Gene/Protein Disease Symptom Drug Enzyme Compound
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Dentistry uses a variety of different polymer materials. Dental polymer materials are based on methacrylate, its polymer, and polyelectrolytes. The setting of restorative materials and adhesives is initiated chemically by mixing two components or by light. In both cases, polymerisation is incomplete and monomers, not reacted, release. Studies have documented that monomers may cause a wide range of adverse health effects such as irritation to skin, eyes or mucous membranes, allergic dermatitis, asthma, parenthesise in the fingers, and disturbances from central nervous system such as; headache, pain in the extremities, nausea, loss of appetite, fatigue, sleep disturbances, irritability, loss of memory and changes in blood parameters. Dental personnel are occupationally exposed when handling the non reacted monomers. The use of gloves do not give enough protection as monomers, released from the material, easily penetrate all gloves used in dentistry. Face masks do not prevent inhalation of monomers. Ordinary glasses do not protect the eyes against vapor from monomers. The result from this study demonstrate the need for the development of ergonomic procedures and practices for safe handling of such materials in dental clinics.
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PMID:Use of polymer materials in dental clinics, case study. 941 12

We reported a case of adult-onset citrullinemia associated with hypertrigliceridemia and diabetes mellitus. A 24-year-old female was healthy until recently. She first felt intermittent headaches and nausea. Then she noticed memory loss and tiredness. Abnormal behavior such as getting lost on the way from her company sometimes occurred. She came to our hospital because these symptoms had been getting worse. Neurologically she had a very mild disturbed consciousness. An EEG recording showed diffuse slow wave with high amplitude. MR image of the brain showed hyper-intensity in globus pallidus with T1-weighted image. Plasma citrullin level was very high. Plasma ammonia and triglyceride showed a moderately high level. Using biopsied liver tissues, the enzymes of the urea cycle were analyzed. Argininosuccinate synthetase activity was extremely low. Because of clinical course and the result of liver biopsy, the patient was diagnosed as type 2 citrullinemia. A low protein diet was started, but intermittent nausea and consciousness disturbance did not improve. A partial liver transplantation was performed. The living donor was her father, a 50-year-old male, who had normal liver function. After the liver transplantation, all neurological signs soon disappeared. Plasma citrulline, ammonia and triglyceride normalized rapidly. An EEG recording became normal, and the hyper-intensity in globus pallidus with T1-weighted MR image disappeared two months after surgery. Liver transplantation should be planned as soon as possible in a type 2 citrullinemia patient.
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PMID:[Liver transplantation in type II citrullinemia]. 1065 68

Primary hyperparathyroidism is the most common cause of hypercalcemia and 80-85% of the patients have parathyroid tumors. The purpose of this retrospective review was to analyse whether differences exist between patients with parathyroid tumors treated in the 1980s and 1990s. Between 1980-1997, 253 patients underwent initial surgical neck exploration for hyperfunctioning parathyroid tumors. Renal (polyuria, nocturia, renal colic due to lithiasis), rheumatologic (bone and joint pain), neurological (fatigue, memory loss, depression) and gastrointestinal (dyspepsia, anorexia, nausea) symptoms were recorded and main biochemical parameters were measured. In all patients one or more preoperative localization procedures were carried out prior to successful parathyroidectomy, and the confirmation of imaging findings was obtained after surgery. The patients were divided in two groups. Group A: 121 (47.8%) patients who underwent surgery from 1980-1989; Group B: 132 (52.2%) patients in whom parathyroidectomy was performed from 1990-1997. There were no differences (p=NS) between the two groups in average age, preoperative serum creatinine and intact-PTH levels. Symptoms were most common in Group A, and pre-operative serum calcium levels were significantly lower in Group B. Ultrasonography (n=191) sensitivity did not improve significantly (82.8% vs 82.9%), but positive predictive value (PPV) was higher (89.8% vs 96.0%). CT-scan (n=73) sensitivity was 79.2% and 82.6%, and PPV was 95.0% and 100% in Groups A and B, respectively. 201Tl/99mTc subtraction scintigraphy (n=111, Group A) was 84.6% sensitive (PPV=92.6%) whereas 99mTc-sestamibi scanning (n=90, Group B) was 85.1% sensitive (PPV=96.1%). In conclusion, the clinical features of parathyroid tumors has changed in the nineties and increasing asymptomatic pHPT rate has been found. Although sensitivity and PPV of preoperative localization procedures has improved moderately, at present noninvasive techniques may offer excellent results and should be used in all patients with suspected parathyroid tumors.
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PMID:Tumors of the parathyroid glands. Changes in clinical features and in noninvasive localization studies sensitivity. 1084 Sep 29

Alzheimer's disease is, in part, characterised by the loss of neurones in the basal forebrain cholinergic cells that project to the cerebral cortex and hippocampus. These impairments have correlated with the memory loss noted in dementia of the Alzheimer's type. This 'cholinergic hypothesis' has led to the rational design of drugs to enhance or stimulate acetylcholine-mediated neurotransmission. Early acetylcholinesterase inhibitors, such as tacrine and physostigmine, are poorly tolerated and have a short duration of action. Rivastigmine is a centrally-selective acetylcholinesterase inhibitor with a relatively long duration of action and is a 'pseudo-irreversible' cholinesterase inhibitor due to slow dissociation of a carbamoyl derivative from the esteratic site of acetylcholinesterase. Preclinical studies confirmed the central selectivity of the drug and its distribution into the cerebrospinal fluid (CSF). Early studies demonstrated that rivastigmine improved cognition and was relatively well-tolerated at moderate doses. Clinical investigations of rivastigmine administered at doses of 6 - 12 mg/day significantly improved cognition, as measured by the ADAS-Cog score, and activities of daily living, as measured by the Progressive Deterioration Scale. Significant global improvements were also noted as measured by the Clinician's Interview Based Impression of Change that required the use of caregiver information. The most frequent adverse effects noted in clinical trials were consistent with peripheral cholinergic stimulation and included nausea, vomiting, abdominal pain, dizziness and diarrhoea. These effects were dose-related and minimised by slow dose-escalation upon initiation of therapy. Rivastigmine undergoes minimal metabolism by the cytochrome P450 system. As a result, it has few drug interactions. The drug is currently marketed widely in over 60 countries worldwide. In the United States, the drug received 'approvable' status subsequent to the NDA filing, and should be available later this year.
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PMID:Rivastigmine, a brain-region selective acetylcholinesterase inhibitor for treating Alzheimer's disease: review and current status. 1113 19

Clinical symptoms and self-reported health status in persons reporting multiple chemical sensitivities (MCS) are presented from a 9-year follow-up study. Eighteen (69%) subjects from a sample of 26 persons originally interviewed in 1988 were followed up in 1997 and given structured interviews and self-report questionnaires. In terms of psychiatric diagnosis, 15 (83%) met DSM-IV criteria for a lifetime mood disorder, 10 (56%) for a lifetime anxiety disorder, and 10 (56%) for a lifetime somatoform disorder. Seven (39%) of subjects met criteria for a personality disorder using the Personality Diagnostic Questionnaire-IV. Self-report data from the Illness Behavior Questionnaire and Symptom Checklist-90-Revised show little change from 1988. The 10 most frequent complaints attributed to MCS were headache, memory loss, forgetfulness, sore throat, joint aches, trouble thinking, shortness of breath, back pain, muscle aches, and nausea. Global assessment showed that 2 (11%) had "remitted", 8 (45%) were "much" or "very much" improved, 6 (33%) were "improved", and 2 (11%) were "unchanged/worse". Mean scores on the SF-36 health survey showed that, compared to U.S. population means, subjects reported worse physical functioning, more bodily pain, worse general health, worse social functioning, and more emotional-role impairment; self-reported mental health was better than the U.S. population mean. All subjects maintained a belief that they had MCS; 16 (89%) acknowledged that the diagnosis was controversial. It is concluded that the subjects remain strongly committed to their diagnosis of MCS. Most have improved since their original interview, but many remain symptomatic and continue to report ongoing lifestyle changes.
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PMID:The Iowa follow-up of chemically sensitive persons. 1200 35

A survey study using questionnaire was conducted in 530 people (270 men, 260 women) living or not in vicinity of cellular phone base stations, on 18 Non Specific Health Symptoms. Comparisons of complaints frequencies (CHI-SQUARE test with Yates correction) in relation with distance from base station and sex, show significant (p < 0.05) increase as compared to people living > 300 m or not exposed to base station, till 300 m for tiredness, 200 m for headache, sleep disturbance, discomfort, etc. 100 m for irritability, depression, loss of memory, dizziness, libido decrease, etc. Women significantly more often than men (p < 0.05) complained of headache, nausea, loss of appetite, sleep disturbance, depression, discomfort and visual perturbations. This first study on symptoms experienced by people living in vicinity of base stations shows that, in view of radioprotection, minimal distance of people from cellular phone base stations should not be < 300 m.
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PMID:[Investigation on the health of people living near mobile telephone relay stations: I/Incidence according to distance and sex]. 1216 54

There is increasing evidence of permanent sequalae from acute organophosphate poisoning. We report on accidental diazinon overexposure with acute organophosphate poisoning through cutaneous absorption and inhalation followed by persistent neurological effects. In addition, we observed skeletal and endocrine effects likely attributable to the diazinon poisoning. A family of seven was exposed to diazinon in June 1999 over a two-day period. The pesticide company mistakenly used diazinon to heavily spray the inside of the home instead of permethrin. The applicator applied the pesticide over the entire surface of the floor, carpeting, furniture, and clothing in closets to eradicate an infestation of fleas. Acute symptoms in the family members included headaches, nausea, skin irritation, runny nose, and vomiting. The family was first evaluated at 3 months and then 3 years after the acute poisoning. There were persisting neurological symptoms of memory loss, decreased concentration, irritability, and personality changes of varying degrees in all family members. Objective neurological findings of impaired balance, reaction time, color vision, slotted pegboards and trials making were present in the three older children who could be tested. Neuropsychological evaluation revealed evidence of organic brain dysfunction in all seven family members. Bone growth difficulties are present in four of five children. One child has delayed menarche.
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PMID:Health effects of diazinon on a family. 1546 49

Pellagra is a systemic disturbance caused by a cellular deficiency of niacin, resulting from inadequate dietary nicotinic acid and/or its precursors, the essential amino-acid tryptophan. In Europe and North America cases of pellagra are rarely encountered, but in some developing countries this disease is frequent, and is the most frequent clinical feature of nutritional deficiency of adult. The principal causes of pellagra are: nutritional niacin deficiency; chronic alcoholism; gastro-intestinal malabsorption; some medications (5-fluoro-uracil, isoniazid, pyrazinamide ehtionamide, 6-mercaptopurine, hydantoins, phenobarbital and chloramphenicol). The diagnosis of pellagra is based on the patient's history and the presence of "3 D syndrome": dermatitis, diarrhea, and dementia. The dermatitis caused by pellagra is a bilaterally symmetrical erythema at the sites of solar exposure. The dermatitis begins in the form of an erythema with acute or intermittent onset gradually changing to an exsudative eruption on the dorsa of the hand, face, neck, and chest with pruritus and burning. Acute dermatitis of pellagra resembles sunburn in the first stages, sometimes with vesicles and bullae. The gastro-intestinal disturbances are: anorexia, nausea, epigastric discomfort and chronic or recurrent diarrhea. Anorexia and malabsorbative diarrhea lead to a state of malnutrition and cachexia. Stools are typically watery, but occasionally can be bloody and mucoid. Neuropsychologic manifestation included photophobia, asthenia, depression, hallucinations, confusions, memory loss and psychosis. As pellagra advances, patient become disoriented, confused and delirious; then stuporous and finally die. Pathological changes in the skin is non-specific, there are no chemical tests available to definitively diagnose pellagra. However low levels of urinary excretion of N-methylnicotinamide and pyridone indicates niacin deficiency. The treatment of pellagra consisted to exogenous administration of niacin or nicotinamide cures. Topical management of skin lesions with emollients may reduce discomfort. The therapy should also include other B vitamins, zinc and magnesium as well as a diet rich in calories. The prevention is based in the nutritional education (food sources of niacin: eggs, bran, peanuts, meat, poultry, fish, red meat, legumes and seeds), and the eviction of alcohol.
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PMID:[Pellagra]. 1620 85

A colloid cyst, also called a neuroepithelial cyst, is a slow-growing, benign tumor that occurs in the anterior third ventricle. The cyst typically blocks the foramen of Monro, causing obstructive hydrocephalus involving only the lateral ventricles. The most common presenting sign and symptom of a colloid cyst is headache. Less common presenting signs and symptoms include nausea, vomiting, memory loss, mental status changes, gait disorder, and visual disturbances. Surgical resection is the recommended treatment. Meticulous baseline and ongoing neurological assessments are of paramount importance in the care of a patient with a colloid cyst to promote optimal patient outcomes.
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PMID:Colloid cyst: a case study. 1848 40

OBJECTIVES: 5-Fluorouracil (5-FU) is an integral part of treatment of GI malignancies. While normal DPD enzyme activity is rate limiting in 5-FU catabolism, its deficiency could increase concentrations of bioavailable 5-FU anabolic products leading to 5-FU related toxicity syndrome. METHODOLOGY: Twenty-three patients were tested for DPD deficiency after excessive toxicities from 5-FU and/or capecitabine. DPD activity was evaluated by Peripheral Blood Mononuclear Cell (PBMC) radioassay, genotyping of DPYD gene by Denaturing High Performance Liquid Chromatography (DHPLC), or 2-(13)C uracil breath test (UraBT). RESULTS: Of 23 patients with excessive toxicities from 5-FU and/or capecitabine, 7 (30%) were DPD deficient with a median age of 66 years, M:F ratio = 1.3:1 and ethnicities included Caucasian (71%), African-American (14%) and South-Asian (14%). DPD activity ranged from 0.064 - 0.18nmol/min/mg. Three patients were treated with bolus 5-FU/LV, two with capecitabine, and two with high dose bolus 5-FU with 2', 3', 5'-tri-O-acetyluridine. Toxicities included mucositis (71%), diarrhea (43%), skin rash (43%), memory loss/altered mental status (43%), cytopenias (43%), nausea (29%), hypotension (14%), respiratory distress (14%) and acute renal failure (14%) Re-challenge with capecitabine in one patient after the Mayo regimen caused grade 3 hand-foot syndrome. Genotypic analysis of the DPYD gene in one patient with severe leucopenia demonstrated a heterozygous mutation (IVS14+1 G>A, DPYD). The UraBT in two patients of 112.8; PDR of 49.4%) and borderline normal values revealed 1 to be DPD-deficient (DOB(50) of 130.9; PDR of 52.5%) in a second patient. There were 2 toxicity-related deaths among (DOB(50) DPD-deficient patients (28%). CONCLUSIONS: DPD deficiency was observed in several ethnicities. Akin to 5-FU, capecitabine can also lead to severe toxicities in DPD-deficient patients. Screening patients for DPD deficiency prior to administration of 5-FU or capecitabine using UraBT could potentially lower risk of toxicity. Future studies should validate this technique.
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PMID:DIHYDROPYRIMIDINE DEHYDROGENASE DEFICIENCY (DPD) IN GI MALIGNANCIES: EXPERIENCE OF 4-YEARS. 1884 42


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