Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Methylmalonic acidemia (MMA) is an inherited organic acidemia usually present with recurrent episodes of acute illness. A typical episode is ushered in with ketonuria and vomiting, followed by acidosis, dehydration, and lethargy, leading, in the absence of aggressive treatment, to coma and death. We report an infant with MMA presented with diabetes symptoms. A 13-month-old girl complained of polydipsia, diuresis, and loss of weight. She had clinical signs of diabetic ketoacidosis such as dehydration, deep sighing respiration, smell of ketones, lethargy, and vomiting. Laboratory analysis showed hyperglycemia with acidosis and ketonuria. She was treated with parenteral fluid, electrolyte, and insulin infusion. Two days after her discharge, after having a meal rich in protein, she was brought unconscious with hepatomegaly, severe acidosis, ketonuria, and mild hyperammonemia. The absence of hyperglycemia and the presence of neurologic findings suggested organic acidemia. MMA was diagnosed because of methylmalonic aciduria and elevated C3 carnitine esters. Cranial magnetic resonance imaging (MRI) showed increased uptake of radiocontrast material in the basal ganglia bilaterally. A homozygous mutation in exon 4 of the MMAA gene was found in mutation analysis and confirmed the diagnosis of cblA-deficient MMA. Neurologic regression was improved with treatment of low-protein diet, vitamin B12, and l-carnitine. In patients born to consanguineous parents who admit during infancy with severe acidosis refractory to treatment, organic acidemias should be kept in mind, even they have high blood glucose. The definitive diagnosis is important because it may allow a specific treatment and a favorable evolution to prevent the sequelae.
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PMID:Methylmalonic acidemia mimicking diabetic ketoacidosis in an infant. 2154 77

A 6 yr old pregnant Yorkshire terrier bitch presented 62 days after mating with an acute history of vomiting and coughing. The owners also reported that the dog was polyuric and polydypsic for the last 2 weeks. Complete blood count, serum biochemistry, and urinalysis revealed hyperglycemia, ketonemia, ketonuria, and metabolic acidosis. Diabetic ketoacidosis was diagnosed and after emergency treatment, including fluid therapy, prophylactic antibiotics, and regular insulin, the bitch whelped six healthy normal puppies. Two weeks after treatment, the bitch was clinically normal with normal fructosamine levels. To the authors' knowledge, this is the first reported case of gestational diabetes mellitus in a small breed dog.
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PMID:Gestational diabetes mellitus with diabetic ketoacidosis in a Yorkshire terrier bitch. 2167 34

Neonatal diabetes mellitus (NDM) is a rare disorder. A one-month-old boy presented with vomiting, hyperglycemia (968 mg/dl [53.8 mmol/L]), severe acetonemia, and metabolic acidosis (pH 6.95, HCO3-4.2 mmol/L). A second child (three months of age) presented with upper respiratory tract symptoms and a plasma glucose level of 835 mg/dl, without acetonemia or acidosis. Both were hospitalized and managed with intravenous fluids and then discharged on insulin. Genetic testing identified the presence of the de nova V59M and E322K activating mutations in the KCNJ11 gene encoding the sulphonylurea/potassium channel (Kir6.2 subunit) of the insulin beta cell. Both patients were switched to glibenclamide and remain off insulin. To our knowledge, these are the first children in Puerto Rico identified with NDM secondary to a KCNJ11 activating mutation. We conclude that NDM secondary to KCNJ11/Kir6.2 activating mutations, although unusual, should be considered in similar cases since patients with these mutations could come off insulin.
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PMID:Neonatal diabetes mellitus: description of two Puerto Rican children with KCNJ11 activating gene mutation. 2168 53

Severe hypokalemia is a potentially life-threatening disorder and is associated with variable degrees of skeletal muscle weakness, even to the point of paralysis. On rare occasions, diaphragmatic paralysis from hypokalemia can lead to respiratory arrest. There may also be decreased motility of smooth muscle, manifesting with ileus or urinary retention. Rarely, severe hypokalemia may result in rhabdomyolysis. Other manifestations of severe hypokalemia include alteration of cardiac tissue excitability and conduction. Hypokalemia can produce electrocardiographic changes such as U waves, T-wave flattening, and arrhythmias, especially if the patient is taking digoxin. Common causes of hypokalemia include extrarenal potassium losses (vomiting and diarrhea) and renal potassium losses (eg, hyperaldosteronism, renal tubular acidosis, severe hyperglycemia, potassium-depleting diuretics) as well as hypokalemia due to potassium shifts (eg, insulin administration, catecholamine excess, familial periodic hypokalemic paralysis, thyrotoxic hypokalemic paralysis). Although the extent of diuretic misuse in professional bodybuilding is unknown, it may be regarded as substantial. Hence, diuretics must always be considered as a cause of hypokalemic paralysis in bodybuilders.
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PMID:Hypokalemic paralysis in a professional bodybuilder. 2315 15

Motion sickness is caused by exposure to unfamiliar motions and typical symptoms of motion sickness include nausea and vomiting. To observe the metabolic and hormonal differences between nausea/vomiting (NAV) subjects and non-nausea/vomiting (NNV) ones, and to understand how the differences in metabolites and hormones affect the tolerance of organism to acceleration, 60 volunteers were exposed to repetitive acceleration using a 6-degree-of-freedom ship motion simulator. Meanwhile, 36 rats were randomly divided into three groups: an acceleration model group (n=14, exposed to acceleration), insulin group (n=14, intraperitoneal injection of insulin 30 min before exposure to acceleration), and control group (n=8). Gas chromatography coupled to time-of-flight mass spectrometry (GC-TOF/MS) was applied to analyze the serum metabolites in human subjects. Serum glucocorticoid, insulin, and glucagon levels were determined by radioimmunoassay in the NAV and NNV subjects as well as in rats, and serum epinephrine level was determined by ELISA. After acceleration exposure, 9 metabolites, including L-histidine, L-ornithine, L-serine, L-tyrosine, pyroglutamic acid, fumaric acid, urea, n-dodecanoic acid and n-tetradecanoic acid, had different changes in the NAV and NNV groups. The serum levels of 4-hydroxy-L-proline, glucose, oleic acid and urea were significantly higher in the NAV group than in the NNV group after exposure; however, only the elevation degree of serum glucose was significantly greater in the NAV group than in the NNV group (P<0.05). Serum cortisol and epinephrine were increased in both groups. Before exposure, insulin level in the NAV group was significantly lower than that in the NNV group (P<0.05). After rotation exposure, rat serum glucose in the insulin group was significantly lower than that in the acceleration model group (P<0.001), and the motion sickness index was significantly lower than that in the acceleration model group (P<0.05). Our study provides the first evidence that stable glucose level can help to relieve gastrointestinal symptoms in motion sickness, and suggests that acute hyperglycemia is related to gastrointestinal symptoms in motion sickness.
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PMID:Acute hyperglycemia is related to gastrointestinal symptoms in motion sickness: an experimental study. 2190 24

Postoperative nausea and vomiting (PONV) is a common annoying experience after surgery. The overall incidence of PONV in adults is 20-30%; the incidence rate in patients of high-risk groups can be as high as 70-80%. Children are not exempted from attacking either; the incidence rate in children above the age of 3 is more than 40%. The incidence slowly drops after puberty, sharing the same rate with adults. Dexamethasone can be effective in preventing PONV in adults and children. Compared with other preventive medications, dexamethasone has equal or even better efficacy in reducing the incidence of PONV and has the advantages of low cost and longer effectiveness as well. Although the action mechanism of dexamethasone is hitherto not fully understood, animal studies have confirmed that the vomiting center in the brain stem plays a central role. A combination of dexamethasone with other antiemetics is more effective than any single drug alone. Additionally, the use of dexamethasone to prevent nausea and vomiting triggered by intravenous or epidural morphine for pain control can also offer a good therapeutic effect. To date, clinically, dexamethasone as a preventative drug against PONV has not caused fatal outcome; therefore, it is generally considered to be an effective and safe antiemetic. Nevertheless, its use in this regard may lead to adverse effects, principally postoperative hyperglycemia and infection.
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PMID:Dexamethasone prevents postoperative nausea and vomiting: benefit versus risk. 2198 66

Fructose-1,6-diphosphatase (FDPase) enzyme deficiency is a rare inherited metabolic disease. Affected patients usually present with metabolic crisis including hypoglycemia, acidosis, ketonuria, and hyperuricemia. A previously healthy 8-month-old male infant presented with fever, vomiting, and hypoactivity. He had tachycardia, tachypnea, and a tendency to sleep. The patient had signs of severe dehydration and shock. Laboratory findings revealed significant lactic acidosis, hyperuricemia, hyperglycemia, elevated liver enzyme level, and hyperlipidemia. The urine analysis had evidence of glycosuria and ketonuria. Hyperuricemia, lactic acidemia, and hyperglycemia persisted despite insulin infusion, adequate hydration, and perfusion. Consequently, peritoneal dialysis was started. About 12 hours after dialysis, his metabolic derangements were normalized, and clinical status was improved dramatically. His metabolic disease workup was compatible with FDPase deficiency. Here, we described a metabolic attack of FDPase deficiency presented with hyperglycemia mimicking diabetic ketoacidosis.
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PMID:Gluconeogenesis defect presenting with resistant hyperglycemia and acidosis mimicking diabetic ketoacidosis. 2215 80

Patients with impaired nutritional status may show increased risk of hematopoietic stem cell transplantation (HSCT)-related complications. This study was conducted to determine whether body mass index (BMI) and other body composition parameters, such as lean body mass index (LBMI) and body fat mass (BFM), are associated with early post-transplantation toxicity and mortality in allogeneic HSCT recipients. The records of 71 patients diagnosed with acute myeloid leukemia (AML), acute lymphoblastic leukemia (ALL), chronic myeloid leukemia (CML), or myelodysplastic leukemia (MDS) who had undergone allogeneic HSCT with a conditioning regimen of busulfan-cyclophosphamide (Bu-Cy), between September 2003 and January 2009 at the Stem Cell Transplantation Unit of Gazi University Hospital were retrospectively evaluated. BMI was found to be negatively correlated with the NCI grade of mucositis, cardiotoxicity, emesis, and hyperglycemia, and with the number of erythrocyte transfusions. LBMI was also negatively correlated with the number of erythrocyte transfusions, cardiotoxicity, emesis, and hyperglycemia. BFM was negatively correlated with the day of neutrophil engraftment, and NCI grade of mucositis. Nutritional status did not have an impact on overall survival (OS), progression-free survival (PFS), or 100-day transplant related mortality (TRM).
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PMID:The role of body mass index and other body composition parameters in early post-transplant complications in patients undergoing allogeneic stem cell transplantation with busulfan-cyclophosphamide conditioning. 2216 Aug 35

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

Octreotide is an octapeptide that mimics natural somatostatin pharmacologically. It is a potent inhibitor of growth hormone, glucagon and insulin, which is used for treatment of acromegaly, symptomatic treatment of carsinoid tumours, and vasoactive intestinal peptide secreting tumors. It is also used for chylothorax, chemotherapy induced diarrhea and, as it inhibits the exocrine production of pancreatic enzymes, for acute and chronic pancreatitis. Gallbladder stones, diarrhea, nausea, vomiting, hypoglycemia/hyperglycemia, headache, and abdominal discomfort are some of the common adverse effects of octreotide and it may rarely cause anaphylaxis. We present here a child who had chronic pancreatitis and had an anaphylactic reaction to octreotide. To our knowledge this is the first pediatric case of anaphylaxis with octreotide who was successfully desensitized.
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PMID:A pediatric case of anaphylaxis due to octreotide. 2229 17


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