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)

The rationale behind combination therapy relates to the fact that when two different classes of agents are combined, they may provide complementary, additive, or synergistic antihypertensive effects through different mechanisms. Lower doses of two drugs, which provide blood pressure reduction similar to higher doses of one drug, may enhance tolerability and improve compliance. Investigative efforts have been undertaken to explore fixed-dose combinations of drugs that do not include diuretics. The first nondiuretic fixed-dose combinations are an angiotensin-converting enzyme (ACE) inhibitor-calcium antagonist combination or a beta-blocker-calcium antagonist combination. The rationale for an ACE inhibitor-calcium antagonist combination is based on the fact that both drugs reduce vasoconstriction through different mechanisms. The ACE inhibitor largely attenuates vasoconstriction through augmentation of vasodilatory kinins and reduction of the vasoconstrictive effect of angiotensin II, whereas the calcium antagonists, through attenuating the transmembrane flux of calcium, inhibit calcium-mediated electromechanical coupling in contractile tissue in response to numerous stimuli. Moreover, both classes of drugs facilitate salt and water excretion by the kidney through different mechanisms. The ACE inhibitor restores the renal-adrenal response to salt loading, whereas the calcium antagonist possesses intrinsic natriuretic properties through poorly described mechanisms of inhibiting renal tubular salt and water reabsorption. The combination of a beta-blocker and dihydropyridine calcium antagonist is logical due to the different antihypertensive mechanisms of these drugs without risk of cardiac conduction abnormalities. There is evidence in clinical trials that ACE inhibitors may offset one of the major side effects associated with calcium antagonist therapy: pedal edema. Although the studies are small and the observations subjective, there is consistent evidence that the combination may provide an opportunity to reduce the likelihood of this common clinical problem. There is also evidence of reduced calcium antagonist-associated constipation and headache with this type of drug combination, likely because lower doses of this agent are used in combination with ACE inhibitors. However, there is no published evidence that calcium antagonists reduce the cough associated with the ACE inhibitor.
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PMID:The rationale for combination versus single-entity therapy in hypertension. 979 51

A case of human ehrlichiosis (caused by infection with Ehrlichia chaffeensis) is presented. The patient was a female Naval Academy midshipman with a 26-day history of daily field training with the U.S. Marines near Quantico, Virginia. She presented with a several-day history of myalgias, fever, and frontal headache. During her clinical course, she developed fever to 104 degrees F, dry cough, dyspnea on exertion, arthralgias, and nephrotic syndrome. She did not develop a rash. Laboratory studies were significant for thrombocytopenia, equivocal Lyme enzyme immunosorbent assay with a negative confirmatory western immunoblot, equivocal Rocky Mountain spotted fever acute serology without a convalescent increase in immunoglobulin G, and immunoglobulin G/immunoglobulin M serology positive for human monocytic ehrlichiosis. She manifested known sequelae for this emerging disease, including dyspnea, pedal edema, increased transminases, and nephrotic syndrome.
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PMID:A Naval Academy midshipman with ehrlichiosis after summer field exercises in Quantico, Virginia. 1127 20

With the availability of better treatment and prophylactic regimens for the infectious complications of human immunodeficiency virus (HIV), the non-infectious complications are gaining greater attention. HIV-related pulmonary arterial hypertension (HIV-PAH) is one of these. The incidence of HIV-PAH is estimated at 0.5% of HIV-infected individuals. The pathogenesis remains unclear. Patients present with symptoms as diverse as progressive shortness of breath, pedal edema, dry cough, fatigue, syncope, as well as chest pain. Chest X-ray always shows cardiomegaly and prominent pulmonary artery, and evidence of right ventricular hypertrophy can be seen from the electrocardiogram. The pulmonary arterial systolic pressure, diastolic pressure and pulmonary vascular resistance from right heart catheterization are increased. There are a few small studies showing the benefit of prostacyclin analog (epoprostenol and iloprost) and bosentan. The role of antiretrovirals remains controversial, as do those of other agents such as calcium channel blockers and anticoagulants. The prognosis of HIV-PAH is grave. Two thirds of HIV-PAH related mortality is usually secondary to consequences of pulmonary hypertension, with the worst survival noted in New York Heart Association (NYHA) functional class III-IV. The probability of survival in one series was 73%, 60% and 47% at one, two and three years, respectively.
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PMID:HIV-related pulmonary hypertension. 1719 95

Cancer survivors who have received cardiotoxic chemotherapy or mediastinal radiation have an increased risk of developing cardiovascular late effects. Cardiac functioning should be evaluated during follow-up exams based on the patient's risk factors, cardiac symptoms, and type of cancer treatment received. Signs and symptoms indicative of cardiovascular late effects include dyspnea, fatigue, tachycardia, nonproductive cough, neck vein distention, coarse breath sounds, and pedal edema.
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PMID:Cardiovascular late effects. 1843

Pulmonary hypertension is defined by a mean pulmonary artery pressure greater than 25 mm Hg. Chronic thromboembolic pulmonary hypertension (CTEPH) is defined as pulmonary hypertension in the presence of an organized thrombus within the pulmonary vascular bed that persists at least 3 months after the onset of anticoagulant therapy. Because CTEPH is potentially curable by surgical endarterectomy, correct identification of patients with this form of pulmonary hypertension and an accurate assessment of surgical candidacy are essential to provide optimal care. Patients most commonly present with symptoms of exertional dyspnea and otherwise unexplained decline in exercise capacity. Atypical chest pain, a nonproductive cough, and episodic hemoptysis are observed less frequently. With more advanced disease, patients often develop symptoms suggestive of right ventricular compromise. Physical examination findings are minimal early in the course of this disease, but as pulmonary hypertension progresses, may include nonspecific finding of right ventricular failure, such as a tricuspid regurgitation murmur, pedal edema, and jugular venous distention. Chest radiographs may suggest pulmonary hypertension, but are neither sensitive nor specific for the diagnosis. Radioisotopic ventilation-perfusion scanning is sensitive for detecting CTEPH, making it a valuable screening study. Conventional catheter-based pulmonary angiography retains an important role in establishing the presence and extent of chronic thromboembolic disease. However, computed tomographic and magnetic resonance imaging are playing a growing diagnostic role. Innovative technologies such as dual-energy computed tomography, dynamic contrast-enhanced magnetic resonance imaging, and optical coherence tomography show promise for contributing diagnostic information and assisting in the preoperative characterization of patients with CTEPH.
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PMID:Diagnostic Evaluation of Chronic Thromboembolic Pulmonary Hypertension. 2757 Oct 4

BACKGROUND Pulmonary alveolar microlithiasis is an autosomal recessive disease in which a mutation in the SLC34A2 gene that codes for a sodium phosphate type IIb transporter protein (expressed in human epithelial tissues and functions in the clearance of phosphate ions) leads to the formation of extensive pulmonary intra-alveolar microliths. The subsequent characteristic clinical features of dyspnea and hypoxia are a manifestation of these microliths. There have been fewer than 1000 cases of pulmonary alveolar microlithiasis reported worldwide, and there have been 19 reported lung-transplanted patients. CASE REPORT A 49-year-old Saudi male patient presented with longstanding history of easy fatigability and tiredness on exertion since he was 16 years old. Throughout his follow-up in different hospitals (1986-1989), tuberculosis and pulmonary fibrosis were suspected. The patient was lost to follow-up between 1989 and 2001. In 2002, he presented to the emergency room with coughing, shortness of breath on exertion, abdominal swelling, and pedal edema. An investigation with chest x-rays, CT scan, electrocardiogram, and an echocardiogram was conducted. After referral to a tertiary care center, the patient was diagnosed with pulmonary alveolar microlithiasis. He subsequently developed pulmonary hypertension and polycythemia and therefore received a bilateral lung transplant in 2016. Following the lung transplant, he developed a mild reperfusion injury and tonic-clonic seizures, requiring ICU admission. After a successful extubatation with stable vitals and good recovery, he was discharged home in stable condition with planned follow-up. CONCLUSIONS We report a case of pulmonary alveolar microlithiasis successfully treated with a bilateral lung transplant. Although pulmonary alveolar microlithiasis is a rare entity, healthcare providers should consider it in the differential diagnoses of parenchymal lung diseases and differentiate it from tuberculosis and pulmonary fibrosis.
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PMID:Pulmonary Hypertension and Polycythemia Secondary to Pulmonary Alveolar Microlithiasis Treated with Sequential Bilateral Lung Transplant: A Case Study and Literature Review. 3135 64

A 77-year-old woman with obstructive sleep apnea presented with a 3-week history of leg swelling and dyspnea on exertion. She had a dry cough and lost 10 kg over the past 2 years. Examination revealed elevated jugular venous pressure, reduced air entry in the left lower-lung field, and pedal edema. Imaging with chest computed tomography revealed a giant pedunculated left atrial myxoma to be the cause of her severe pulmonary hypertension, which was reversible with treatment.
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PMID:Severe, Reversible Pulmonary Hypertension From Giant Pedunculated Left Atrial Myxoma. 3147 95