Pov D
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What does POVD mean as an abbreviation? 2 popular meanings of POVD abbreviation:
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Learn more about the genes associated with Pulmonary veno-occlusive disease
Isolated pulmonary venous sclerosis Obstructive disease of the pulmonary veins Pulmonary venoocclusive disease PVOD Venous form of primary pulmonary hypertension
Genetic and Rare Diseases Information Center
Pulmonary venoocclusive disease
Patient Support and Advocacy Resources
Disease InfoSearch
National Organization for Rare Disorders (NORD)
Research Studies from ClinicalTrials.gov
ClinicalTrials.gov
Scientific Articles on PubMed
PubMed
Eyries M, Montani D, Girerd B, Perret C, Leroy A, Lonjou C, Chelghoum N,
Coulet F, Bonnet D, Dorfmüller P, Fadel E, Sitbon O, Simonneau G, Tregouët DA,
Humbert M, Soubrier F. EIF2AK4 mutations cause pulmonary veno-occlusive disease,
a recessive form of pulmonary hypertension. Nat Genet. 2014 Jan;46(1):65-9. doi:
10.1038/ng.2844. Epub 2013 Dec 1. Citation on PubMed
Mandel J, Mark EJ, Hales CA. Pulmonary veno-occlusive disease. Am J Respir
Crit Care Med. 2000 Nov;162(5):1964-73. Review. Citation on PubMed
Montani D, Achouh L, Dorfmüller P, Le Pavec J, Sztrymf B, Tchérakian C,
Rabiller A, Haque R, Sitbon O, Jaïs X, Dartevelle P, Maître S, Capron F, Musset
D, Simonneau G, Humbert M. Pulmonary veno-occlusive disease: clinical,
functional, radiologic, and hemodynamic characteristics and outcome of 24 cases
confirmed by histology. Medicine (Baltimore). 2008 Jul;87(4):220-233. doi:
10.1097/MD.0b013e31818193bb. Citation on PubMed
Runo JR, Vnencak-Jones CL, Prince M, Loyd JE, Wheeler L, Robbins IM, Lane KB,
Newman JH, Johnson J, Nichols WC, Phillips JA 3rd. Pulmonary veno-occlusive
disease caused by an inherited mutation in bone morphogenetic protein receptor
II. Am J Respir Crit Care Med. 2003 Mar 15;167(6):889-94. Epub 2002 Nov 21.
Citation on PubMed
Genetic Disorders
Pulmonary Hypertension
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National Library of Medicine
8600 Rockville Pike, Bethesda, MD 20894
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National Institutes of Health
Pulmonary veno-occlusive disease (PVOD) is characterized by the blockage (occlusion) of the blood vessels that carry oxygen-rich (oxygenated) blood from the lungs to the heart (the pulmonary veins). The occlusion is caused by a buildup of abnormal fibrous tissue in the small veins in the lungs , which narrows the vessels and impairs blood flow. Because blood flow through the lungs is difficult, pressure rises in the vessels that carry blood that needs to be oxygenated to the lungs from the heart ( the pulmonary arteries ). Increased pressure in these vessels is known as pulmonary arterial hypertension .
The problems with blood flow in PVOD also impair the delivery of oxygenated blood to the rest of the body, which leads to the signs and symptoms of the condition. Shortness of breath (dyspnea) and tiredness (fatigue) during exertion are the most common symptoms of this condition. Other common features include dizziness, a lack of energy (lethargy), difficulty breathing when lying down, and a cough that does not go away. As the condition worsens, affected individuals can develop a bluish tint to the skin (cyanosis), chest pains, fainting spells, and an accumulation of fluid in the lungs ( pulmonary edema ).
Certain features commonly seen in people with PVOD can be identified using a test called a CT scan. One of these features, which is seen in the lungs of affected individuals, is an abnormality described as centrilobular ground-glass opacities. Affected individuals also have abnormal thickening of certain tissues in the lungs, which is described as septal lines. In addition, lymph nodes in the chest (mediastinal lymph nodes) are abnormally enlarged in people with PVOD.
PVOD can begin at any age, and the blood flow problems worsen over time. Because of the increased blood pressure in the pulmonary arteries, the heart must work harder than normal to pump blood to the lungs, which can eventually lead to fatal heart failure. Most people with this severe disorder do not live more than 2 years after diagnosis.
The exact prevalence of PVOD is unknown. Many cases are likely misdiagnosed as idiopathic pulmonary arterial hypertension, which is increased blood pressure in the pulmonary arteries without a known cause. Research suggests that 5 to 25 percent of people diagnosed with idiopathic pulmonary arterial hypertension have PVOD. Based on these numbers, PVOD is thought to affect an estimated 1 to 2 per 10 million people.
The primary genetic cause of PVOD is mutations in the EIF2AK4 gene. Mutations in other genes may cause a small percentage of cases. Other suspected causes of PVOD include viral infection and exposure to toxic chemicals, including certain chemotherapy drugs.
The protein produced from the EIF2AK4 gene helps cells respond appropriately to changes that could damage the cell. For example, when the level of protein building blocks ( amino acids ) in a cell falls too low, the activity of the EIF2AK4 protein helps reduce the production of other proteins, which conserves amino acids. The EIF2AK4 gene mutations involved in PVOD likely eliminate functional EIF2AK4 protein; however, it is unknown how absence of this protein's function leads to the pulmonary vessel abnormalities that underlie PVOD.
When caused by mutations in the EIF2AK4 gene, PVOD is inherited in an a utosomal recessive pattern , which means both copies of the gene in each cell have mutations. The parents of an individual with an autosomal recessive condition each carry one copy of the mutated gene, but they typically do not show signs and symptoms of the condition.
In contrast, when caused by mutations in another gene, the condition can have an autosomal dominant pattern of inheritance, which means one copy of the altered gene in each cell is sufficient to cause the disorder. In these cases, one parent of an affected individual typically has increased blood pressure in the vessels of the lungs.
The information on this site should not be used as a substitute for professional medical care or advice. Contact a health care provider if you have questions about your health.
Anatomy of the respiratory system, showing the trachea and both lungs and their lobes and airways. Lymph nodes and the diaphragm are also shown. Oxygen is inhaled into the lungs and passes through the thin membranes of the alveoli and into the bloodstream (see inset).
Credit: Alila Medical Media/Shutterstock.com
Amino acids are a set of 20 different molecules used to build proteins. Proteins consist of one or more chains of amino acids called polypeptides. The sequence of the amino acid chain causes the polypeptide to fold into a shape that is biologically active. The amino acid sequences of proteins are encoded in the genes.
Credit: U.S. National Library of Medicine
Credit: U.S. National Library of Medicine
From Wikipedia, the free encyclopedia
Shortness of breath
Fatigue
Fainting
Hemoptysis
Difficulty breathing ( lying flat)
Chest pain
Cyanosis
Hepatosplenic congestion
Pulmonary veno-occlusive disease ( PVOD ) is a rare form of pulmonary hypertension caused by progressive blockage of the small veins in the lungs. [2] The blockage leads to high blood pressures in the arteries of the lungs, which, in turn, leads to heart failure . The disease is progressive and fatal, with median survival of about 2 years from the time of diagnosis to death. [3] The definitive therapy is lung transplantation . [4]
The symptoms for pulmonary veno-occlusive disease are the following: [2] [5]
The genetic cause of pulmonary veno-occlusive disease is mutations in EIF2AK4 gene. Though this does not mean other possible causes do not exist, such as viral infection and risk of toxic chemicals ( chemotherapy drugs). [6]
Pulmonary veno-occlusive disease may have a genetic basis. Published reports have indicated fatal occurrences that appeared to possess a familial pattern, more to the point, a germline mutation. [7] The pathophysiology of veno-occlusive disease culminates in occlusion of the pulmonary blood vessels . This could be due to edematous tissue (sclerotic fibrous tissue). Thickening is identified in lobular septal veins, also dilatation of lymphatics happens. Furthermore, alveolar capillaries become dilated (due to back-pressure). [8]
Pulmonary veno-occlusive disease can only be well diagnosed with a lung biopsy. CT scans may show characteristic findings such as ground-glass opacities in centrilobular distribution, and mediastinal lymphadenopathy , but these findings are non-specific and may be seen in other conditions. However, pulmonary hypertension (revealed via physical examination), in the presence of pleural effusion (done via CT scan) usually indicates a diagnosis of pulmonary veno-occlusive disease. The prognosis indicates usually a 2-year (24 month) life expectancy after diagnosis. [9] [10]
Treatments for primary pulmonary hypertension such as prostacyclins and endothelin receptor antagonists can be fatal in people with PVOD due to the development of severe pulmonary edema , and worsening symptoms after initiation of these medications may be a clue to the diagnosis of pulmonary veno-occlusive disease. [7]
The definitive therapy is lung transplantation , though transplant rejection is always a possibility, in this measures must be taken in terms of appropriate treatment and medication. [11] [12]
Pulmonary venoocclusive disease is rare, difficult to diagnose, and probably frequently misdiagnosed as idiopathic pulmonary arterial hypertension. Prevalence in parts of Europe is estimated to be 0.1-0.2 cases per million. [13]
PVOD appears to occur as frequently in men as in women, and age at diagnosis ranges from 7–74 years with a median of 39 years. [13] PVOD may occur in patients with associated diseases such as HIV , bone marrow transplantation , and connective tissue diseases . [13] PVOD has also been associated with several chemotherapy regimens such as bleomycin , BCNU , and mitomycin . [13]
Obstructive disease of the pulmonary veins [1]
Pulmonary veno-occlusive disease-Intimal fibrosis with marked narrowing of lumen of a large pulmonary vein
Narrow pulmonary vein, Pulmonary artery hypertension [2]
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