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      Hydroxocobalamin as Rescue Therapy in a Patient With Refractory Amlodipine-Induced Vasoplegia

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          Abstract

          Vasoplegic syndrome is a type of distributive shock characterized by mean arterial pressure of less than 65 mmHg, with normal to high cardiac output and often refractory to fluid resuscitation, high doses of intravenous vasopressors, and inotropes. It is usually observed after cardiac and solid organ transplantation surgeries.

          Here, we report a 56-year-old female patient who presented with a profound vasoplegia manifesting as lethargy and confusion in the setting of amlodipine toxicity. This case of severe vasoplegia was refractory to all conditional lines of medical management reported in the literature. The mainstay treatment modalities for vasoplegia include volume resuscitation, catecholamines, vasopressin, angiotensin II, and possibly methylene blue in unresponsive cases. Our patient was given hydroxocobalamin in favor of methylene blue, given the history of serotonin reuptake inhibitors use, which would have caused a life-threatening serotonin syndrome. Hydroxycobolamine resulted in a dramatic clinical recovery, suggesting its potentially significant role in refractory vasoplegia.

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          Most cited references47

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          Hydrogen sulfide as endothelium-derived hyperpolarizing factor sulfhydrates potassium channels.

          Nitric oxide, the classic endothelium-derived relaxing factor (EDRF), acts through cyclic GMP and calcium without notably affecting membrane potential. A major component of EDRF activity derives from hyperpolarization and is termed endothelium-derived hyperpolarizing factor (EDHF). Hydrogen sulfide (H(2)S) is a prominent EDRF, since mice lacking its biosynthetic enzyme, cystathionine γ-lyase (CSE), display pronounced hypertension with deficient vasorelaxant responses to acetylcholine. The purpose of this study was to determine if H(2)S is a major physiological EDHF. We now show that H(2)S is a major EDHF because in blood vessels of CSE-deleted mice, hyperpolarization is virtually abolished. H(2)S acts by covalently modifying (sulfhydrating) the ATP-sensitive potassium channel, as mutating the site of sulfhydration prevents H(2)S-elicited hyperpolarization. The endothelial intermediate conductance (IK(Ca)) and small conductance (SK(Ca)) potassium channels mediate in part the effects of H(2)S, as selective IK(Ca) and SK(Ca) channel inhibitors, charybdotoxin and apamin, inhibit glibenclamide-insensitive, H(2)S-induced vasorelaxation. H(2)S is a major EDHF that causes vascular endothelial and smooth muscle cell hyperpolarization and vasorelaxation by activating the ATP-sensitive, intermediate conductance and small conductance potassium channels through cysteine S-sulfhydration. Because EDHF activity is a principal determinant of vasorelaxation in numerous vascular beds, drugs influencing H(2)S biosynthesis offer therapeutic potential.
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            How I treat cobalamin (vitamin B12) deficiency.

            The challenges in medical management of cobalamin deficiency lie in attention to the unique pathophysiology that underlies cobalamin deficiency, more than in the mechanics of therapy. The central physiologic principles are that clinically important deficiency is more likely to occur (and progress) when intrinsic factor-driven absorption fails than when diet is poor and that most causes take years to produce clinically obvious deficiency. Transient defects have little clinical impact. The key management principle is the importance of follow-up, which also requires knowing how the deficiency arose. The virtues of these principles are not always fully appreciated. Recent developments have made diagnosis and management more difficult by diminishing the ability to determine cobalamin absorption status. Clinicians must also grapple with premature medicalization of isolated, mild biochemical changes that added many asymptomatic cases of still undetermined medical relevance to their caseload, often expanded by inflated cobalamin level criteria. The potential for misattribution of cobalamin-unrelated presentations to nongermane cobalamin and metabolite abnormalities has grown. Pathophysiologically based management requires systematic attention to each of its individual components: correctly diagnosing cobalamin deficiency, reversing it, defining its underlying cause, preventing relapse, managing the underlying disorder and its complications, and educating the patient.
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              Cell response to surgery.

              To describe the profound alterations in host immunity that are produced by major surgery as demonstrated by experimental and clinical studies, and to evaluate the benefits of therapeutic strategies aimed at attenuating perioperative immune dysfunction. A review of the English-language literature was conducted, incorporating searches of the MEDLINE, EMBASE, and Cochrane collaboration databases to identify laboratory and clinical studies investigating the cellular response to surgery. Original articles and case reports describing immune dysfunction secondary to surgical trauma were included. The results were compiled to show outcomes of different studies and were compared. Current evidence indicates that the early systemic inflammatory response syndrome observed after major surgery that is characterized by proinflammatory cytokine release, microcirculatory disturbance, and cell-mediated immune dysfunction is followed by a compensatory anti-inflammatory response syndrome, which predisposes the patient to opportunistic infection, multiple organ dysfunction syndrome, and death. Because there are currently no effective treatment options for multiple organ dysfunction syndrome, measures to prevent its onset should be initiated at an early stage. Accumulating experimental evidence suggests that targeted therapeutic strategies involving immunomodulatory agents such as interferon gamma, granulocyte colony-stimulating factor, the prostaglandin E(2) antagonist, indomethacin, and pentoxifylline may be used for the treatment of systemic inflammatory response syndrome to prevent the onset of multiple organ dysfunction syndrome. Surgical trauma produces profound immunological dysfunction. Therapeutic strategies directed at restoring immune homeostasis should aim to redress the physiological proinflammatory-anti-inflammatory cell imbalance associated with major surgery.
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                Author and article information

                Journal
                Cureus
                Cureus
                2168-8184
                Cureus
                Cureus (Palo Alto (CA) )
                2168-8184
                1 May 2023
                May 2023
                : 15
                : 5
                : e38400
                Affiliations
                [1 ] Internal Medicine, Al-Quds University, Jerusalem, PSE
                [2 ] Respiratory Institute, Cleveland Clinic, Cleveland, USA
                [3 ] Faculty of Medicine, An Najah National University, Nablus, PSE
                [4 ] Pediatrics, Al Makassed Hospital, Jerusalem, PSE
                Author notes
                Article
                10.7759/cureus.38400
                10231868
                59e59012-ee12-49a2-80f7-0a4284135ef0
                Copyright © 2023, Ayasa et al.

                This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                : 1 May 2023
                Categories
                Emergency Medicine
                Internal Medicine
                Substance Use and Addiction

                amlodipine poisoning,hydroxocobalamin,vasopressors,distributive shock,vasoplegia

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