1/11. Inhaled corticosteroids and churg-strauss syndrome: a report of five cases.churg-strauss syndrome is an eosinophil-associated, small vessel granulomatous vasculitis, characterized by late onset asthma, upper airways disease, eosinophilia, and clinical manifestations of systemic vasculitis. Several cases of churg-strauss syndrome have been recognized in patients treated with cysteinyl leukotriene-receptor antagonists and weaned off systemic corticosteroids. These cases have led to a general warning on the possible development of Churg-Strauss syndrome after taking cysteinyl leukotriene-receptor antagonists. The authors report five cases of churg-strauss syndrome in severe steroid dependent asthmatics in whom inhaled corticosteroids allowed systemic corticosteroid withdrawal. It is concluded that physicians should monitor patients carefully when severe asthma is controlled with any substance allowing withdrawal from (or even avoidance) of systemic corticosteroids. case-control studies should identify more precisely the risk factors of churg-strauss syndrome.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
2/11. Asthma therapies and churg-strauss syndrome.The pulmonary vasculitides are a group of rare but serious disorders that require early recognition, accurate diagnosis, and effective therapy. churg-strauss syndrome (CSS) is classified as small vessel vasculitis. Four different definitions for the diagnosis of CSS have been developed: (1) the pathologic criteria put forth by Churg and Strauss, (2) the criteria based on clinical grounds from Lanham and colleagues, (3) the criteria based on clinical grounds from the American College of rheumatology, and (4) the criteria from the Chapel Hill consensus Conference, which closely concur with the Churg and Strauss definition. It is apparent that cessation, diminution, or even a switch from low-dose systemic to inhaled corticosteroid therapy can precipitate the appearance of CSS. The term forme fruste has been used to indicate that the signs and symptoms of CSS were (inadvertently) suppressed by cortico-steroids. The clinical risk factors for CSS are moderately severe or severe asthma, chronic sinusitis, or reductions in systemic corticosteroid therapy. Differential diagnosis, treatment, and ongoing monitoring of CSS therapeutic responses are reviewed. The introduction of leukotriene modifiers and high-potency inhaled corticosteroids have allowed control of asthma symptoms, which results in avoidance or reduction in oral corticosteroid use. The advent of these agents has been associated with reports of CSS appearing in patients with asthma. The available data regarding the association of CSS and antiasthma agents are most consistent with the unmasking of a previously contained pathologic condition (forme-fruste CSS) or disease that progresses because systemic corticosteroids were avoided. Early recognition and immunosuppressive therapy are the keystones of successful treatment of this rare disorder.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
3/11. churg-strauss syndrome associated with the leukotriene antagonist montelukast.churg-strauss syndrome (CSS) is a disseminated small vessel vasculitis characterized by late-onset asthma, upper airways disease, eosinophilia and late neurological manifestations such as peripheral neuropathy. Recently, several cases of CSS have been reported in patients treated with leukotriene antagonists after weaning corticosteroids. We describe a case of CSS developed while the patient was receiving montelukast for asthma treatment, after corticosteroids withdrawal. A causal relationship between montelukast therapy and CSS is hypothesized.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
4/11. A right-sided aortic arch misdiagnosed as asthma since childhood.Congenital malformation of the aortic arch complex occurs in 3% of humans. These vascular aberrations result from embryonic structures that persist when there is incomplete atrophy or regression during normal development. Typically, anomalies of the aortic arch do not cause respiratory symptoms. However, in some individuals, the unusual position of the remnant vessels may compress the airway and cause airflow limitation. As might be expected, a symptomatic vascular anomaly is most often clinically apparent in childhood. We report an adult male with exertional dyspnea who had been diagnosed with asthma since childhood. After his symptoms proved refractory to newer asthmatic therapy, he was referred for further evaluation. Bronchial hyperactivity was not present with objective testing, and compression of his trachea by a right-sided aortic arch was confirmed with appropriate imaging studies. This report illustrates the need to confirm the diagnosis of asthma with objective measures of airflow and reminds the clinician that a congenital vascular aberrancy may initially elude diagnosis.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
5/11. angiolymphoid hyperplasia with eosinophilia (epithelioid hemangioma) of the lung: a clinicopathologic and immunohistochemical study of two cases.Two cases of primary angiolymphoid hyperplasia with eosinophilia (epithelioid hemangioma) (ALHE/EH) of the lung are described. Both patients are white, a 60-year-old man and a 27-year-old woman. One patient had a long-standing history of asthma, and the other had symptomatology related to the pulmonary mass. Wedge resections were performed in both cases, and both lesions shared similar histopathologic changes, mainly the presence of a tumor mass with a marked presence of eosinophils in the background, lymphoid hyperplasia, and marked proliferations of small-caliber vessels. Immunohistochemical studies using leukocyte common antigen, L-26, and UCHL-1 nicely stained the lymphoid component of the lesion, and CD31 clearly outlined the vascular component of the process. Clinical follow-up demonstrated that the woman died of status asthmaticus, and the man was alive and well 1 year after surgical resection of the lesion. Both cases highlight the ubiquitous distribution of ALHE/EH and underscore the importance of keeping these lesions in the differential diagnosis of vascular and lymphoid lesions of the lung.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
6/11. Endoscopic observation of peripheral airway lesions.Peripheral airways of 2 mm or less in diameter were observed in 142 patients by means of an ultrathin bronchofiberscope measuring 1.8 mm in outside diameter. On the basis of the observed and photographed endoscopic findings, an endoscopic classification of peripheral airway lesions was proposed. The endoscopic findings showed changes in the bronchial wall consisting of reddening, pallor, absence of mucosal luster, edema, engorgement of blood vessels, irregular mucosal surface, and elevated mucosa. In the lumen, stenosis, obstruction, ectasis, and deformation due to pressure were recognized, in addition to excessive secretion and pigmentation as morphologic abnormalities or abnormal findings at bifurcation.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
7/11. serum sickness triggered by anaphylaxis: a complication of immunotherapy.An 8-year-old boy developed anaphylaxis after receiving his maintenance dose of immunotherapy and proceeded to display the signs and symptoms of serum sickness. These consisted of fever, arthralgia, arthritis, urticaria followed by a hemorrhagic palpable rash, edema, lymphadenopathy, splenomegaly, abdominal pain, proteinuria, and neurologic manifestations consistent with vascular compromise of the posterior cerebral circulation. A skin biopsy specimen revealed perivascular infiltrates of lymphocytes and few polymorphonuclear neutrophils. The timing of events in this patient suggests that immunotherapy initiated a chain of events beginning with anaphylaxis and leading to serum sickness. It is hypothesized that the enhanced vascular permeability that accompanied the anaphylaxis allowed immune complexes that may have preexisted in the circulation to deposit in the blood vessels of the patient. These complexes may or may not have been related to the immunotherapy itself. Because antihistamines are known to prevent the induction of serum sickness, early and aggressive treatment of anaphylaxis during immunotherapy may prevent the occurrence of immune complex disease.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
8/11. Cutaneous clinicopathologic correlation of allergic granulomatosis.Allergic granulomatosis is a distinct clinical syndrome occurring in adults with asthma, eosinophilia, and multisystem vasculitis. Atopy and drug sensitivity are other important features. The skin reactions are most commonly nodular and inflammatory lesions. A unique feature is the deep papulonodules, which may occur singly on the scalp or symmetrically on the extremities. Cutaneous findings may range from purpura to urticaria and ulceration. The most common histologic finding is the extravascular granuloma; however, necrotizing vasculitis of small vessels is seen, as well as periarteritis nodosa involving larger vessels of the skin. This varied histologic and clinical spectrum seen in patients with systemic allergic granulomatosis is a reflection of a unique host response to multiple antigens. The cutaneous findings imply that allergic granulomatosis probably represents a unique host response to the same causative and pathogenetic factors as are usually found in periarteritis nodosa and necrotizing vasculitis.- - - - - - - - - - ranking = 2keywords = vessel (Clic here for more details about this article) |
9/11. Inflammatory bronchial polyps associated with asthma.We report a case of inflammatory bronchial polyps associated with asthma in a 10-year-old boy. He expelled about 50 polyps varying in size from 0.4 to 1.8 cm without difficulty. Microscopically, the polyps were lined by columnar epithelium supported by stroma consisting of a loose connective tissue with many capillary vessels and a chronic inflammatory infiltration composed mainly of lymphocytes, plasma cells, and eosinophils. The blood and urine laboratory data were normal except for blood eosinophilia of 3% to 10%, and a chest roentgenogram that showed a left perihilar small nodular lesion and a small irregular area in the right upper lobe. Test results of pulmonary function and blood gases were normal. The association of bronchial inflammatory polyps with asthma and the clinical manifestation in this patient is very uncommon.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
10/11. IgA2-alveolitis and eosinophilic pneumonia--a possibly virus-triggered allergy.A case of severe therapy-resistant asthma in a young girl with a duration of two years prior to death is reported. At autopsy antibodies of the IgA2-subtype were demonstrated in the lungs on the alveolar basement membranes. We were able to demonstrate intracellular virus-like structures by electron microscopy; this virus infection is taken to be the cause of antibody production. Following antigen-antibody reaction a non-complement-mediated eosinophilic pneumonia with numerous macrophages developed. This inflammatory reaction showed the injurious effect of eosinophilic granulocytes causing fibrinoid necrosis; this is confirmed by the pronounced depletion of the Charcot-Leyden-granules, equivalent to the release of the major basic protein and the Charcot-Leyden crystal protein. death was caused by IgA2 deposition in the myocardial vessels with consequent eosinophilic myocarditis.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
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