Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0231835 (tachypnea)
 2,543 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A special type of respiratory distress syndrome has been described in connection with fractures of the long bones, called fat embolism syndrome. In addition to the respiratory signs - tachypnoea, hypoxaemia and snow storm infiltrations in the chest x-ray films- the syndrome consists of petechiae, thrombocytopenia, cerebral disturbances, pyrexia etc. The respiratory insufficiency in this syndrome may be explained by a coagulation disorder, in which the release of tissue thromboplastins from the traumatized tissues results in an interstitial pneumonitis and peripheral thrombocytopenia. Accumulation of fat in the lung microvasculature has been observed both clinically and post morten. The importance of fat for the pathogenesis of the syndrome is not clear, but fat globuli are present in quantities, which are not encountered in other types of post-traumatic pulmonary insufficiency. Careful observation of a patient with multiple fractures is the cornerstone of early diagnosis. Cautions handling and early stabilization of fractures reduce the tissue trauma and may thus reduce the manifestations of the fat embolism syndrome. Respiratory assistance is given when necessary, and most often the syndrome is self-resolving. Fulminant cases with increasing symptomatology are treated with methylprednisolone and respirator.
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PMID:Fat embolism syndrome: etiology, pathogenesis and treatment. 693

A pediatric patient is reported who experienced fatal progressive pulmonary fibrosis as a complication of 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) therapy. The patient received a cumulative dosage of 1.29 g (1.72 g/m2) over a two-year period as adjuvant therapy for a medulloblastoma. Two and one-half years after cessation of therapy, cough, tachypnea and fatigue were noted. Progressive pulmonary insufficiency developed. Pulmonary pathologic findings included interstitial fibrosis and alveolar dysplasia. Other cases of BCNU pulmonary toxicity are cited from the medical literature.
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PMID:Pulmonary fibrosis: a complication of 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) therapy. 727 34

This paper is a review of the patients with pulmonary thromboembolism hospitalized at General hospital in Teanj starting from the first case recorded in 1980 till now and 172 patients were subjects of this study. Thromboembolism was a direct cause of death in 43.7% (75 patients). Clinical and laboratory records, etiology, chest radiography, ECG data of 89 patients hospitalised and treated in the last five years were analyzed in detail. The most frequent symptoms were dyspnea and tachypnea, often accompanied with other symptoms (84.2%), chest pain (65.2%), cough (52.4%), tachycardia (40.5%), hemoptysis (25.8%). At 74% of patients with pulmonary thromboembolism a significant simultaneous increase of all examined enzymes, except CPK was found. Pulmonary insufficiency (global or partial) was found at 75% of patients. According to our results, in 57.2% of the subjects the pathologic changes on Radiography (infiltrates of the lung, with or without affection of the pleura and changed position of diaphragm) were found, and 70.9% had changes on the ECG.
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PMID:[Clinical aspects of pulmonary thromboembolism]. 1032 Oct 63

Retinoic acid syndrome is a potentially life-threatening complication of therapy for acute promyelocytic leukemia (APL) with all-transretinoic acid (ATRA). The case of a 55-year old male patient admitted to the hospital because of a bleeding diathesis is reported. APL was diagnosed and he underwent treatment with idarubicin and ATRA (GIMEMA protocol); 24 hrs after ATRA treatment he developed retinoic acid syndrome and was admitted to the Intensive Care Unit because of severe respiratory insufficiency (dyspnoea, tachypnea and severe hypoxemia (SpO2 75%). Pulmonary insufficiency was treated non-invasively with CPAP and the patient recovered from pulmonary distress one week later.
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PMID:[Retinoic acid syndrome. Severe respiratory insufficiency treated with CPAP]. 1096 36

We report 4 cases of late onset glycogen storage disease type II (GSD II) or Pompe disease (OMIM #232300), under enzyme replacement therapy (ERT) with recombinant human acid alpha glucosidase (rh-GAA, OMIM *606800). In these 4 cases, we focused on the case of a 28-years-old man, whose condition at the ERT starting was the worst and resulted in poor prognosis. The autopsy was done under his family's permission, and revealed severe accumulation of glycogen in his muscle, especially diaphragm or iliopsoas, and pulmonary veno-occlusive disease (PVOD) which resulted in severe pulmonary hypertension (PH). This is the first report of PVOD as the cause of PH in Pompe disease. We studied this case comparing to another 3 cases of late onset Pompe disease under the same course of ERT in our hospital, and the average data of the group of late onset Pompe disease with severe pulmonary insufficiency receiving ERT, supposed that low score of the body mass index (BMI) on the baseline, the presence of specific genotype (p.R600C), and signs of pulmonary dysfunction suggesting PH (tachypnea, ultrasound cardiography data) were factors that influenced the prognosis. For a better prognosis in the late onset Pompe disease, an early diagnosis for the early start of ERT before the onset of respiratory failure should be important, and the deliberate management and care should be needed even after the ERT start, especially for severe cases including pulmonary dysfunction.
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PMID:Prognostic factors for the late onset Pompe disease with enzyme replacement therapy: from our experience of 4 cases including an autopsy case. 2048 40