Bariatric surgery is the most efficacious treatment for obesity, though it is not free from complications. Preoperative conditioning has proved beneficial in various clinical contexts, but the evidence is scarce on the role of prehabilitation in bariatric surgery. We describe the protocol and pilot study of a randomized (ratio 1:1), parallel, controlled trial assessing the effect of a physical conditioning and respiratory muscle training programme, added to a standard 8-week group intervention based on therapeutical education and cognitive-behavioural therapy, in patients awaiting bariatric surgery. The primary outcome is preoperative weight-loss. Secondary outcomes include associated comorbidity, eating behaviour, physical activity, quality of life, and short-term postoperative complications. A pilot sample of 15 participants has been randomized to the intervention or control groups and their baseline features and results are described. Only 5 patients completed the group programme and returned for assessment. Measures to improve adherence will be implemented and once the COVID-19 pandemic allows, the clinical trial will start. This is the first randomized, clinical trial assessing the effect of physical and respiratory prehabilitation, added to standard group education and cognitive-behavioural intervention in obese patients on the waiting list for bariatric surgery. Clinical Trial Registration: NCT0404636.

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Introduction and Objective:Pheochromocytoma is often diagnosed in the workup of a patient with severe, refractory hypertension, but nowadays many silent pheochromocytomas are diagnosed in the workup of an incidental adrenal mass. Anxiety is also a common symptom in patients with pheochromocytoma and occasionally may be the only clinical manifestation. Hereby we describe the case of a patient with a severe refractory anxiety disorder as a bizarre presentation of pheochromocytoma.Design and Methods:Review of the patient's records and of the relevant literature.Results (Case Description):A 67-year old woman was referred to our Endocrinology Clinic for the workup of an incidental left adrenal mass found in an abdominal CT ordered in the nephrolithiasis workup after a renal colic. The patient had no previous relevant history of somatic disease. She had been suffering from anxiety disorder since she was 50, beginning with climacteric symptoms (hot flashes, irritability and mood swings) followed by severe anxiety, frequent panic attacks, insomnia and inability to concentrate. Hormonal replacement therapy had been ineffective. In the following 17 years she had consulted many public and private psychiatrists and had been treated with combinations of anxiolytic and antidepressant drugs including lormetazepam, clonazepam, bromazepam, vortioxetine, quetiapine, venlafaxine, agomelatine, risperidone, mirtazapine, but the patient's anxiety symptoms kept deteriorating. BP up to 180/110 mmHg and tachycardia up to 130 bpm had been recorded during anxiety crises but ABPM ruled out sustained hypertension or tachycardia. After the finding of the adrenal lesion the diagnostic process was straightforward. It was a solid, heterogeneous mass of about 6 cm diameter, with necrotic areas and mean densitometry of 86 UH. The lab workup showed normal creatinine and potassium, suppressed cortisol after 1 mg dexamethasone, normal ACTH, aldosterone, renin and aldosterone/renin ratio, but plasma metanephrines were above 5x the upper normal limit (634/2423 pg/mL). A MIBG scan confirmed intense uptake in the left adrenal area without abnormal extra-adrenal deposits. After standard preparation, the tumor was laparoscopically removed without complications. 1 month after the surgery plasma metanephrines were normal and the anxiety symptoms had vanished almost totally, but the patient kept taking a low dose of risperidone (1.5 mg/day) as a maintenance therapy; BP and HR remained normalConclusions:Pheochromocytoma/paraganglioma should be included in the workup of patients with severe anxiety disorder, especially when refractory to treatment.

Objective:The antihypertensive effect of SGLT2 inhibitors has been mostly overlooked, but in patients with type 2 diabetes mellitus (T2DM) and uncontrolled hypertension empagliflozin elicits a powerful systolic blood pressure (SBP) lowering effect, often attributed to diuretic/natriuretic effect and/or weight loss (WL), but other mechanisms are possible. We sought to retrospectively study the impact of the initiation of empagliflozin therapy on SBP in patients living with T2DM and uncontrolled hypertension in a real-world setting, and to assess its relationship with previous diuretic and other classes of antihypertensive therapy, and with weight loss during treatment.Design and Methods:Retrospective analysis of the SBP, weight and antihypertensive medication data in patients with T2DM who initiated empagliflozin therapy while having sitting office SBP > 140 mmHg. Mediation analyses with WL as mediator were performed post-hoc to quantify the relative contribution of WL to SBP reduction. Consent was obtained from all included subjects. Patients who changed their antihypertensive medication simultaneously with empagliflozin initiation were excluded.Results:Data were obtained from 198 patients (59.6% female, age 63.2 ± 8.9 years) from the visit in which empagliflozin (largely 10 mg/day) was started and the following one (3–4 months afterwards). Baseline BMI was 31.7 ± 8.5 Kg/m2. Baseline SBP was 166 ± 17 mmHg. 112 patients had ACEI/ARB, 76 diuretic, 69 calcium antagonist, 32 alpha-blocker and 29 beta-blocker therapy. The SBP reduction was 7.2 ± 5.7 mmHg (p = 0.012, paired t-test). The Figure shows comparisons by number and classes of antihypertensive drugs, with no significant differences for SBP reduction. The WL was 3.2 ± 1.7 kg, and it correlated significantly with the SBP reduction (Pearson's r: 0.22, p = 0.0012). The mediation analyses showed that a SBP reduction of 1.5 ± 0.9 mmHg was mediated by WL while 5.7 ± 4.9 mmHg was WL-independent.Conclusions:Empagliflozin initiation elicited a clinically relevant SBP decrease in patients with T2DM and uncontrolled hypertension. The number and classes of previous antihypertensive effects did not modify the SBP reduction. In particular, previous diuretic treatment does not attenuate it, suggesting that the diuretic effect is not the main driver of SBP reduction with empagliflozin. Also, the contribution of WL seems modest, implying alternative mechanisms for SBP reductions with empagliflozin; improvement of endothelial function and/or arterial stiffness and many others have been suggested.

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