This study aimed to evaluate the prevalence of thyroid dysfunction in elderly subjects attending an outpatient clinic at a tertiary hospital and to assess whether subclinical hypothyroidism (SCH) or aging affected activities of daily living (ADLs), instrumental activities of daily living (IADLs), cognitive status, or depressive symptoms. This crosssectional study included 411 patients recruited in the outpatient geriatric setting. 48 subjects reported levothyroxine use and were evaluated separately. After excluding subjects with diseases or drugs which could influence thyroid status, the 284 subjects remaining were classified as having euthyroidism (n = 235, 82.8 %), subclinical hypothyroidism (n = 43, 15.1 %), subclinical hyperthyroidism (n = 4, 1.4 %), or overt hyperthyroidism (n = 2, 0.7 %). ADLs and IADLs were assessed using the Katz Index (ranging from 0 [independence] to 6 [dependence in all activities]) and Health Assessment Questionnaire (ranging from 0 to 3 [severely disabled]), respectively. Cognition was assessed using the mini mental state depressive symptoms that were assessed using the Geriatric depression scale or cornell scale for depression in dementia. SCH did not reduce performance in ADLs or IADLs in elderly subjects as a whole, but was an independent protective factor against dependence in ADLs (OR = 0.196 [0.045–0.853]; p = 0.003) and IADLs (OR = 0.060 [0.010–0.361]; p = 0.002) in subjects aged ≥85 years. Very old subjects with SCH showed better performance in ADLs than did those with euthyroidism (Katz Index: 0.9 ± 1.6 [median: 0.5] vs. 1.7 ± 1.7 [1.0], p = 0.024; HAQ: 1.2 ± 0.8 [0.9] vs. 1.8 ± 1.0 [1.9], p = 0.015). This putative protective effect of SCH was not found in subjects aged <85 years. The number of falls, number of medications used, depressive symptoms, and cognitive impairment did not differ among thyroid status groups, regardless of age. In conclusion, SCH does not have impact functional performance in the elderly population as a whole, but was associated with better functional status in subjects aged ≥85 years.

Background: Cushing's syndrome is rare during pregnancy and more commonly due to adrenal pathology, in contrast to the non-pregnant population. Increased levels of cortisol-binding globulin and placental production of corticotropin-releasing hormone and adrenocorticotropic hormone complicate the diagnostic strategies usually employed.Case: A 32-year-old G1P0 at 15/40 gestation presented with severe peripheral oedema and excessive weight gain. Examination revealed pitting oedema to the abdominal wall, wide violaceous striae, moon facies and acne. Cortisol excess was confirmed with elevated 24 h urinary free cortisol, raised midnight salivary cortisol and lack of diurnal variation. Adrenocorticotropic hormone ranged between 22 and 36 pg/ml (5-8 pmol/L). Fetal ultrasound confirmed a single live intrauterine gestation with an incidental finding of a maternal left adrenal mass. Magnetic resonance imaging confirmed an adrenal mass measuring 3.0 Â 4.4 Â 4.1 cm. She underwent a laparoscopic left adrenalectomy at 18 weeks' gestation without complication. Her postoperative cortisol level was undetectable. Hydrocortisone replacement was commenced with slow weaning as an outpatient. Histology was consistent with an adrenal adenoma. Immunohistochemistry revealed strong staining for the luteinising hormone/choriogonadotropin receptor, and expression of the luteinising hormone/choriogonadotropin receptor gene was in the range seen in normal ovary. DNA analysis revealed a mutation in GNAS encoding the Ga subunit in the cyclic adenosine monophosphate pathway. Conclusion:Cushing's syndrome may present in pregnancy as a result of hCG acting on the luteinising hormone/choriogonadotropin receptor overexpression by the adenoma amplifying the aberrant cyclic adenosine monophosphate signaling implicated in the development of cortisol-secreting adenomas. KeywordsCushing's, pregnancy, adrenal adenoma, luteinising hormone/choriogonadotropin receptor, GNAS CaseCushing's syndrome (CS) in pregnancy is uncommon; it is associated with high rates of maternal diabetes, fracture, pre-eclampsia, fetal morbidity and fetal mortality. 1 We report a case of Cushing's rapidly progressing in pregnancy and characterise the underlying molecular pathogenesis. This case illustrates the difficulties encountered in the workup of Cushing's in pregnancy and the complications that can ensue.A 32-year-old Chinese woman, gravida 1 para 0, presented at 15 weeks' gestation with severe peripheral oedema and excessive weight gain of 30 kg over two months. She had been previously well, conceived naturally and was on no regular medications.On examination, the most striking feature was pitting oedema to the top of her thighs, which hindered her mobility, with wide violaceous striae over her calves and lower abdomen (Figure 1(a)). She had a moon like facies with acne but no hirsutism.Initial biochemistry revealed hypokalaemia (3.0 nmol/L; RR 3.5-5.0 mmol/L) with hypoalbuminaemia (2.5 g/dL; RR 3.5-4.5 g/dL). An abdominal ultrasound confirmed a single live intraute...