Chronic Atherosclerotic Mesenteric Ischemia That Started to Develop Symptoms Just after Anaphylaxis

Abstract

An 83-year-old woman was referred to our emergency department with acute urticaria and sudden shortness of breath approximately 30 min after taking rectal diclofenac potassium for lumbago. After treatment with adrenaline and corticosteroids, the patient became hemodynamically stable and left the hospital on the next day. She attended our hospital 1 week after the onset of anaphylaxis because of repeated postprandial epigastric pain. No abnormal lesions were found in endoscopy. Radiographic selective catheter angiography revealed chronic mesenteric ischemia caused by atherosclerosis and abundant collateral arteries between the celiac trunk, the superior mesenteric artery and the inferior mesenteric artery. Patients with chronic mesenteric ischemia usually present with a clinical syndrome characterized by painful abdominal cramps and colic occurring typically during the postprandial phase. Fear of eating resulted in malnutrition. She was prescribed proton pump inhibitor, digestants, anticholinergic agents, serine protease inhibitors, prokinetics, antiplatelet agents and transdermal nitroglycerin intermittently, but these had no beneficial effects. It was most probable that this patient with chronic atherosclerotic mesenteric ischemia was suffering from functional abdominal pain syndrome induced by anaphylaxis. Since psychiatric disorders were associated with alterations in the processing of visceral sensation, we facilitated the patient’s understanding of functional abdominal pain syndrome with the psychologist. Postprandial abdominal pain gradually faded after administration of these drugs and the patient left the hospital. Developing a satisfactory patient-physician relationship was considered more effective for the management of persistent abdominal pain caused by complicated mechanisms.

Kounis syndrome: an update on epidemiology, pathogenesis, diagnosis and therapeutic management

“…Recent research has shown that Kounis like syndromes can affect the mesenteric [26] and cerebral arteries [27]. The coronary arteries, the heart and the entire arterial system seem to be vulnerable to allergic, hypersensitivity, anaphylactic, and/or anaphylactoid events and physicians should be alert for its consequences.…”

Histamine induced coronary artery spasm, fish consumption and Kounis syndrome

“…Platelets bearing high and low affinity FCγRI, FCγRII, FCεRI and FCεRII receptors are also involved [6]. Recently, Kounis-like syndromes have been described that affect the cerebral [7] and mesenteric arteries [8]. Mast cells influence decisively the inflammatory process via a vicious inflammatory cycle where mast cells activate macrophages and enhance T cell activation, macrophage protein-1a activates mast cells, CD 169(+) macrophages activate CD8 T cells, T-cells mediate mast cell activation and proliferation and regulate macrophage activity.…”

Kounis syndrome

“…nitrates), and calcium channel blockers. [3,8] • Type 2 variant: apply the acute coro nary event protocol and administer cortico steroids, antihistamines, vasodila tors (e.g. nitrates), and calcium channel blockers when appropriate.…”

“…In addition to coronary arterial involvement, Kounis syndrome com prises other arterial systems with similar physiologies, such as mesenteric and cerebral circulation resulting in ischaemia/infarction of the vital organs. [3,4] The incidence of Kounis syndrome is difficult to establish owing to the number of potential instigating factors and its relatively infrequent documentation in the literature. It remains unclear whether the reported lower rates of the condition are the direct result of underdiagnosis.…”