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 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The objective of the study was to evaluate the phosphate-binding efficacy, side effects, and cost of therapy of calcium ketoglutarate granulate as compared with calcium carbonate tablets in patients on chronic hemodialysis. The study design used was a randomized, crossover open trial, and the main outcome measurements were plasma ionized calcium levels, plasma phosphate levels, plasma intact parathyroid hormone (PTH) levels, requirements for supplemental aluminum-aminoacetate therapy, patient tolerance, and cost of therapy. Nineteen patients on chronic hemodialysis were treated with a dialysate calcium concentration of 1.25 mmol/L and a fixed alfacalcidol dose for at least 2 months. All had previously tolerated therapy with calcium carbonate. Of the 19 patients included, 10 completed both treatment arms. After 12 weeks of therapy, the mean (+/-SEM) plasma ionized calcium level was significantly lower in the ketoglutarate arm compared with the calcium carbonate arm (4.8+/-0.1 mg/dL v 5.2+/-0.1 mg/dL; P = 0.004), whereas the mean plasma phosphate (4.5+/-0.3 mg/dL v 5.1+/-0.1 mg/dL) and PTH levels (266+/-125 pg/mL v 301+/-148 pg/mL) did not differ significantly between the two treatment arms. Supplemental aluminum-aminoacetate was not required during calcium ketoglutarate treatment, while two patients needed this supplement when treated with calcium carbonate. Five of 17 (29%) patients were withdrawn from calcium ketoglutarate therapy within 1 to 2 weeks due to intolerance (anorexia, vomiting, diarrhea, general uneasiness), whereas the remaining 12 patients did not experience any side effects at all. The five patients with calcium ketoglutarate intolerance all had pre-existing gastrointestinal symptoms; four of them had received treatment with cimetidine or omeprazol before inclusion into the study. Calculations based on median doses after 12 weeks showed that the cost of the therapy in Denmark was 10 times higher for calcium ketoglutarate compared with calcium carbonate (US$6.00/d v US$0.65/d). Calcium ketoglutarate may be an effective and safe alternative to treatment with aluminum-containing phosphate binders in patients on hemodialysis who are intolerant of calcium carbonate or acetate because of hypercalcemia. However, care must be exercised when dealing with patients with pre-existing gastrointestinal discomfort. Due to the high cost of the therapy, calcium ketoglutarate should be used only for selected patients.
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PMID:Randomized crossover study comparing the phosphate-binding efficacy of calcium ketoglutarate versus calcium carbonate in patients on chronic hemodialysis. 946 96

Metabolic alkalosis is a primary pathophysiologic event characterized by the gain of bicarbonate or the loss of nonvolatile acid from extracellular fluid. The kidney preserves normal acid-base balance by two mechanisms: bicarbonate reclamation, mainly in the proximal tubule, and bicarbonate generation, predominantly in the distal nephron. Bicarbonate reclamation is mediated mainly by a Na(+)-H(+) antiporter and to a smaller extent by the H(+)-ATPase (adenosine triphosphate-ase). The principal factors affecting HCO3(-) reabsorption include effective arterial blood volume, glomerular filtration rate, chloride, and potassium. Bicarbonate regeneration is primarily affected by distal Na(+) delivery and reabsorption, aldosterone, arterial pH, and arterial partial pressure of carbon dioxide. To generate metabolic alkalosis, either a gain of base or a loss of acid must occur. The loss of acid may be via the gastrointestinal tract or via the kidney. Excess base may be gained by oral or parenteral HCO3(-) administration or by lactate, acetate, or citrate administration. Factors that help maintain metabolic alkalosis include decreased glomerular filtration rate, volume contraction, hypokalemia, hypochloremia, and aldosterone excess. Clinical states associated with metabolic alkalosis are vomiting, mineralocorticoid excess, the adrenogenital syndrome, licorice ingestion, diuretic administration, and Bartter's and Gitelman's syndromes. The effects of metabolic alkalosis on the body are variable and include effects on the central nervous system, myocardium, skeletal muscle, and liver. Treatment of this disorder is simple, once the pathophysiology of the cause is delineated. Therapy consists of reversing the contributory factors that are promoting the alkalosis and, in severe cases, administration of carbonic anhydrase inhibitors, acid infusion, and low bicarbonate dialysis.
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PMID:Metabolic alkalosis. 1126 55

Some plants contain glycoside compounds which determine cardiovascular symptoms similar to those observed after acute toxic digoxin administration. The present case report involves a patient who showed important cardiovascular symptoms following the ingestion of Thevetia nereifolia/peruviana seeds. About 30 min after ingestion, a 65-year-old man presented with dizziness, giddiness, numbness and a burning sensation, diarrhea, sweating, vomiting and ECG changes. At the time of admission he presented with tremors; his body temperature was 37 degrees C, and blood analysis gave the following results: K 5.6 mEq/l, myoglobin 176 IU, troponin T 0.10 ng/ml, PO2 69 mmHg, PCO2 37.4 mmHg, pH 7.33, HCO3- 19.9 mEq/l, hemoglobin 14.8 g/dl, saturation 92.5%. Echocardiography showed a left ventricle with normal global and segmentary contractility. The following days, the patient showed a reduction, until total resolution, of the atrioventricular block and of the alterations of the ST segment. The ectopic beats also resolved; K value before discharge was 4.4 mEq/l. On the third day, the serum levels of digoxin were 0.15 ng/ml. This case report is important because it describes all the cardiovascular and non-cardiovascular signs of glycoside toxicity in an adult patient who accidentally swallowed only two seeds (non-fatal dose) of Thevetia.
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PMID:Cardiovascular glycoside-like intoxication following ingestion of Thevetia nereifolia/peruviana seeds: a case report. 1192 13

The carbonic acid/bicarbonate system, as defined by the Henderson-Hasselbach (H-H) equation, has traditionally formed the centrepiece of the presentation of acid/base physiology in nursing education. However, an alternative approach to describe acid/base physiology was proposed by Peter Stewart in 1983. Stewart determined, using the physiochemical principles of dissociation equilibrium, electroneutrality and conservation of mass, that hydrogen ion concentration [H+] was dependent upon the difference between the concentrations of strong cations and strong anions in a solution (the strong ion difference or SID), concentration of weak acid anions, and the partial pressure of carbon dioxide in plasma. Therefore, a change in pH (the [H+] expressed as its negative log) indicates that there must be a change in one of these independent variables, and not simply explained by movement of hydrogen ions or bicarbonate into or out of the body fluids. An analysis of the complex acid/base derangements commonly seen in the critically ill can be achieved using this approach. The acid/base consequences of vomiting, gastric aspiration, diarrhoea, diuretic therapy, the infusion of large volumes of normal saline, the contribution of lactate, and the effects of methanol and ethylene glycol poisoning can all be more readily understood considering Stewart's explanation of acid/base balance. This paper outlines this alternative approach and provides some examples for the intensive care setting.
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PMID:Introduction to an alternate view of acid/base balance: the strong ion difference or Stewart approach. 1224 Jun 97

Nine cats that had surgical treatment for obstructive cholelithiasis were reviewed to evaluate clinical signs, diagnostic test results, and outcome after surgery. Common clinical signs included progressive vomiting (9/9), dehydration (9/9), anorexia (6/9), icterus (5/9), and lethargy (4/9). Five cats had a cholecystectomy performed, one cat had a cholecystotomy, and three cats had a biliary diversion procedure. Four of the cats that had a cholecystectomy had no recurrence of vomiting or anorexia. The majority of cats (7/9) had multiple choleliths, which were radiopaque and most commonly composed of calcium carbonate. Seven cats were diagnosed with cholangiohepatitis, and four of these cats did not need long-term medical therapy. Most cats (7/9) survived long term postsurgery (mean, 21 months; median, 24 months) without additional medical therapy, while the two cats with concurrent hepatic lipidosis died. Cholecystectomy appeared to have low morbidity with good clinical success.
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PMID:The surgical treatment of cholelithiasis in cats: a study of nine cases. 1202 16

A 70-year-old Japanese woman with renal dysfunction under hemodialysis presented with vomiting and chill with fever. Over the previous 24 weeks she had been taking 75 mg of ranitidine after hemodialysis. Other medications taken were prednisolone, furosemide, alpha-calcidol, amlodipine and calcium carbonate. Before starting ranitidine, she had been treated with famotidine for about 2 years without complication. Hematological inspection on admission revealed agranulocytosis with WBC of 400/mm3. Ranitidine was discontinued and granulocyte colony-stimulating factor (G-CSF) was started. On Day 3, laboratory data showed slight improvement of cytopenia with WBC of 1,000/mm3. On Day 6, her hemogram showed marked improvement with WBC of 11,700/mm3 and G-CSF was discontinued. She was discharged on Day 10. Several cases describing ranitidine-induced cytopenia are associated with the use of ranitidine at a dose of 150 mg/day or higher, and adverse reactions were found within 2-35 days after beginning ranitidine treatment. In the case described here, however, the adverse reaction occurred after a longer treatment period with ranitidine at a lower dose. In conclusion, ranitidine should be administered with great caution to patients with severe renal dysfunction.
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PMID:Agranulocytosis possibly caused by ranitidine in a patient with renal failure. 1269 89

This study was designed to evaluate possible organ and system disorders associated with experimentally induced levamisole poisoning in dogs. For this purpose, twelve clinically healthy dogs of different ages, sexes and breeds were used. They were divided into two equal groups (Group A and Group B) and given levamisole orally at a dose of 25 mg/kg of body weight daily for three days. The dogs in Group B were also injected with atropin sulphate (0.04 mg/kg of body weight) subcutaneously (sc) 1 hour after each administration of levamisole. Routine clinical examinations were made and some haematological, biochemical and blood gas parameters were established at various times after administration of levamisole. The dogs in Group A developed severe neurological signs, gastric haemorrhage, bloody vomiting, colic, anaemia and four dogs died. In Group B these signs were mild and only one dog died. Levamisole poisoning was characterised by a significant reduction in the total number of red blood cells (RBCs), concentration of haemoglobin (Hb) and packed cell volume (PCV), and by anaemia. Peripheral blood pH, actual bicarbonate of plasma (HCO3), actual base excess (BE), partial pressure of oxygen (pO2) and saturated oxygen (O2SAT) increased in both groups of animals and these dogs developed metabolic alkalosis 48 hours after the first administration of levamisole. The results of the study also show that levamisole poisoning in dogs causes a significant increase in the activity of serum alanine aminotransferase (ALT) and of alkaline phosphatase (AP) and in the concentration of urea in both Group A and Group B. In the study, atropin sulphate reduced the severity of the clinical signs and the number of deaths, but it was not alone sufficient to remedy levamisole poisoning in dogs.
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PMID:The effects of levamisole poisoning on the haematological and biochemical parameters in dogs. 1503 67

Ecstasy, the popular name for 3,4-methylenedioxymethamphetamine (MDMA), is a synthetic amphetamine derivative. It stimulates the sympathetic nervous system, producing serious adverse effects on the cardiovascular system. We present a 20-year-old female patient, who developed subarachnoid hemorrhage (SAH) and death following MDMA and coingestion with other drugs. She suffered from severe headache followed by vomiting, and conscious change 5 hours after an intake of 1 tablet MDMA and other drugs at a dance club. Her blood pressure was 226/164 mmHg, pulse rate 164/min, respiratory rate 30/min on arrival at our emergency department. Diffuse rales were heard over both lung fields. Both pupils' sizes were 4 mm, with sluggish reaction to light. A 12 lead electrocardiograph showed sinus tachycardia, ST depression in the inferior leads and V4 to V6 precordial leads. Laboratory findings revealed normal except a slightly raised white cell count and glucose. Arterial blood gas analysis showed pH was 7.333, with PaCO2 24.6 mmHg, PaO2 151.7 mmHg and HCO3 12.8 mmol/L. Chest x-ray revealed acute pulmonary edema. Urgent computerized tomography scanning of the head demonstrated SAH. Her condition continued to deteriorate, and went to deep coma and shock status. She expired on the second day although we treated aggressively.
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PMID:Subarachnoid hemorrhage and death following coingestion of MDMA with other drugs. 1577 90

Lithium (Eskalith) is commonly used in the treatment of depressive and bipolar affective disorders, in a population at relatively high risk for overdose. Lithium may help correct a chemical imbalance in the brain; however, it has a comparatively narrow therapeutic index. Thus, lithium intoxication is a frequent complication of chronic lithium therapy. The central nervous system (CNS) is the major organ system affected, although the renal, gastrointestinal (GI), endocrine, and cardiovascular (CV) systems also may be involved. Here we present a forty-two-year-old Caucasian female with altered mental status, inability to eat, speak or walk properly, with shaking and vomiting for three days. Past medical history was significant for hepatitis C and bipolar disorder. Vital signs were within normal limits. Physical exam revealed a patient with aphasia, tremor, and an expressionless face, able to make eye contact and move all four extremities. However, she was unable to follow commands and she expressed rigidity of extremities, mild tachycardia, and stupor. Severely elevated serum lithium levels were found. A diagnosis of severe lithium toxicity was made and the patient was admitted to the telemetry unit. Intravenous hydration with normal saline was initiated as the patient had normal kidney function, and urinary output was monitored. All psychotropic medications were held except for a benzodiazepine. In the meantime the patient developed acute respiratory distress, was intubated on clinical grounds and was transferred to the intensive care unit. Acute cardiogenic pulmonary edema and other causes of respiratory distress were ruled out; diagnosis of Adult Respiratory Distress Syndrome (ARDS) was made. After two months of mechanical ventilation, the patient was stabilized. Mental status, vital signs, and all laboratory parameters including thyroid function tests, normalized. The patient was transferred to a rehabilitation center. This is a rare case of ARDS associated with lithium intoxication.
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PMID:Prolonged requirement for ventilatory support in a patient with Eskalith overdose. 1641 84

Metabolic alkalosis is a primary pathophysiologic event characterized by the gain of bicarbonate or the loss of nonvolatile acid from extracellular fluid. The kidney preserves normal acid-base balance by two mechanisms: bicarbonate reclamation mainly in the proximal tubule and bicarbonate generation predominantly in the distal nephron. Bicarbonate reclamation is mediated mainly by a Na-H antiporter and to a smaller extent by the H-ATPase. The principal factors affecting HCO 3 reabsorption include effective arterial blood volume, glomerular filtration rate, chloride, and potassium. Bicarbonate regeneration is primarily affected by distal Na delivery and reabsorption, aldosterone, arterial pH, and arterial pCO2. To generate metabolic alkalosis, either a gain of base or a loss of acid, must occur. The loss of acid may be via the GI tract or by the kidney. Excess base may be gained by oral or parenteral HCO 3 administration or by lactate, acetate, or citrate administration. Factors that help maintain metabolic alkalosis include decreased glomerular filtration rate (GFR), volume contraction, hypokalemia, hypochloremia, and aldosterone excess. Clinical states associated with metabolic alkalosis are vomiting, mineralocorticoid excess, the adrenogenital syndrome, licorice ingestion, diuretic administration, and Bartter's and Gitelma's Syndromes. The effects of metabolic alkalosis on the body are varied and include effects on the central nervous system, myocardium, skeletal muscle, and the liver. Treatment of this disorder is simple, once the pathophysiology of the cause is delineated. Therapy consists of reversing the contributory factors promoting alkalosis and in severe cases, administration of carbonic anhydrase inhibitors, acid infusion, and low bicarbonate dialysis.
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PMID:Metabolic alkalosis. 1673 46


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