Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 36-year-old man with a history of asthma visited an outpatient clinic complaining of high fever and general fatigue, and was diagnosed as having influenza type A by influenza antigen test. Laboratory findings revealed mild inflammation, mild acidemia, and hypercapnea with radiologic infiltrations in the right lung, and remarkable wheezes in both lungs were heard on auscultation. He was diagnosed with asthma exacerbation and having influenza pneumonia, and was referred to us. Therapy was begun with oseltamivir for influenza infection and intravenous infusions of betamethasone and aminophylline with non-invasive pulmonary ventilation for asthma exacerbation and acute respiratory failure. Although he was weaned from mechanical ventilation and his general condition became good, electrocardiogram showed sinus bradycardia and negative T waves in V1-4 without any symptoms. Blood test and echocardiography showed almost normal findings except for slight elevation of LDH and AST. Influenza A antigen was already confirmed and he was diagnosed as having influenza myocarditis clinically. Although it is well known that influenza can cause asthma exacerbation and encephalopathy, influenza myocarditis is regarded as rare by physicians. In fact, the number of case reports about influenza myocarditis is few. Myocarditis may not appear to be serious, but could cause fatal arrhythmia and heart failure. All clinicians should be aware of the overall clinical picture and the possibility of severe complications of myocarditis caused by flu infection.
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PMID:A case of asthma-complicated influenza myocarditis. 2094 21

The syndrome of inappropriate secretion of antidiuretic hormone (SIADH)/syndrome of inappropriate antidiuresis is characterized by a hypotonic hyponatremia, with an insufficiently diluted urine given the plasmatic hypoosmolality, in the absence of hypovolemia (with or without a third space), hypotension, renal or heart failure, cirrhosis of the liver, hypothyroidism, adrenal insufficiency, vomiting, or other non-osmotic stimuli of ADH secretion. The response of ADH to the infusion of hypertonic saline divides SIADH into 4 different types. In type D, there is no alteration in ADH secretion. Rather, the defect is the maintained permeability of kidney aquaporin-2 channels to water. Activating mutations of the V2 receptor have been identified. The most frequent cause of SIADH is the use of drugs that induce secretion of the hormone. Old age is per se a risk factor for its development. SIADH is underdiagnosed, and hospitalization often worsens the clinical situation, due to an iatrogenic excess in the use of oral and i.v. liquids, often hypotonic, together with a reduction in salt intake. Treatment is directed towards normalization of natremia when possible, together with the avoidance of both hyponatremic encephalopathy as well as the osmotic demyelinization syndrome. Cases of "appropriate" secretion of ADH with normovolemic hyponatremia and high mortality rates should be treated with the same urgency as SIADH--such is the case of post-surgical hyponatremia.
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PMID:[Current considerations in syndrome of inappropriate secretion of antidiuretic hormone/syndrome of inappropriate antidiuresis]. 2113 Sep 59

This review considers the 250+ papers concerning the association of the angiotensin converting enzyme (ACE) gene insertion/deletion polymorphism (rs1799752) and various disease conditions published in 2009. The deletion allele occurs in approximately 55% of the population and is associated with increased activity of the ACE enzyme. It might be predicted that the D allele, therefore, might be associated with pathologies involving increased activity of the renin-angiotensin system. The D allele was seen to be associated with an increased risk of hypertension, pre-eclampsia, heart failure, cerebral infarct, diabetic nephropathy, encephalopathy, asthma, severe hypoglycaemia in diabetes, gastric cancer (in Caucasians) and poor prognosis following kidney transplant. On the positive side, the D allele appears to offer protection against schizophrenia and chronic periodontitis and confers greater up-per-body strength in old age. The I allele, meanwhile, offers improved endurance/athletic performance and aerobic capacity as determined by lung function tests, although it does increase the risk of oral squamous cell carcinoma and obstructive sleep apnoea in hypertensives.
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PMID:Implications of the angiotensin converting enzyme gene insertion/deletion polymorphism in health and disease: a snapshot review. 2153 87

The clinical presentation of beriberi can be quite varied. In the extreme form, profound cardiovascular involvement leads to circulatory collapse and death. This case report is of a 72 year-old male who was admitted to the Neurology inpatient ward with progressive bilateral lower extremity weakness and parasthesia. He subsequently developed pulmonary edema and high output cardiac failure requiring intubation and blood pressure support. With the constellation of peripheral neuropathy, encephalopathy, ophthalmoplegia, unexplained heart failure, and lactic acidosis, thiamine deficiency was suspected. He was empirically initiated on thiamine replacement therapy and his thiamine level pre-therapy was found to be 23 nmol/L (Normal: 80-150 nmol/L), consistent with the diagnosis of beriberi. Cardiovascular magnetic resonance (CMR) showed severe left ventricular systolic dysfunction, markedly increased myocardial T2, and minimal late gadolinium enhancement (LGE). After 5 days of daily 100 mg IV thiamine and supportive care, the hypotension resolved and the patient was extubated and was released from the hospital 3 weeks later. Our case shows via CMR profound myocardial edema associated with wet beriberi.
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PMID:Cardiovascular magnetic resonance in wet beriberi. 2183 1

Clinico-instrumental characteristics of arterial hypertension, liable to the ishemic stroke were studied. The pecularities of clinical, neurological picture of disease and results of instrumental methods of examination were determined. These peculiarities let to educe the course of arterial hypertension, liable to the ishemic stroke. This course appeared because of hypertensional macroangiopathy during 3-5 years, two atherosclerotic stenosis of brachiocephalic arteria, occlusions and stenosis of these arterias, left ventricular hypertrophy of hypodynamic type, circulatory dynamics against the bad daily profile of arterial pressure and/or increased variability of arterial pressure accompanied with ischemic attacks, signs of chronicle heart failure and circulatory encephalopathy. The scheme of the examination of patients with AH during the long-term examination with the goal of prophylaxis IS was offered.
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PMID:[Clinico-instrumental characteristics of arterial hypertension, liable to the ishemic stroke]. 2189 79

Patients with infective endocarditis (IE) are generally referred to the intensive care unit (ICU) for one or more organ dysfunctions caused by complications of IE. Neurologic events are frequent causes of ICU admission in patients with IE. They can arise through various mechanisms consisting of stroke or transient ischemic attack, cerebral hemorrhage, mycotic aneurysm, meningitis, cerebral abscess, or encephalopathy. Most complications occur early during the course of IE and are a hallmark of left-sided abnormalities of native or prosthetic valves. Occlusion of cerebral arteries, with stroke or transient ischemic attack, accounts for 40% to 50% of the central nervous system complications of IE. CT scan is the most easily feasible neuroimaging in critically unstable patients. However, magnetic resonance imaging is more sensitive and when performed should follow a standardized protocol. In patients with ischemic stroke who are already receiving oral anticoagulant therapy, this treatment should be replaced by unfractionated heparin for at least 2 weeks with a close monitoring of coagulation tests. Mounting evidence shows that, for both complicated left-sided native valve endocarditis and Staphylococcus aureus prosthetic valve endocarditis, valve replacement combined with medical therapy is associated with a better outcome than medical treatment alone. In a recent series, approximately 50% of patients underwent valve replacement during the acute phase of IE before completion of antibiotic treatment. After a neurological event, most patients have at least one indication for cardiac surgery. Recent data from literature suggest that after a stroke, surgery indicated for heart failure, uncontrolled infection, abscess, or persisting high emboli risk should not be delayed, provided that the patient is not comatose or has no severe deficit. Neurologic complications of IE contribute to a severe prognosis in ICU patients. However, patients with only silent or transient stroke had a better prognosis than patients with symptomatic events. In addition, more than neurologic event per se, a better predictor of mortality is neurologic dysfunction, which is associated with location and extension of brain damage. Patients with severe neurological impairment and those with brain hemorrhage have the worse outcome.
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PMID:Management of neurological complications of infective endocarditis in ICU patients. 2190 36

Neurologic dysfunction complicates the course of 10-40% of left-side infective endocarditis (IE). In right-sided IE, instead, when systemic emboli occur, paradoxical embolism should be considered. The spectrum of neurologic events includes embolic cerebrovascular complication (CVC), intracranial haemorrhage, ruptured mycotic aneurysm, transient ischaemic attack (TIA), meningitis, encephalopathy and brain abscess. Cardiopulmonary bypass might exacerbate neurological deficits due to: heparinization and secondary cerebral haemorrhage; hypotension and cerebral oedema in areas of the disrupted blood brain barrier. A best evidence topic was written according to a structured protocol. The question addressed was, whether there is an optimal timing for surgery in IE with CVCs. One hundred papers were found using the reported search criteria, and out of these 20 papers, provided the best evidence to answer the clinical question. The authors, journal, date and country of publication, patient group studied, study type, relevant outcomes and results were tabulated. We found that evidence is conflicting because of lack of controlled studies. The optimal timing for the valve replacement depends on the type of neurological complication and the urgency of the operation. The new 2009 Guidelines on the prevention, diagnosis, and treatment of infective endocarditis (IE) recommend a multidisciplinary approach and to wait for 1-2 weeks of antibiotics treatment before performing cardiac surgery. However, early surgery is indicated in: heart failure (class 1 B), uncontrolled infection (class 1 B) and prevention of embolic events (class 1B/C). After a stroke, surgery should not be delayed as long as coma is absent and cerebral haemorrhage has been excluded by cranial CT (class IIa level B). After a TIA or a silent cerebral embolism, surgery is recommended without delay (class 1 level B). In intracranial haemorrhage (ICH), surgery must be postponed for at least 1 month (class 1 level C). Surgery for prosthetic valve endocarditis (PVE) follows the general principles outlined for native valve IE. Every patient should have a repeated head CT scan immediately before the operation to rule out a preoperative haemorrhagic transformation of a brain infarction. The presence of a haematoma warrants neurosurgical consultation and consideration of cerebral angiography to rule out a mycotic aneurysm.
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PMID:What is the optimal timing for surgery in infective endocarditis with cerebrovascular complications? 2210 25

Antidiuretic hormone (ADH), or arginine vasopressin (AVP), is primarily regulated through plasma osmolarity, as well as non-osmotic stimuli including blood volume and stress. Links between water-electrolyte and carbohydrate metabolism have also been recently demonstrated. AVP acts via the intermediary of three types of receptors: V1a, or V1, which exerts vasoconstrictive effects; pituitary gland V1b, or V3, which participates in the secretion of ACTH; and renal V2, which reduces the excretion of pure water by combining with water channels (aquaporin 2). Antidiuresis syndrome is a form of euvolaemic, hypoosmolar hyponatraemia, which is characterised by a negative free water clearance with inappropriate urine osmolality and intracellular hyper-hydration in the absence of renal, adrenal and thyroid insufficiency. Ninety percent of cases of antidiuresis syndrome occur in association with hypersecretion of vasopressin, while vasopressin is undetectable in 10% of cases. Thus the term "antidiuresis syndrome" is more appropriate than the classic name "syndrome of inappropriate ADH secretion" (SIADH). The clinical symptoms, morbidity and mortality of hyponatraemia are related to its severity, as well as to the rapidity of its onset and duration. Even in cases of moderate hyponatraemia that are considered asymptomatic, there is a very high risk of falls due to gait and attention disorders, as well as rhabdomyolysis, which increases the fracture risk. The aetiological diagnosis of hyponatraemia is based on the analysis of calculated or measured plasma osmolality (POsm), as well as blood volume (skin tenting of dehydration, oedema). Hyperglycaemia and hypertriglyceridaemia lead to hyper- and normoosmolar hyponatraemia, respectively. Salt loss of gastrointestinal, renal, cutaneous and sometimes cerebral origin is hypovolaemic, hypoosmolar hyponatraemia (skin tenting), whereas oedema is present with hypervolaemic, hypoosmolar hyponatraemia of heart failure, nephrotic syndrome and cirrhosis. Some endocrinopathies (glucocorticoid deficiency and hypothyroidism) are associated with euvolaemic, hypoosmolar hyponatraemia, which must be distinguished from SIADH. Independent of adrenal insufficiency, isolated hypoaldosteronism can also be accompanied by hypersecretion of vasopressin secondary to hypovolaemia, which responds to mineralocorticoid administration. The causes of SIADH are classic: neoplastic (notably small-cell lung cancer), iatrogenic (particularly psychoactive drugs, chemotherapy), lung and cerebral. Some causes have been recently described: familial hyponatraemia via X-linked recessive disease caused by an activating mutation of the vasopressin 2 receptor; and corticotropin insufficiency related to drug interference between some inhaled glucocorticoids and cytochrome p450 inhibitors, such as the antiretroviral drugs and itraconazole, etc. SIADH in marathon runners exposes them to a risk of hypotonic encephalopathy with fatal cerebral oedema. SIADH treatment is based on water restriction and demeclocycline. V2 receptor antagonists are still not marketed in France. These aquaretics seem effective clinically and biologically, without demonstrated improvement to date of mortality in eu- and hypervolaemic hyponatraemia. Obviously treatment of a corticotropic deficit, even subtle, should not be overlooked, as well as the introduction of fludrocortisone in isolated hypoaldosteronism and discontinuation of iatrogenic drugs.
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PMID:Hyponatremia and antidiuresis syndrome. 2211 69

Clinical efficacy of combined therapy including the use of rifaximin and L-ornithin-l-aspartate, as well as the dynamics of the biochemical indices, the manifestation levels of portal-systemic-encephalopathy and intestinal microbiocynosis were investigated in patients with chronic cardiac insufficiency of ischemic genesis and hobnail liver. The combined therapy resulted in improvement of the patients clinical state, lower levels of the portal-systemic encephalopathy manifectation by decreasing hyperammonium, normalization of the large intestine microflora, and blood serum biochemical parameters.
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PMID:[Optimization of treatment of patients with chronic cardiac insufficiency of the ischemic genesis and hobnail liver]. 2214 33

The mid-aortic syndrome is an uncommon clinical condition characterized by severe narrowing of the descending aorta, usually with involvement of its renal and visceral branches, presenting with uncontrollably elevated blood pressures of the upper body, renal and cardiac failure, intestinal ischemia, encephalopathy symptoms and claudication of the lower limbs, although clinical presentation is variable. In this article we report the case of an eleven-year-old patient with the initial diagnosis of a mid-aortic syndrome and present the computed tomography angiography pictures and reconstructions before and after surgical therapy.
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PMID:Mid-aortic syndrome: computed tomography angiography depicting extensive collateral circulation in an 11-year-old patient with thoracoabdominal aortic coarctation. 2240 32


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