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)

A syndrome of pulmonary alveolar septal calcinosis, pneumothorax, and pneumomediastinum, leading to rapidly progressive acute respiratory insufficiency and death was observed in 2 children with acute lymphoblastic leukemia (ALL). Primary clinical and radiological considerations in these patients were pulmonary edema and infection, and the diagnosis of pulmonary alveolar septal calcification was established only at autopsy. One patient, a 15-year-old girl, was found also to have parathyroid hyperplasia typical of familial hyperparathyroidism. The other, a 16-month-old girl, showed osteitis fibrosa of the bones and parathyroid hyperplasia of secondary type, suggesting that the pulmonary calcinosis resulted from hypercalcemia caused by a parathormone or prostaglandin-secreting tumor. The cause of pneumothorax and pneumomediastinum may have been rupture of calcified alveolar septa induced by high PEEP during ventilation of these patients. Other possible mechanisms contributing to hypercalcemia and pulmonary calcinosis in children with acute leukemia include bone resorption due to marrow infiltration, immobilization syndrome, renal failure, and administration of calcium, phosphate, or bicarbonate. This complication of acute leukemia in childhood is rare (2 patients in 430 autopsied over the period 1961-1982 at Childrens Hospital of Los Angeles). How often the process can be reversed if diagnosed before severe respiratory insufficiency is present is not known.
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PMID:Pulmonary alveolar septal calcinosis causing progressive respiratory failure in acute lymphoblastic leukemia in childhood. 347 56

Pulmonary calcinosis is a recognized complication of renal failure. The resulting pulmonary compromise may be severe or even fatal. The potential contribution of hypercalcemia, hyperphosphatemia, and increased calcium-phosphorus product to the development of pulmonary calcinosis has been controversial. We describe four patients (ages 2 1/4 to 18 years) who had severe pulmonary calcinosis and respiratory failure within three to five days after renal transplantation. Initial clinical and roentgenographic findings suggested noncardiogenic pulmonary edema. Marked pulmonary hypertension was present in the two patients in whom pulmonary artery pressure data were available. Other clinical features in common included poor allograft function with persistent uremia requiring dialysis and evidence of moderate to severe secondary hyperparathyroidism. In three of the patients, the calcium-phosphorus product increased markedly after transplantation, to peak values of 122 to 147. This increase occurred at the same time as the onset of respiratory failure. Peak serum calcium levels were 10.0 to 11.0 mg/dL and peak serum phosphorus levels were 9.2 to 13.5 mg/dL. All patients died of respiratory failure five to 58 days after transplantation. The posttransplantation period may be a time of increased risk of potentially fatal pulmonary calcinosis in pediatric renal transplant recipients. The diagnosis should be considered in any patient with respiratory failure of unknown cause following renal transplantation.
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PMID:Pulmonary calcinosis after renal transplantation in pediatric patients. 352 Dec 66

The pathological findings in the lungs and related organs of 26 patients (21 female, 5 male) with systemic lupus erythematosus (SLE), with onset of disease before age 20 years, were reviewed. Several categories of lung lesions were found. Chronic interstitial pneumonitis was present in all 26 patients and was severe in 5. Acute pneumonia was present in 20, mild in 13, moderate in 2, and severe in 5. Alveolar hemorrhage, massive enough to cause death in 5, was seen in 18 patients, and pulmonary edema was found in 13. Fourteen patients had hyaline membranes indicative of acute alveolar damage (DAD), 12 had alveolitis obliterans, indicative of prior episodes of DAD, and 9 had bronchiolitis obliterans. Other parenchymal lesions were mild interstitial fibrosis in 12, alveolar hemosiderosis and alveolar overinflation in 10 each, and alveolar septal calcinosis with chronic renal insufficiency in 3. Pleural effusion, pleuritis, or pleural thickening were noted in 15 of 26, 6 of 23, and 7 of 23 evaluable patients, respectively. Vascular lesions were present in 16 as intimal thickening (9), thromboemboli (8), medial hypertrophy (6), calcinosis (3), and vasculitis (2). A previously unreported lesion was chronic (proliferative) peribronchitis, noted in 11 patients. Diaphragmatic lesions included mild variation in fiber size in 7, mild fibrosis in 2, and calcinosis in 1 of 13 evaluable patients. Correlation of the above lesions with previously described lung syndromes in SLE such as lupus pneumonitis, hemorrhagic lung disease, chronic interstitial fibrosis, lupus cor pulmonale, pleurisy, and "shrinking lung syndrome" are discussed.
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PMID:Pulmonary lesions in childhood onset systemic lupus erythematosus: analysis of 26 cases, and summary of literature. 360 12

Pulmonary opacities following orthotopic liver transplantation (OLT) are frequent due to pneumonia, infarction, or pulmonary edema. Metastatic pulmonary calcifications are present as persistent opacities that may mimic these conditions. In a series of 91 patients who underwent OLT, chest radiographs of 77 were reviewed and pulmonary calcinosis was seen in 4 (5.2%). Pulmonary calcinosis may be due to a variety of conditions, including dystrophic calcification in damaged lung and primary or secondary hyperparathyroidism. In this series, patients with pulmonary calcinosis had significantly higher levels of serum phosphate and calcium postoperatively and had received more intraoperative platelets and other blood products containing exogenous calcium than other patients. Pulmonary calcinosis should be considered in patients following OLT when stable, nonspecific pulmonary opacities are present. CT or radionuclide studies will aid in confirming this diagnosis.
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PMID:Pulmonary calcinosis following orthotopic liver transplantation. 824 29

Pulmonary arterial hypertension (PAH) is commonly associated with the CREST (calcinosis, Raynaud phenomenon, esophageal dysmotility, sclerodactyly, telangiectasia) syndrome. Inhaled nitric oxide (iNO) is often used to assess acute vasoresponsiveness in patients with PAH, and reports of adverse reactions have been infrequent. We describe two of nine patients with PAH and CREST syndrome who had pulmonary edema develop during acute iNO testing. This complication was not encountered in the 46 patients with other forms of PAH tested with iNO. We suggest that iNO should be used with caution, if at all, to test acute vasoreactivity in patients with CREST syndrome.
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PMID:Pulmonary edema caused by inhaled nitric oxide therapy in two patients with pulmonary hypertension associated with the CREST syndrome. 1183 88