Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Zygomycosis is an uncommon but frequently fatal infection and occurs mostly in immunosuppressed hosts, whereas approximately 50% of zygomycosis occurs in diabetic patients. The current patient initially presented with persistent pulmonary edema secondary to renal failure. This was the last of four admissions within 1 year for this 68-year-old woman, for whom the chief complaints were shortness of breath and chest pain. Her past medical history included insulin-requiring type 2 diabetes and hypertension for 10 years, and chronic heart and renal failure. She was previously admitted to the hospital for what appeared to be pulmonary edema secondary to renal failure. In the last admission the patient developed pulmonary hemorrhage and metabolic acidosis. Transbronchial biopsy was performed, showing irregular fungal hyphae in the blood vessels, morphologically consistent with zygomycosis. Central nervous system computed tomography also revealed a large infarct in the cerebral hemisphere. The patient died on the seventh hospital day. At autopsy three organs were extensively involved by zygomycosis: (i) lungs were diffusely hemorrhagic with acute infarcts; (ii) pericardium had fibrotic inflammation; and (iii) the left cerebral hemisphere, cerebellum and pons had large hemorrhagic infarct by zygomycosis infection. Corticosteroid medication and hemodialysis triggered increasing hyperglycemia, metabolic acidosis and iron overload, which contributed to zygomycosis infection that subsequently spread to the heart and brain as a rare consequence.
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PMID:Zygomycosis involving lungs, heart and brain, superimposed on pulmonary edema. 1582 46

Coronavirus disease-19 (COVID-19) has been regarded as an infective-inflammatory disease, which affects mainly lungs. More recently, a multi-organ involvement has been highlighted, with different pathways of injury. A hemoglobinopathy, hypoxia and cell iron overload might have a possible additional role. Scientific literature has pointed out two potential pathophysiological mechanisms: i) severe acute respiratory syndrome-coronavirus-2 (SARS-CoV- 2) interaction with hemoglobin molecule, through CD147, CD26 and other receptors located on erythrocyte and/or blood cell precursors; ii) hepcidin-mimetic action of a viral spike protein, inducing ferroportin blockage. In this translational medicinebased narrative review, the following pathologic metabolic pathways, deriving from hemoglobin denaturation and iron metabolism dysregulation, are highlighted: i) decrease of functioning hemoglobin quote; ii) iron overload in cell/tissue (hyperferritinemia); iii) release of free toxic circulating heme; iv) hypoxemia and systemic hypoxia; v) reduction of nitric oxide; vi) coagulation activation; vii) ferroptosis with oxidative stress and lipoperoxidation; viii) mitochondrial degeneration and apoptosis. A few clinical syndromes may follow, such as pulmonary edema based on arterial vasoconstriction and altered alveolo-capillary barrier, sideroblastic-like anemia, endotheliitis, vasospastic acrosyndrome, and arterio- venous thromboembolism. We speculated that in COVID-19, beyond the classical pulmonary immune-inflammation view, the occurrence of an oxygen-deprived blood disease, with iron metabolism dysregulation, should be taken in consideration. A more comprehensive diagnostic/therapeutic approach to COVID-19 is proposed, including potential adjuvant interventions aimed at improving hemoglobin dysfunction, iron over-deposit and generalized hypoxic state.
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PMID:COVID-19: hemoglobin, iron, and hypoxia beyond inflammation. A narrative review. 3250 58