Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A wheelchair-bound 61-year-old diabetic man with amyotrophic lateral sclerosis (ALS) developed sudden respiratory failure. Specific findings for hypoxemia and hypocapnia were incompatible with type II respiratory failure seen in the terminal stages of ALS. 'Economy class syndrome' was diagnosed, with massive thrombosis in the pulmonary arteries and deep vein thrombosis. This case offers a warning for long-term wheelchair users, particularly hypoxemic ALS patients, regarding the risks of treatable pulmonary thromboembolism.
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PMID:Wheelchair economy class syndrome in amyotrophic lateral sclerosis. 1648 7

We describe the case of a 61-year-old male patient, in which the search for the cause of chronic respiratory failure, severe pulmonary hypertension and secondary erythrocytosis resulted in a diagnosis of combined pulmonary fibrosis and emphysema (CPFE). This is a unique, recently characterised syndrome with upper-lobe emphysema and pulmonary fibrosis of the lower lungs. The cause is unknown, but one of the main risk factor remains smoking. The patient was a heavy smoker (over 40 pack-years). He complained of dyspnoea on exertion and cough. Physical examination revealed basal crackles and cyanosis. The patient had severe reduction in diffusing capacity, out of proportion to his lung volumes (DLCO 27% of predicted value, FEV1 2.95 l (100%), FVC 4.41 l (118%), FEV1/FVC (66%). The blood gas showed hypoxemia (pO2 37 mm Hg), hypocapnia and respiratory alkalosis. Diagnosis was based on chest computer tomography, which revealed upper lobe emphysema and lower lobe ground glass changes and honeycombing. Severe pulmonary hypertension (SPAP 80 mm Hg) was confirmed by echocardiography and right cardiac catherisation. The patient received long-term oxygen therapy, inhaled corticosteroid and Ca-blocker.
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PMID:[Combined pulmonary fibrosis and emphysema - case report and literature review]. 1946 58

Amyopathic dermatomyositis (ADM) is a clinical subtype of dermatomyositis, characterized by the absence of motor weakness and the presence of normal muscle enzyme levels. ADM is sometimes accompanied by neoplasm or interstitial pneumonia that shows a rapid progressive course both of them are associated with a poor prognosis. A 56-year-old woman with no medical history was referred to the department of medicine because of arthralgia with a remarkable weight loss. She also complained of rapidly progressive dyspnea, cough and photosensitivity. Physical examination on admission showed scaly erythema on the dorsum of the hands (Gottron sign) and periorbital edema with a purplish appearance (heliotropic rash), arthritis, but no muscle weakness. Auscultation of the chest identified audible fine crackles on the lower aspects of both lungs. Results of laboratory findings on admission revealed a lymphopenia. The serum creatine kinase and serum lactate dehydrogenase concentration were normal. IRM muscle and electromyography were normal. Antinuclear antibody was positive 1:80 and anti-Jo-1 antibody and other autoantibodies to specific antigens were all negative. High resolution computed tomographic chest scans also revealed diffuse ground-glass opacities in both lungs with basilar predominance. Arterial blood gas analysis revealed hypoxia and hypocapnia. LBA was not performed because of the deterioration of respiratory symptoms. There was no neoplasm associated. The diagnosis of ADM complicated with ADM rapidly progressive interstitial pneumonia was made. Despite of IV methylprednisolone pulse therapy (1g*day-1 for 3 days) and cyclophosphamide, she died by respiratory failure.
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PMID:[Interstitial pneumonia complicating amyopathic dermatomyositis: a case report]. 1999 56

Supplementary oxygen is routinely administered to patients, even those with adequate oxygen saturations, in the belief that it increases oxygen delivery. But oxygen delivery depends not just on arterial oxygen content but also on perfusion. It is not widely recognized that hyperoxia causes vasoconstriction, either directly or through hyperoxia-induced hypocapnia. If perfusion decreases more than arterial oxygen content increases during hyperoxia, then regional oxygen delivery decreases. This mechanism, and not (just) that attributed to reactive oxygen species, is likely to contribute to the worse outcomes in patients given high-concentration oxygen in the treatment of myocardial infarction, in postcardiac arrest, in stroke, in neonatal resuscitation and in the critically ill. The mechanism may also contribute to the increased risk of mortality in acute exacerbations of chronic obstructive pulmonary disease, in which worsening respiratory failure plays a predominant role. To avoid these effects, hyperoxia and hypocapnia should be avoided, with oxygen administered only to patients with evidence of hypoxemia and at a dose that relieves hypoxemia without causing hyperoxia.
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PMID:Supplementary oxygen for nonhypoxemic patients: O2 much of a good thing? 2172 34

This report presents the case of a 67-year-old woman affected by glioblastoma. After a few days of adjuvant therapy with temozolomide and prophylaxis with trimetrophin-sulfamethoxazolo to prevent Pneumocystis Jiroveci, she had progressive and rapid worsening of symptoms with weakness, dyspnea and orthopnea. She had peripheral edema and proximal hyposthenia of the lower limbs. Chest CT showed bilateral ground-glass opacities and laboratory exams revealed hypoxemia and hypocapnia, an initial reduction in platelet and white blood cells, and an elevation of LDH, AST, ALT, and active urinary sediment. Blood cultures, bronchoalveolar lavage (BAL) data and transbronchial biopsy showed no infections, and in particular no evidence of Pneumocystis Jiroveci pneumonia. Histological examination revealed a typical pattern of AIP. She was treated with broad-spectrum antibiotics and high-dose steroids. The symptoms worsened and respiratory failure required mechanical ventilation. The pneumonia was not responsive to medical or invasive care. She died after ten days of hospitalization. At present very little can be found in the literature about lung toxicity caused by temozolomide. This case can be added as a new report describing this risk. The combination therapy with temozolamide and trimetophin-sulfamethoxazolo could have a synergistic action inducing various forms of pulmonary toxicity. ESTABLISHED FACTS: Acute interstitial pneumonia is a common manifestation of lung toxicity caused by drugs. The clinical course is favorable with a good response to corticosteroids. NOVEL INSIGHT: This is the first fatal case of lung toxicity caused by Temozolomide. Clinicians must be aware that a combination therapy including trimetophin-sulfamethoxazolo could have a synergistic action in inducing pulmonary toxicity.
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PMID:A fatal case of acute interstitial pneumonia (AIP) in a woman affected by glioblastoma. 2441 Mar 8

Paroxysmal Vocal Cords Dysfunction(PVCD), also known as paradoxical vocal cord motion, is abnormal adduction of the vocal cords during inspiration. Like asthma, PCVD can be triggered by breathing in lung irritants, upper respiratory infection or exercise. However, unlike asthma, PCVD is not an immune system reaction and does not involve the lower airways. Treatment for the two conditions differs. Plasma lactate levels are usually associated with acidosis and an increased risk of poor outcome and are described in a number of disease states of circulatory and/or respiratory failure. In patients with psychogenic hyperventilation, high lactates are associated with hypocapnia and alkalosis and should not necessarily be considered as an adverse sign. We describe a case of a young patient with PCVD mimicking asthma with high plasma lactate and discuss the mechanisms involved.
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PMID:Hyperventilation-related hyperlactataemia in a case of paroxysmal vocal cord dysfunction. 2897 1


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