Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A positive ferric chloride reaction was found at routine examination of the urine of a 14 year old mentally normal girl, admitted for complaints of headache and other meningitis-like symptoms. It turned out that she excreted permanently increased amounts of phenylpyruvic, phenyllactic and o-hydroxyphenylacetic acids, but phenylacetic acid (free plus conjugated) was normal. Fasting serum phenylalanine was not increased nor was urinary phenylalanine. On loading with L-phenylalanine (100 mg/kg) a normal serum phenylalanine response followed, but urinary phenylpyruvic, phenyllactic and o-hydroxyphenylacetic acids increased further. Phenylacetic acid responded too, but remained in the normal range. In addition to the above-mentioned abnormalities the urine contained a still unidentified abnormal acid, which also increased after loading with phenylalanine. Her 12 year old healthy sister showed the same chemical abnormality. Two older brothers and the parents had normal excretions. The enzyme defect has not been identified. As a possibility the defective decarboxylation of phenylpyruvic acid is proposed.
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PMID:Permanent chemical phenylketonuria and a normal phenylalanine tolerance in two sisters with a normal mental development. 118 53

Ten healthy volunteers with no history of aspartame intolerance (6 men and 4 women, aged 21-36 years) received a single dose of aspartame (15 mg/kg body weight in capsules) or matching placebo in a randomized, double-blind crossover study. Eleven blood samples collected over 24 hours were analyzed for plasma glucose and amino acid concentrations. The following variables were evaluated at 1, 2, 4, 8, and 24 hours post-dosage: changes in mood measured on visual analog scales, cognitive function determined by digit-symbol substitution test (DSST) and arithmetic test scores, and reaction time measured with a brake-pedal reaction timer. Memory was tested at 2 and 24 hours after dosage based on recall of standardized 16-item word lists. No significant differences between aspartame and placebo were found in measures of sedation, hunger, headache, reaction-time, cognition, or memory at any time during the study. Plasma phenylalanine levels were significantly higher following aspartame (P less than .01) than with placebo between 1 and 6 hours postdosage, reaching a maximum difference of +3.36 mumols/dl at 2 hours. Plasma glucose concentrations were not significantly different between aspartame and placebo. The results of this study suggest that following a single 15 mg/kg dose of aspartame, no detectable effects are observed in a group of healthy volunteers with no history of aspartame intolerance, despite significant increases in plasma phenylalanine concentrations.
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PMID:The neuropsychiatric effects of aspartame in normal volunteers. 234 57

Both complement (C) and neutrophils (PMN) are activated in critically ill patients. To evaluate the role of endotoxin in this response, we studied C activation products and PMN cell surface receptors in seven normal subjects before and after endotoxin (USRef 20 U/kg) or saline solution administered on separate occasions. By 4 hours, with endotoxin only, all subjects had myalgia, headache, an increase in body temperature and heart rate, and leukocytosis that returned to normal by 24 hours. At the same time, PMN cell surface receptors for the complement opsonin C3b increased, as measured by indirect immunofluorescence, rising to 251 +/- 44% of baseline by 4 hours (p less than 0.01) and remaining elevated at 24 hours (237 +/- 16%, p less than 0.01). PMN receptors for iC3b increased to 308 +/- 49% of baseline by 4 hours (p less than 0.02) and returned to normal by 24 hours. There was no change in plasma of C3a desArg, C4a desArg, and C5a desArg (4 hours: mean C3a: 153.4 +/- 11.5 ng/ml versus 176.2 +/- 16.2 ng/ml for saline solution, p = ns; C4a: 159.6 +/- 32 ng/ml versus 151.4 +/- 21 ng/ml, p = ns; C5a: undetectable). To confirm the lack of C activation, we examined PMN chemotaxis (CTX) to C5a for any impairment caused by prior in vivo exposure to C5a. CTX to C5a was unaffected (4 hours: 109% +/- 22% of normal versus 114% +/- 10% for saline solution, p = ns). PMN CTX to formyl-methionyl-leucine-phenylalanine and PMN phagocytosis and killing of S. aureus were also unaffected by endotoxin. Thus, a single dose of endotoxin produced a subjective febrile illness and precipitated sustained PMN activation as indicated by increased PMN cell surface complement receptor number in the absence of C activation.
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PMID:A single dose of endotoxin activates neutrophils without activating complement. 330 97

Normotensive and hypertensive headache sufferers were treated with D-phenylalanine, aprotinin or captopril--all inhibitors of endogenous opioid degradation. Inconsistent results were obtained using D-phenylalanine and aprotinin (acute administration at the start of a migraine attack). Satisfactory results were obtained by prophylactic treatment with captopril (an inhibitor of the angiotensin converting enzyme and of the dipeptidyl carboxypeptidase--an enkephalin inactivating enzyme) compared with conventional drugs such as methysergide, lisuride, pizotifen, clonidine and beta-blocking agents. Excellent results were obtained with captopril on patients suffering from headache and arterial hypertension who had experienced no relief from beta-blocking agents and clonidine. Captopril could thus be a drug of choice in the therapy of headache associated with essential hypertension.
Cephalalgia 1981 Dec
PMID:Enkephalinase inhibition relieves pain syndromes of central dysnociception (migraine and related headache). 618 94

G-CSF (granulocyte-colony stimulating factor) is one of the cytokines which increase and activate neutrophils. These effects have been confirmed by a lot of clinical studies. Although only few side effects have been reported so far, we saw a patient with hypertension, facial edema, and severe headache after G-CSF administration. We have measured the sticking strength of leukocytes to the walls of narrow pores in modified Nuclepore filtration method of Kikuchi, in various clinical situations, and we have denoted the pore filtration time as the rheological activity of leukocytes (RAL). In this study, we tried to measure RALs of patients after G-CSF administration (60-100 micrograms) and to compare them with those of non-treated normal individuals. We also checked serum levels of granulocyte elastase in the patients. In the static state (in which neutrophils were not stimulated), RALs of the patients were 8.0 +/- 1.5sec. [N = 8], and those of the controls were 3.8 +/- 1.6sec. [N = 21] (p < 0.001). In the activated state (in which neutrophils were stimulated by formyl-methionyl-leucyl-phenylalanine), PALs of patients were quite high, i.e. those of the patients and controls were 592 +/- 322sec. and 69 +/- 62sec., respectively (p < 0.001). In all cases given G-CSF, the serum levels of granulocyte elastase were above the normal range. In view of our results, we it is possible that highly activated leukocytes would injure tissue and then induce organ failure and several symptoms, as in this study.
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PMID:[Leukocyte activity and occurrence of tissue injury by G-CSF]. 768 59

A Phase I trial was conducted to investigate the clinical toxicity, pharmacokinetics, and chemiluminescence (CL) responses of alveolar macrophages (AMs), peripheral blood neutrophils, and monocytes after subcutaneous injection of recombinant interferon-gamma (rIFN-gamma). Six patients with lung cancer received rIFN-gamma subcutaneously as single doses of 0.2, 0.6, and 1.8 mg. Bronchoalveolar lavage was performed three times: 21 h before as well as 6-7 and 27 h after injection. Serum samples were taken five times during the 27-h follow-up. IFN concentrations were measured from alveolar epithelial lining fluid (ELF) and serum by using an antiviral bioassay. IFN-gamma was not detectable in ELF after subcutaneous injection. AMs did not effect an increase in CL responses to N-formyl-methionyl-leucyl-phenylalanine or to phosphate-buffered saline. Circulating IFN-gamma was detectable at 3-12 h after an injection of 1.8 mg of rIFN-gamma, the highest dose given. CL responses of peripheral blood monocytes increased in all patients after injection, whereas the responses of neutrophils were less clear-cut. All patients developed systemic side effects such as transient fever, nausea, headaches, and flu-like symptoms. The findings suggest that rIFN-gamma passes poorly from the blood to the pulmonary alveoli. On the basis of this and our previous findings of increased CL responses in AMs and measurable IFN concentrations in ELF after inhalation of rIFN-gamma, we recommend inhalation rather than the parenteral route of IFN-gamma for the treatment of respiratory diseases.
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PMID:Subcutaneously administered recombinant interferon-gamma in humans: pharmacokinetics and effects on chemiluminescence responses of alveolar macrophages, blood neutrophils, and monocytes. 806 1

Amino acid levels in plasma were measured by amino acid autoanalyser in 130 convulsive children. The levels of taurine, serine and tryptophan were significantly lower in convulsive children as compared to normal control; in contrast, isoleucine, homocystine, GABA, histidine, arginine and ammonia were higher. The children with paroxysmal disorders (headache, dizziness and abdominal epilepsy) had the highest levels of isoleucine, histidine and arginine and the lowest levels of glutamate and cystein. Clinical seizure activity within 6 months prior to the test seemed to have no obvious effect on the plasma amino acid pattern, except for the levels of glycine and arginine tended to return to normal, and the level of GABA was significantly increased in patients with the seizure being controlled. The patients treated with carbamazepin as a single anticonvulsant had the highest GABA level compared to those with other anticonvulsants. Hyperglycinemia and hyperammonaemia were also noted in patients who took valproic acid. The levels of serine, isoleucine and phenylalanine in the CSF within 6 hours after convulsion were significantly lower than the normal control; while asparagine, tyrosine, lysine and arginine were significantly higher. The concentration of ammonia in the CSF was also elevated after convulsion as compared to the normal control. Amino acids play an important role in the generation of epilepsy and recently there has been an increasing number of studies to help determine their effects during an epileptic attack. However, there still is much debate and controversy on this topic. Therefore, further studies are needed and researchers should carefully consider factors that might affect the accurate assessment of the results.
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PMID:Alteration of amino acid in plasma and cerebrospinal fluid of children with seizure disorders. 851 Jan 96

A 32-year-old man of Irish descent presented with severe progressive headache and sensorineural hearing loss. MRI/magnetic resonance angiography head scans were normal. A length-dependent sensorimotor peripheral neuropathy with autonomic dysfunction predated these symptoms. Systemic organ involvement and transthyretin (TTR) amyloid immunostaining of bone marrow and fat aspirate were documented. Direct DNA sequencing revealed both the normal TTT (phenylalanine) and a new variant TCT (serine) at position 44 of the TTR gene. This case expands the genotypic and phenotypic variability within TTR amyloidosis.
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PMID:Transthyretin amyloidosis (serine 44) with headache, hearing loss, and peripheral neuropathy. 981 83

Over 20 years have elapsed since aspartame was approved by regulatory agencies as a sweetener and flavor enhancer. The safety of aspartame and its metabolic constituents was established through extensive toxicology studies in laboratory animals, using much greater doses than people could possibly consume. Its safety was further confirmed through studies in several human subpopulations, including healthy infants, children, adolescents, and adults; obese individuals; diabetics; lactating women; and individuals heterozygous (PKUH) for the genetic disease phenylketonuria (PKU) who have a decreased ability to metabolize the essential amino acid, phenylalanine. Several scientific issues continued to be raised after approval, largely as a concern for theoretical toxicity from its metabolic components--the amino acids, aspartate and phenylalanine, and methanol--even though dietary exposure to these components is much greater than from aspartame. Nonetheless, additional research, including evaluations of possible associations between aspartame and headaches, seizures, behavior, cognition, and mood as well as allergic-type reactions and use by potentially sensitive subpopulations, has continued after approval. These findings are reviewed here. The safety testing of aspartame has gone well beyond that required to evaluate the safety of a food additive. When all the research on aspartame, including evaluations in both the premarketing and postmarketing periods, is examined as a whole, it is clear that aspartame is safe, and there are no unresolved questions regarding its safety under conditions of intended use.
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PMID:Aspartame: review of safety. 1218 Apr 94

During 1967-1983, the Maternal and Child Health Division of the Public Health Services funded a collaborative study of 211 newborn infants identified on newborn screening as having phenylketonuria (PKU). Subsequently, financial support was provided by the National Institute of Child Health and Human Development (NICHD). The infants were treated with a phenylalanine (Phe)-restricted diet to age 6 years and then randomized either to continue the diet or to discontinue dietary treatment altogether. One hundred and twenty-five of the 211 children were then followed until 10 years of age. In 1998, NICHD scheduled a Consensus Development Conference on Phenylketonuria and initiated a study to follow up the participants from the original Collaborative Study to evaluate their present medical, nutritional, psychological, and socioeconomic status. Fourteen of the original clinics (1967-1983) participated in the Follow-up Study effort. Each clinic director was provided with a list of PKU subjects who had completed the original study (1967-1983), and was asked to evaluate as many as possible using a uniform protocol and data collection forms. In a subset of cases, magnetic resonance imaging and spectroscopy (MRI/MRS) were performed to study brain Phe concentrations. The medical evaluations revealed that the subjects who maintained a phenylalanine-restricted diet reported fewer problems than the diet discontinuers, who had an increased rate of eczema, asthma, mental disorders, headache, hyperactivity and hypoactivity. Psychological data showed that lower intellectual and achievement test scores were associated with dietary discontinuation and with higher childhood and adult blood Phe concentrations. Abnormal MRI results were associated with higher brain Phe concentrations. Early dietary discontinuation for subjects with PKU is associated with poorer outcomes not only in intellectual ability, but also in achievement test scores and increased rates of medical and behavioural problems.
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PMID:Phenylketonuria in adulthood: a collaborative study. 1240 83


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