Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although the conditions that cause hypoglycemia in adults may also be present in infants and children, there are many entities unique to the pediatric age group. This reflects the delicate balance that exists in the newborn and young child between glucose production and utilization. During fasting in infants and children, hepatic glucose production is normally two to three times that of adults when expressed on the basis of weight. In the newborn and young infants, hypoglycemia usually presents with irritability, feeding difficulties, lethargy, cyanosis, tachypnea, and/or hypothermia rather than the typical adrenergic or neuroglucopenic symptoms seen in the adult. The hypoglycemia may be due to abnormalities in hormone secretion, substrate interconversion, or mobilization of metabolic fuels. The hypoglycemia associated with hyperinsulinemia may be transient neonatal, sustained, or drug-induced. Inborn errors of metabolism caused by enzymatic defects are responsible for hypoglycemia associated with abnormalities of production and utilization of metabolic fuels. These can involve carbohydrate, protein, and fat metabolism. In addition, there may be acquired or transient defects in carbohydrate metabolism secondary to other diseases or ingestion of certain substances. Finally ketotic hypoglycemia appears to be due to abnormalities in substrate availability. A variety of tests are useful for establishing the etiologic basis of the hypoglycemia, and the appropriate treatment depends upon the underlying cause.
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PMID:Hypoglycemia in infants and children. 264 28

Mania is a psychiatric illness that often requires immediate intervention, and the pregnant manic patient presents a therapeutic dilemma. Use of psychotropic medications during pregnancy may cause three complications: teratogenesis, neonatal toxicity, and behavioral toxicity. The literature contains few well-controlled studies for psychotropic medications in bipolar or other psychiatric populations and those often lack a control group or do not consider confounding factors such as other drug use. Pharmacologic alternatives include antipsychotics, lithium, carbamazepine, and benzodiazepines. Although studies and case reports describe fetal malformations in infants exposed in utero to psychotropic medications, the data are conflicting as to the nature of anomalies and risk of their occurrence. Malformations can occur in almost every organ system; however, the cardiovascular type are of major concern after lithium exposure during the first trimester and oral clefts after benzodiazepine exposure. Antipsychotic exposure can produce extrapyramidal symptoms in the neonate and lithium has been associated with neonatal cyanosis, lethargy, flaccidity, and non-toxic goiter. A neonatal abstinence syndrome has occurred after maternal benzodiazepine consumption. Behavioral toxicity is more difficult to assess, as long-term follow-up is needed. To date, evidence for behavioral toxicity in children exposed to lithium or antipsychotics in utero is lacking. Few specific guidelines for using psychotropic medications in an acutely manic pregnant patient exist. Current symptoms, past response, and the stage of gestation all must be considered. Complete elimination of symptoms may not be the goal. A team approach is essential in treatment of such a complex and challenging patient.
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PMID:Pharmacologic management of acute mania in pregnancy. 265 79

A 3-day-old girl had a syndrome of lethargy and lactic acidosis. Pregnancy and delivery had been normal; there was no consanguinity or family history of neuromuscular disease. At age 4 1/2 months, she had generalized weakness, hypotonia, areflexia, and macroglossia. She developed cyanosis and respiratory failure, and marked cardiomegaly was noted. She died at age 8 1/2 months of cardiac arrest. Results from a muscle biopsy specimen obtained at age 4 1/2 months showed ragged-red fibers and increased glycogen and lipid droplets. With the cytochrome c oxidase reaction, only 5% of the fibers stained positively in the biopsy specimen. Cytochrome c oxidase activity was 7.3% of normal in muscle mitochondria and 12.2% of normal in heart mitochondria. Reduced-minus-oxidized cytochrome spectra showed lack of the cytochrome aa3 peak. Immunotitration using antibodies against purified human heart cytochrome c oxidase showed normal amount of cross-reacting material in both heart and muscle. The genetic error could have involved a cytochrome c oxidase isozyme common to heart and muscle.
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PMID:Myopathy and fatal cardiopathy due to cytochrome c oxidase deficiency. 302 95

Nine- to ten-week-old, male castrated, specific pathogen-free derived pigs, weighing 34 to 42 kg, were exposed to a T-2 toxin aerosol (390 micrograms/liter, 1.5 microM mass median aerodynamic diameter) for a time period which allowed an amount equivalent to 8 mg/kg to be nebulized (six pigs). Control animals (five pigs) were exposed to an equivalent amount of the nebulized vehicle. Pigs were immunized subcutaneously with sheep red blood cells on Days 0 and 21. Whole blood and serum samples were taken periodically for clinical pathologic and immunologic studies. Pigs were closely observed, and daily rectal temperatures and weekly weights were measured. The T-2-treated pigs vomited and exhibited cyanosis, anorexia, lethargy, lateral recumbency, slightly elevated rectal temperature, and depressed body weight gain. The lymphocyte count decreased while the neutrophil count increased. The concentrations of total serum protein and hemoglobin declined. There was a marked increase in serum alkaline phosphatase activity on Day 1, followed by a marked and persistent decrease. Mitogen-induced (Con A, PHA, and PWM) blastogenic responses of peripheral blood mononuclear cells and hemagglutination titers to SRBC were also transiently decreased. Thus, inhalation exposure of pigs to a sublethal dose of T-2 toxin caused clinical signs of toxicity and adverse effects on clinical pathologic parameters and immune responses; however, most of these effects were short-lived. The changes described in our study resemble those reported in pigs given T-2 toxin by intravascular injection.
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PMID:Experimental T-2 toxicosis in swine following inhalation exposure: clinical signs and effects on hematology, serum biochemistry, and immune response. 320 8

The case of a 3-week-old male infant is described. After receiving an iatrogenic overdose of metoclopramide (1.0 mg/kg every six hours) throughout a 36-hour period for the treatment of suspected gastroesophageal reflux, he became cyanotic, lethargic, and irritable, he fed poorly, and he had diarrhea and respiratory distress. Methemoglobinemia (20.5%) and reduced oxyhemoglobin saturation (79%) were identified. The patient had an excellent clinical response following a single IV dose of methylene blue. Subsequently, methemoglobin reductase activity was normal and there was no measurable hemoglobin M. The diagnosis of methemoglobinemia should be considered in any infant receiving large doses of metoclopramide who has clinical findings of cyanosis, ashen color, or a history of lethargy and/or motor restlessness.
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PMID:Metoclopramide-induced methemoglobinemia. 340 65

We report the results of a two-part study examining the frequency of symptoms and other findings associated with neonatal polycythemia. In the first part of the investigation, we evaluated the occurrence and features of the disorder in a cohort of 3,768 infants born at our institution that had been screened for the disorder during a 4-year period. Fifty-five infants (1.46%) had neonatal polycythemia. Of these infants, 85% had features associated with the disorder. Frequent signs and symptoms included "feeding problems" (21.8%), plethora (20.0%), lethargy (14.5%), cyanosis (14.5%), respiratory distress (9.1%), jitteriness (7.3%), and hypotonia (7.3%). Other findings included hypoglycemia (40.0%) and hyperbilirubinemia (21.8%). Of the polycythemic infants, 14.5% had no clinical symptoms or associated laboratory abnormalities. In the second portion of the study, we reviewed the features of polycythemia in all infants so diagnosed who were born in United States Army hospitals, worldwide, during a 5-year period. There were 220,050 infants born during this period; 932 (0.42%) were diagnosed as having neonatal polycythemia. Frequent findings were hyperbilirubinemia (33.5%), hypoglycemia (13.0%), and respiratory distress (6.6%). In this large group, only 13 (1.4%) had necrotizing enterocolitis, and nine (1.0%) were thrombocytopenic. Several findings among the 932 infants were unexpected. Six of the infants (only one premature) had intracranial hemorrhages. Additionally, three of the 932 had gonadal dysgenesis and three had cystic fibrosis. We found that premature infants were not less prone to having polycythemia and that the overall frequency of the disorder was less than that which has been previously reported.
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PMID:Neonatal polycythemia: frequency of clinical manifestations and other associated findings. 372 98

Four infants with Down syndrome developed cor pulmonale and heart failure in association with chronic upper airway obstruction. Features of the sleep apnea syndrome were conspicuous; namely, noisy breathing with retraction, cyanosis and frequent apnea during sleep, and daytime lethargy and somnolence. The clinical picture masqueraded as cyanotic congenital heart disease. Arterial blood gas analyses revealed alveolar hypoventilation, especially during sleep. The nature of the obstructive element was variable. Adenoidectomy provided partial relief in one patient, and tonsillectomy and adenoidectomy resulted in temporary improvement in two others. Three patients were markedly benefitted by tracheostomy. Functional inspiratory pharyngeal closure was demonstrated fluorographically in one patient. Infants with Down syndrome may be predisposed to upper airway obstruction by virtue of hypoplasia of facial and oropharyngeal structures and generalized hypotonia. Additional obstructive elements may be contributed by hypertrophied lymphoid tissue, excessive secretions, and glossoptosis. Removal of the obstructive element is helpful, but functional obstruction may only be relieved by tracheostomy.
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PMID:Alveolar hypoventilation and cor pulmonale associated with chronic airway obstruction in infants with Down syndrome. 645 3

A fatal case of poisoning by a mixture of methanol and ethylene glycol is described. A 72-year-old man was hospitalized when he was found stuporous to semicomatose, and despite massive bicarbonate therapy, died 36 hr after the admission. While the presence of numerous oxalate crystals in urine strongly suggested ethylene glycol intoxication, the GC analysis of the liquid the patient ingested revealed that he presumably drunk about 150 to 200 ml of a mixture of methanol (80%) and ethylene glycol (20%), the amount well over the lowest lethal dose when the additiveness of toxicity was considered. Retrospective evaluation of the signs suggested that while some of them such as oxalate crystalluria, elevated CPK, hypocalcemia, renal failure are attributable to the toxicity of ethylene glycol, others including elevated serum amylase and cyanosis are indicative of methanol poisoning. Disturbed consciousness was considered to be of metabolic origin; the high anion gap observed (38.2 mEq/liter) may be due not only to lactic acidosis but also to acidogenicity of the two chemicals ingested. The importance of gas chromatographic analysis for identification of the causative chemical(s) is stressed.
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PMID:A case of poisoning by a mixture of methanol and ethylene glycol. 667 Jan 3

We report here on a case of primary alveolar hypoventilation in a 9 yr old child. From the age of 8 years, the patient has suffered from episodes of bronchopneumonia associated with severe respiratory insufficiency and lethargy. After recovery, cyanosis developed during the night and, later on, during the day. On two occasions, serious respiratory depression followed ketamine sedation for cardiac catheterization and total anaesthesia for cerebral angiography. Pulmonary function tests showed normal volumes and normal mechanics of breathing; blood gas analysis revealed a slight hypercapnic acidosis and hypoxia. The ventilatory response to CO2 was virtually absent, whereas voluntary hyperventilation normalized blood gas values. A polygraphic recording during sleep showed a marked worsening of hypoventilation, which occurred soon after falling asleep and continued throughout all sleep stages; sporadic central apnoeas, at times prolonged, were recorded only during light sleep. The patient, now 14 yr old, is maintained in satisfactory condition with low flow nocturnal oxygen administration combined with the use of a body respirator during sleep twice a week.
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PMID:A polygraphic study of one case of primary alveolar hypoventilation (Ondine's curse). 672 66

Active pulmonary vasoconstriction and subsequent right-to-left atrial and/or ductal shunting of venous blood may influence the course of many neonatal cardiorespiratory disorders. The term "persistent fetal circulation" has been applied to these infants. This report concerns the late occurrence of fetal circulation after major intraabdominal operative procedures in two neonates. The first patient was a full-term, 3.6-kg infant with a covered, large liver-containing omphalocele. Cyanosis, hypoxia, and a right-to-left shunt were present at birth, but were improved by 24 hr of life. Primary repair was delayed for 6 days, in the belief that fetal circulation was unlikely to recur. On day 7, primary fascial closure of the omphalocele was followed by severe hypoxia secondary to right-to-left shunt, documented to be due to postoperative fetal circulation (POFC). The second was a 1600-g premature infant who was well until noted to be lethargic on the fourth day of life. Radiologic findings of pneumoperitoneum led to laparotomy and closure of a spontaneous gastric perforation. Twenty-four hours later the patient developed severe hypoxia and a right-to-left shunt at the atrial level was documented with contrast echocardiogram, again supporting the diagnosis of POFC. Each patient survived and has a normal heart. Both patients responded to hyperventilation and/or tolazoline therapy. Contrast echocardiography was a helpful, noninvasive means of establishing the diagnosis. This diagnosis should be considered in postoperative neonates after more common cardiac and pulmonary causes of hypoxia are excluded.
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PMID:Postoperative fetal circulation: POFC. 717 45


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