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Male hypogonadism-rebadged by some as testosterone deficiency syndrome-is a clinical and biochemical diagnosis of increasing worldwide interest. Organic male hypogonadism-usually permanent-is well-established, but aging men may also exhibit lower serum testosterone levels; principally due to burden of extra-gonadal comorbidities such as obesity, diabetes and metabolic syndrome, but with an underlying intact hypothalamo-pituitary-testicular (HPT) axis capable of springing back into operation once comorbidities are addressed. Despite encouraging observational data and plausible theoretical underpinning, evidence for efficacy and safety of testosterone in this "aging" group of men is lacking; addressing comorbid illnesses remains the key priority instead. Nevertheless, in recent years, accumulation of misleading information online has triggered a global tsunami of testosterone prescriptions. Despite this, many men with organic hypogonadism remain undiagnosed or untreated; many more face a diagnostic odyssey before achieving care by the appropriate specialist. As testosterone therapy is not without risk several clinical practice guidelines have been published specialist societies to guide physicians on best practice. However, these are heterogeneous in key areas, reflecting divergent approaches to the same evidence basis. Herein, we navigate the major clinical practice guidelines on male hypogonadism and test their respective recommendations against current best evidence.

IntroductionPhaeochromocytomas/paragangliomas (PHAEO/PG) are linked to hereditary syndromes including Neurofibromatosis type 1 (NF-1). Current guidelines do not recommend biochemical screening for PHAEO/PG in asymptomatic or normotensive patients with NF-1. This strategy may miss preventable morbidities in those patients who ultimately present with symptomatic PHAEO/PG. Our aim was to review the literature and extract data on mode of presentation and the incidence of reported adverse outcomes.MethodsPubMed and EMBASE literature search using the keywords ‘Phaeochromocytoma’, ‘Paraganglioma’ and ‘Neurofibromatosis’ was performed looking for reported cases from 2000 to 2018.ResultsSeventy-three reports of NF-1 patients with PHAEO/PG were found. Patients were predominately women (n = 40) with a median age of 46 years (range 16–82). PHAEO/PG was found incidentally in most patients, 36/73 did not present with typical symptoms while 27 patients were normotensive at diagnosis. Thirty-one patients had adverse outcomes including metastases and death.ConclusionGiven the protean presentation of PHAEO/PG, relying on symptomology and blood pressure status as triggers for screening, is associated with adverse outcomes. Further studies are required to ascertain whether biochemical screening in asymptomatic and normotensive patients with NF-1 can reduce the rate of adverse outcomes.

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Summary Oral calcium salts are recommended for the treatment of chronic hypoparathyroidism (HypoPT), although dosimetry is variable between individual patients and clinicians. However, patient feedback on calcium salts can be negative, particularly due to gastrointestinal side effects and hypercalciuria‐related complications. We begin with a clinical case of a HypoPT patient taking oral calcium salts following thyroid surgery, who requested support in reducing her dose of these with a view to stopping entirely. To evaluate her request, we first describe the usual treatment of HypoPT according to current guidance and then present data from (a) a case note review of a cohort of 24 HypoPT patients managed with a “no calcium” treatment regimen by single physician (b) a comprehensive online survey of HypoPT patients’ treatment and experiences (n = 330). The case note review found that target range serum calcium levels were successfully achieved in all 24 patients since transitioning to a “no calcium” regimen, without any breakthrough hypocalcaemia‐related symptoms, the development of new renal stones, the occurrence of calcium‐related hospital admissions or the finding of significant hypercalciuria. The online survey identified 36% of HypoPT patients who continued to take activated vitamin D, but had discontinued calcium supplements. HypoPT patients not currently taking calcium reported a significantly lower prevalence of adverse effects and outcomes, both compared with their previous experiences whilst taking calcium and also compared with the 64% of patients who continued to take oral calcium. We conclude that, subject to methodological limitations, there are significant issues of tolerability arising from conventional calcium‐based treatment regimens for patients with chronic HypoPT. For selected patients, it may be reasonable to facilitate a managed therapeutic transition to “no calcium” regimen, and we also propose that calcium‐based regimes be prospectively evaluated against calcium‐free (or calcium‐low) alternatives.

Chronic obstructive pulmonary disease (COPD) and diabetes mellitus (DM) are chronic health conditions with significant impacts on quality and extent of life. People with COPD and DM appear to have worse outcomes in each of the comorbid conditions. Treatment with corticosteroids in acute exacerbation of COPD (AECOPD) has been shown to reduce treatment failure and exacerbation relapse, and to shorten length of hospital stay, but not to affect the inexorable gradual worsening of lung function. Treatment with corticosteroids can lead to a wide spectrum of side effects and complications, including worsening hyperglycemia and deterioration of diabetes control in those with pre-existing DM. The relationship between COPD and DM is rather complex and accumulating evidence indicates a distinct phenotype of the comorbid state. Several randomized controlled trials on corticosteroid treatment in AECOPD excluded people with DM or did not report on outcomes in this subgroup. As such, the perceived benefits of corticosteroids in AECOPD in people with DM have not been validated. In people with COPD and DM, the detrimental side effects of corticosteroids are guaranteed, while the benefits are not confirmed and only presumed based on extrapolation from the general COPD population. Therefore, the potential for harm when prescribing corticosteroids for AECOPD in people with DM cannot be excluded.

We describe a case of a 35-year-old woman who presented with bilateral leg weakness and encephalopathy while on long-term valproate therapy. She was diagnosed with valproate-induced encephalopathy due to carnitine deficiency. Clinical improvement occurred with oral carnitine supplementation. Our case report highlights the importance of considering carnitine deficiency in patients presenting with unexplained neurological signs while on long-term valproate treatment.