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

Acute fatty liver of pregnancy (AFLP), rare and potentially fatal disease, is considered as obstetric emergency. The perinatologist must be familiar with this complication of pregnancy because early diagnosis, prompt delivery and supportive care is the mainstay of therapy. When pregnant woman has nausea or vomiting, abdominal pain and jaundice, increased transaminase activity, coagulopathy and hypoglycemia during third trimester AFLP should be suspected. Mothers who have experienced AFLP must be informed of the possibility recurrence and undergo close surveillance in the next pregnancy.
 ...
PMID:[Acute fatty liver in pregnancy: treatment, prognosis, rules of management]. 1058 7

Hereditary fructose intolerance (HFI) is an autosomal recessive disease caused by catalytic deficiency of aldolase B (fructose-1, 6-bisphosphate aldolase). Herein we report on a case of hereditary fructose intolerance with initial presentation of episodic unconsciousness, seizure, hypoglycemia, hepatomegaly, and abnormal liver function since the patient was 11 months old. She was diagnosed as Reye's-like syndrome according to a liver biopsy done at 20 months of age. As she grew up, cold sweating, abdominal pain or gastrointestinal discomfort shortly after the intake of fruits was noted and she developed an aversion to fruits, vegetables and sweet-tasting foods. At 9 years of age, a fructose tolerance test signified a positive result that induced hypoglycemia, transient hypophosphatemia, hyperuricaemia, elevation of serum magnesium, and accumulation of lactic acid. Appropriate dietary management and precautions were recommended. The patient has been symptom-free and exhibited normal growth and development when followed up to 12 years of age.
 ...
PMID:Hereditary fructose intolerance presenting as Reye's-like syndrome: report of one case. 1102 Oct 9

Although migraine is the main chronic headache in childhood and adolescence, it remains extensively misdiagnosed. Schematically, migraine is a severe headache evolving by stereotyped attacks frequently associated with marked digestive symptoms (nausea, vomiting, abdominal pain). Throbbing pain, sensitivity to sound, and light (and sometimes odors) are frequent additional symptoms. The attack is sometimes preceded by a visual or sensory aura. Rest brings relief, and sleep often ends the attack. Childhood migraine prevalence varies between 5 and 10%. Migraine episodes are frequently triggered by several factors: emotional stress (school pressure, vexation, excitement, upset), hypoglycemia, lack or excess of sleep (weekend migraine), sensory stimulation (loud noise, bright light, strong odor, heat or cold, etc.), sympathetic stimulation (sport, physical exercise). Attack treatments must be given at an early stage, oral ibuprofen (10 mg/kg) being particularly recommended. If the oral route is not available because of nausea or vomiting, rectal or nasal routes have then to be used. Non-pharmacological treatments (biofeedback and interventions combining progressive muscle relaxation) have demonstrated good efficacy as prophylactic measures. Daily prophylactic pharmacological treatments are prescribed as the second line after failure of non-pharmacological treatments.
 ...
PMID:[Migraine, misunderstood pathology in children]. 1102 9

In childhood and adolescence, migraine is the main essential chronic headache. This diagnosis is extensively underestimated and misdiagnosed in pediatric population. Lacks of specific biologic marker, specific investigation or brain imaging reduce these clinical entities too often to a psychological illness. Migraine is a severe headache evolving by stereotyped crises associated with marked digestive symptoms (nausea and vomiting); throbbing pain, sensitivity to sound, light are usual symptoms; the attack is sometimes preceded by a visual or sensory aura. During attacks, pain intensity is severe, most of children must lie down. Abdominal pain is frequently associated, rest brings relief and sleep ends often the attack. The prevalence of the migraine varies between 5p.100 and 10p.100 in childhood. At childhood, headache duration is quite often shorter than in adult population, it is more often frontal, bilateral (2/3 of cases) that one-sided. Migraine is a disabling illness: children with migraine lost more school days in a school year, than a matched control group. Migraine episodes are frequently triggered by several factors: emotional stress (school pressure, vexation, excitement: upset), hypoglycemia, lack of sleep or excess (week end migraine), sensorial stimulation (loud noise, bright light, strong odor, heat or cold.), sympathetic stimulation (sport, physical exercise). Attack treatments must be given at the early beginning of the crisis; oral dose of ibuprofen (10mg/kg) is recommended. If the oral route in not available when nausea or vomiting occurs, the rectal or nasal routes have then to be used. Non pharmacological treatments (biofeedback and interventions combining progressive muscle relaxation) have shown to have good efficacy as prophylactic measure. Daily prophylactic pharmacological treatments are prescribed in second line after failure of non-pharmacological treatment.
 ...
PMID:[Migraine and chronic headache in children]. 1113 52

Anorectics and bulimics often complain sleep onset insomnia and disrupted sleep. During awakenings bulimics can have binges. Conversely, eating disorders can be a clinical expression of a concomitantly occurring sleep disorder. Two clinical entities have been recently described: the Night Eating Syndrome (NES) and the Sleep Related Eating Disorders. The main goal of this literature review was to better characterize the relationships between eating disorders and sleep disturbances. No specific EEG sleep pattern emerges in anorectic and bulimic patients. However, all studies include several methodological limitations: a few number of patients, heterogeneous patient groups, various diagnostic criteria. The results of studies evaluating the impact of depression on sleep EEG in eating disorder patients are also subject to controversy. The only study examining the relationship between sleep EEG and morphological alterations in anorectics and normal weight bulimics shows that patients with enlarged cerebrospinal fluid spaces spent more time in slow wave sleep and that the duration of rapid eye movement (REM) sleep was reduced. The ventricular brain ratio was negatively correlated with REM sleep. The Night Eating Syndrome consists in insomnia, binge eating and morning anorexia. Other criteria are proposed to characterize the NES: more than 50% of the daily energy intake is consumed after the last evening meal, awakenings at least once a night, repetition of the provisional criteria for more than 3 months, subjects do not meet criteria for bulimia nervosa or binge eating disorder. Patients have no amnesia nor alteration of alertness, and no other sleep disorder. There is no modification of sleep EEG except sleep maintenance. The prevalence of the NES is 1.5% in the general population. Some neuroendocrine disturbances have been found in the NES. The delimitation with eating disorders is not yet clearly established. If it shares the compulsive features with eating disorders, particularly the "Binge Eating Disorder", and occurs during full awakenings, the night eating syndrome may be recognized as a specific eating disorder. The sleep related eating syndrome is also characterized by compulsive binge eating during awakenings. But in this case, night eating is linked with a reduced consciousness and sleep disorders, mainly somnambulism. Patients never experience hunger, abdominal pain, nausea or hypoglycemia. Night-eating takes place invariant across weekdays, weekend and vacations. Patients consumed high caloric foods and fluids but never alcohol and purging does not occur. Diurnal bulimia is frequently associated with the sleep-related eating disorder. In conclusion, the sleep related eating disorder seems rather be a clinical subtype of sleep disorders whereas the NES could be considered as an eating disorder.
 ...
PMID:[Correlation between eating disorders and sleep disturbances]. 1176 Jun 92

Pancreatic neuroendocrine tumors rarely undergo cystic degeneration leading to a radiologic appearance, which is often interpreted as a pancreatic mucinous cystadenoma or pseudocyst. We reviewed our experience with 38 neuroendocrine tumors, four of which were cystic, and 24 other cystic pancreatic tumors (mucinous cystadenoma [n = 5], cystadenocarcinoma [n = 6], serous cystadenoma [n = 3], solid/cystic papillary neoplasm [n = 3], intraductal papillary mucinous tumor [n = 6], and mucinous adenocarcinoma [n = 1]) managed operatively between 1990 and 2000. This review was undertaken to identify clinical and pathologic features useful for preoperative diagnosis of cystic neuroendocrine tumors. Two of the four patients with cystic neuroendocrine tumors presented with abdominal pain, one patient was asymptomatic, and one patient had hypoglycemia. Three of the four cystic neuroendocrine tumors were identified by CT scan, and none were biopsied preoperatively. Preoperative diagnoses included mucinous cystadenoma in two patients (n = 2), pancreatic cystic neoplasm in one patient, (n = 1) and insulinoma in one patient (n = 1). All four cystic neuroendocrine tumors were benign and were completely resected (distal pancreatectomy [n = 2], enucleation [n = 2]). Cystic neuroendocrine tumors are difficult to diagnose preoperatively because the majority of these tumors are nonfunctional, and CT does not differentiate these tumors from other cystic neoplasms. Cystic neuroendocrine tumors represent a subgroup of pancreatic cystic and neuroendocrine tumors with malignant potential. Their high resectability rate further supports the role of surgical exploration and resection in the treatment of pancreatic cystic neoplasms.
 ...
PMID:Cystic pancreatic neuroendocrine tumors: is preoperative diagnosis possible? 1198 20

A 36-year-old woman presented with right upper quadrant abdominal pain, weight loss and attacks of severe sweating. She was known to have a chronic hepatitis B infection. A large hepatocellular carcinoma was diagnosed complicated by recurrent episodes of hypoglycaemia. Serum insulin, insulin-like growth factor (IGF-I) and growth hormone levels proved to be low, with increased serum levels of big-IGF-II. This is indicative of non-islet cell tumour hypoglycaemia. The patient received prednisone which resulted in an improvement in the blood glucose values but the morning hypoglycaemia remained, so that nightly intravenous glucose administration continued to be necessary. Therefore, growth hormone was added to the treatment which resulted in a complete disappearance of the hypoglycaemias. The patient died within 6 months of the diagnosis having been established.
 ...
PMID:[Hepatocellular carcinoma complicated by non-islet cell tumor hypoglycemia]. 1203 25

Severe or complicated malaria is defined by infestation by Plasmodium falciparum into all red blood cells, especially those in the brain, causing coma and repeated convulsions; severe anemia (6 g/dl hemoglobin, 20% hematocrit); renal insufficiency (265 mcmol/l creatinine, 400 ml/day diuresis); pulmonary edema; hypoglycemia (2.2 ml/l or 0.4 g/l); shock; diffuse hemorrhaging; massive hemoglobinuria; and blood acidosis. Other possible symptoms of severe malaria are clouded thinking, changes in behavior, and inability to focus. It is most common in people with no immunity to malaria (children aged 4 and travelers in endemic zones). Pregnancy, splenectomy, corticotherapy, or poorly maintained immunity status favor severe anemia in adults. Sources of chloroquine-resistant P. falciparum have existed since 1960. Resistance has since expanded from Southeast Asia and South America to Africa, posing treatment problems. Malaria usually begins with fever (40 or more degrees Celsius), headaches, muscular pain, digestive troubles (e.g., diarrhea, nausea, or vomiting), and abdominal pain. In suspected cases of malaria, a blood sample or a thick blood smear as well as treatment (even in the absence of parasitological proof) needs to be done as soon as possible. Intravenous quinine diluted in a 5-10% glucose solution should be delivered at a rate of 24 mg/kg/day. In the case of severe jaundice, the dose should be cut in half beginning 8 hours after treatment began. If intravenous delivery is impossible, intramuscular delivery should be done. Corticosteroids, anticoagulants, and aspirin are contraindicated. In 2-4 days, oral administration (chloroquine, halofantrine, or mefloquine) is warranted. 20% of malaria-related deaths among patients who receive treatment are due to complications of the central nervous system. Protection against mosquito bites prevents malaria. Chemoprophylaxis in endemic zones should be limited to short trips to malaria zones or to pregnant women.
 ...
PMID:[Severe malaria]. 1229 Jan 83

Gastrointestinal symptoms such as nausea and vomiting, heartburn, abdominal pain, diarrhoea, constipation and faecal incontinence are common in patients with diabetes. Diabetes gastroenteropathy is a clinically relevant problem. In addition to the increased morbidity it causes, it results in severely impaired metabolic control, which in turn increases the risk of hyper-/hypoglycaemia. Moreover, the poorly controlled blood glucose level increases the risk of secondary diabetes complications, namely, retinopathy, nephropathy, neuropathy and cardiovascular affection. Gastrointestinal symptoms may also cause malnutrition in patients with diabetes, which, together with the disturbed immune defence in diabetes, may cause intercurrent infections. Gastrointestinal symptoms in patients with diabetes are attributed to disturbed gastrointestinal motility. Gastrointestinal dysmotility in diabetes is believed to be caused by autonomic neuropathy and/or hyperglycaemia. The neuroendocrine system of the gut secretes peptides/amines that play an important role in regulating gastrointestinal motility. It is conceivable, therefore, to assume that a disturbance in this regulatory system may contribute to the pathogenesis of gastrointestinal complications in diabetes. The present review gives an updated overview of the abnormalities in the gastrointestinal neuroendocrine system in diabetes, speculates upon the possible role of these abnormalities in the pathogenesis of diabetes gastroenteropathy and, finally, predicts the possible clinical implications of these findings.
 ...
PMID:The possible role of the gut neuroendocrine system in diabetes gastroenteropathy. 1237 Nov 43

Functioning gastroenteropancreatic endocrine tumors produce and secrete different substances that can be detected in the plasma and cause hormone-related syndromes. Symptoms such as diarrhea associated either with typical skin rash or peptic ulcer disease may be suggestive of the presence of intestinal carcinoid or gastrinoma. Other clinical manifestations such as severe hypoglycemia, diabetes, necrolytic erythema and gallbladder disease may also indicate an endocrine tumor. Sometimes, patients present no, or just vague, symptoms such as dyspepsia or abdominal pain and nonfunctioning endocrine tumors in these patients can be found incidentally during diagnostic imaging procedures or at operation. Usually, the diagnosis is established by the measurement of the specific tumor marker in the plasma and, sometimes, in the urine. In some cases, normal basal hormone levels are observed even in the presence of typical symptoms. Therefore, stimulatory tests such as the secretin test for gastrinomas are required to establish the diagnosis. General markers for the diagnosis of gastroenteropancreatic endocrine tumors are also available. Among these, chromogranin A has proved to be of great value for diagnosing nonfunctioning tumors and is considered the most sensitive general marker. The availability of both specific and general markers as well as stimulatory tests may enable the clinician to diagnose functioning gastroenteropancreatic endocrine tumors at an early stage and to recognize nonfunctioning tumors.
 ...
PMID:Biochemical diagnosis of gastroenteropancreatic endocrine tumors. 1271 97


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>