The detrimental role of inducible nitric oxide synthase in the pulmonary edema caused by hypercalcemia in conscious rats and isolated lungs

Chen, Hsing I.; Yeh, Diana; Kao, Shang Jyh

doi:10.1007/s11373-007-9211-1

Cited by 21 publications

(9 citation statements)

References 43 publications

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“…In vitro, raised nitrate/nitrite, free radicals, proinflammatory cytokines, procalcitonin and inducible nitric oxide synthase activity suggest that hypercalcaemia induces a sepsis-like syndrome. 4 Acute kidney injury is a more established complication of hypercalcaemia, for example in milk-alkali syndrome. However, overall, it remains a rare cause for renal failure.…”

Section: Discussionmentioning

confidence: 99%

A case of multi-organ failure due to hyperparathyroidism-related hypercalcaemia

Cummings

Vannahme

Stanworth

2019

Journal of the Intensive Care Society

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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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Section: Discussionmentioning

confidence: 99%

A case of multi-organ failure due to hyperparathyroidism-related hypercalcaemia

Cummings

Vannahme

Stanworth

2019

Journal of the Intensive Care Society

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“…A second theory emphasizes the importance of altered blood brain barrier function resulting from a combination of endothelial dysfunction, hypoperfusion and vasoconstriction (24). Hypercalcemia and elevated PTH levels have been shown to induce the production of vascular endothelial growth factor (VEGF) and nitric oxide (NO) by way of which they can alter vascular permeability (25,26,27) as mentioned in the second theory. In PRES, symptoms develop sub-acutely or acutely, often with seizures at onset (24).…”

Section: Discussionmentioning

confidence: 99%

Parathyroid Adenoma Complicated with Severe Hypercalcemia, Encephalopathy and Pancreatitis

Okaygün¹,

Sav²,

Mousa³

et al. 2015

tjem

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Abs tract ÖzetPrimary hyperparathyroidism is the most frequent cause of hypercalcemia in adults. Primary hyperparathyroidism generally leads to mildmoderate hypercalcemia. Severe hypercalcemia in these cases is rare. Coexistence of severe hypercalcemia and hypercalcemic encephalopathy is very unusual with very limited number of reported cases. Our case is a 50-year-old female who presented to the emergency department with the complaints of nausea and severe abdominal pain. Her serum calcium level was 19.7 mg/dL (8.8-10.2 mg/dL) and her PTH level was 73.5 ng/ dL (15-65) on presentation. After her hospitalization, she was treated with saline infusions and furosemide, however, her calcium level increased to 22.4 mg/dL. Her calcium levels were also refractory to subcutaneous calcitonin 200 mg twice a day and zoledronic acid 4 mg. Ultrasonography of the neck revealed a 3.2x2.7x4.6 cm mass suspicious for a left parathyroid adenoma hardly being distinguished from a left thyroid nodule. Considering her general situation getting worse despite maximum medical treatment, she underwent an emergency parathyroidectomy and total thyroidectomy. Early postoperatively, the patient's general condition deteriorated reaching a precoma state. Cranial computed tomography (CT) at this point revealed periventricular ischemia compatible with metabolic encephalopathy. During the follow-up postoperatively, the patient's serum calcium levels normalized eventually requiring active vitamin D and calcium pills and she no longer had symptoms of encephalopathy. The pathology specimen was reported as a parathyroid neoplasm compatible with atypical parathyroid adenoma. Although mild-moderate hypercalcemia is frequent in primary hyperparathyroidism, it should be noted that it can be severe and refractory to maximum medical treatment requiring emergency surgical intervention. In addition, not being one of the most frequent reasons, severe hypercalcemia due to primary hyperparathyroidism should be considered as an important cause of metabolic encephalopathy. Turk Jem 2015; 19: 105-108Erişkinlerde hiperkalseminin en sık görülen sebebi primer hiperparatiroididir. Primer hiperparatiroidinin yol açtığı kalsiyum yüksekliği genellikle ılımlıdır. Bu olgularda ciddi hiperkalsemi seyrektir. Bu olgularda ciddi hiperkalsemi ile birlikte hiperkalsemik ensefalopati birlikteliği seyrek görülmekte olup sınırlı sayıda olgu sunumu literatürde bildirilmiştir. Elli yaşındaki kadın olgumuz bulantı ve ciddi karın ağrısı şikayeti ile acil servise başvurusunda serum kalsiyum düzeyi 19,7 mg/dL (8,8-10,2 mg/dL) ve serum PTH düzeyi 73,5 (13-65) ng/dL olarak saptandı. Hastaneye yatışının ardından serum fizyolojik infüzyonu ve furosemid tedavisine rağmen kalsiyum düzeyi 22,4 mg/dL'ye kadar yükseldi. Kalsitonin günde 2 kez 200 mg subkutan ve zoledronik asit 4 mg intravenöz verilmesi sonrası da yanıt alınamadı. Boyun ultrasonografisinde sol lob inferiorunda tiroid nodülünden zor ayrılabilen ve paratiroid ile uyumlu olabilecek 3,2x2,7x4,6 cm kitle izlendi. Genel durumunun tedaviye ...

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“…We proposed that hypercalcemia produced a sepsis-like syndrome. The ALI caused by hypercalcemia may involve NO and iNOS [85] .…”

Section: Investigations On Ali/ards In Our Laboratorymentioning

confidence: 99%

Acute respiratory distress syndrome and lung injury: Pathogenetic mechanism and therapeutic implication

Kao

Chen

2012

WJCCM

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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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The detrimental role of inducible nitric oxide synthase in the pulmonary edema caused by hypercalcemia in conscious rats and isolated lungs

Cited by 21 publications

References 43 publications

A case of multi-organ failure due to hyperparathyroidism-related hypercalcaemia

A case of multi-organ failure due to hyperparathyroidism-related hypercalcaemia

Parathyroid Adenoma Complicated with Severe Hypercalcemia, Encephalopathy and Pancreatitis

Acute respiratory distress syndrome and lung injury: Pathogenetic mechanism and therapeutic implication

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