Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0000737 (abdominal pain)
 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cefdinir is an extended-spectrum, third-generation cephalosporin that may be used for treatment of acute otitis media in patients allergic to penicillin. When administered with iron-containing products, including infant formulas, cefdinir or one of its metabolites may bind to ferric ions, forming a nonabsorbable complex that imparts a reddish color to the stool. We describe a 9-month-old infant with failure to thrive and acute otitis media who developed an erythematous maculopapular rash during treatment with amoxicillin-clavulanate. His antibiotic therapy was changed to cefdinir. Five days into a 10-day course of therapy, the infant's mother brought him to the pediatric clinic and reported the appearance of red stools. He had no associated gastrointestinal symptoms (vomiting, abdominal pain, or diarrhea). His hematocrit and hemoglobin level were normal, and Clostridium difficile antigen studies and tests for species of Shigella, Salmonella, and Camphylobacter as well as ova and parasites were all negative. Cefdinir was discontinued, and his stools returned to normal within 48 hours. Three weeks later, he again received cefdinir for recurrent otitis media. Red stools reappeared 48 hours later, were determined to be guaiac negative, and resolved within hours of drug discontinuation. During both occurrences of red stools, the infant had been breastfed and was receiving supplemental feedings with an iron-containing infant formula. In the product labeling of cefdinir, this adverse event is described as a consequence of the drug-drug interaction; however, it is not listed in the adverse drug reaction section of the labeling. As such, one may miss the association between cefdinir and reddish stools when investigating this event as a potential adverse reaction to cefdinir. When using the Naranjo adverse drug reaction probability scale to assess causality in our patient's case, this adverse drug reaction was determined as highly probable. As this infant had been breastfed, the use of a supplemental iron-containing infant formula was not identified as a potential contributing factor until the second occurrence of red stools. Health care professionals should review the entire product labeling, including the drug-drug interaction section, when investigating a potential adverse drug reaction. With the recent approval of generic formulations of cefdinir, clinicians should be aware of this drug-drug interaction with iron-containing products to prevent unnecessary alarm by parents and caregivers, as well as costly medical evaluations for gastrointestinal bleeding.
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PMID:Nonbloody, red stools from coadministration of cefdinir and iron-supplemented infant formulas. 1844 64

Cyclic vomiting syndrome (CVS) is a disorder characterized by recurrent, stereotypic episodes of incapacitating nausea, vomiting, and other symptoms, separated by intervals of comparative wellness. Associated symptoms include nausea, abdominal pain, headache, and motion sickness. Recently, CVS was categorized as a migraine. Case 1 was a girl aged 4 years and 11 months, who had frequent and severe episodes of vomiting since she was 3 years old. The diagnosis of CVS was established on the basis of clinical symptoms and laboratory data. Her electroencephalogram was normal. Prophylactic therapy using a single drug such as amitriptyline, carbamazepine, phenytoin, cyproheptadine, valproate sodium or phenobarbital was not effective. However, her recurring vomiting disappeared with prophylactic therapy using valproate sodium and phenobarbital. Case 2 was a boy aged 10 years and 7 months, who had frequent episodes of vomiting since he was 1 year and 10 months old. He had been receiving intravenous hyperalimentation therapy at home since infancy because of frequent vomiting and failure to thrive. His electroencephalogram showed no abnormality. Prophylactic therapy using a single drug such as diazepam, phenytoin, valproate sodium or phenobarbital was not effective. However, his recurring vomiting disappeared with prophylactic therapy using valproate sodium and phenobarbital. There were no adverse effects in both patients. The combination therapy with valproate sodium (20 - 26 mg/kg/day) and phenobarbital (4 - 5 mg/kg/day) was effective as a prophylactic therapy in these two patients. The combination therapy with valproate sodium and phanobarbital for prophylaxis of vomiting may be helpful in patients with intractable CVS.
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PMID:[The effect of prophylactic therapy with valproate sodium and phenobarbital in two patients with cyclic vomiting syndrome]. 1880 88

Congenital diaphragmatic hernia (CDH) presents a wide spectrum of anatomical variants and clinical pictures depending on the topography and dimensions of the diaphragmatic defect and on the patient age. Most CDH cases acutely present with tachypnea, cyanosis, and respiratory failure within the first minutes to hours of life. Despite significant advances in neonatal medicine, this congenital anomaly still presents a high mortality rate, especially for associated malformations. On the other hand, there is a rare subset of CDH patients who present outside the neonatal period. The most common symptoms of late-presenting CDH include recurrent pulmonary infections, dyspnea, wheezing, abdominal pain, failure to thrive, vomiting, diarrhea and anorexia. Although late-presenting CDH generally presents good prognosis after early surgical correction, misdiagnosis is quite frequent because of its wide spectrum of clinical manifestations. The following case report describes a six-month-old infant presenting with acute respiratory distress and vomiting caused by late-presenting left-sided CDH.
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PMID:Acute respiratory distress for late-presenting congenital diaphragmatic hernia. 1910 55

Hereditary fructose intolerance (HFI) is an under-recognized, preventable life-threatening condition. It is an autosomal recessive disorder with subnormal activity of aldolase B in the liver, kidney and small bowel. Symptoms are present only after the ingestion of fructose, which leads to brisk hypoglycemia, and an individual with continued ingestion will exhibit vomiting, abdominal pain, failure to thrive, and renal and liver failure. A diagnosis of HFI was made in a 50-year-old woman on the basis of medical history, response to IV fructose intolerance test, demonstration of aldolase B activity reduction in duodenal biopsy, and molecular analysis of leukocyte DNA by PCR showed homozygosity for two doses of mutant gene. HFI may remain undiagnosed until adult life and may lead to disastrous complications following inadvertent fructose or sorbitol infusion. Several lethal episodes of HFI following sorbitol and fructose infusion have been reported. The diagnosis can only be suspected by taking a careful dietary history, and this can present serious complications.
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PMID:Adult hereditary fructose intolerance. 1945 88

Chronic intussusception is a treatable cause of failure to thrive. It is an uncommon condition often diagnosed late. The presenting features differ from acute intussusception. Chronic intussusception presents with a varying combination of abdominal pain, vomiting, weight loss/failure to thrive, diarrhea, and blood per rectum. An abdominal mass may or may not be palpable. The classic triad of abdominal pain, vomiting, and blood per rectum is uncommon. The purpose of this report is to present a small series of 3 cases and review 19 previously reported cases of chronic intussusception. Considering the diagnosis of chronic intussusception in children who present with failure to thrive and recurrent nonspecific abdominal symptoms is emphasized.
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PMID:Just another case of diarrhea and vomiting? 1952 66

Gastrointestinal motility disorders can develop in neurologically impaired children and those with congenital malformations of the gut. It is characterized by moderate to severe abdominal pain, vomiting, and failure to thrive. Antral dysmotility after fundoplication and increased sympathetic over activity are 2 factors associated with this condition that make it difficult to treat. This paper proposes a management strategy using metoclopramide, celiac plexus blockade, and thoracic splanchnectomy. It reviews our experience with 11 patients.
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PMID:New tools in the treatment of motility disorders in children. 1978 10

Ghrelin is predominately produced in the stomach, but new findings indicate that the intestinal wall is an important source of the hormone. In patients with shortbowel syndrome, reduction in the intestinal tissue resulted in a decrease in the circulating ghrelin levels. Since in celiac disease (CD) intestinal mucosa atrophy is the main finding, alterations in duodenal ghrelin-positive cell population can be expected. The aim of the study was to evaluate the density of ghrelin-positive cells in the duodenum of CD children and its relationship with body mass index (BMI) and clinical presentation. The study included 31 consecutive patients with newly diagnosed CD [BMI SD scores (BMISDS) -0.926+/-1.496]. The control group consisted of 21 children (BMISDS -0.517+/-1.186], diagnosed with growth retardation, anemia or abdominal pain. All the patients underwent endoscopy with biopsy samples taken from distal duodenum. Immunohistochemistry was performed using rabbit anti- ghrelin (human) antiserum. The number of ghrelin-positive cells in the duodenum was significantly higher in children with CD than in controls (14.82+/-11.12 vs 5.69+/-5.02, p<0.0013). The density of ghrelin-positive cells in the duodenum did not correlate with age, pubertal status, BMISDS or clinical presentation. In the duodenum of CD children, the number of ghrelin-positive cells is increased compared with the control patients. The population of ghrelin-positive cells in the duodenum does not simply reflect an altered mucosal morphology or failure to thrive but is under the influence of other conditions.
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PMID:The ghrelin-positive cells number is increased in duodenum in children with celiac disease. 1979 98

Bariatric surgery dramatically alters the normal stomach anatomy resulting in a significant incidence of hiatal hernia and gastroesophageal reflux disease. Although the majority of patients remain asymptomatic, many complain of severe heartburn refractory to medical management and additional highly atypical symptoms. Here, we describe the diagnosis and treatment regarding four cases of symptomatic hiatal hernia following bariatric surgery presenting with atypical symptoms in the University Hospital, USA. Four patients presented following laparoscopic Roux-en-Y gastric bypass or duodenal switch/pancreaticobiliary bypass (DS) with disabling and intractable midepigastric abdominal pain characterized as severe and radiating to the jaw, left shoulder, and midscapular area. The pain in all cases was described as paroxysmal and not necessarily associated with eating. All four patients also experienced nausea, vomiting, and failure to thrive at various intervals following laparoscopic bariatric surgery. Routine workup failed to produce any clear mechanical cause of these symptoms. However, complimentary use of multidetector CT and upper gastrointestinal contrast studies eventually revealed the diagnosis of hiatal hernia. Exploration identified the presence of a type I hiatal hernia in all four patients, with the stomach staple lines densely adherent to the diaphragm and parietal peritoneum. Operative intervention led to immediate and complete resolution of symptoms. The presence of a hiatal hernia following bariatric surgery can present with highly atypical symptoms that do not resolve without operative intervention. Recognition of this problem should lead to the consideration of surgery in cases where patients are dependent on artificial nutritional support and whose symptoms are poorly controlled with medication alone.
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PMID:Diagnosis and treatment of atypical presentations of hiatal hernia following bariatric surgery. 1985 36

Overlap in the clinical presentation of pediatric granulomatous inflammatory bowel disease may be substantial, depending on the mode of presentation. Chronic granulomatous disease (CGD) may present with granulomatous colitis, perianal abscesses, hepatic abscesses or granulomas, failure to thrive, and obstruction of the gastrointestinal tract (including esophageal strictures and dysmotility, delayed gastric emptying, and small bowel obstruction). Anemia, thrombocytosis, elevated C-reactive protein and erythrocyte sedimentation rate, and hypoalbuminemia are nonspecific and may occur in any of the granulomatous inflammatory bowel diseases. In histology, macrophages with cytoplasmic inclusions will be rather specific for CGD. Sarcoidosis may present with abdominal pain or discomfort, diarrhea, weight loss, growth failure, delayed puberty, erythema nodosum, arthritis, uveitis, and hepatic granulomata. Only in 55% of the patients will angiotensin-converting enzyme be elevated. The noncaseating epithelioid granulomata will be unspecific. Bronchoalveolar lymphocytosis and abnormalities in pulmonary function are reported in sarcoidosis and in Crohn disease (CD) and CGD. Importantly, patients with CD may present with granulomatous lung disease, fibrosing alveolitis, and drug-induced pneumonitis. Sarcoidosis and concomitant gastrointestinal CD have been reported in patients, as well as coexistence of CD and sarcoidosis in siblings. Common susceptibility loci have been identified in CD and sarcoidosis. CD and CGD share defects in the defense mechanisms against different microbes. In the present review, common features and essential differences are discussed in clinical presentation and diagnostics--including histology--in CGD, sarcoidosis, and CD, together with 2 other granulomatous inflammatory bowel diseases, namely abdominal tuberculosis and Hermansky-Pudlak syndrome. Instructions for specific diagnosis and respective treatments are provided.
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PMID:Overlap, common features, and essential differences in pediatric granulomatous inflammatory bowel disease. 2068 5

Ten per cent of girls and 3% of boys will have had a UTI by 16 years of age. The majority are acute, isolated illnesses that resolve quickly, with no long-term implications for the patient. However, UTIs may be associated with underlying congenital abnormalities, and recurrent infections can lead to renal scarring. UTI is defined as bacteriuria in the presence of symptoms. Asymptomatic bacteriuria does not require treatment or investigation. The presentation of UTI is extremely variable. The only way to differentiate a UTI from a viral infection is by testing the urine and this should be carried out within 24 hours in children with non-specific fever. UTIs can also present with vomiting, failure to thrive or persistent irritability. A urine infection in the presence of any of the above symptoms is a pyelonephritis (upper UTI). Children may also present with classical symptoms of cystitis (lower UTI) such as urinary frequency, dysuria and abdominal pain. Most children with UTI, even if febrile, can be managed in the community. If the initial assessment shows a high risk of serious illness, there should be an urgent referral to a paediatrician. The same applies to infants under three months with suspected UTI. It is better to obtain a urine sample by the clean catch method, rather than using urine pads or bags. Leucocyte esterase and nitrite dipsticks are not reliable in children under three, so a negative dipstick does not rule out UTI. Not every child needs to be referred after a first UTI. However, they should all be evaluated to help determine which require renal imaging as well as identifying triggers for recurrence. GPs are central to the identification of children at risk of renal pathology. All children who are diagnosed and treated for a UTI must be assessed for risk of renal abnormalities and/or recurrence.
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PMID:GPs should evaluate all children following UTI. 2081 9


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