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)

Over a period of 6 years, 58 patients aged between 55 +/- 16 years have been treated for post-intubation tracheal stenosis (STPI). These patients were characterised by their frequency of an underlying respiratory or cardiac failure, a duration of intubation which was sometimes short and a delay between the extubation and the detection of stenosis which was les than one month in about one half of the cases. Thirty of the 58 patients presented with respiratory distress on admission. All the stenoses were treated initially by mechanical dilatation using a rigid bronchoscope. Radial incisions using an Nd-Yag laser were performed when necessary to facilitate the dilatation. The great majority of stenoses which were not fitted up with a tracheal endoprosthesis (EPT) at the first attempt recurred, leading to repeated therapeutic bronchoscopies (221 sessions in all). Fitting an EPT (Dumon prosthesis) was necessary in 35 cases on 12 occasions at the first attempt with the first bronchoscopy, and 23 times following a recurrence. Amongst the recurring stenoses a stabilisation was obtained at the price of repeated dilatations (4.3 sessions on average in only nine patients). Seven patients finally had a surgical resection and anastamosis of the trachea, of whom four had a transitory instillation of an EPT for the stenosis. The removal of the EPT was later attempted in 11 patients. Four did not present with any symptomatic recurrence. The secondary migration of the EPT is in practice one of the main inconveniences of the silicon prosthesis (8 cases now experienced). Our approach, which used to favour the mechanical dilatation has lead to a relatively high number of failures and thus to repeated bronchoscopies. This has lead us to re-define our therapeutic approach. The current schema which we propose is in the course of being validated in which we use EPT and surgical repair of the trachea more often. Only short stenoses (less than 1 cm) with a diaphragm are treated by dilatation and laser. The others are fitted initially with an EPT. The final management is guided by the progress in the stenosis, the tolerance of the endoprosthesis and the operability of the patients.
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PMID:[Endoscopic treatment of post-intubation tracheal stenosis. Apropos of 58 cases]. 867 52

The elimination of caffeine was investigated in a 1860 g, 31 week gestation neonate, following the accidental administration of a 160 mg.kg-1 dose. The first serum concentration measured was 217.5 mg.l-1 at 36.5 h after dosing. Fitting of time-concentration data was performed using non-linear regression with MKMODEL. A first order elimination model was superior to a mixed order model. Parameter estimates were: clearance 0.01 l.h-1, volume of distribution 1.17 litres, elimination half-life 81 h. Toxic manifestations included hypertonia, sweating, tachycardia, cardiac failure, pulmonary oedema and metabolic disturbances (metabolic acidosis, hyperglycaemia and creatine kinase elevation). An unusual feature of this infant's illness course was gastric dilatation. These signs resolved by day 7 at a serum concentration of 60-70 mg.l-1. Caffeine clearance has traditionally been reported as either an absolute value or as directly proportional to body weight. The per kilogram model gives an erroneous impression that clearance is greatest in early childhood and then decreases with age until adult rates are reached in late adolescence. Age-related clearance values reported in the literature were reviewed using an allometric 3/4 power model. This size model demonstrates that clearance increases in infancy and reaches adult rates within the first three months of life.
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PMID:Caffeine overdose in a premature infant: clinical course and pharmacokinetics. 1038 69

Ca(2+) binding to cardiac troponin C (cTnC) triggers contraction in heart muscle. In heart failure, myofilaments response to Ca(2+) are often altered and compounds that sensitize the myofilaments to Ca(2+) possess therapeutic value in this syndrome. One of the most potent and selective Ca(2+) sensitizers is the thiadiazinone derivative EMD 57033, which increases myocardial contractile function both in vivo and in vitro and interacts with cTnC in vitro. We have determined the NMR structure of the 1:1 complex between Ca(2+)-saturated C-domain of human cTnC (cCTnC) and EMD 57033. Favorable hydrophobic interactions between the drug and the protein position EMD 57033 in the hydrophobic cleft of the protein. The drug molecule is orientated such that the chiral group of EMD 57033 fits deep in the hydrophobic pocket and makes several key contacts with the protein. This stereospecific interaction explains why the (-)-enantiomer of EMD 57033 is inactive. Titrations of the cCTnC.EMD 57033 complex with two regions of cardiac troponin I (cTnI(34-71) and cTnI(128-147)) reveal that the drug does not share a common binding epitope with cTnI(128-147) but is completely displaced by cTnI(34-71). These results have important implications for elucidating the mechanism of the Ca(2+) sensitizing effect of EMD 57033 in cardiac muscle contraction.
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PMID:Structure of the C-domain of human cardiac troponin C in complex with the Ca2+ sensitizing drug EMD 57033. 1132 96

During the neonatal period, inborn errors of metabolism mostly present with an overwhelming illness that requires prompt diagnosis and both supportive and specific treatments. The most frequent situations are due to branched-chain organic acidurias that present with ketoacidosis and urea cycle defects that are characterized by hyperammonaemia. During both situations, toxin removal procedures and nutritional support with a free-protein and high-energy diet are pivotal treatments. In patients presenting with hypoglycaemia blood glucose levels must be corrected. Progress following glucose provision is useful in recognizing the disorders that are mainly implicated. Hyperinsulinism requires high-glucose infusion. Glycogen storage diseases and gluconeogenesis defects are easily treated with a permanent glucose provision while hypoglycaemias quickly recur. In patients with galactosaemia, hereditary fructose intolerance or tyrosinaemia type I, the presentation is dominated by a liver failure requiring galactose and fructose exclusion associated with a low-protein diet. Many patients with beta-oxidation defects may present with hypoglycaemia that is usually easily corrected. The precise diagnosis can be easily missed in those patients that do well in the following weeks but may develop cardiac failure, arrhythmia and/or liver failure. Patients presenting with intractable convulsions, vitamin responsiveness to biotin, pyridoxine and folate must be considered.
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PMID:Management and emergency treatments of neonates with a suspicion of inborn errors of metabolism. 1206 35

Fever is often an indication of a serious illness in children. In areas endemic to malaria, hospital workers should check a febrile child for malaria parasites. Children with a fever associated with meningitis or malaria need immediate attention. To diagnose meningitis: microscopic examination of cerebrospinal fluid obtained by lumbar puncture is the only reliable method. If a febrile child also has a stiff neck, health workers should immediately administer antibiotic treatment without waiting for the results of the lumbar puncture. If available and in epidemic situations, oily chloramphenicol may be administered, since it is effective in a single dose. Treatment with other antibiotics should last for 10 days in children and 14-21 days for young infants. To diagnose malaria in endemic areas: laboratory technicians should examine thick and thin blood films of sick children with fever. Health workers must consider as medical emergencies children who have a slide positive for malaria parasites plus severe anemia, hypoglycemia, deep rapid breathing, any indication of kidney malfunction or failure, or altered consciousness. They should begin antimalarial treatment with quinine, the drug of choice for severe and complicated malaria. In cases of convulsions lasting longer than 5 minutes, health workers should administer anticonvulsants and take actions to prevent aspiration pneumonia. If the fever persists for 14 days or if the child does not emerge from unconsciousness and someone in the family has active tuberculosis, health workers should consider tuberculous meningitis. If a child with malaria has low hemoglobin levels (5 g/dl) and many malaria parasites in the blood and is in heart failure, a blood transfusion (15-20 ml/kg whole blood over 4 hours) and infusion of 1 mg/kg fursemide (to prevent cardiac failure) are needed. If the preceding case has pulmonary edema, a single dose of fursemide at the same dosage is needed to prevent overloading of the circulation. Health workers should closely monitor that intravenous fluids not exacerbate brain swelling.
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PMID:Managing meningitis and severe malaria. 1229 72

Pulmonary edema is the primary danger in cardiac patients who undergo abortion by intra-amniotic instillation of hypertonic saline solution. The intra-amniotic saline has not been considered safe for induction of abortion in the 2nd trimester of pregnancy due to either immediate or late complications. Side effects range from vomiting, diarrhea, and headaches to severe septicaemea, convulsions, hemorrhage, disseminated intra-vascular coagulation, and pulmonary edema. Pulmonary edema is often unanticipated in women with "tight" mitral stenosis which was unrecognized in pregnancy. Organic lesion in the heart is often undetected prior to instillation of hypertonic saline which could subsequently cause cardiac failure and lung edema.
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PMID:Unanticipated complications of intra amniotic saline. 1233 31

We report here the case of a 44-year-old woman with thrombocytopenia, anemia, convulsions, hyperprolactinemia, and galactorrhea. The patient died of cardiac failure. Autopsy revealed PAS-positive and von Willebrand factor-positive microthrombi in the arterioles and capillaries of many organs, mainly in the heart and brain, confirming the clinical diagnosis of thrombotic thrombocytopenic purpura. In the pituitary, a prolactin-producing adenoma was identified. To our knowledge, thrombotic thrombocytopenic purpura accompanied by a prolactin-secreting pituitary adenoma has not yet been described. The question of whether the association between the vascular changes and the pituitary adenoma is incidental or causal cannot be answered. Further studies are required to determine whether prolactin released from the pituitary tumor in excess played a role in the formation of microthrombi causing multiple organ failure and the demise of the patient.
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PMID:Thrombotic thrombocytopenic purpura associated with a prolactin-producing pituitary adenoma. 1294 91

Alkavervir (Veriloid(R)), a new derivative of veratrum viride was used in the treatment of hypertension in ten children with acute nephritis. The patients had a variety of complications associated with hypertension-heart failure, convulsions, vomiting and headache. In all of them the blood pressure decreased soon after the drug was given.
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PMID:Hypertension in childhood; treatment of acute nephritis with a derivative of veratrum viride. 1331 38

Ethyl alcohol (ethanol) is readily absorbed from all parts of the gastrointestinal tract due to its hydrophilic potential. The biological effects in humans refer to practically every organ and system. The basic enzyme involved in its oxidation is alcohol dehydrogenase. Another important metabolic pathway is the Microsomal Ethanol-Oxidizing System (MEOS). Toxic effect on basic cell functions is produced both by ethanol and acetic aldehyde, its oxidation product which accounts for most of the acute and delayed effects of ethanol toxicity. In acute ethanol intoxication's the CNS symptoms are the first to manifest. Ethanol affects the CNS functions mainly through stimulating opiate and benzodiazepine receptors and a number of neurotransmitters. However, the attempts to diminish the toxic effects of ethanol on CNS by blocking the affected receptors have proved to be ineffective. In acute poisoning a basic essential is to sustain vital functions by following the principles of intensive care. Each case of acute ethanol intoxication must be subject to neurological examination for possible cerebro-cranial traumas. The diagnostics and treatment procedures should take account of the possible symptoms: convulsions, respiratory and cardiac failure, hypoglycemia, hypothermia, and severe gastric dysfunction. Vital signs monitoring and control of acid-base and water-electrolyte balance are a must. The toxic properties of ethanol metabolites can be particularly hazardous to patients treated with disulfiram. The patients who develop "antabuse response" should be given immediately iron and vitamin C intravenously.
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PMID:[Biological and toxic effects of ethanol: diagnostics and treatment of acute poisonings]. 1456 85

Two decades of research from CONSENSUS to CHARM using modulators of the renin-angiotensin-aldosterone system (RAAS) in chronic heart failure (CHF) patients have shown convincing clinical benefits, but the majority of clinicians prescribing these drugs are still unclear about what mechanisms are responsible for the observed benefits. Of the candidate mechanisms hitherto proposed, there emerges a theme that best fits the spectrum of known factors from pathophysiology of heart failure to how the drugs enhance longevity of patients. This concept can be summarised as follows: after the onset of heart failure, neurohormones are activated resulting in raised levels of angiotensin, aldosterone and catecholamines, which are all known cardiotoxic agents. Cumulatively over time, they are responsible for accelerated cardiomyocyte attrition, manifesting as a faster reduction of cardiac pumping reserve, leading to worsening heart failure, more neurohormonal activation, thus propagating a vicious cycle spiralling towards an earlier fatality. The vicious cycle can be interrupted by dampening the excessive neurohormonal activities, thereby minimising cardiomyocyte losses and preserving cardiac functional reserve for longer. This culminates in maintenance of a reasonable quality of life and enhanced longevity. Such a mechanistic understanding would enable clinicians to have a better perspective on how to apply data from various clinical trials involving these drugs into clinical practice, to optimise and tailor therapy to the individual patient so that each patient can gain maximal benefits.
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PMID:From CONSENSUS to CHARM--how do ACEI and ARB produce clinical benefits in CHF? 1606 Nov 32


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