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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyperemesis gravidarum is an extreme form of nausea and vomiting during pregnancy. Its presenting symptoms include vomiting, disturbed nutrition, electrolyte imbalance, ketosis, extreme weight loss, renal and/or liver damage. It is rare for a hyperemesis gravidarum patient to present with jaundice, hyperthyroidism and idiopathic acute pancreatitis during the same hospitalization period. Here, we report such a case. A 25-year-old pregnant woman without underlying liver or thyroid disease was admitted due to jaundice noted for 2 days at 8 weeks of gestational age. Hyperthyroidism symptoms of tachycardia and finger tremor also bothered her. After treatment with parenteral fluid and antithyroid agents, her clinical condition improved. However, an episode of idiopathic pancreatitis occurred after nausea and vomiting subsided. Bowel rest with parenteral fluid and nutrition supplement was given and the increased pancreatic enzyme level gradually subsided. Follow-up liver and thyroid function were normal after gestational age of 26 weeks. She delivered a healthy female baby without low birth body weight at gestational age of 39 weeks. Rapid diagnosis and supportive care are important for the hyperemesis gravidarum patient with the complication of acute pancreatitis.
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PMID:Hyperemesis gravidarum presenting as jaundice and transient hyperthyroidism complicated with acute pancreatitis. 1581 35

As anyone else, diabetic patients are confronted to professional or private travels. This article is meant to gather some practical recommendations to allow patients to travel safely. All travels must be thoroughly prepared and diabetes must stabilised at best before departure. To avoid severe hypoglycaemias and ketosis are the medical objectives. It is therefore essential that patients take with them their injection material and a sufficient carbohydrate back up. The prevention of diarrheas and vomiting, as well as the adaptation of treatment to jet-lag and all kind of physical activity are necessary to have a nice travel. Some specific aspects of travelling by car, boat or plane are discussed.
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PMID:[Diabetics travelling]. 1596 25

Isovaleric acidemia (IVA), a rare recessive autosomal disorder, is caused by isovaleryl-CoA dehydrogenase (IVD) deficiency. IVA may present with symptoms during the acute stage of severe metabolic acidosis, ketosis, vomiting, and altered mental status. With the help of newborn screening (NBS) by tandem mass spectrometry (MS/MS), IVA can now be diagnosed presymptomatically. According to statistic data, the incidence of IVA in Taiwan was about 1/365,000. In this study, six IVA patients from five families were investigated and followed-up clinically. As for the timing, two patients were found before MS technique introduced to Taiwan, the others were identified after MS/MS applied to NBS. The blood level of C5-carnitine in our patients was 7.43-18.96 microM (with upper limit in our laboratory <0.51 microM) and all of their urines contained raised amounts of 3-hydroxyisovaleric acid and isovalerylglycine. Molecular analysis of their IVD gene revealed six mutation profiles, among which the 149G-->A (Arg21His) and 1174 C-->T (Arg363Cys) mutations have been reported previously, while the other four mutations, 386A-->G (His100Arg), 347C-->T (Ser87Phe), 1007G-->A (Cys307Tyr) and 1199A-->G (Tyr371Cys), were first reported. Specially, we found 1199A-->G (Tyr371Cys) mutated was a common recurring missense mutation in our population (4 in 10 mutant alleles).
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PMID:Genetic mutation profile of isovaleric acidemia patients in Taiwan. 1702 10

Propionic acidemia is an autosomal recessive disorder as a result of a deficient activity of propionyl-CoA carboxylase. Propionyl CoA is metabolized by propionyl-CoA carboxylase to methylmalonyl CoA. Propionic acidemia is a major cause of ketotic hyperglycinemia. This disorder is characterized by episodic vomiting, dehydratation, feeding intolerante, lethargy, hypotonia, metabolic acidosis, ketosis and hyperammonemia. The patient presented herein was a full-term female newborn with encephalopathy in the first days of life. She presented hypoglycemia, metabolic acidosis with increased anion gap, ketosis, hyperammonemia, anemia, leukopenia and thrombocytopenia. The brain ultrasonography was normal. The tandem mass expectrometry done by Pediatrix was abnormal, with the acylcarnitine results consistent with an organic acidemia. The parents are consanguineus and have a history of abortus, miscarriage and neonatal death, characteristics suggestive of the presence of genetic defects.
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PMID:[Neonatal onset of organic acidemia (propionic) diagnosed by tandem mass spectrometry]. 1864 57

Diabetic ketoacidosis (DKA) is associated with disturbances of acid base, fluid balance and electrolytes. Much of the established literature states that the fluid deficit in someone presenting with DKA is in the region of 6-8 l of fluid (about 100 ml/Kg), and this needs to be the fluid volume that is replaced in the first 24 h following admission to hospital. The physiology of fluid loss in DKA is complex. In summary, however, as blood glucose levels rise, the renal threshold for active glucose reabsorbtion is exceeded leading to glucose loss in the urine. This leads to an osmotic diuresis, and thus dehydration if oral intake is insufficient. Further losses are accounted for by hyperventilation, sweating and vomiting. With the older insulins--such as soluble human insulins, the duration of action was 8-10 h, with a peak of action at approximately 2-4 h after subcutaneous injection. Because very low insulin concentrations are sufficient to prevent ketone production, and because insulin concentrations would stay sufficiently high enough to do this, ketones would not be formed for up to 10 h after the last injection. Furthermore, concentrations of ketones sufficiently high enough to make a person unwell may take several more hours to develop. However, during this time, as insulin concentrations declined, blood glucose levels would increase, eventually overcoming the renal threshold, causing the renal diuresis and subsequent dehydration. Thus, on human soluble insulin, there is the opportunity to become profoundly dehydrated prior to the onset of significant ketoacidosis. The new rapid acting analogue insulins have durations of action of between 4 and 6 h. Thus the individual would become absolutely insulin deficient relatively quicker than with human soluble insulin. In this circumstance, the blood glucose would not have time to rise as high as with human soluble insulin deficiency before significant ketosis develops, thus leading to a lesser degree of dehydration. New rapid acting insulin analogues are becoming more widely used. This suggests that the volumes needed to replace those lost prior to the onset of significant DKA may be lower.
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PMID:People with type 1 diabetes using short acting analogue insulins are less dehydrated than those with using human soluble insulin prior to onset of diabetic ketoacidosis. 1869 27

Mitochondrial acetoacetyl-CoA thiolase deficiency (or beta-ketothiolase deficiency) is a rare metabolic disorder characterized by acute episodes of severe acidosis and ketosis. A case is presented of an 18-month-old boy who presented with vomiting and diarrhoea and was found to be markedly acidotic. When the acidosis persisted despite saline fluid boluses and bicarbonate correction, further investigations were undertaken. Routine biochemical investigation revealed detectable salicylate concentrations despite the parents denying its administration, which initially caused some diagnostic confusion. The results of urine organic acid analysis, however, confirmed that the diagnosis of mitochondrial acetoacetyl-CoA thiolase deficiency. The high concentrations of acetoacetate present in the patient's sample resulted in a false-positive reaction in the Trinder assay for salicylate.
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PMID:An unusual cause of interference in a salicylate assay caused by mitochondrial acetoacetyl-CoA thiolase deficiency. 1875 30

The medium-chain triglyceride diet (MCTD) is a variant of the classic 4:1 ketogenic diet (KD) introduced in 1971 by Huttenlocher as an attempt to improve the palatability of the KD by allowing more carbohydrates yet preserving ketosis. Although initially found to be equally effective as the classic KD, use of the MCTD declined because of frequent gastrointestinal side effects such as cramps, diarrhea, and vomiting. Recently, we have used the MCTD in more than 50 patients. We have found excellent seizure control, similar to the classic KD, and with careful monitoring, we have encountered minimal side effects. The MCTD should remain a viable dietary option for children with refractory epilepsy who have large appetites, can tolerate more calories, or cannot accept the restrictions of the classic KD.
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PMID:Medium-chain triglyceride (MCT) ketogenic therapy. 1904 83

3-Hydroxy-3-methylglutaric aciduria is a rare disorder of organic acid metabolism caused by 3-hydroxy-3-methylglutaryl-coenzyme A lyase deficiency. The disorder was common in neonatal or infant period. Here a case of late onset 3-hydroxy-3-methylglutaric aciduria complicated by leucodystrophy was reported. The patient was a 7-year-old boy. He presented with progressive headache, drowsiness and vomiting. Hepatic lesions, ketosis and leucopenia were found. Symmetrical diffused leucodystrophy was shown by MRI. Blood levels of isovalerylcarnitine and acetylcarnitine increased significantly. Urinary levels of 3-hydroxy-3-methylglutaric, 3-methylglutaconic, 3-hydroxyglutaric acids and 3-methyl-crotonylglycine increased significantly. Symptoms were released by intravenous infusion of L-carnitine and glucose. After treatment for 6 months, urinary levels of 3-hydroxy-3-methylglutaric aciduria decreased in the boy and his health improved.
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PMID:[Leucodystrophy induced by late onset 3-hydroxy-3-methylglutaric aciduria]. 2157 45

A 2-year-old boy was admitted with diagnosis of diabetes debut, with blood glucose of 500 mg% on admission, without ketosis or metabolic acidosis. He also presented bilious vomiting and brownish bloody stools. He was operated with a presumptive diagnosis of acute intestinal obstruction. The final diagnosis was volvulus, secondary to congenital malrotation. After surgery, he normalized blood sugar levels. The clinical setting was assumed as hyperglycemia without ketosis, with characteristic of severity caused by stress, secondary to volvulus in malrotation. This association has not yet been described.
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PMID:[Intestinal malrotation with volvulus associated with severe stress hyperglycemia]. 2223 80

Starvation ketosis outside pregnancy is rare and infrequently causes a severe acidosis. Placental production of hormones, including glucagon and human placental lactogen, leads to the insulin resistance that is seen in pregnancy, which in turn increases susceptibility to ketosis particularly in the third trimester. Starvation ketoacidosis in pregnancy has been reported and is usually precipitated by a period of severe vomiting. Ketoacidosis is likely to have important implications for fetal survival as ketoacidosis in women with type 1 diabetes mellitus is associated with intrauterine death. This article features four cases of women with vomiting in the third trimester of pregnancy associated with a severe metabolic acidosis. The mechanism underlying ketogenesis, the evidence for accelerated ketogenesis in pregnancy and other similar published cases are reviewed. A proposed strategy for management of these women is presented.
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PMID:Starvation ketoacidosis in pregnancy. 2313 45


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