Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Granulocyte-colony stimulating factor (G-CSF), a hematopoietic growth factor, is widely used to accelerate recovery from neutropenia after severe chemotherapy, both decreasing the risk of infection and mobilizing peripheral blood stem cells. Adverse effects occur with G-CSF use in approximately 30% of cases, comprised predominantly of bone pain, headache, and general fatigue. Pulmonary toxicity is very rare. Here, we describe a healthy donor for allogeneic hematopoietic stem cell transplantation who developed acute lung injury (ALI) after 4 days of G-CSF administration. Among the serum cytokines examined, only Interleukin (IL)-1beta level was elevated in this case. As a high level of IL-1beta was detected at the onset of ALI, on day 4 after G-CSF administration, and decreased to below the level of detection on day 11, it is possible in a certain part that IL-1beta was involved in the onset of G-CSF-related ALI in the present case. Granulocyte-colony stimulating factor (G-CSF) is commonly administered to healthy donors to mobilize peripheral blood stem cells (PBSC) for allogeneic hematopoietic stem cell transplantation (allo-HSCT). Adverse events from G-CSF use in healthy donors have been described in approximately 30% of cases, and are comprised predominantly of bone pain, headache, and general fatigue. Pulmonary complications caused by G-CSF include cough, dyspnea, and interstitial or alveolar pulmonary edema with mild-to-severe deterioration of blood oxygen level. Few cases of acute respiratory distress syndrome (ARDS) following G-CSF administration have been reported. The present report describes a healthy donor for allo-HSCT with acute lung injury (ALI) after 4 days of G-CSF administration. The cytokine-related mechanisms of G-CSF administration that contribute to ALI are discussed.
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PMID:Acute lung Injury in a healthy donor during mobilization of peripheral blood stem cells using granulocyte-colony stimulating factor alone. 1575 51

Pulmonary edema occurring in divers using a self-contained underwater breathing apparatus (scuba) is an uncommon, probably under-reported, but potentially life-threatening and recurrent condition. We report six episodes of pulmonary edema in five scuba divers seen during a period of 15 months. The four men and one woman ranged in age from 37 to 56 years and two were treated for hypertension. Symptoms were mostly dyspnea onset at depth, cough, hemoptysis and hypoxemia, which in the recurrent case led to cardiac arrest and death. All cases occurred in rather cold water. Findings on thoracic computed tomography (CT) scanning ranged from pleural effusion to ground-glass opacities restricted to a few areas of the lung. The complex underlying mechanisms that would contribute to a raised transalveolar pressure or to a disruption of the blood-gas barrier are discussed. It is important for emergency care providers to be aware of this syndrome for prompt recognition and optimal treatment.
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PMID:Pulmonary edema in scuba divers: recurrence and fatal outcome. 1579 13

Fumonisin B(1) (FB(1)) is a mycotoxin produced by Fusarium verticillioides and F. proliferatum that commonly occurs in maize. In swine, consumption of contaminated feed induces liver damage and pulmonary edema. Pasteurella multocida is a secondary pathogen, which can generate a respiratory disorder in predisposed pigs. In this study, we examined the effect of oral exposure to fumonisin-containing culture material on lung inflammation caused by P. multocida. Piglets received by gavage a crude extract of fumonisin, 0.5mg FB(1)/kg body weight/day, for 7 days. One day later, the animals were instilled intratracheally with a non toxin producing type A strain of P. multocida and followed up for 13 additional days. Pig weight and cough frequency were measured throughout the experiment. Lung lesions, bronchoalveolar lavage fluid (BALF) cell composition and the expression of inflammatory cytokines were evaluated at the autopsy. Ingestion of fumonisin culture material or infection with P. multocida did not affect weight gain, induced no clinical sign or lung lesion, and only had minimal effect on BALF cell composition. Ingestion of mycotoxin extract increased the expression of IL-8, IL-18 and IFN-gamma mRNA compared with P. multocida infection that increased the expression of TNF-alpha. The combined treatment with fumonisin culture material and P. multocida delayed growth, induced cough, and increased BALF total cells, macrophages and lymphocytes. Lung lesions were significantly enhanced in these animals and consisted of subacute interstitial pneumonia. TNF-alpha, IFN-gamma and IL-18 mRNA expression was also increased. Taken together, our data showed that fumonisin culture material is a predisposing factor to lung inflammation. These results may have implications for humans and animals consuming FB(1) contaminated food or feed.
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PMID:Oral exposure to culture material extract containing fumonisins predisposes swine to the development of pneumonitis caused by Pasteurellamultocida. 1597 25

An 81-year-old man was referred to our hospital for the treatment for left spontaneous pneumothorax. A chest X-ray revealed a left-sided total pneumothorax and complete collapse of the lung. After intravenous administration of methylprednisolone, a 16 Fr chest tube was inserted, and drainage was started without negative pressure suction. Four hours after chest tube insertion, the patient's condition deteriorated. He complained severe cough and dyspnea, and pulse oximetry reading was 70%. A repeat chest X-ray demonstrated diffuse reexpansion pulmonary edema (RPE) on the left. After mechanical ventilation and intravenous infusion therapy with sivelestat sodium hydrate, methylprednisolone and ulinastatin were started, P(O2)/ Fi(O2) ratio improved rapidly. He was extubated on hospital day 6 and was discharged after pleurodesis for the pneumothorax. This case suggests that sivelestat sodium hydrate may be useful for the treatment for RPE.
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PMID:[Clinical experience of sivelestat sodium hydrate for severe reexpansion pulmonary edema; report of a case]. 1623 53

A case of negative pressure bilateral pulmonary edema in a 28 years old healthy female patient, scheduled for diagnostic pelvic laparoscopy for infertility. Following extubation and apparent recovery from anesthesia, she had strong inspiratory efforts due to airway obstruction caused by coughing and laryngeal spasm, that lead to negative pressure bilateral pulmonary edema. The pulmonary edema disappeared within few hours. She was breathing spontaneously through CPAP system (mask-bag-expiratory valve). Diuretics and lungs physiotherapy helped in controlling patient's complication.
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PMID:Bilateral negative airway pressure pulmonary edema (NPPE)--a case report--. 1638 Dec 68

20 children, diagnosed with scrub typhus who attended Chiang Rai Regional Hospital during a period of 6 months from June 2003 to December 2003, were studied prospectively. All cases were serologically proved to be scrub typhus by using Dipstick or indirect immunofluorescent antibody (IFA) technique. The most common clinical feature was eschar (75%). Others included hepatomegaly (65%), cough (60%), lymphadenopathy (40%), tachypnea (35%), constipation (25%), abdominal pain (20%), edema (20%), splenomegaly (15%), vomiting (15%), rash (15%) and petichia (5%) respectively. Chest radiography showed abnormalities in 85% with mostly bilateral interstitial infiltrations. Elevated of SGOT: SGPT were detected in 18 (90%) and 15 (75%) cases. Hypoalbuminemia was detected in 12 (60%) cases. Complete blood count showed PMN leukocytosis (> 60%) in 12 (60%) cases, lymphocytosis (> 40%) and atypical lymphocytosis (> 5%) in 1 (5%) case each and thrombocytopenia in 16 (80%) cases. The Weil-Felix test was positive in 1 (5%) case. Complications were pneumonia with or without pulmonary edema, meningitis and shock. Chloramphenicol and doxycycline were successfully treated and roxithromycin was not effective.
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PMID:Clinical study of 20 children with scrub typhus at Chiang Rai Regional Hospital. 1651 87

An unusual case of fibrosing mediastinitis with obstruction of the inferior and superior left pulmonary veins and severe narrowing of the right pulmonary artery, disclosed after unilateral pulmonary edema, is described. The 18-year-old male patient had a long history of cough, progressive dyspnea and recurrent hemoptysis and the possible diagnosis of "interstitial fibrosis" from a previous lung biopsy. The diagnosis and the pulmonary vessels involvement were suspected after right heart catheterization combined with transesophageal echocardiography and confirmed during urgent thoracotomy and at postmortem examination.
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PMID:Unilateral pulmonary edema due to pulmonary venous obstruction from fibrosing mediastinitis. 1652 Jan 36

A unique case of HAPE precipitating diabetic ketoacidosis in a previously undiagnosed Type 2 diabetic is reported. A 39-year-old male, previously well, was admitted at a hospital situated at a height of 3500 m with complaints of increasing breathlessness on effort, cough, and fever of short duration, 5 days after high altitude reascent. Examination at admission revealed a febrile (38 degrees C) patient with tachycardia (104/min), SaO2 was 82% (on supplemental oxygen), chest examination revealed bilateral crackles in all lung fields, and chest radiograph demonstrated bilateral fluffy heterogeneous opacities in all zones. He was diagnosed as suffering from high altitude pulmonary edema. The patient did not show adequate improvement despite conventional treatment for HAPE with supplemental oxygen and rest. Investigations revealed leucocytosis, and urinalysis revealed glycosuria and ketonuria. Subsequent arterial blood gas analysis revealed that acidemia and serum glucose levels were raised. He was thereafter managed as for HAPE and DKA and recovered in 2 weeks. The patient has been on regular follow-up with satisfactory glycemic control with oral hypoglycemic agents.
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PMID:Diabetic ketoacidosis in an undiagnosed diabetic precipitated by high altitude pulmonary edema. 1654 71

The use of fluorine compounds in various areas of medicine, particularly in dentistry, as well as in agriculture and industry became very popular in the second half of the 20th century. Fluorine owed this widespread acceptance to observations that its compounds stimulate ossification processes and reduce the prevalence of caries. Unfortunately, growing expectations overshadowed the truth regarding interactions of fluoride on the molecular level. The fact was often ignored that fluoride is toxic, even though laboratory data stood for a careful approach to the benefits of usage. Excessive exposure to fluoride may lead to acute poisoning, hyperemia, cerebral edema, and degeneration of the liver and kidneys. Acute intoxication through the airways produces coughing, choking, and chills, followed by fever and pulmonary edema. Concentrated solutions of fluorine compounds produce difficult to heal necrotic lesions. In spite of these dramatic symptoms, acute intoxications are relatively rare; the more common finding is chronic intoxication attributable to the universal presence of fluorine compounds in the environment. The first noticeable signs of excessive exposure to fluoride in contaminated water, air, and food products include discolorations of the enamel. Dental fluorosis during tooth growth and loss of dentition in adulthood are two consequences of chronic intoxication with fluorine compounds. Abnormalities in mineralization processes affect by and large the osteoarticular system and are associated with changes in the density and structure of the bone presenting as irregular mineralization of the osteoid. Fluorine compounds also act on the organic part of supporting tissues, including collagen and other proteins, and on cells of the connective tissue. These interactions reduce the content of collagen proteins, modify the structure and regularity of collagen fibers, and induce mineralization of collagen. Interactions with cells produce transient activation of osteoblasts, stimulate fibroblasts to produce collagenase, and trigger toxic reactions in osteocytes and chondrocytes of trabecular bone. Growing deformations of the skeleton reduce mobility and result in permanent crippling of the patient. Fluoride increases the mass of non-collagen proteins such as proteoglycans and glucosaminoglycans, accelerating skin aging even though protein biosynthesis is generally suppressed. The final outcome includes progressive vascular lesions and disorders of energy metabolism in muscles. In conclusions, the use of fluoride, particularly by dentists and pediatricians, must be controlled and adapted to individual needs. It is worth remembering that fluoride: is the cause of disability due to bone deformations and abnormalities in the musculoskeletal system; reduces the incidence of caries but do not protect against tooth loss; exerts an adverse effect of metabolic processes in the skin; accelerates calcification of vessels and thus reduces their elasticity; inhibits bioenergetic reactions, in particular oxidative phosphorylation, reducing physical activity of muscles. These findings suggest that fluorine may be yet another factor in accelerated aging and revive the dispute started more than two and half thousand years ago whether aging is a physiologic or pathologic process. The understanding of factors modifying the process of aging is the basis for preventive measures aimed at extending life and maintaining full psychosocial activity.
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PMID:[Fluorine as a factor in premature aging]. 1689 76

Almost one mountain trekker or climber out of two develops several symptoms of high altitude illness after a rapid ascent (> 300 m/day) to an altitude above 4000 m. Individual susceptibility is the most important determinant for the occurrence of high altitude pulmonary oedema (HAPE). Symptoms associated with HAPE are incapacitating fatigue, chest tightness, dyspnoea at the slightest effort, orthopnoea, and cough with due to haemoptysis in an advanced stage of the disease pink frothy sputum. The hallmark of HAPE is an excessively elevated pulmonary artery pressure (mean pressures of 35 and 55 mm Hg), which precedes the development of pulmonary oedema. Elevated pulmonary capillary pressure and protein- as well as red blood cell-rich oedema fluid without signs of inflammation in its early stage are characteristic findings. Furthermore, decreased fluid clearance from the alveoli may contribute to this non-cardiogenic pulmonary oedema. Immediate descent or supplemental oxygen and nifedipine are recommended until descent is possible. Susceptible individuals can prevent HAPE by slow ascent: an average gain of altitude not exceeding 400 m/day above an altitude of 2500 m. If progressive high altitude acclimatization is not possible, a prophylaxis with nifedipine should be recommended.
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PMID:High altitude-induced pulmonary oedema. 1690 89


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