Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anorexia nervosa and bulimia nervosa are eating disorders characterized by gross disturbances in eating behavior. Recently these disorders have reached near-epidemic proportions, affecting approximately 1.2 million adolescent and young adult females in the United States. The incidence in males is considerably less, and the prevalence rate has remained fixed at 5 percent during the last five years. The estimates of mortality range between 1 and 15 percent and are equally divided between medical complications (electrolyte disturbance, acute kidney failure, cardiac complications) and suicide. Successful treatment requires a combination of aggressive medical management, psychotherapy, behavioral management, food-intake management and nutritional counseling. This requires health care providers to understand 1) the psychological ramifications of these disorders, 2) the types of depression associated with them, 3) antidepressants used and therapeutic dosages, 4) correction of nutritional deficiencies, 5) outpatient management and 6) indications for hospitalization (inpatient management).
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PMID:Anorexia nervosa, bulimia nervosa: causal theories and treatment. 218 95

Acute causes and chronic risk factors for the development of acute renal failure were analyzed in prospective acquired data of 261 patients in a medical ICU. The population was divided into a group requiring dialysis treatment for established renal failure (n = 95) and a collective maintaining mild renal insufficiency (n = 166). Bivariate and linear discriminant analyses revealed that, above all, variables related to bacterial infections (sepsis and administration of antibiotic agents) and pancreatitis contributed to the discrimination, followed by bleeding, volume depletion, and chronic liver disease in the discriminant function. Bivariate analysis also yielded significant results for mechanical ventilation, CNS depression, and surgery. The importance of the nephrotoxic properties of aminoglycosides may be outweighed by their role as an indicator of severe infectious disease. The overall correct classification rate of the discriminant function was 78.5%, which reflects the importance of the predictor variables, but does not allow individual predictions.
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PMID:Impairment of renal function in medical intensive care: predictability of acute renal failure. 218 66

Nonsalicylate, nonsteroidal anti-inflammatory drugs (NSAIDs) can be divided into 4 chemical classes: acetic acids, fenamic acids, oxicams and propionic acids. Most NSAID overdoses result in a benign outcome. Of 50,614 exposures reported to poison centres in the United States in a 2-year period, 131 (0.26%) had a major outcome, with 10 deaths. Despite the generally mild effects reported in large patient series, isolated case reports have documented serious toxicity, such as seizures, hypotension, apnoea, coma and renal failure. The majority of these consequences occur after ingestion of substantial quantities by adults attempting suicide. Rarely, with ibuprofen and piroxicam, children who ingest small amounts in accidental exposure develop serious toxicity. Typical signs and symptoms of NSAID overdose include nausea, vomiting, headache, drowsiness, blurred vision and dizziness. Seizures are rarely documented across all NSAID classes, with the exception of mefenamic acid (where seizures occur in over one-third of cases), or following massive ingestion of other agents. Drugs in the propionic acid group have produced metabolic acidosis, respiratory depression and coma in severe cases. Ibuprofen is the agent with the most published data on overdose, probably because it is available without a prescription in many countries. Symptoms are unlikely after ingestion of 100 mg/kg or less, and are usually not life-threatening unless more than 400 mg/kg is ingested. There is some relationship between plasma concentrations and the potential for development of symptoms, but plasma concentrations have no impact on treatment decisions. Treatment of NSAID overdose is entirely supportive. Recent trends in emergency department procedures regarding gastric decontamination are evolving towards the recommended administration of activated charcoal without gastric emptying in patients presenting more than 1 hour after ingestion, although gastric lavage, followed by administration of activated charcoal, may be advisable in patients who present earlier. Home administration of syrup of ipecac is still recommended if treatment is given shortly after ingestion, with a few exceptions: for example, ipecac is contraindicated after ingestion of mefenamic acid or ibuprofen in amounts greater than 400 mg/kg. Urine alkalinisation and diuresis have been recommended to enhance the elimination of NSAIDs, based on a pKa in the range of 3 to 5. However, because the drugs are universally highly protein bound, with little unchanged renal excretion, this technique is not likely to be beneficial. Haemodialysis is also unlikely to enhance elimination, but may be required if oliguric renal failure develops. Multiple dose activated charcoal may be useful in enhancing elimination of NSAIDs with long half-lives, such as piroxicam and sulindac.
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PMID:Toxic effects of nonsteroidal anti-inflammatory drugs in overdose. An overview of recent evidence on clinical effects and dose-response relationships. 219 51

More than a century ago, Jonathan Hutchingson, a surgeon-dermatologist, identified the first case of sarcoidosis at King's College, London. The disease is now known as a commonplace multisystem disorder characterized by the formation of noncaseating granulomata. The diagnosis of sarcoidosis is established by recognizing clinicoradiologic findings and providing histologic evidence of non-caseating granuloma. Serum angiotensin converting enzyme levels are high in about two thirds of the patients and hypercalcemia is a feature in one of every ten victims of sarcoidosis. Immunologic abnormalities include depression of cutaneous delayed-type hypersensitivity, accumulation of T-cells at the site of activity, hyperactive B-cells, and the presence of circulating immune complexes. The course and prognosis of the disease usually correlate with the mode of onset. An acute onset with erythema nodosum indicates a good prognosis and spontaneous resolution; whereas, an insidious onset may be followed by relentless, progressive fibrosis. Mortality and morbidity are caused by pulmonary fibrosis, cardiac arrhythmias, renal failure, neurologic involvement, and blindness. Corticosteroids and chloroquine relieve symptoms and suppress inflammation and granuloma formation.
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PMID:Sarcoidosis. 220 9

Patients with end stage renal failure have been shown to have higher basal concentrations of plasma arginine vasopressin than subjects with normal renal function. Immunoreactive vasopressin was detected in plasma from patients with severe chronic renal failure and a healthy subject at an elution volume identical to that previously determined with synthetic vasopressin. Assay of all fractions yielded identical chromatograms in the renal failure and healthy control groups. We conclude that the plasma immunoreactive vasopressin in end stage renal failure plasma coelutes with synthetic vasopressin and that the elevated concentrations found in these patients are not due to non-specific depression of binding in the vasopressin radioimmunoassay by circulating substances in renal failure.
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PMID:Immunoreactive vasopressin in end stage renal failure. 225 98

1. A 43-year-old male developed acute kidney failure due to ethylene glycol poisoning. He was treated with bicarbonate to combat metabolic acidosis, ethanol as an antimetabolite and haemodialysis to remove the glycol and its toxic metabolites. He was kept on a respirator and sedated with morphine. Peritoneal dialysis was given for 36 d. Following sedation with morphine for 11 d, the patient was given naloxone and then extubated. The antidote had to be continued for 14 d to prevent respiratory depression, until kidney function improved. 2. Only morphine-6-glucuronide (M-6-G) was found in the plasma and CSF at concentrations which might explain the opioid effects observed in the patient during the days after the cessation of morphine treatment. The ratio of the area under the concentration-time curve (AUC) of morphine-3-glucuronide (M-3-G) to M-6-G was 2:1. The elimination half-lives of M-3-G and M-6-G were 55 and 82 h, respectively. The clearance data indicate that most of the glucuronides were eliminated by peritoneal dialysis during renal failure. 3. The data suggest that M-6-G exerts opioid effects and is retained in acute kidney failure. Morphine should therefore not be used preferentially as a sedative/analgesic in pronounced kidney failure.
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PMID:Morphine-6-glucuronide might mediate the prolonged opioid effect of morphine in acute renal failure. 226 Dec 46

Serum magnesium (Mg) was measured in 6,252 patients; in 1,246 (19.9%) the value was abnormal. Hypermagnesemia (serum Mg greater than or equal to 3.9 mg/dl) was observed in 51 patients (0.8%) and hypomagnesemia (Mg less than or equal to 1.5 mg/dl) in 165 (2.6%). Hypermagnesemia was found in patients with renal failure treated with Mg-containing antacids or cathartics, or with eclamptic convulsions treated with Mg sulfate. The most frequent clinical finding of hypermagnesemia was urinary disturbance, although various other neurological signs and symptoms were observed. Hypomagnesemia was seen in patients with various diseases such as cancer, hepatic cirrhosis, cerebrovascular disease, and generally poor condition. Abnormalities of electrolytes other than Mg were also frequently observed. The most common clinical findings of hypomagnesemia were personality changes and depression. The differentiation from psychiatric disease is important.
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PMID:An analysis of hypermagnesemia and hypomagnesemia. 227 20

Retrospective analysis of 58 burn patients (greater than or equal to 60% TBSA) were performed. 38 patients associated with MSOF according to the criteria stated by Eiseman. Glucose and osmolality were examined continuously in all patients. Glucose was determined by using a glucose oxidase method, and osmolality by freezing-point depression method. We investigated the relationship between the incidence of MSOF and changes in glucose and osmolality in burn patients. The present study showed that, (1) Glucose and osmolality were significantly higher in group of MSOF than group of non-MSOF from the third day postburn. (2) The elevation of glucose and osmolality in patients with MSOF dominated about four days earlier than the development of MSOF. (3) The osmolality was markedly higher after renal failure than before, but the glucose was not. (4) The incidence rate of MSOF increased as the elevation of glucose and osmolality. This paper suggested that, (1) The hypermetabolic situation of posttrauma is one of the important causes of MSOF. (2) The occurrence of acute renal failure induced metabolic disturbance and had an adverse effect on other organs. (3) Continuous determination of glucose and osmolality in severe trauma patients may be useful in the early diagnosis of MSOF.
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PMID:[Changes in blood glucose and plasma osmolality in postburn multiple system organ failure]. 227 60

Quinidine, procainamide and disopyramide are antiarrhythmic drugs in the class 1A category. These drugs have a low toxic to therapeutic ratio, and their use is associated with a number of serious adverse effects during long term therapy and life-threatening sequelae following acute overdose. Class 1A agents inhibit the fast inward sodium current and decrease the maximum rate of rise and amplitude of the cardiac action potential. Prolonged Q-T interval and, to a lesser extent, QRS duration may be observed at therapeutic concentrations of quinidine. With increasing plasma concentrations, progressive depression of automaticity and conduction velocity occur. 'Quinidine syncope' (a transient loss of consciousness due to paroxysmal ventricular tachycardia, frequently of the torsade de pointes type) occurs with therapeutic dosing, often in the first few days of therapy. Extracardiac adverse effects of quinidine include potentially intolerable gastrointestinal effects and hypersensitivity reactions such as fever, rash, blood dyscrasias and hepatitis. Procainamide produces electrophysiological changes that are similar to those of quinidine, although Q-T interval prolongation with the former is less pronounced at therapeutic concentrations. Hypersensitivity reactions including fever, rash and (more seriously) agranulocytosis are associated with procainamide, and a frequent adverse effect requiring cessation of therapy is the development of systemic lupus erythematosus. Of the 3 drugs, disopyramide has the most pronounced negative inotropic effects, which are especially significant in patients with pre-existing left ventricular dysfunction. As with quinidine, unexpected 'disopyramide syncope' at therapeutic concentrations has been described. Anticholinergic side effects are common with this drug and may require cessation of therapy. Disopyramide therapy may unpredictably induce severe hypoglycaemia. Severe intoxication with the class 1A agents may result from acute accidental or intentional overdose, or from accumulation of the drugs during long term therapy. Acute overdose can result in severe disturbances of cardiac conduction and hypotension, frequently accompanied by central nervous system toxicity. Decreased renal function can cause significant accumulation of procainamide and its active metabolite acecainide (N-acetyl-procainamide), resulting in severe intoxication. Mild to moderate renal dysfunction is less likely to lead to quinidine or disopyramide intoxication, unless renal failure is severe or concurrent hepatic dysfunction is present. Management of acute intoxication with class 1A drugs includes gut decontamination with provision of respiratory support and treatment of seizures as needed. Hypertonic sodium bicarbonate, by antagonising the inhibitory effect of quinidine on sodium conductance, may reverse many or all manifestations of cardiovascular toxicity.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Poisoning due to class IA antiarrhythmic drugs. Quinidine, procainamide and disopyramide. 228 95

Renal failure has both medical and psychological implications. Indeed, various psychiatric problems related to end-stage renal disease have been reported in the literature; however, the focus has been on anxiety and depression. While previous research has dealt with the comparisons of patients with renal failure, few studies have investigated the comparison of renal patients with psychiatric and general medical patients. The present study compared renal patients (N = 24) with a group of depressed psychiatric patients (N = 24) and a group of general medical patients (N = 24) on the MMPI. The results suggested that the renal group presented a psychological profile that more closely resembled that of the depressed psychiatric group than that of patients with other chronic medical conditions.
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PMID:MMPI differences for renal, psychiatric, and general medical patients. 232 1


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