Cases reported "Hypertension, Pulmonary"

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1/31. Diffuse alveolar hemorrhage syndrome due to 'silent' mitral valve regurgitation.

    A variety of clinical diseases are associated with diffuse alveolar hemorrhage. Although mitral valve disease can cause hemoptysis, it rarely is associated with diffuse alveolar hemorrhage at presentation. A 49-year-old woman was admitted to the hospital with the abrupt onset of fever, anemia, dyspnea, azotemia, and diffuse alveolar infiltrates. Two-dimensional echocardiography done several months earlier to evaluate atypical chest pain had been unremarkable. Fiberoptic bronchoscopy 2 days after admission to the hospital revealed fresh blood throughout the tracheobronchial tree. The infiltrates resolved rapidly and completely during systemic steroid therapy only to reappear as the steroids were tapered, suggesting a beneficial therapeutic response. Results of serologic evaluation were negative. Transbronchial biopsies showed inflammation and hemosiderin-laden macrophages; no specific diagnosis was established. The patient was scheduled for open lung biopsy. The surgeon was concerned about the history of chest pain and requested placement of a pulmonary artery catheter, which revealed severe pulmonary hypertension. Transesophageal echocardiography and subsequent cardiac catheterization showed severe mitral regurgitation. mitral valve replacement resulted in complete elimination of symptoms.
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2/31. Pulmonary hypertension associated with pulmonary occlusive vasculopathy after allogeneic bone marrow transplantation.

    BACKGROUND: Pulmonary vasculature abnormalities, including pulmonary veno-occlusive disease, have been demonstrated in marrow allograft recipients. However, it is often difficult to make a correct diagnosis of pulmonary lesions. methods: An open lung biopsy was performed on a patient who developed severe pulmonary hypertension after bone marrow transplantation for T-cell lymphoma. RESULTS: An open lung biopsy specimen demonstrated pulmonary arterial occlusion due to intimal fibrosis and veno-occlusion. The most striking alteration was partial to complete occlusion of the small arteries by fibrous proliferation of the intima. CONCLUSION: High-dose preparative chemotherapy and radiation before transplantation are thought to have contributed to the development of vasculopathy in this patient, because arterial occlusion by intimal fibrosis and atypical veno-occlusion are often associated with lung injury due to chemoradiation. An open lung biopsy is essential for diagnosing pulmonary vascular disease presenting signs compatible with posttransplantation pulmonary hypertension.
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3/31. Detection of chlamydia pneumoniae in unexplained pulmonary hypertension.

    The pathogenesis of primary pulmonary hypertension is still unclear. The case of a 68-yr-old female patient who complained of recurrent dizzy spells and collapses over a period of 6 weeks and died of global cardiac failure is presented. autopsy revealed severe pulmonary hypertension, slight chronic bronchitis, and bronchiolitis as well as intra-alveolar accumulation of macrophages. Chlamydiae were detected within the pulmonary arteries and in intramural and intra-alveolar macrophages by immunofluorescence, confocal laser scanning microscopy, scanning and transmission electron microscopy. Nested-polymerase chain reaction (PCR) and nonradioactive deoxyribonucleic acid (dna) hybridization of PCR products from pulmonary arteries revealed chlamydia pneumoniae dna. chlamydia pneumoniae has already been detected in atherosclerosis and in pulmonary emphysema. It can induce proliferation of smooth muscle cells. chlamydia pneumoniae might be relevant in aggravation of primary pulmonary hypertension and might perhaps be a trigger factor in some cases.
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4/31. Idiopathic severe pulmonary hypertension in an infant with pulmonary infection.

    We report a 5-month-old infant who showed typical echocardiographic findings of primary pulmonary hypertension without the typical histopathological findings and who recovered from severe pulmonary hypertension. Histopathological findings revealed mild thickening of small pulmonary arteries and activated macrophages in the lung. Some cases with idiopathic severe pulmonary hypertension in infants are associated with pulmonary infection.
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5/31. Pulmonary arterial occlusive disease following chemotherapy and bone marrow transplantation for leukaemia.

    Cancer treatment is not known to cause obstructive lesions in the pulmonary artery. We report the case of an 8-year-old girl in whom apparent primary pulmonary hypertension developed shortly after chemotherapy and bone marrow transplantation for myelomonocytic leukaemia (LAME 91 protocol). Cardiac catheterisation showed, at baseline, severe precapillary pulmonary hypertension (mean pulmonary arterial pressure 49 mm Hg) with an increase in pulmonary vascular resistance (23.3 U/m(2)). Prostacyclin infusion demonstrated a 49% reduction and diltiazem infusion a 30% reduction in pulmonary vascular resistance without significant modification of systemic vascular resistance or cardiac output. Significant improvement in functional status was obtained with oral diltiazem. Follow-up cardiac catheterisation 3 months later showed a maintained haemodynamic improvement. CONCLUSION: pulmonary arterial occlusive disease should be added to the list of complications likely to occur after cancer chemotherapy. In addition, our report demonstrates that the pulmonary vasodilator response of vasodilating agents should be tested in such patients.
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6/31. Pulmonary capillary hemangiomatosis associated with primary pulmonary hypertension: report of 2 new cases and review of 35 cases from the literature.

    Pulmonary capillary hemangiomatosis (PCH) is a rare cause of primary pulmonary hypertension characterized by thin-walled microvessels infiltrating the peribronchial and perivascular interstitium, the lung parenchyma, and the pleura. These proliferating microvessels are prone to bleeding, resulting in accumulation of hemosiderin-laden macrophages in alveolar spaces. Here we report 2 cases of PCH with pulmonary hypertension, 1 of them associated with mechanical intravascular hemolysis, a feature previously reported in other hemangiomatous diseases, but not in PCH. Case 2 was diagnosed by pulmonary biopsy; to our knowledge the patient is the second adult to be treated with interferon alpha-2a. review of the literature identified 35 patients with PCH and pulmonary hypertension. The prognosis is poor and median survival was 3 years from the first clinical manifestation. dyspnea and right heart failure are the most common findings of the disease. hemoptysis, pleural effusion, acropachy, and signs of pulmonary capillary hypertension are less common. Chest X-ray or computed tomography scan usually shows evidence of interstitial infiltrates, pulmonary nodules, or pleural effusion. Hemodynamic features include normal wedge pressures. Radiologic and hemodynamic findings are undifferentiated from those of pulmonary veno-occlusive disease but differ from other causes of primary pulmonary hypertension. epoprostenol therapy, considered the treatment of choice in patients with primary pulmonary hypertension, may produce pulmonary edema and is contraindicated in patients with PCH. Regression of lesions was reported in 1 patient treated with interferon therapy and 2 other patients stabilized, including our second patient. PCH was treated successfully by lung transplantation in 5 cases. Early recognition of PCH in patients with suspected primary pulmonary hypertension is possible based on clinical and radiologic characteristics. diagnosis by pulmonary biopsy is essential for allowing appropriate treatment.
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7/31. pulmonary veno-occlusive disease caused by an inherited mutation in bone morphogenetic protein receptor II.

    pulmonary veno-occlusive disease (PVOD) is a rare form of pulmonary hypertension in which the vascular changes originate in the small pulmonary veins and venules. The pathogenesis is unknown and any link with primary pulmonary hypertension (PPH) has been speculative. Mutations in the bone morphogenetic protein receptor II (BMPR2) gene have been identified in at least 50% of familial cases and in 25% of sporadic cases of PPH. We report a patient with documented PVOD whose mother had severe pulmonary hypertension. Sequencing of the patient's BMPR2 coding region revealed a del44C mutation in Exon 1 that is predicted to encode for a truncated protein. Analysis of dna from family members suggests that this mutation was transmitted by the proband's mother to two of her four children. The finding of PVOD associated with a BMPR2 mutation reveals a possible pathogenetic connection with PPH.
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8/31. herpes simplex type 2 pneumonia.

    Extensive reviews of pulmonary infections in AIDS have reported few herpetic infections. Generally these infections are due to herpes simplex type 1. pneumonia due to herpes type 2 is extremely rare. We describe a 40 year-old hiv positive woman who complained of fever, cough and dyspnea for seven years. She had signs of heart failure and the appearance of her genital vesicles was highly suggestive of genital herpes. echocardiography showed marked pulmonary hypertension, right ventricular hypertrophy and tricuspid insufficiency. After a few days of hospitalization she was treated with Aciclovir and later with ganciclovir. An open pulmonary biopsy revealed an interstitial inflammation, localized in the alveolar walls. Some pulmonary arteries had widened walls and focal hyaline degeneration. immunohistochemistry indicated that the nuclei had herpes simplex virus type 2 in many endothelial cells (including vessels with widened walls), macrophages in the alveolar septa and pneumocytes. There was clinical improvement after treatment for herpes. We concluded that as a consequence of herpes infection, endothelial involvement and interstitial inflammation supervene, with thickening of vascular walls and partial obliteration of the vessel lumen. A direct consequence of these changes in pulmonary vasculature was pulmonary hypertension followed by heart failure.
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9/31. cardiovascular abnormalities associated with the Stuve-Wiedemann syndrome.

    The Stuve-Wiedemann syndrome (SWS) is a congenital bone dysplasia characterized by camptodactyly with ulnar deviation and congenital bowing of the long bones. Affected patients present with respiratory difficulties in the neonatal period or later and recurrent episodes of hyperthermia. The typical radiological findings are bowing of the long bones of the lower limbs, wide metaphyses with decreased density, and abnormal trabecular pattern. Generally, respiratory insufficiency and hyperthermia are reported to be the cause of death. We report on two sibs with SWS, who died from severe pulmonary hypertension with pulmonary artery wall abnormality. We suggest a common pathophysiological process, which could explain the cardiovascular findings that we observed immediately after birth in the two affected sibs. We hypothesize that the severe pulmonary hypertension due to the arterial wall abnormality could explain the neonatal death of these two children.
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10/31. Primary pulmonary hypertension after amfepramone (diethylpropion) with BMPR2 mutation.

    Primary pulmonary hypertension (PPH) is characterised by sustained elevations of pulmonary arterial pressure without a demonstrable cause, leading to right ventricular failure and death. Hereditary mutations in the bone morphogenetic protein receptor type II (BMPR2) gene result in familial PPH transmitted as an autosomal dominant trait, albeit with low penetrance. The causes in cases without a BMPR2 mutation are unknown, but a syndrome of pulmonary arterial hypertension (PAH) similar to hereditary PPH is associated with systemic connective tissue disease, congenital heart disease, portal hypertension, and human immunodeficiency virus infection, or with the use of appetite-suppressant drugs. The authors identified a BMPR2 gene mutation in a 27-yr-old female who developed PAH after a short course of the appetite-suppressant drug amfepramone (diethylpropion). This allowed molecular genetic counselling and prevention of potentially harmful drug exposure in the patient's son treated for attention deficit disorder with methylphenidate, an amphetamine-related drug. No BMPR2 mutation was found in four additional, unrelated patients with appetite suppressant-related PPH. The findings provide strong evidence that amfepramone can trigger primary pulmonary hypertension in a bone morphogenetic protein receptor type II gene mutation carrier, and indicate that other genes are probably implicated in genetic susceptibility to appetite suppressants.
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