Pulmonary hypertension (PH) is a progressive disorder characterized by a chronic in-crease in pulmonary arterial pressure, frequently resulting in right-sided heart failure and potentially death. Co-existing medical conditions are important factors in PH, since they not only result in the genesis of the disorder, but may also contribute to its progression. Various studies have assessed the impact of thyroid disorders and other endocrine conditions (namely estrogen exposure, obesity, and diabetes mellitus) on the progression of PH. The complex interactions that hormones may have with the cardiovascular system and pulmonary vascular bed can create several pathogenetic routes that could explain the effects of endocrine disorders on PH development and evolution. The aim of this review is to summarize current knowledge on the role of concomitant thyroid disorders, obesity, diabetes mellitus, and estrogen exposure as potential modifiers for PH, and especially for pulmonary arterial hypertension, and to discuss possible pathogenetic routes linking them with PH. This information could be valuable for practicing clinicians so as to better evaluate and/or treat concomitant endocrine conditions in the PH population.

IntroductionThe potential additive benefits of rehabilitation beyond spontaneous recovery post-COVID-19 currently remain unknown.MethodsIn this prospective, interventional, non-randomised parallel assignment two-arm study, we investigated the effects of an 8-week rehabilitation programme (Rehab, n=25) added to usual care (UC) versus UC (n=27) on respiratory symptoms, fatigue, functional capacity, mental health and health-related quality of life in patients with COVID-19 pneumonia, 6–8 weeks post-hospital discharge. The rehabilitation programme included exercise, education, dietary and psychological support. Patients with chronic obstructive pulmonary disease, respiratory and heart failure were excluded from the study.ResultsAt baseline, groups were not different in mean age (56 years), gender (53% female), intensive care unit admission (61%), intubation (39%), days of hospitalisation (25), number of symptoms (9) and number of comorbidities (1.4). Baseline evaluation was conducted at median (IQR) 76 (27) days after symptoms onset. Groups were not different regarding baseline evaluation outcomes. At 8 weeks, Rehab showed significantly greater improvement in COPD Assessment Test by a mean±SEM (95% CI) 7.07±1.36 (4.29–9.84), p <0.001andall three fatigue questionnaires: Chalder-Likert: 5.65±1.27 (3.04–8.25), p <0.001; bimodal: 3.04±0.86 (1.28–4.79), p=0.001; Functional Assessment of Chronic Illness Therapy: 6.37±2.09 (2.08–10.65), p=0.005 and Fatigue Severity Scale: 1.36±0.433 (0.47–2.25), p=0.004. At 8 weeks rehab also showed significantly greater improvment in Short Physical Performance Battery: 1.13±0.33 (0.46–1.79), p=0.002; Hospital Anxiety and Depression Scale (HADS)Anxiety: 2.93±1.01 (0.67–5.18), p=0.013; Beck Depression Inventory: 7.81±3.07 (1.52–14.09), p=0.017; Montreal Cognitive Assessment: 2.83±0.63 (1.5–4.14), p <0.001; EuroQol (EQ-5D-5L) Utility Index: 0.21±0.05 (0.1–0.32), p=0.001 and Visual Analogue Scale: 6.57±3.21 (0.2–13.16), p=0.043. Both groups significantly improved 6-min walking distance by approximately 60 m and pulmonary function measures, whereas post-traumatic stress disorder measurement IES-R (Impact of Event Scale, Revised) and HADS-Depression score were not different between groups at 8 weeks. A 16% attrition rate was observed in the rehabilitation group exhibiting a threefold increase in training workload. There were no adverse effects reported during exercise training.DiscussionThese findings highlight the added value of rehabilitation post-COVID-19 to amplify the natural course of physical and mental recovery that otherwise would remain incomplete with UC.

We present the case of a 28-year-old African man with multiple hospitalizations during the past two years due to worsening shortness of breath. The initial work-up revealed recurrent pulmonary embolism and interstitial lung disease (ILD). The diagnosis of primary Sjogren syndrome was established and a lung biopsy demonstrated cellular non-specific interstitial pneumonia (NSIP). Proper treatment of NSIP was partially effective and respiratory failure persisted, implying additional pathology to NSIP. Further evaluation revealed pulmonary hypertension that required treatment with pulmonary vasodilators.