GONZÁLEZ ALVAREZ Felipe, ESTAÑOL VIDAL Bruno, GONZÁLEZ HERMOSILLO Jesús Antonio, PEÑA ANDRADE Eduardo, SALAZAR CALDERÓN Guadalupe Estrella, ACEVES BUENDIA Jose de Jesus
INTRODUCTION
Post-COVID-19 condition (PCC) is a multisystemic disorder defined as the persistence or appearance of new symptoms 3 months after the onset of COVID-19 with at least 2 months of duration [1]. One of the most reported symptoms is postural tachycardia, which may be caused by Postural Orthostatic Tachycardia Syntome (POTS) [2]. POTS is further classified into hyperadrenergic, neuropathic and hypovolemic subtypes. Hyperadrenergic POTS is defined as an increase in >30 bpm in HR with an increase >10 mmHg in SBP and the presence of elevated serum norepinephrine levels (>600 pg/ml) during orhostatism (3). Its physiopathology remains unclear, although Mast Cell Activation Syndrome (MCAS) may coexist, as they may develop after viral infections [4]. MCAS is a disease characterized by recurrent MC activation, in which MC mediators are released more abundantly and frequently [5].
CASE PRESENTATION
A 26-year old male was studied following a year-long history of palpitations, presyncope and fatigue, which began two months after recovery from mild COVID-19. Subsequently, he noticed the appearance of a generalized, pruriginous rash after a pre-syncopal episode. Few weeks later, the patient reported angioedema after a presyncopal episode (Figure 1). A Head-Up tilt test (HUTT) (Figure A) was performed, which showed orthostatic tachycardia (a) and hypertension (b) suggesting hyperadrenergic POTS. Beta[1]blocker was started, which worsened symptoms and was therefore discontinued. MCAS was suspected based on a history of rash and angioedema in accordance with orthostatic intolerance symptoms. A trial with histamine blocker (Loratadine 10 mg/12 hrs) was initiated, achieving remission of symptoms after a few weeks. A new HUTT was performed, showing a significant reduction in blood pressure (Figure B) during orthostatism compared with the previous HUTT.
DISCUSSION
SARS-CoV-2 can infect the Central Nervous System (CNS) through: a) olfactory nerve infiltration; b) haematogenous dissemination; c) transinaptically; and d) through the choroid plexus of the ventricular system. Interestingly, the ACE-2 receptor is richly expressed in the brainstem, which is the constitutive receptor for SARS-CoV2. [6]. Matschke et al. showed in post-mortem studies of deceased COVID-19 patients the presence of gliosis and astrogliosis in the brainstem, close the nuclei that control sympathetic activity [7]. Malfunction of these nuclei could give rise to sympathetic hyperactivity. Sympathetic activity releases predominantly norepinephrine (NE) through sympathetic nerve endings, which share notable proximity to the MC [8]. MC expresses different receptors, including adrenergic receptors [9]. As a result, sympathetic release of NE can be sensed by MC. MC liberates pre-stored mediators, mostly with vasodilator effects (e.g., histamine, bradykinin, tryptase), and its association with POTS can be explained as follows: upon vasodilation, blood redistribution occurs, diminishing venous return and cardiac output, which is sensed by the carotid and aorta, causing increased baroreflex activation and enhancing sympathetic activity [10] (Figure C). Besides, MC may degranulate by direct linkage with SARS-CoV-2 as they express the angiotensin-converting enzyme type 2 (ACE 2) [11]. There isn’t a standardized pharmacological approach. Symptomatic treatment along with non-pharmacological interventions are the basis of the PCC treatment until now [8]. A specific group of patients suffering from Hyperadrenergic POTS and MCAS in the PCC context can benefit from MC-targeted therapy, including MC stabilizers (e.g., sodium cromoglycate), mast cell activation blockages (e.g., antihistamines), and MC mediator’s blockers (e.g., antihistamines, antileukotryens) [12]. More studies are needed to determine the concrete treatment approach for these patients.
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