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)

The study of serum from a patient with C2 deficiency is described. The patient had an episode of pneumococcal meningitis at 5 mo of age with seizures and transient hemiparesis and apparent purpuric skin lesions. He was first admitted to the University of Minnesota Hospitals at 10 yr of age following the discovery of proteinuria accidentally by his mother. Since then he has been admitted repeatedly to this hospital with numerous clinical findings including arthralgia, recurrent abdominal pain, proteinuria, membranous nephropathy, malar butterfly rash, seizures, personality aberrations, and recurrent fever. In June 1971, the patient developed positive DNA and DNP antibodies and positive LE cells. When the C profile was studied before and after recognition of lupus, C1q, C1s, and C4 dropped. C3 levels were elevated as were C5, C6, and C7, C3 proactivator had been reduced in the patient even before he developed lupus. Also because of a traumatic renal biopsy leading to a perirenal hematoma, he required surgery and a blood transfusion. 1 h after blood transfusion, a C2 titer of 23 hemolytic units was detected. Almost immediately levels of C3, C5, C6, and C7 dropped, C8 and C9 remained elevated. The addition of C2 from normal blood permitted dramatic activation of C3. These findings support the view that the rare deficiency in production of C2 predisposes to serious susceptibility to infection, vascular and mesenchymal disease as well as to renal disease and a lupus syndrome.
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PMID:C2 deficiency. Development of lupus erythematosus. 457 55

Valproic acid represents a new class of anticonvulsants that are widely employed in the management of many types of seizure disorders. Compared with other anticonvulsants, it has been considered relatively free of adverse effects. Recently, acute hepatic failure has been ascribed to valproic acid. Now experience is accumulating that implicates this agent in causing pancreatitis. Contributing to this evidence, the patient described herein had well-documented, recurrent pancreatitis while he was taking valproic acid. Nonspecific vomiting and abdominal pain frequently occur with valproic acid; however, pancreatitis must be considered whenever these symptoms are severe or protracted.
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PMID:Recurrent pancreatitis induced by valproic acid. A case report and review of the literature. 616 6

Cerebral cysticercosis was studied in 131 children. The patients were divided into two groups, confirmed and probable cysticercosis. The clinical picture may be divided into two stages: initial stage of acute invasion and chronic encephalitic stage. Symptoms in the initial stage are headache, vomiting, fever, myalgia, abdominal pain, seizures and psychotic reactions. In the initial stage only cerebral edema can be seen in the computed tomography (CT) scan. In the chronic stage, variability of symptomatology is great, and it is in this phase that cysticerci can be seen in the CT scan. Only 66 out of the 131 patients studied had CT performed. The computed tomographic sequence of parenchymatous brain cysticercosis is described. A feature not previously reported was the presence of transient arterial hypertension due to cerebral cysticercosis found in four cases.
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PMID:Clinical manifestations and sequential computed tomography scans of cerebral cysticercosis in childhood. 661 86

Out of 858 epileptic patients, 24 had painful seizures. Three distinct groups emerged: (1) those with unilateral pain in the face, arm, leg or trunk (Unilateral Group)--10 cases; (2) a Cephalic Group with pain restricted to the head--11 cases; and (3) an Abdominal Group with central abdominal pain--3 cases. Unilateral pain consistently implicated ictal involvement of the contralateral rolandic region at the time of pain. In most cases it was probably due to involvement of the primary somatosensory cortex (SI). Cephalic pain did not localize the site of seizure origin. In most cases it probably arose by a vascular mechanism. Abdominal ictal pain reflected temporal lobe epileptic activity in our cases. The mechanism of its production is uncertain, but it is unlikely to be due to a peripheral (for example gastrointestinal) mechanism.
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PMID:Painful epileptic seizures. 664 Feb 68

Cerebral origin of relapsing paroxysmal abdominal pains is discussed in the light of six case histories, other personal observations and the literature. The pains are assumed to be due to locally limited epileptic discharges in areas of the cortex where the digestive tract is represented. When the neuronal discharges reach other brain formations, multisymptomatic, partial or generalized epileptic seizures occur. In such cases, therefore, the abdominal symptomatology is either a first stage or a rudiment of a more complex course of attack, and should not be considered as the expression of a particular form of epilepsy that might be termed abdominal epilepsy. Difficulties regarding differential diagnosis ensue in the case of migraine with abdominal symptomatology. The latter should be taken into account when relapsing attacks of abdominal pain, which cannot be explained gastroenterologically, persist for hours and alternate with headache. In case of doubt, a family history of migraine confirms the diagnosis.
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PMID:[Recurring paroxysmal abdominal pains of cerebral origin]. 679 44

A retrospective method was used to estimate the incidence of recurring motion-sickness, cyclic vomiting and abdominal pain considered as different manifestations of a so-called periodic syndrome in 100 migraine sufferers, 100 epileptics and 100 control subjects in the pediatric age group. Such recurrent symptoms are significantly more frequent in those suffering from migraine than in the other two groups. Examination of subgroups of patients affected by particular forms of migraine (classical and common) and of epilepsy (generalized seizures, simple partial seizures, complex partial seizures) contributed little new to our understanding of the nature of periodic syndrome. It is concluded that the above symptoms of periodic syndrome should generally be considered as manifestations of a migrainous rather than of an epileptic disorder.
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PMID:Cyclic vomiting and recurrent abdominal pains as migraine or epileptic equivalents. 687 85

After an upper respiratory tract infection an eight months old infant developed a severe hemolytic uremic syndrome with anemia, thrombocytopenia and anuria. Remarkable was a lesion of the erythrocytes by neuraminidase producing microorganisms. By early hemodialysis, blood transfusions and accurate fluid therapy the acute stage could be managed. The proceeding course was complicated by hypertension, seizures, coma, abdominal pain attacks and a fibrinous hemorrhagic pericarditis, which made an incomplete pericardectomy necessary. Although it came again to diuresis a severe chronic renal failure with its concluding effects as anemia, acidosis, hypertension and inanition resulted. After a four months period the patient died of biventricular congestive heart failure.
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PMID:[Severe course of a hemolytic-uremic syndrome]. 715 51

Subacute lead encephalopathy due a chronic poisoning was present in a 6 year-old child. Neurologic features (coma, seizures, CSF abnormalities) began after 2 weeks of vomiting, abdominal pain and constipation. Diagnosis was confirmed by studies of porphyrin metabolism. Lead poisoning following pica in childhood has rarely been reported in France. Its pathogenesis, main features, diagnosis and treatment are reviewed.
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PMID:[Lead poisoning revealed by severe encephalopathy : pica does exist in France (author's transl)]. 731 73

A retrospective chart review for the 1993 calendar year identified 187 children with cerebral malaria admitted to a large teaching hospital in central Ghana, West Africa. The most common clinical presentation was fever, sensorial depression and convulsions in young children experiencing their first episode of malaria. One-half had splenomegaly. Additional features, seen in decreasing frequency, were hepatomegaly, vomiting, abdominal pain and headache. Long term sequelae were identified in 9% and mortality in 6%. Risk factors for central nervous system disease were negative history for previous malaria (P < 0.005) and a high percentage of parasitemia (P < 0.001). Death or long term sequelae were associated with multiple seizures and prolonged sensorial depression. The incidence of malaria is currently increasing in Western Africa and young children are more likely than older children to develop severe disease.
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PMID:Cerebral malaria in children. 760 9

Hereditary coproporphyria (Hepatic coproporphyria: HCP); HCP is the rarest and least recognized among hepatic porphyrias and is characterised by an excess of faecal and urinary excretion of coproporphyrin (mainly isomer III). The deficiency is in coproporphyrinogen oxidase. HCP was first described by Berger and Goldberg in 1955 and was considered an asymptomatic biochemical abnormality. It later became evident that HCP could provoke acute attacks similar to those of acute intermittent porphyria (AIP) and variegate porphyria (VP). Such episodes are often provoked by barbiturates, sulphonamides and other drugs, and include automatic symptoms (hypertension, tachycardia, abdominal pain, constipation), central (epileptic seizures, mental disturbances) and peripheral nervous system dysfunction. During acute attacks, urinary ALA (delta-aminole-vulinic acid) and PBG (porphobilinogen) are elevated just as in AIP and VP, however, a marked elevation of faecal COPRO (coproporphyrin) is diagnostic of HCP. Laparoscopic finding of our case showed a map-like appearance of the liver surface with slightly depressed dark-bluish areas and reddish-brown areas. The liver biopsy specimen showed red fluorescence under ultraviolet light. On HE staining, hydropic degeneration of the hepatocytes and many brown granules in the hepatocytes were seen. A part of the granules stained positive for iron. Schmorl's stain showed many needle-shaped crystallines. Erythropoietic coproporphyria (ECP); Heilmeyer and Clotten have described that elevated PROTO (protoporphyrin) and COPRO were found in the RBC of the patient. Topi et al. described two brothers with cutaneous photosensitivity similar to that of erythropoietic protoporphyria, but with elevated RBC PROTO and COPRO III in both. Very little is known about this disease.
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PMID:[Hereditary coproporphyria (Hepatic coproporphyria), Erythropoietic coproporphyria]. 761 59


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