Adherence to prescription medications is critical for both remission from schizophrenia and control of physical comorbidities. While schizophrenia with comorbid hypothyroidism is common, there is little research on adherence to hypothyroidism treatment in this population. The current study used a retrospective, matched case-control design. The cohort included 1,252 patients diagnosed with schizophrenia according to ICD-10 and 3,756 controls matched for gender, age, socioeconomic status and ethnicity without diagnosis of schizophrenia. All data were retrieved from the electronic medical database of a large health maintenance organization. Retrieved data included demographics, thyroid functionality test results and prescribed medications. Measures of adherence to therapy were used for analyses as were data from follow-ups of patients with hypothyroidism. A diagnosis of hypothyroidism was found in 299 patients, 115 of whom were also diagnosed with schizophrenia. The 184 without schizophrenia constituted the control group. No statistically significant differences were found between the two groups regarding prescriptions for L-thyroxin and TSH levels and number of TSH tests. Adherence of patients with schizophrenia to hypothyroidism treatment was found to be as good as that of individuals without a schizophrenia diagnosis.

The aim of the present study was to determine and elaborate on all changes in old-aged (OA) versus young-aged (YA) rat thyroids by using stereological, ultrastructural, hormonal, and gene expression analyses. We used 4- and 24-month-old male Wistar rats in our evaluation, presenting all changes in comparison with YA rats. Results showed that the thyroid parenchyma was characterized by higher absolute volumes of the gland, colloid, epithelium, and interstitium by 135, 135, 140, and 142% (p < 0.05) respectively, while the relative volumes of colloid and glands were unchanged. Ultrastructural analysis revealed less active glands, with smaller amounts of lysosomes, thyroglobulin (Tg) granules, and microvilli in the luminal colloid. Optical density values for thyroid peroxidase (TPO), Tg, and vascular-endothelial growth factor immunostaining remained unchanged; however, TPO and Tg exhibited visually stronger expression in small active follicles. Thyroxine (T4)-Tg, the relative intensity of fluorescence (RIF), serum T4, and the sodium-iodide symporter immunohistochemical and gene expressions decreased by 20, 40, 29, and 31% (p < 0.05), respectively, in OA thyroids. Pituitary thyroid-stimulating hormone (TSH) RIF increased by 44% (p < 0.05), but the TSH serum concentration remained unchanged. In conclusion, the obtained results indicate depression of the thyroid gland synthetic and secretory capacity with advanced age.

The thyrotropin (TSH) and prolactin (PRL) responses to protirelin (TRH) were studied in 62 female unipolar depressive patients, 24 delusional (psychotic) and 38 nondelusional (Diagnostic and Statistical Manual [DSM]-III-R criteria). The TSH response to TRH was blunted (≤6 μlU/mL) in ten of the 24 delusional (41.6%) and in 18 of the 38 nondelusional (47.4%) patients, the difference being not significant. The TSH and PRL responses to TRH, calculated as area under the curve, were not different between the two groups. Similar results were obtained when the response patterns were compared by repeated measure analysis of covariance.

We studied circadian thyrotropin (TSH) and prolactin (PRL) response to synthetic thyrotropin-releasing-hormone (protirelin) infusion (200μg IV) at 8 am and 11 pm in 35 drug-free inpatients with DSM III-R Major Depressive Episode and in 22 hospitalized controls. In each group, maximum TSH and PRL responses were lower at 8 am than at 11 pm. The difference between 11 pm-ΔTSH and 8 am-ΔJTSH (ΔΔTSH) was significantly lower in depressed patients compared to controls. No such blunting was observed in PRL responses to protirelin in depressed patients. In the overall population, TSH response to protirelin (ie8 am-ΔTSH, 11 pm-ΔTSH, ΔΔTSH) correlated significantly with TSH circadian parameters (ie mesor and amplitude). These correlations were also observed with PRL (except for ΔΔPRL). TSH mesor and amplitude were lower in depressives than in controls. In contrast, PRL mesor and amplitude were not significantly different between diagnostic groups. ΔΔTSH is thus a chronobiological refinement to the measure of thyroid axis dysfunction in major depression. The blunted TSH response to protirelin suggests that the TRH receptors of the pituitary thyrotrophs are hyposensitive in major depression.

The objective of this research is to determine the prevalence and risk factors for primary hypothyroidism in a sample of Canadian seniors. The Canadian Study of Health and Aging (CSHA) was a prevalence survey of seniors living at home and in long-term care facilities (n = 10,263). Detailed clinical examinations were conducted on 2,914 seniors, of which 1,415 had serum TSH levels measured.The ten Canadian Provinces were grouped into five geographic regions (Atlantic, Quebec, Ontario, Prairies and British Columbia). Only seniors who underwent detailed clinical examinations (n = 2,914) are included. Hypothyroidism was defined as seniors taking thyroid hormone replacement or seniors having a serum TSH level greater than 10 mU/L. An estimated 9.6 per cent of seniors had hypothyroidism, 5.1 per cent were inadequately treated and 2.1 per cent were untreated. Age, gender, cultural background, geographic region and place of residence were potential risk factors for hypothyroidism. Hypothyroidism was found to be a prevalent problem in this population.

La participation des rythmes biologiques circadiens à la pathogénie de la dépression repose sur une série d’arguments cliniques, thérapeutiques et biologiques. La recrudescence matinale des symptômes dépressifs oriente vers une anomalie de l’organisation temporelle. Les aspects épidémiologiques de la dépression ou des suicides évoquent, quant à eux, l’existence de recrudescence saisonnière dans laquelle les facteurs naturels de synchronisation pourraient jouer un role. De plus, les thérapeutiques de la dépression agissent directement sur les horloges biologiques, qu’il s’agisse des manipulations du cycle veille/sommeil, de la photothérapie ou des antidépresseurs.

Notre étude longitudinale a permis de comparer les rythmes circadiens de cortisol, de TSH et de mélatonine plasmatique chez des sujets déprimés (n = 16), chez des sujets en rémission clinique (n = 15) ainsi que chez des sujets sains (n = 16). Nos résultats montrent de profondes perturbations du système circadien endocrinien en période dépressive. L’anomalie essentielle semble porter sur l’amplitude des rythmes, les sécrétions nocturnes de TSH et de mélatonine étant effondrées chez les sujets dépressifs. Ces perturbations disparaissent avec l’amélioration clinique des sujets.

Nos résultats confirment, dans une certaine mesure, les interrelations temporelles et fonctionnelles qui existent entre les sécrétions de cortisol, de TSH et de mélatonine. Par ailleurs, l’absence de décalage horaire de la position des rythmes étudiés incite à nuancer l’hypothèse d’une désynchronisation biologique dans la dépression pour privilégier une défaillance des mécanismes de couplage entre les facteurs synchronisants de l’environnement et les oscillateurs centraux. Dans cette perspective, les traitements de la dépression tels que les manipulations du cycle veille/sommeil, la photothérapie ainsi que les tricycliques semblent agir sur ces mécanismes de transmission de l’information temporelle soit en augmentant artificiellement leur intensité, soit en abaissant le seuil de perception. Cette hypothèse pourrait aboutir à concevoir de nouveaux outils thérapeutiques des troubles de l’humeur.