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Enomoto Y, Matsuda Y, Nagamine Y, Goto T. Venoarterial-extra corporeal membrane oxygenation-assisted parathyroidectomy for hypercalcemic crisis due to parathyroid carcinoma complicated by severe circulatory and respiratory failure: a case report. JA Clin Rep 2023; 9:14. [PMID: 36914845 PMCID: PMC10011232 DOI: 10.1186/s40981-023-00606-y] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/28/2022] [Revised: 03/04/2023] [Accepted: 03/07/2023] [Indexed: 03/16/2023] Open
Abstract
BACKGROUND Hypercalcemia crisis is a rare but severe form of hypercalcemia complicated by multiple organ failure. Hypercalcemia crisis due to hyperparathyroidism is commonly caused by a parathyroid tumor, which often requires surgical resection. However, there are no clear recommendations on when the surgery should be performed. CASE PRESENTATION A 64-year-old female patient developed hyperparathyroidism due to a parathyroid tumor and hypercalcemic crisis, which was complicated by severe circulatory and respiratory failure refractory to medical therapy, and an emergent surgery was planned to resect the parathyroid tumor. To prevent intraoperative circulatory and respiratory collapse, venoarterial-extra corporeal membrane oxygenation (VA-ECMO) was introduced, resulting in a safe operation and anesthetic management. CONCLUSIONS In patients with hypercalcemic crisis complicated by severe circulatory and respiratory failure, induction of prophylactic VA-ECMO was useful for safe anesthetic management. Surgical resection should be performed as soon as the diagnosis is made before VA-ECMO is required.
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Affiliation(s)
- Yuria Enomoto
- Department of Anesthesiology and Critical Care Medicine, Yokohama City University Hospital, 3-9 Fukuura, Kanazawa-Ku, Kanagawa, 236-0004, Yokohama, Japan
| | - Yuko Matsuda
- Department of Anesthesiology and Critical Care Medicine, Yokohama City University Hospital, 3-9 Fukuura, Kanazawa-Ku, Kanagawa, 236-0004, Yokohama, Japan
| | - Yusuke Nagamine
- Department of Anesthesiology and Critical Care Medicine, Yokohama City University Hospital, 3-9 Fukuura, Kanazawa-Ku, Kanagawa, 236-0004, Yokohama, Japan.
| | - Takahisa Goto
- Department of Anesthesiology and Critical Care Medicine, Yokohama City University Hospital, 3-9 Fukuura, Kanazawa-Ku, Kanagawa, 236-0004, Yokohama, Japan
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Latha K, Rao S, Sakamoto K, Watford WT. Tumor Progression Locus 2 Protects against Acute Respiratory Distress Syndrome in Influenza A Virus-Infected Mice. Microbiol Spectr 2022; 10:e0113622. [PMID: 35980186 PMCID: PMC9604045 DOI: 10.1128/spectrum.01136-22] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/04/2022] [Accepted: 06/16/2022] [Indexed: 12/30/2022] Open
Abstract
Excessive inflammation in patients with severe influenza disease may lead to acute lung injury that results in acute respiratory distress syndrome (ARDS). ARDS is associated with alveolar damage and pulmonary edema that severely impair gas exchange, leading to hypoxia. With no existing FDA-approved treatment for ARDS, it is important to understand the factors that lead to virus-induced ARDS development to improve prevention, diagnosis, and treatment. We have previously shown that mice deficient in the serine-threonine mitogen-activated protein kinase, Tpl2 (MAP3K8 or COT), succumb to infection with a typically low-pathogenicity strain of influenza A virus (IAV; HKX31, H3N2 [x31]). The goal of the current study was to evaluate influenza A virus-infected Tpl2-/- mice clinically and histopathologically to gain insight into the disease mechanism. We hypothesized that Tpl2-/- mice succumb to IAV infection due to development of ARDS-like disease and pulmonary dysfunction. We observed prominent signs of alveolar septal necrosis, hyaline membranes, pleuritis, edema, and higher lactate dehydrogenase (LDH) levels in the lungs of IAV-infected Tpl2-/- mice compared to wild-type (WT) mice from 7 to 9 days postinfection (dpi). Notably, WT mice showed signs of regenerating epithelium, indicative of repair and recovery, that were reduced in Tpl2-/- mice. Furthermore, biomarkers associated with human ARDS cases were upregulated in Tpl2-/- mice at 7 dpi, demonstrating an ARDS-like phenotype in Tpl2-/- mice in response to IAV infection. IMPORTANCE This study demonstrates the protective role of the serine-threonine mitogen-activated protein kinase, Tpl2, in influenza virus pathogenesis and reveals that host Tpl2 deficiency is sufficient to convert a low-pathogenicity influenza A virus infection into severe influenza disease that resembles ARDS, both histopathologically and transcriptionally. The IAV-infected Tpl2-/- mouse thereby represents a novel murine model for studying ARDS-like disease that could improve our understanding of this aggressive disease and assist in the design of better diagnostics and treatments.
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Affiliation(s)
- Krishna Latha
- Department of Infectious Diseases, University of Georgia, Athens, Georgia, USA
| | - Sanjana Rao
- Department of Genetics, University of Georgia, Athens, Georgia, USA
| | - Kaori Sakamoto
- Department of Pathology, University of Georgia, Athens, Georgia, USA
| | - Wendy T. Watford
- Department of Infectious Diseases, University of Georgia, Athens, Georgia, USA
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Zagkotsis G, Markou M, Papanikolaou P, Sabanis N. Acute Respiratory Distress Syndrome Induced by Parathyroid Storm. Cureus 2021; 13:e12881. [PMID: 33633910 PMCID: PMC7899288 DOI: 10.7759/cureus.12881] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/19/2022] Open
Abstract
Hypercalcemic crisis associated with the development of acute respiratory distress syndrome (ARDS) has been rarely documented in the literature. Most cases have been described in patients suffering from malignancies or renal failure with the presence of metastatic calcifications being a prominent feature. Only three cases of ARDS have been reported to date in patients with hypercalcemic crisis due to primary hyperparathyroidism (PHPT). Herein, we report a 72-year-old patient with PHPT that presented with severe hypercalcemic crisis and developed ARDS. He had mild chronic kidney disease and at presentation he had extremely high levels of serum calcium (22.5 mg/dl) and parathormone (3822 pg/ml). After receiving medical treatment for hypercalcemia and the initiation of hemodialysis, he developed ARDS with a fatal outcome, without the presence of pancreatitis, sepsis or heart failure. Although very rare, ARDS should be taken into account as a possible complication of parathyroid crisis, especially in patients with excessive calcium and parathormone levels.
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Affiliation(s)
| | - Maria Markou
- Endocrinology, "Evaggelismos" General Hospital of Athens, Athens, GRC
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Pal R, Dutta A, Agrawal K, Jain N, Dutta P, Bhansali A, Behera A, Bhadada SK. Primary Hyperparathyroidism Presenting as Posterior Reversible Encephalopathy Syndrome: A Report of Two Cases. J Clin Res Pediatr Endocrinol 2020; 12:432-438. [PMID: 32129057 PMCID: PMC7711632 DOI: 10.4274/jcrpe.galenos.2020.2019.0181] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/01/2022] Open
Abstract
Posterior reversible encephalopathy syndrome (PRES) is a clinico-radiological entity characterized by subcortical vasogenic edema presenting with acute neurological symptoms. Common precipitating causes include renal failure, pre-eclampsia/eclampsia, post-organ transplant, and cytotoxic drugs. Hypercalcemia is a rare cause of PRES; most cases occur in the setting of severe hypercalcemia secondary to malignancy or iatrogenic vitamin D/calcium overdose. Primary hyperparathyroidism (PHPT), as a cause of PRES, is an oddity. We report two cases of adolescent PHPT presenting with generalized tonic-clonic seizures and altered sensorium. On evaluation, both had hypertension, severe hypercalcemia (serum calcium 14.1 mg/dL and 14.5 mg/dL, respectively) and elevated parathyroid hormone levels. Magnetic resonance imaging (MRI) revealed T2/fluid-attenuated inversion recovery hyperintensities located predominantly in the parieto-occipital regions, suggestive of PRES. Identification and excision of parathyroid adenoma led to the restoration of normocalcemia. Neurological symptoms and MRI changes improved subsequently. An extensive literature search revealed only four cases of PHPTassociated PRES; none of them being in the pediatric/adolescent age group. The predominant clinical manifestations were seizures and altered sensorium. All had severe hypercalcemia; three had hypertension at presentation, while one was normotensive. Parathyroid adenomectomy led to normalization of serum calcium and resolution of neurological symptoms and radiological changes. Thus, severe hypercalcemia, although rare in PHPT, can lead to hypercalcemic crisis precipitating acute hypertension that can result in cerebral endothelial dysfunction with the breakdown of the blood-brain barrier, culminating in PRES. We therefore recommend that serum calcium levels should be checked in all patients with PRES and that PHPT be regarded as a differential diagnosis in those with underlying hypercalcemia.
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Affiliation(s)
- Rimesh Pal
- Post Graduate Institute of Medical Training and Research, Clinic of Endocrinology, Chandigarh, India
| | - Aditya Dutta
- Post Graduate Institute of Medical Training and Research, Clinic of Endocrinology, Chandigarh, India
| | - Kanhaiya Agrawal
- Post Graduate Institute of Medical Training and Research, Clinic of Endocrinology, Chandigarh, India
| | - Nimisha Jain
- Post Graduate Institute of Medical Training and Research, Clinic of Endocrinology, Chandigarh, India
| | - Pinaki Dutta
- Post Graduate Institute of Medical Training and Research, Clinic of Endocrinology, Chandigarh, India
| | - Anil Bhansali
- Post Graduate Institute of Medical Training and Research, Clinic of Endocrinology, Chandigarh, India
| | - Arunanshu Behera
- Post Graduate Institute of Medical Training and Research, Clinic of General Surgery, Chandigarh, India
| | - Sanjay Kumar Bhadada
- Post Graduate Institute of Medical Training and Research, Clinic of Endocrinology, Chandigarh, India,* Address for Correspondence: Post Graduate Institute of Medical Training and Research, Clinic of Endocrinology, Chandigarh, India Phone: +91 9876602448 E-mail:
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Cummings D, Vannahme M, Stanworth H. A case of multi-organ failure due to hyperparathyroidism-related hypercalcaemia. J Intensive Care Soc 2020; 21:274-277. [PMID: 32782468 DOI: 10.1177/1751143719832179] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/17/2022] Open
Abstract
Albeit still rare, hypercalcaemia has been linked to pulmonary oedema in solid organ malignancy and chronic renal failure. However to date, there is only one case report linking pulmonary oedema to hypercalcaemia secondary to primary hyperparathyroidism. Case presentation A 60-year-old male presented to the emergency department with a history of confusion and collapse. Investigations revealed initial serum calcium of over 5 mmol/L. He subsequently developed widespread bilateral chest infiltrates with increasing oxygen requirements and an acute kidney injury. On day 9, continuous haemodiafiltration was commenced; however, hypercalcaemia proved resistant to maximal therapy. His initial parathyroid hormone (PTH) level measured 371 ng/L, and an ultrasound of his neck revealed a 2 × 2.5 cm parathyroid mass in the inferior neck. An acute parathyroidectomy was performed following which his chest infiltrates resolved and serum calcium levels returned to within normal range. Conclusions This case highlights primary hyperparathyroidism and the resulting hypercalcaemia as a sole cause for multi-organ failure in an otherwise well patient.
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A rare case of parathyroid crisis with respiratory failure successfully treated using extracorporeal membrane oxygenation. Respir Med Case Rep 2020; 30:101088. [PMID: 32455106 PMCID: PMC7236054 DOI: 10.1016/j.rmcr.2020.101088] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/11/2020] [Revised: 05/07/2020] [Accepted: 05/07/2020] [Indexed: 11/21/2022] Open
Abstract
Parathyroid crisis, which might occur during the natural history of primary hyperparathyroidism, presents fatal hypercalcemia. Although hyperparathyroidism is known to cause metastatic pulmonary calcification, parathyroid crisis with respiratory failure is rarely reported. Here, we present a case of parathyroid crisis with respiratory failure due to parathyroid adenoma. For the first 2 weeks after admission to our hospital, the patient was treated with hydration, calcium-lowering agents, dialysis and extracorporeal membrane oxygenation, with gradual improvement in her respiratory condition as blood calcium levels decreased. However, she still needed oxygen even after that. Therefore, parathyroidectomy was performed on day 48, and she no longer needed oxygen after the surgery. Chest computed tomography scan also demonstrated improvement in pulmonary calcification, although it did not completely disappear even 4 months after parathyroidectomy. Parathyroid crisis is an endocrine emergency, and its possibility should be considered in patients with respiratory failure with hypercalcemia.
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Camara-Lemarroy CR, Gonzalez-Moreno EI, Ortiz-Corona JDJ, Yeverino-Castro SG, Sanchez-Cardenas M, Nuñez-Aguirre S, Villarreal-Alarcon MA, Galarza-Delgado DA. Posterior reversible encephalopathy syndrome due to malignant hypercalcemia: physiopathological considerations. J Clin Endocrinol Metab 2014; 99:1112-6. [PMID: 24476076 DOI: 10.1210/jc.2013-3487] [Citation(s) in RCA: 25] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/03/2023]
Abstract
CONTEXT Posterior reversible encephalopathy syndrome (PRES) is a neurological entity characterized by seizures, headache, and reversible subcortical vasogenic edema. It is associated with many etiologies, most often hypertension, chronic renal failure, and chemotherapy. Hypercalcemia is rarely associated with PRES. OBJECTIVE The aim of this study is to describe and discuss a case of PRES that developed in a patient with malignant hypercalcemia, with emphasis on the possible pathophysiological mechanisms involved. PATIENTS AND METHODS A 38-year-old woman presented with altered mental status. She had a 2-month history of lumbar pain of moderate intensity, weight loss, and gastrointestinal complaints, in addition to a mass in her left breast. Her corrected serum calcium was 14.5 mg/dL. She was normotensive, had no focalizing signs, and her cerebrospinal fluid was normal. Despite treatment, her neurological state did not resolve, and she developed severe headaches at day 4 of her admission. Brain magnetic resonance imaging showed a bilateral and symmetric hyperintensity in the occipital and parietal lobes on T2-weighted and fluid-attenuated inversion recovery imaging, a characteristic highly suggestive of PRES. After correction of hypercalcemia, her symptoms and imaging abnormalities resolved. CONCLUSIONS The development of PRES in the setting of severe hypercalcemia is extremely rare. Hypercalcemia could lead to PRES in the absence of hypertension by various mechanisms, including vasospasm, endothelial dysfunction, and an inflammatory state. A high index of suspicion is needed in this setting because hypercalcemia can lead to neurological symptomatology, and prompt diagnosis is essential for adequate treatment.
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Affiliation(s)
- Carlos R Camara-Lemarroy
- Departamento de Medicina Interna, Hospital Universitario "Dr. José E. González," Universidad Autónoma de Nuevo León, Monterrey, N.L. México, Madero y Gonzalitos S/N, Monterrey NL 64460, México
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Abstract
The objectives of this study were to determine whether type 2 diabetic mice would exhibit a more severe renal impact of hemorrhagic shock (HS) based on a recently described model of acute kidney injury and to determine the impact of HS on renal responses to hypoxia. We induced HS or sham procedure in type 2 diabetic and obese db/db mice. Creatininemia, glomerular filtration rate, urine output, histologic injury score, and kidney inductible molecule 1 mRNA were used to investigate the renal impact of HS. Tissular hypoxia and its impact were quantified using pimonidazole immunostaining and mRNA of hypoxic inducible factor, vascular endothelial growth factor receptors 1 and 2, Tie-2, endothelial nitric oxide synthase, and inducible nitric oxide synthase. Diabetic mice exhibiting mild diabetic nephropathy express hypoxic signals at baseline. The renal impact of HS was more severe in diabetic mice, with a worsening of tissular hypoxia and an altered response to hypoxia. Furthermore, endothelial nitric oxide synthase was highly overexpressed in diabetic shocked mice when compared with nondiabetic shocked mice. Renal impact of HS in type 2 diabetic mice is more intense than in nondiabetic ones. Preexisting hypoxia during diabetes could result in a renal preconditioning that modifies endothelial and tissular responses to acute kidney injury.
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Acute lung injury and acute respiratory distress syndrome: experimental and clinical investigations. J Geriatr Cardiol 2012; 8:44-54. [PMID: 22783284 PMCID: PMC3390060 DOI: 10.3724/sp.j.1263.2011.00044] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/06/2011] [Revised: 03/12/2011] [Accepted: 03/19/2011] [Indexed: 01/11/2023] Open
Abstract
Acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) can be associated with various disorders. Recent investigation has involved clinical studies in collaboration with clinical investigators and pathologists on the pathogenetic mechanisms of ALI or ARDS caused by various disorders. This literature review includes a brief historical retrospective of ALI/ARDS, the neurogenic pulmonary edema due to head injury, the long-term experimental studies and clinical investigations from our laboratory, the detrimental role of NO, the risk factors, and the possible pathogenetic mechanisms as well as therapeutic regimen for ALI/ARDS.
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Chen CF, Wang D, Leu FJ, Chen HI. The protective role of nitric oxide and nitric oxide synthases in whole-body hyperthermia-induced hepatic injury in rats. Int J Hyperthermia 2012; 28:421-30. [DOI: 10.3109/02656736.2012.677928] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/13/2022] Open
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Su CF, Kao SJ, Chen HI. Acute respiratory distress syndrome and lung injury: Pathogenetic mechanism and therapeutic implication. World J Crit Care Med 2012; 1:50-60. [PMID: 24701402 PMCID: PMC3953859 DOI: 10.5492/wjccm.v1.i2.50] [Citation(s) in RCA: 26] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/27/2011] [Revised: 10/14/2011] [Accepted: 03/10/2012] [Indexed: 02/06/2023] Open
Abstract
To review possible mechanisms and therapeutics for acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). ALI/ARDS causes high mortality. The risk factors include head injury, intracranial disorders, sepsis, infections and others. Investigations have indicated the detrimental role of nitric oxide (NO) through the inducible NO synthase (iNOS). The possible therapeutic regimen includes extracorporeal membrane oxygenation, prone position, fluid and hemodynamic management and permissive hypercapnic acidosis etc. Other pharmacological treatments are anti-inflammatory and/or antimicrobial agents, inhalation of NO, glucocorticoids, surfactant therapy and agents facilitating lung water resolution and ion transports. β-adrenergic agonists are able to accelerate lung fluid and ion removal and to stimulate surfactant secretion. In conscious rats, regular exercise training alleviates the endotoxin-induced ALI. Propofol and N-acetylcysteine exert protective effect on the ALI induced by endotoxin. Insulin possesses anti-inflammatory effect. Pentobarbital is capable of reducing the endotoxin-induced ALI. In addition, nicotinamide or niacinamide abrogates the ALI caused by ischemia/reperfusion or endotoxemia. This review includes historical retrospective of ALI/ARDS, the neurogenic pulmonary edema due to head injury, the detrimental role of NO, the risk factors, and the possible pathogenetic mechanisms as well as therapeutic regimen for ALI/ARDS.
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Affiliation(s)
- Chain-Fa Su
- Chain-Fa Su, Department of Neurosurgery, Tzu Chi University Hospital, Hualien 97004, Taiwan, China
| | - Shang Jyh Kao
- Chain-Fa Su, Department of Neurosurgery, Tzu Chi University Hospital, Hualien 97004, Taiwan, China
| | - Hsing I Chen
- Chain-Fa Su, Department of Neurosurgery, Tzu Chi University Hospital, Hualien 97004, Taiwan, China
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Lin CC, Liu PH, Kao SJ, Chen HI. Effects of phorbol myristate acetate and sivelestat on the lung injury caused by fat embolism in isolated lungs. J Biomed Sci 2012; 19:3. [PMID: 22216930 PMCID: PMC3265425 DOI: 10.1186/1423-0127-19-3] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/04/2011] [Accepted: 01/05/2012] [Indexed: 11/10/2022] Open
Abstract
Background Fat embolism syndrome (FES) associated with acute lung injury (ALI) is a clinical condition following long bone fracture. We have reported 14 victims due to ALI with FES. Our laboratory has developed an animal model that produced fat emboli (FE). The major purpose of this study was to test whether neutrophil activation with phorbol myristate acetate (PMA) and inhibition with sivelestat (SVT) exert protection on the lung. Methods The lungs of Sprague-Dawley rats were isolated and perfused. FE was produced by addition of corn oil micelles into the lung perfusate. PMA and SVT were given simultaneously with FE. Parameters such as lung weight/body weight ratio, LW gain, exhaled nitric oxide (NO), protein concentration in bronchoalveolar lavage relating to ALI were measured. The neutrophil elastase (NE), myeloperoxidase, malondialdehyde and phopholipase A2 activity were determined. We also measured the nitrate/nitrite, methyl guanidine (MG), and cytokines. Pulmonary arterial pressure and microvascular permeability were assessed. Lung pathology was examined and scored. The inducible and endothelial NO synthase (iNOS and eNOS) were detected. Results FE caused ALI and increased biochemical factors. The challenge also resulted in pulmonary hypertension and increased microvascular permeability. The NE appeared to be the first to reach its peak at 1 hr, followed by other factors. Coadministration with PMA exacerbated the FE-induced changes, while SVT attenuated the effects of FE. Conclusions The FE-induced lung changes were enhanced by PMA, while SVT had the opposite effect. Sivelestat, a neutrophil inhibitor may be a therapeutic choice for patients with acute respiratory distress syndrome (ARDS) following fat embolism.
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Affiliation(s)
- Chia-Chih Lin
- Department of Physical Education and Kinesiology, National Dong Hwa University, Hualien, Taiwan
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A hyperparathyroid case with pulmonary edema: can hypercalcemia trigger pulmonary edema? Am J Emerg Med 2011; 30:512.e1-3. [PMID: 21354747 DOI: 10.1016/j.ajem.2010.12.033] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/24/2010] [Accepted: 12/25/2010] [Indexed: 11/22/2022] Open
Abstract
Most cases of pulmonary edema presenting with hypercalcemia are associated with malignant hypercalcemia and related with metastatic calcification. Most patients have predisposing factors such as hematological and solid organ malignancies and chronic renal failure. Pulmonary edema, induced by moderate hypercalcemia, which is associated with primary hyperparathyroidism, has not been reported previously. A 72-year-old female patient was admitted to the emergency service with pulmonary edema and moderate hypercalcemia because of primary hyperparathyroidism. In this presented case, we have discussed the 72-year-old female patient admitted with acute pulmonary edema who had primary hyperparathyroidism.
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Biomedical vignette. J Biomed Sci 2008. [PMCID: PMC7101994 DOI: 10.1007/s11373-008-9234-2] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/28/2022] Open
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