The role of the endocrine system on the immune response, especially in the lung, remains poorly understood. Hormones play a crucial role in the development, homeostasis, metabolism, and response to the environment of cells and tissues. Major infectious and metabolic diseases, such as tuberculosis and diabetes, continue to converge, necessitating the development of a clearer understanding of the immune and endocrine interactions that occur in the lung. Research in bacterial respiratory infections is at a critical point, where the limitations in identifying and developing antibiotics is becoming more profound. Hormone receptors on alveolar and immune cells may provide a plethora of targets for host-directed therapy. This review discusses the interactions between the immune and endocrine systems in the lung. We describe hormone receptors currently identified in the lungs, focusing on the effect hormones have on the pulmonary immune response. Altered endocrine responses in the lung affect the balance between pro- and anti-inflammatory immune responses and play a role in the response to infection in the lung. While some hormones, such as leptin, resistin and lipocalin-2 promote pro-inflammatory responses and immune cell infiltration, others including adiponectin and ghrelin reduce inflammation and promote anti-inflammatory cell responses. Furthermore, type 2 diabetes as a major endocrine disease presents with altered immune responses leading to susceptibility to lung infections, such as tuberculosis. A better understanding of these interactions will expand our knowledge of the mechanisms at play in susceptibility to infectious diseases and may reveal opportunities for the development of host-directed therapies.

Pre-existing diabetes mellitus (DM), hyperglycaemia and obesity emerged as prognostic factors in severe Coronavirus disease 2019 . To date, no published South African studies report on the incidence, presentation and outcomes of DM and diabetic ketoacidosis (DKA) during the COVID-19 pandemic. Objective: To reflect on the diagnosis, management, obstacles to care and outcome of four patients who were admitted to Tygerberg Hospital, Cape Town, South Africa. The outcome of these cases that presented consecutively with DKA and COVID-19 between May and July 2020 are discussed, the presentation, management and long-term considerations with specific reference to DKA and COVID-19 are reviewed. Results: Three of the four patients had newly diagnosed DM. These patients presented with non-specific symptoms and signs leading to a diagnosis of both DKA and COVID-19. The single surviving patient in this series was known to have pre-existing DM but discontinued his insulin upon becoming unwell. One patient required insulin therapy at the time of initial presentation a week or two prior to the current admission but received metformin instead. She was diagnosed with COVID-19 after having poor glycaemic control for over one week, after which insulin was initiated. Ultimately she died as a result of severe hypokalaemia. One patient primarily had respiratory complaints, severe COVID-19 pneumonia and received concomitant dexamethasone. Glycaemic control in this patient was complicated by both hypo-and hyperglycaemia. Conclusion: These cases highlight the management challenges faced by many developing countries, and identify the missed opportunities in persons presenting with COVID-19 and hyperglycaemic emergencies.

Subacute thyroiditis is a granulomatous inflammatory disorder often triggered by a preceding viral infection. Patients typically present with complaints of anterior neck pain associated with a tender enlarged thyroid gland. The coronaviruses have never before been implicated in the aetiology of subacute thyroiditis. It is postulated that the pathogenesis related to thyroid disease in Coronavirus disease 2019 (COVID-19) is multifactorial. Contributory factors include effects of the virus-related cytokine storm and direct action of the virus on SARS-CoV-2 receptors in the thyroid. This article further reviews the association between thyroiditis and COVID-19. The clinical characteristics, diagnostic workup and management of a patient who presented with subacute thyroiditis following COVID-19 are discussed. Furthermore, complications are entertained and suggestions for the management of thyroiditis following COVID-19 are provided.

Background Hormone therapy in transgender individuals may impact processes that lead to changes in biochemical analytes, and therefore reference intervals. Currently, few reference interval studies are available for the transgender population. We determined biochemical reference intervals for transgender individuals receiving hormone therapy. Methods Our retrospective, laboratory-based, observational study included healthy transgender males ( N = 24) and transgender females ( N = 84) on hormone therapy. Various biochemical reference intervals were established for each cohort and compared to their cisgender counterparts. Results We detected significant differences in reference intervals for sodium, 139–142 mmol/L vs. 136–145 mmol/L when comparing transgender males (TM) with cisgender males (CM). The following significant changes in upper reference limits (URL) for TM versus CM were detected, ALP (URL: 96 U/L vs. 128 U/L), GGT (URL: 27 U/L vs. 67 U/L) and testosterone (URL: 46.7 nmol/L vs. 29.0 nmol/L), respectively. Moreover, when comparing transgender female (TF) to cisgender female (CF), significant differences in creatinine (URL: 117 μmol/L vs. 90 μmol/L), albumin (lower reference limit: 41 g/L, vs. 35 g/L), AST (URL: 50 U/L vs. 35 U/L), ALP (URL: 118 U/L vs. 98 U/L) and oestradiol (URL: 934 pmol/L vs. 213 pmol/L) were noted, respectively. Significantly higher LDL-C was observed for TM on hormone treatment, compared to baseline (2.9 mmol/L vs. 2.2 mmol/L, p <0.01). Conclusions Biochemical results for TM and TF receiving hormone therapy can be evaluated against our transgender-specific reference intervals for some analytes, while others can be compared to their identified gender reference intervals.