Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

CASE DESCRIPTION-A 12-week-old female English Springer Spaniel was evaluated for lethargy, vomiting, and pyrexia 1 week after treatment of patent ductus arteriosus (PDA) via coil occlusion. CLINICAL FINDINGS-Test results were consistent with septicemia, and the assumption was made that the PDA occlusion coils were infected. Radiography revealed partial migration of the coil mass into the pulmonary artery and signs of congestive heart failure. TREATMENT AND OUTCOME-After successful treatment of the septicemia and heart failure, surgical removal of the coils and resection of the PDA were undertaken. Although the coil that embolized to the pulmonary vasculature was left in place, the dog's clinical signs resolved. CLINICAL RELEVANCE-This case highlights the fact that as PDA coil occlusion devices become more widely used in dogs, practitioners must be prepared to treat implant infections aggressively, with both medical and surgical interventions if necessary.
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PMID:Septicemia in a young dog following treatment of patent ductus arteriosus via coil occlusion. 1678 81

Vomiting and abdominal pain are common pediatric complaints encountered by emergency physicians. The differential diagnosis of abdominal pain is extensive. Herein, we report 2 cases with fatal myocarditis who initially presented with abdominal pain and vomiting. Both cases were presented with abdominal pain, vomiting, and loose stools. On arrival at our emergency department, hypotension, tachycardia, and cyanotic extremities were found. Their serum troponin-I levels were elevated. The echocardiogram demonstrated poor left ventricular performance and a decreased ejection fraction. In both cases, an arrhythmia and a coma developed within hours and were shortly followed by death. The clinical presentations of acute myocarditis are variable, ranging from an initial mild discomfort to acute progressive heart failure, and at times, even death. Abdominal pain may be a manifestation of systemic disease, an extra-abdominal lesion, or myocarditis. Although myocarditis associated with abdominal pain or vomiting remains a diagnostic challenge to physicians, it should be considered in the differential diagnosis of children with gastritis and hypotension or who are refractory to rehydration therapy.
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PMID:Myocarditis presenting as gastritis in children. 1680 47

The seas and oceans around Australia harbour numerous venomous jellyfish. Chironex fleckeri, the box jellyfish, is the most lethal causing rapid cardiorespiratory depression and although its venom has been characterised, its toxins remain to be identified. A moderately effective antivenom exists which is also partially effective against another chirodropid, Chiropsalmus sp. Numerous carybdeids, some unidentified, cause less severe illness, including Carybdea rastoni whose toxins CrTX-A and CrTX-B are large proteins. Carukia barnesi, another small carybdeid is one cause of the 'Irukandji' syndrome which includes delayed pain from severe muscle cramping, vomiting, anxiety, restlessness, sweating and prostration, and occasionally severe hypertension and acute cardiac failure. The syndrome is in part caused by release of catecholamines but the cause of heart failure is undefined. The venom contains a sodium channel modulator. Two species of Physalia are present and although one is potentially lethal, has not caused death in Australian waters. Other significant genera of jellyfish include Tamoya, Pelagia, Cyanea, Aurelia and Chyrosaora.
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PMID:Australian venomous jellyfish, envenomation syndromes, toxins and therapy. 1692 89

Hypoglycaemia is the commonest metabolic abnormality faced by diabetic patients on hypoglycaemic therapy including insulin. Diabetic keto-acidosis (DKA) requires prompt diagnosis and all patients arriving emergency with dehydration, shock, coma, severe respiratory difficulty and evidence of any major illness should be tested for capillary blood glucose (CBG) and urinary ketones urgently not to miss DKA. Hyperosmolar non-ketotic state complicates elderly type 2 diabetes with intercurrent infections (respiratory tract infection is commonest) characterised by severe dehydration, severe hyperglycaemia and absence of acidosis and vomiting. Lactic acidosis is extremely rare; may be compounded with comorbidities like tissue hypoxia, septic shock, heart failure--metformin usage inadvertently may precipitate the condition.
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PMID:Metabolic emergencies in diabetes. 1705 69

Istaroxime is a new luso-inotropic compound selected for the treatment of acute heart failure syndromes, which reduces sodium-potassium adenosine triphosphatase (ATPase) activity and stimulates the sarcoplasmic calcium ATPase isoform 2 reuptake function. The aim of this study was to evaluate the safety profile of istaroxime. For this purpose, istaroxime was administered during a 24-hour infusion to conscious dogs with chronic heart failure and to genetically cardiomyopathic BIO TO.2 hamsters for 34 weeks orally. The parameters recorded were arrhythmic events and hemodynamic effects in dogs and mortality in hamsters. In dogs, istaroxime at 1, 3, and 4 microg/kg per min did not trigger arrhythmic events or magnify preexisting events. It increased left ventricular (LV) dP/dtmax (about 50% at 3 microg/kg per min) and LV-dP/dtmax (about 20% at 3 microg/kg per min) without changing heart rate, blood pressure, or double product. At 4 microg/kg per min, istaroxime increased dP/dtmax>100% but induced intense emesis in all animals. In cardiomyopathic hamsters, the dose of 30 mg/kg prolonged the survival rate to 32%. In conclusion, istaroxime seems to be a promising and safe new drug for improving cardiac performance in the failing heart.
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PMID:Istaroxime: a new luso-inotropic agent for heart failure. 1723 2

Niemann-Pick Disease (NPD) is a heterogeneous group of autosomal recessive disorders characterized by progressive accumulation of sphingomyelin and cholesterol in lysosomes. Six types of NPD have been described based on clinical presentation and involved organs. The primary defect in NPD types A and B is a deficiency of lysosomal acid sphingomyelinase (ASM). We present a case of a 5-year-old boy with type B NPD who had severe clinical manifestations, including heart involvement. He was first admitted to the hospital at 2 months because of vomiting, refusal to feed, lethargy, hepatomegaly and mild transaminasaemia. Liver biopsy at 12 months showed lipid accumulation and fibrosis. Investigations for lysosomal storage disorders revealed increased plasma chitotriosidase (549 nmol/h per ml, normal value 0-150). At 18 months, no detectable ASM activity was observed in cultured fibroblasts (normal range 23-226 nmol/h per mg protein) confirming NPD B. Pulmonary involvement was detected with high-resolution computerized tomography which revealed reticulonodular infiltrations and thickening of the interlobular septa. At 2 years growth retardation and kyphosis were noted. At 2.5 years he manifested neurodevelopment regression, indicating CNS involvement. Cardiac involvement (grade III mitral valve insufficiency) developed at 4 years and heart failure at 5 years. Genetic analysis revealed two mutations: a H421Y mutation that is common in Saudi Arabian and Turkish patients, and a W32X mutation, which has been found in other Mediterranean patients.
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PMID:Acid sphingomyelinase-deficient Niemann-Pick disease: novel findings in a Greek child. 1787 23

Amiodarone chlorhydrate is a diiodated benzofuran derivative, and it is used to treat cardiac rhythm abnormalities. Hepatotoxicity is a relatively uncommon side effect of amiodarone, and symptomatic hepatic dysfunction occurs in fewer than 1% of the patients taking amiodarone. Cirrhosis is a rare complication that's been confirmed in 12 cases. Peripheral neuropathy occurs in 10% of patients taking aminodarone. We report here on an unusual case of amiodarone-induced hepatotoxicity and peripheral neurotoxicity. A 75 year old man with normal liver function was given amiodarone for treating his atrial fibrillation and heart failure. He developed nausea, vomiting, muscle weakness and wasting after 17.8 months therapy with amiodarone (400 mg orally once per day). Liver biopsy showed the presence of foam cells in the hepatic sinusoids and Mallory bodies in the periportal hepatocytes on light microscopy. Sural nerve biopsy showed demyelination, and nerve conduction studies showed mixed sensorimotor polyneuropathy. These observations show the necessity of monitoring the hepatic function and conducting neurologic examination of the patients treated with amiodarone.
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PMID:Amiodarone-induced hepatitis and polyneuropathy. 1793 44

Idiopathic infantile arterial calcification (IIAC) is a rare disorder characterized by extensive calcification of medium and large arteries. We report the case of a 32-week-old infant with hydrops fetalis and heart failure who died at 4 days of age. At autopsy the infant was found to have cardiomegaly, myocardial infarctions and multifocal calcifications of the aorta and arteries in the lungs, heart, thyroid, spleen, and testis. Calcification extended from the internal elastic lamina into the intima and media and was associated with a giant-cell reaction and smooth muscle proliferation. A search of the English language medical literature identified 161 IIAC case reports. Of these, 48% of cases presented in utero or at birth with hydrops fetalis, maternal hydramnios, heart failure, or respiratory distress and 52% present later, at a median age of 3 months, with sudden onset of fever, vomiting, irritability, or respiratory distress in a previously healthy infant. Significantly, 19 of 22 IIAC survivors presented at less than 2 weeks of age, and 15 survivors were treated with diphosphonates.
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PMID:Idiopathic infantile arterial calcification: the spectrum of clinical presentations. 1799 Sep 35

1. The kidneys are the key organs to maintain the balance of the different electrolytes in the body and the acid-base balance. Progressive loss of kidney function results in a number of adaptive and compensatory renal and extrarenal changes that allow homeostasis to be maintained with glomerular filtration rates in the range of 10-25 ml/min. With glomerular filtration rates below 10 ml/min, there are almost always abnormalites in the body's internal environment with clinical repercussions. 2. Water Balance Disorders: In advanced chronic kidney disease (CKD), the range of urine osmolality progressively approaches plasma osmolality and becomes isostenuric. This manifests clinically as symptoms of nocturia and polyuria, especially in tubulointerstitial kidney diseases. Water overload will result in hyponatremia and a decrease in water intake will lead to hypernatremia. Routine analyses of serum Na levels should be performed in all patients with advanced CKD (Strength of Recommendation C). Except in edematous states, a daily fluid intake of 1.5-2 liters should be recommended (Strength of Recommendation C). Hyponatremia does not usually occur with glomerular filtration rates above 10 ml/min (Strength of Recommendation B). If it occurs, an excessive intake of free water should be considered or nonosmotic release of vasopressin by stimuli such as pain, anesthetics, hypoxemia or hypovolemia, or the use of diuretics. Hypernatremia is less frequent than hyponatremia in CKD. It can occur because of the provision of hypertonic parenteral solutions, or more frequently as a consequence of osmotic diuresis due to inadequate water intake during intercurrent disease, or in some circumstance that limits access to water (obtundation, immobility). 3. Sodium Balance Disorders: In CKD, fractional excretion of sodium increases so that absolute sodium excretion is not modified until glomerular filtration rates below 15 ml/min (Strength of Recommendation B). Total body content of sodium is the main determinant of extracellular volume and therefore disturbances in sodium balance will lead to clinical situations of volume depletion or overload: Volume depletion due to renal sodium loss occurs in abrupt restrictions of salt intake in advanced CKD. It occurs more frequently in certain tubulointerstitial kidney diseases (salt losing nephropathies). Volume overload due to sodium retention can occur with glomerular filtration rates below 25 ml/min and leads to edema, arterial hypertension and heart failure. The use of diuretics in volume overload in CKD is useful to force natriuresis (Strength of Recommendation B). Thiazides have little effect in advanced CKD. Loop diuretics are effective and should be used in higher than normal doses (Strength of Recommendation B). The combination of thiazides and loop diuretics can be useful in refractory cases (Strength of Recommendation B). Weight and volume should be monitored regularly in the hospitalized patient with CKD (Strength of Recommendation C). 4. Potassium Balance Disorders: In CKD, the ability of the kidneys to excrete potassium decreases proportionally to the loss of glomerular filtration. Stimulation of aldosterone and the increase in intestinal excretion of potassium are the main adaptive mechanisms to maintain potassium homeostasis until glomerular filtration rates of 10 ml/min. The main causes of hyperkalemia in CKD are the following: Use of drugs that alter the ability of the kidneys to excrete potassium: ACEIs, ARBs, NSAIDs, aldosterone antagonists, nonselective beta-blockers, heparin, trimetoprim, calcineurin inhibitors. Determination of serum potassium two weeks after the initiation of treatment with ACEIs/ARBs is recommended (Strength of Recommendation C). Routine use of aldosterone antagonists in advanced CKD is not recommended (Strength of Recommendation C). Abrupt reduction in glomerular filtration rate: Constipation. Prolonged fasting. Metabolic acidosis. A low-potassium diet is recommended with GFR less than 20 ml/min, or GFR less than 50 ml/min if drugs that raise serum potassium are taken (Strength of Recommendation C). In the absence of symptoms or electrocardiographic abnormalities, review of medications, restriction of dietary potassium and use of oral ion exchange resins are usually sufficient therapeutic measures (Strength of Recommendation C). If symptoms and/or electrocardiographic abnormalities are present, the usual parenteral pharmacological measures should be used (10% calcium gluconate, insulin and glucose, salbutamol, resins, diuretics) (Strength of Recommendation A). Parenteral bicarbonate and ion exchange resins in enemas are not recommended as first-line treatment (Strength of Recommendation C). Hemodialysis should be considered in patients with glomerular filtration rates below 10 ml/min (Strength of Recommendation C). 5. Acid-Base Disorders in CKD: Moderate metabolic acidosis (Bic 16-20) mEq/L is common with glomerular filtration rates below 20 ml/min, and favors bone demineralization due to the release of calcium and phosphate from the bone, chronic hyperventilation, and muscular weakness and atrophy. Its treatment consists of administration of sodium bicarbonate, usually orally (0.5-1 mEq/kg/day), with the goal of achieving a serum bicarbonate level of 22-24 mmol/L (Strength of Recommendation C). Limitation of daily protein intake to less than 1 g/kg/day is also useful (Strength of Recommendation C). Use of sevelamer as a phosphate binder aggravates metabolic acidosis since it favors endogenous acid production and therefore acidosis should be monitored and corrected if it occurs (Strength of Recommendation C). Hypocalcemia should always be corrected before metabolic acidosis in CKD (Strength of Recommendation B). Metabolic acidosis is an infrequent disorder and requires exogenous alkali administration (bicarbonate, phosphate binders) or vomiting.
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PMID:[Electrolyte and acid-base balance disorders in advanced chronic kidney disease]. 1901 44

A rare case of cardiac failure due to hypertensive crisis in pheochromocytoma in a 25-year-old young man is presented. In the Emergency Department the patient complained of persisting headache and vomiting; he was distressed but fully alert, his heart rate was 110 b/min and blood pressure 180/80 mmHg. Few hours after admission, the clinical course suddenly got worse with signs and symptoms of fatal cardiac shock (dyspnoea, cyanosis, pulmonary oedema, hypocontractility of left ventricle). Autopsy revealed a large tumour of the left adrenal gland. Histological examination confirmed macroscopic suspicion of pheochromocytoma. Catecholamine serum levels were analysed by high pressure liquid chromatography (HPLC) with electrochemical detection. The urine contained 35 microg/24 h norepinephrine and 184 microg/24 h epinephrine (normal range < or = 64 and < or = 36 microg/24 h respectively). These laboratory findings impressively demonstrate that the tumour was active, secreting high levels of epinephrine. Cardiac failure due to an acute catecholamine-related hypertensive crisis was established as the cause of death.
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PMID:Cardiac failure due to epinephrine-secreting pheochromocytoma: clinical, laboratory and pathological findings in a sudden death. 1926


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