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)

A non-smoking 76-year-old woman was admitted to our hospital complaining of cough, bloodstained sputum and difficulty in breathing that had developed while she was eating a meal. The initial diagnosis was upper airway obstruction. Her past history revealed no major illness, except that she was under medication for the treatment of hypertension. On examination, chest radiography and computed tomography (CT) scans showed diffuse ground glass opacities in both lungs, and bronchoalveolar lavage studies further yielded findings compatible with pulmonary hemorrhage. The patient's symptoms and hypoxemia improved gradually without any specific treatment. Laboratory data showed no specific underlying cause, such as vasculitis or collagen vascular disease, for the pulmonary hemorrhage. We therefore reached a diagnosis of a negative pressure pulmonary hemorrhage (NPPH) caused by upper airway obstruction. Follow-up examinations after 7 months showed no abnormal findings in the chest radiography or arterial blood gas analysis. To our knowledge, this is the first case of negative pressure pulmonary hemorrhage in japan.
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PMID:[A case of negative pressure pulmonary hemorrhage (NPPH) due to upper airway obstruction induced by asphyxia]. 1283 47

A 45-year-old woman with scleroderma for 15 years duration, rheumatoid arthritis in the past five years, and interstitial pneumonia in the past two years had been followed at OPD. Although sputum had appeared and cough had increased since January 2002, there was no obvious abnormal findings on chest X-ray. Later, as a chest X-ray revealed an infiltrative shadow with cavity in the right lower lung field, we suspected pulmonary tuberculosis and performed the direct smear examination of sputum immediately. As acid-fast bacilli were positive (Gaffky 10) and the polymerase chain reaction (PCR) test was positive for only Mycobacterium avium, we diagnosed the case as pulmonary nontuberculous mycobacterial disease. This case was thought to be pulmonary nontuberculous mycobacterial disease complicated with interstitial pneumonia with collagen vascular disease as a secondary infectious type, and as the cause of the disease, the decrease of the local pulmonary defence mechanism due to pre-existing pulmonary lesions was suspected.
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PMID:[A case of pulmonary Mycobacterium avium complex disease complicated by interstitial pneumonia with collagen vascular disease]. 1293 46

Sirolimus is a recently licensed immunosuppressant for organ transplantation that has been used as basic, adjuvant, or maintenance therapy for prevention of organ rejection. Well-known side effects of this agent are hyperlipidemia and bone marrow suppression. Interstitial pneumonitis is a relatively newly described adverse effect of the drug. A 43-year-old female recipient of a cadaveric kidney developed cough with blood-tinged sputum while receiving sirolimus immunosuppressive therapy. High-resolution computed tomographic scan and chest radiograph revealed interstitial infiltrations over bilateral lower lungs. No evidence of bacterial, fungal, mycobacterial, or viral infection was found and all tests for collagen vascular diseases were negative. Discontinuation of sirolimus resulted in a significant improvement of the lung disease.
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PMID:Sirolimus-induced interstitial pneumonitis in a renal transplant recipient. 1536 50

Idiopathic pulmonary fibrosis (IPF), also termed cryptogenic fibrosing alveolitis, is a clinicopathological syndrome characterised by cough, exertional dyspneoa, basilar crackles, a restrictive defect on pulmonary function tests, honeycombing on high-resolution, thin-section computed tomographic scans and the histological diagnosis of usual interstitial pneumonia on lung biopsy. The course is usually indolent but inexorable. Most patients die of progressive respiratory failure within 3-8 years of the onset of symptoms. Current therapies are of unproven benefit. Although the pathogenesis of IPF has not been elucidated, early concepts focused on lung injury leading to a cycle of chronic alveolar inflammation eventuating in fibrosis and destruction of the lung architecture. Anti-inflammatory therapies employing corticosteroids or immunosuppressive or cytotoxic agents have been disappointing. More recent hypotheses acknowledge that sequential alveolar epithelial cell injury is likely to be a key event in the pathogenesis of IPF, but the cardinal event is an aberrant host response to wound healing. In this context, abnormal epithelial-mesenchymal interactions, altered fibroblast phenotypes, exaggerated fibroblast proliferation, and excessive deposition of collagen and extracellular matrix are pivotal to the fibrotic process. Several clinical trials are currently underway or in the planning stages, and include drugs such as interferon-gamma 1b, pirfenidone, acetylcysteine, etanercept (a tumor necrosis factor-alpha antagonist), bosentan (an endothelin-1 receptor antagonist) and zileuton (a 5-lypoxygenase inhibitor). Future therapeutic strategies should be focused on alveolar epithelial cells aimed at enhancing re-epithelialisation and on fibroblastic/myofibroblastic foci, which play an essential role in the development of IPF. Stem cell progenitors of the alveolar epithelial cells and genetic and epigenetic therapies are attractive future approaches for this and other fibrotic lung disorders.
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PMID:Idiopathic pulmonary fibrosis: pathogenesis and therapeutic approaches. 1496 75

A 47-year-old woman was admitted to our hospital because of dry cough, fever, and subacute, progressive dyspnea. Chest radiography and computed tomography showed ground glass opacities in the lower lung fields. We suspected pneumonia caused by atypical pathogens and administered antibiotics, but they had no effect at all. Histopathologic findings from a transbronchial lung biopsy (TBLB) included intensive infiltration of mononuclear cells and edema on the alveolar wall with no evidence of fibrosis, fibroblasts, hyaline membrane, or granuloma. On the basis of these findings, we suspected interstitial pneumonia, but a surgical lung biopsy was not possible because the patient would not give her consent. After TBLB, corticosteroid was administered repetitively, but dyspnea was deteriorating as the ground glass opacities became more widespread, and tractional bronchiectasis appeared throughout the lung fields. Therefore, we decided to administer cyclophosphamide (CPA). This was very effective: all of her symptoms improved and the ground glass opacities and tractional bronchiectasis disappeared. Though we tapered and then discontinued corticosteroids a few months after CPA, there was no recurrence whatever. No signs suggesting the association of collagen vascular diseases were detected. The effectiveness of CPA in interstitial pneumonia associated with collagen vascular disease is occasionally reported, but the effect on idiopathic interstitial pneumonia, especially in acute and subacute progressive cases, is rarely reported. We think this is an interesting case to consider the availability of CPA in idiopathic interstitial pneumonia with subacute progression.
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PMID:[A case of subacute idiopathic interstitial pneumonia resistant to steroids, successfully treated with cyclophosphamide]. 1565 Dec 74

An autopsy case of fibrotic non-specific interstitial pneumonia (NSIP) is herein reported. A 54-year-old woman was admitted to our hospital because of dry cough and fever that had continued for a month. Her chest radiograph showed diffuse reticular shadows in both lower lung fields. Analyses of bronchoalveolar lavage fluid (BALF) showed an increase in the percentage of lymphocytes and a decrease in CD4/CD8 ratio. Video-assisted thoracoscopic (VATS) lung biopsy revealed that she had fibrotic NSIP. She was treated with corticosteroid with a transient increase in vital capacity, but her condition gradually deteriorated, associated with a decrease in lymphocytes and an increase in CD4/CD8 ratio shown by repeated measurement of BALF. She died 6 years after the diagnosis. The autopsied lungs showed diffuse consolidated lesions predominantly in both lower lung fields, without honeycombing. Histologically, the lung parenchyma was diffusely involved with homogeneous fibrosis, compatible with fibrotic NSIP. However, mononuclear cell infiltration was less severe, and collagen deposition was more extensive than shown by the VATS specimen. There is a possibility that the CD4/CD8 ratio in BALF may reflect the severity of fibrosis in the lung parenchyma. Histological differences between autopsy and biopsy specimens in this case could help to elucidate the natural course of fibrotic NSIP.
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PMID:[An autopsy case of non-specific interstitial pneumonia]. 1605 Apr 63

Organising pneumonia (OP) is a rare syndrome that has been associated with a variety of underlying disorders, including infections, collagen vascular diseases, toxic fumes, cancer, drugs and radiotherapy. Cryptogenic form is also observed. Steroids are usually effective in the treatment of OP, but other treatment regimens have been used as well. We present 5 women with OP, age ranged 57-76 years (mean - 67 years). Two of them were smokers and three were non-smokers. One patient was treated because of hyperthyreosis, one of COPD, and four had a hypertension. Four of them were diagnosed by the open lung biopsy and one by transbronchial lung biopsy. Dyspnoea (100%), cough (100%), fever (80%), weight loss (40%), chest pain (20%), were the most frequently noticed symptoms. All patients had bilateral consolidations with areas of ground glass attenuations at chest x-ray and HRCT. Migratory pattern of them was observed in four patients. Significant elevation of antibodies titers against Chlamydia pneumoniae was revealed in two patients. In all patients clarithromycin in a dose 0.5 g b.d. was administrated. Complete clinical and radiological remission was obtained after 3 months of clarithromycin therapy in 3 patients (one had Chlamydia antibodies). Two patients had not obtained significant improvement during the first two weeks of therapy so prednisolone in a dose 0.5 mg/kg/d was introduced. Also complete remission was noticed in these patients. The observation period ranged from 8 months to 4 years (mean - 34 months). Our study confirms that OP can be treated by the use of clarithromycin. It may be the alternative treatment, particularly for patients in whom probability of adverse reactions in the course of steroid treatment is high.
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PMID:[Organizing pneumonia--own experiences with clarithromycin treatment]. 1632 49

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

CASE 1: A 64-year-old, otherwise healthy woman was referred to the surgery clinic for a presumed umbilical hernia. On physical examination, a cutaneous nodule was noted on the umbilical region and the patient was referred to the dermatology clinic. The patient was reexamined and an erythematous nodule was observed in the umbilicus measuring 2.5 cm in diameter. The patient denied pain, change in bowel habits, or weight loss. There were no other abdominal masses, no sign of ascites, and no regional lymphadenopathy. A skin biopsy from the nodule showed mucinous adenocarcinoma. Immunohistochemical staining was positive for carcinoembryonic antigen, and negative for cytokeratin (CK)7 and CK20. These results were consistent with a Sister Mary Joseph's nodule and led to the diagnosis of an occult colon carcinoma. The patient had no risk factors for colorectal carcinoma. The patient underwent surgery in another hospital, and died 3 months after the initial diagnosis of Sister Mary Joseph's nodule. CASE 2: A 73-year-old woman was referred to the dermatology clinic for evaluation of a painful, ulcerated, 3-cm lesion in the umbilicus (Figure 1). She was otherwise asymptomatic. A skin biopsy showed neoplastic glandular cells infiltrating among collagen bundles (Figure 2). Stainings for mucin and for CK7 were positive, while staining for CK20 was negative. An abdominopelvic CT scan demonstrated a 3.5-cm space-occupying lesion in the liver. Results of gastroscopy, colonoscopy, chest computed tomographic (CT) scan, and mammography were normal. Serum levels of the tumor-associated protein CA125 were elevated to 164 units, while those of CA 19-9 and carcinoembryonic antigen were within normal range. A gynecologic examination and a transvaginal ultrasound were normal. The patient had no personal or family history of any malignancy or any risk factors for developing a carcinoma. The patient was scheduled for a palliative resection of the umbilical nodule, combined with a laparoscopic inspection in search of the undetected primary tumor. She refused surgery and was lost to follow-up. She died 4 months after the initial diagnosis of umbilical metastasis. CASE 3: A 51-year-old man was aware of a silent mass in his umbilicus for 2 years without seeking medical advice. Following 2 weeks of increasing pain in this area, he was referred to the emergency room for a suspected incarcerated umbilical hernia. Surgery revealed a mass attached to the fascia and peritoneal fat. The mass was removed and diagnosed as a poorly differentiated adenocarcinoma, staining positively for carcinoembryonic antigen, and negatively for CK20, CK7, prostate-specific antigen, and prostatic acid phosphatase. Both gastroscopy and colonoscopy failed to detect the primary tumor. An abdominopelvic CT scan was normal, but a CT scan of the chest disclosed a nodule measuring 2.5 x 1.5 cm in the lower lobe of the right lung. On bronchoscopy, it was found to be an invasive adenocarcinoma, consistent with a primary tumor of the lung. The patient was a heavy smoker (45 pack-years). The patient received 4 cycles of combined chemotherapy with carboplatine and gemcitabine, with no improvement. A month later, the patient complained of abdominal pain. Following demonstration of intra-abdominal spread of disease by CT scan, a second line chemotherapy was instituted with paclitaxel. A month later the patient's condition deteriorated and he complained of cough, sweating, and pain along the right leg. A bone scan revealed bone metastases in the right femur and left tibia. Two weeks later he was admitted to the hospital with intestinal obstruction and underwent laparotomy. He had massive intra-abdominal spread of cancer and ascites. Only a palliative colostomy was performed. The patient died 3 weeks later, 9 months after the diagnosis of adenocarcinoma of the lung. The clinical data on the three patients are summarized in Table I.
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PMID:Sister Mary Joseph's nodule as a presenting sign of internal malignancy. 1695 43

Changes in structural support of the urethra and bladder neck have been proposed as important factors in the pathogenesis of stress urinary incontinence (SUI). In this context, we undertook an ultrastructural study on the periurethral connective tissue with an emphasis on incontinent women with normotonic and hypotonic urethras. Small specimens of periurethral connective tissue were obtained by dissection during a tension-free vaginal tape-implantation procedure in 34 stress urinary incontinent postmenopausal women with a normotonic urethra and 9 stress urinary incontinent postmenopausal women with a hypotonic urethra. In the samples taken from stress-incontinent women with a normotonic urethra, intact elastic fibers were closely connected with collagen fibers, smooth muscle cells and fibrocytes. In the samples taken from stress-incontinent women with a hypotonic urethra, we detected irregular fragmented distribution of the elastin within the tissue. We assume that these structural changes lead to functional consequences, such as diminished tissue extensibility and loss of stability surrounding the female urethra. These altered connective tissue properties may affect the mechanism of urethral closure under stress (e.g., coughing) and therefore contribute to the occurrence of SUI with a hypotonic urethra.
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PMID:Changes in the extracellular matrix in periurethral tissue of women with stress urinary incontinence. 1696 46


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