trial). This results in variable follow-up lengths for participants and the data of recurrence status at the end of the trial can be considered as current status data. In this paper, we use a weighted logistic regression model to estimate recurrence rate of adenoma data at the end of the trial. The weights are used to adjust for variable follow-up. We show that logistic regression tends to underestimate recurrence rate. In a simulation study, we show that Kaplan-Meier estimator derived from the right endpoint of the current status data tends to overestimate recurrence rate in contrast to logistic regression and the weighted logistic regression method can produce reasonable estimates of recurrence rate even under a high non-compliance rate compared to conventional logistic regression and Kaplan-Meier estimator. The method described here is illustrated with an example from a colon cancer study.

Adenoma↗