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Biomedical subjects

L L Humphries

Publications and source records attributed to L L Humphries.

At least 19 recordsLinked to original sources
PubMed1999

A role for Helicobacter pylori in the gastrointestinal complaints of eating disorder patients?

UNLABELLED: Eating disorder patients frequently present with gastrointestinal complaints. Helicobacter pylori is an etiologic factor in type B gastritis, gastric and duodenal ulcers, and may cause nausea and anorexia. OBJECTIVE: To determine whether or not there is an increased prevalence of H. pylori infection in patients with eating disorders. METHOD: Serum H. pylori IgG antibody and gastrointestinal symptoms were assessed in 32 patients admitted for inpatient treatment of anorexia nervosa and/or bulimia nervosa. RESULTS: Eating disorder patients did not have an increased rate of detectable serum H. pylori IgG antibody. DISCUSSION: There is not an increased prevalence of H. pylori infection in eating disorder patients. Thus, the increased frequency of gastrointestinal complaints in eating disorder patients cannot be attributed to H. pylori infection.

Adolescent↗
PubMed1996

The cytochrome P450 2D6 (CYP2D6) enzyme polymorphism: screening costs and influence on clinical outcomes in psychiatry.

OBJECTIVES: This study examined factors that affect cost, reliability, and the value of determining the cytochrome P450 2D6 (CYP2D6) polymorphism in clinical practice. STUDY DESIGN: The method of deoxyribonucleic acid isolation, sample preparation, oligonucleotide primers, and polymerase chain reaction procedures were scrutinized for their effect on CYP2D6 genotyping efforts. The determination of the CYP2D6 A, B, D, E, and T alleles was used to identify the deficiency in CYP2D6 expression in 161 individuals phenotyped for CYP2D6 activity with dextromethorphan. The CYP2D6 genotype was assessed in 74 outpatients who had received diagnoses of depression. Eighteen of these patients were screened because of an adverse response to a tricyclic or antidepressant known or suspected to be a CYP2D6 substrate. RESULTS: The CYP2D6 A, B, C, D, E, and T alleles could be detected in 13 hours at a cost of $84 per sample by judicious selection of conditions and procedures. The genotype provided an accurate predictor of CYP2D6 expression in all 134 subjects who expressed the enzyme and in all 27 unrelated individuals phenotyped as deficient in CYP2D6 activity. In the patient group that experienced adverse effects, 44% of all CYP2D6 gene copies contained the A, B, D, E, or T allele(s) associated with inactive CYP2D6 expression. This was more than twice the rate for the occurrence of mutant alleles in the other 56 psychiatric patients (21%) and in 80 random subjects from the general population (20%; p < 0.05). CONCLUSIONS: Screening psychiatric patients for CYP2D6 expression may distinguish metabolic-based therapeutic problems from drug sensitivity caused by other mechanisms.

Antidepressive Agents, Tricyclic↗
PubMed1996

Dietary induced anorexia: a review of involvement of the histaminergic system.

This review examines possible relationships between anorexia, dietary intake and central nervous system histaminergic activity. The hypothesis being reviewed is that one component of normal or pathophysiological neuroregulation of food intake involves histaminergic activity in the central nervous system, as influenced by concentrations and bioperiodicities of histamine and/or histamine receptors. Changes in concentrations of receptors are gender specific. Low protein quality or quantity diets elevate both central histamine and histamine receptors (H1) in rats while significantly decreasing their food intake. When injected with histaminergic antagonists, rats fed low protein diets increase food intake and have improved efficiency of weight gain. This review supports a dual hypotheses: central histaminergic activity is involved in the regulation of food intake, but food intake patterns (including dietary composition or energy content) can modify central histaminergic activity. This review also suggests that modified histamine and/or H1 receptor concentrations are potential mechanisms for elevated central histaminergic activity in food intake-related pathophysiological states. Thus, dietary interventions (clinically- or self-imposed) which modify food intake or diet composition have the potential of affecting the histaminergic system. Also, drugs with antihistaminergic properties have the potential of affecting food intake/weight gain patterns by interfering with normal neurochemical signals.

Adolescent↗
PubMed1996

Gender affects rats' central nervous system histaminergic responses to dietary manipulation.

The histaminergic system (histamine and its H1-receptor) of the central nervous system has been implicated in control of food intake. The reported studies were designed to examine the effects of food restriction and very low (1%) protein diets on central nervous system H1-receptors in male and female rats. In a series of experiments, groups of rats were freely fed a 25% protein diet, a 1% protein diet, or fed the 25% protein diet at 4 g/100 g body weight for 14-20 d. When freely fed 25% protein diets, females had higher whole-brain H1-receptor binding than males on d 1 (female 122.36 +/- 4.53 and male 65.78 +/- 3.82 pmol/g protein; P < 0.001). Changing diets affected central H1-receptor binding in both males and females (P < 0.003). When rats were fed both restricted levels of food and 1% protein diets, the receptor binding of males increased by d 5 whereas that of females decreased by d 5 (P < 0.001). When fed 1% protein diets, females had decreased H1-receptor binding (98.4 +/- 2.38 pmol/g protein) and that in males increased to 119.81 +/- 5.09 pmol/g protein. After 15 d, females had eaten significantly more food than males: females 166 +/- 4.9 g, males 124 +/- 1.9 g (P< 0.0007). Males had a significantly greater weight loss than females: males -28.8 +/- 2.6 g, females -17.08 +/- 0.97 g (P < 0.0007). When fed restricted diets, females had decreased H1-receptor binding (93.81 +/- 5.58 pmol/g) whereas binding in males increased to 111.27 +/- 8.55 pmol/g. Preliminary saturation binding studies indicated that restricted food intake lowered receptor density (females consuming 25% protein: 715 +/- 30 pmol/g protein; female restricted: 467 +/- 28 pmol/g protein, P < 0.05), while 1% protein increased receptor sensitivity, i.e., lowered KD (males consuming 25% protein: 15.3 +/- 1.8 nmol; males fed low protein: 2.8 +/- 0.27 nmol). This study suggests that dietary manipulation affects central H1-receptor binding in a gender-specific manner, thereby modulating central histaminergic activity during food or protein deficit.

Animals↗
PubMed1994

Manipulation of central nervous system histamine or histaminergic receptors (H1) affects food intake in rats.

The reported studies were designed to examine relationships between central nervous system histamine, histaminergic receptors (H1) and food intake in rats. The hypothesis being tested was as follows: "One component of the neuroregulation of food intake involves histaminergic activity in the hypothalamus as influenced by variation of histamine levels and/or H1 receptor concentrations." We performed combinations of dietary, surgical and pharmacological treatments on male or female rats. We fed groups of male or female rats diets containing either 4 g casein/100 g diet (low protein diet) or 25 q casein/100 g diet (normal protein). Rats with surgical ablation of the paraventricular nucleus did not decrease food intake when fed the low protein diet, whereas adrenalectomized rats did. Increasing central histamine levels decreased food intake, whereas decreasing central histamine increased food intake. Rats injected with histaminergic (H1) antagonists lost the ability to detect low protein diet in short-term experiments and had improved efficiency of weight gain. Rats that were fed the low protein diet or pair-fed the normal protein diet had greater H1 receptor concentrations in whole brain preparations when compared with rats fed the normal protein diet. No differences were noted due to gender. Thus, manipulation of histamine levels affected food intake as hypothesized, i.e., increasing central histamine decreased food in rats fed the normal protein diet, whereas decreasing central histamine or blockade of H1 receptors increased food intake in rats fed the low protein diet.

Adrenalectomy↗
PubMed1994

Neurologic complications of anorexia nervosa.

The records of 100 patients with anorexia nervosa were reviewed. Neurologic complications were present in 47 patients. Neuromuscular abnormalities were most common and were present in 45% of patients. Generalized muscle weakness was detected in 43% of patients and peripheral neuropathies in 13%. Less common neurologic complications included headaches (6%), seizures (5%), syncope in the absence of orthostatic hypotension (4%), diplopia (4%), and movement disorders (2%). Neurologic problems due to chronic deficiency diseases were rare; only one patient had symptoms directly attributable to a vitamin B12 deficiency and none had evidence of Wernicke's encephalopathy. In most patients, the neurologic complications were reversed completely after correction of nutritional deficiencies and fluid and electrolyte imbalances.

Adolescent↗
PubMed1993

Gastrointestinal and nutritional aspects of eating disorders.

Anorexia nervosa (AN) and bulimia nervosa (BN) are potentially fatal eating disorders which primarily affect adolescent females. Differentiating eating disorders from primary gastrointestinal (GI) disease may be difficult. GI disorders are common in eating disorder patients, symptomatic complaints being seen in over half. Moreover, many GI diseases sometimes resemble eating disorders. Inflammatory bowel disease, acid peptic diseases, and intestinal motility disorders such as achalasia may mimic eating disorders. However, it is usually possible to distinguish these by applying the diagnostic criteria for eating disorders and by obtaining common biochemical tests. The primary features of AN are profound weight loss due to self starvation and body image distortion; BN is characterized by binge eating and self purging of ingested food by vomiting or laxative abuse. GI complications in eating disorders are common. Recurrent emesis in BN is associated with dental abnormalities, parotid enlargement, and electrolyte disturbances including metabolic alkalosis. Hyperamylasemia of salivary origin is regularly seen, but may lead do an erroneous diagnosis of pancreatitis. Despite the weight loss often seen in eating disorders, serum albumin, cholesterol, and carotene are usually normal. However, serum levels of trace metals such as zinc and copper often are depressed, and hypophosphatemia can occur during refeeding. Patients with eating disorders frequently have gastric emptying abnormalities, causing bloating, postprandial fullness, and vomiting. This usually improves with refeeding, but sometimes treatment with pro-motility agents such as metoclopromide is necessary. Knowledge of the GI manifestations of eating disorders, and a high index of suspicion for one condition masquerading as the other, are required for the correct diagnosis and management of these patients.

Adolescent↗
PubMed1993

Serum insulin-like growth factor-I concentrations in the recovery of patients with anorexia nervosa.

Anorexia nervosa (AN) can result in extreme malnutrition, and these patients frequently require inordinately large amounts of calories to gain weight during refeeding therapy. Insulin-like growth factor-I (IGF-I) is a polypeptide that mediates many of the anabolic effects of growth hormone. Low levels of IGF-I have been associated with malnutrition and can cause poor weight gain. To clarify the potential relationship of IGF-I to weight gain, serial serum IGF-I, retinol-binding protein and prealbumin levels were measured at admission, 2 weeks and 4 weeks, in 14 consecutive consenting patients admitted for treatment of AN. Baseline IGF-I levels were lower in the patients compared to age-matched controls (mean 20.8 +/- 2.5 vs 32.9 +/- 2.9 nmol/L, p < 0.01). In patients with no weight gain, IGF-I levels were static. There was a stepwise increment in the IGF-I values related to weight gain. Retinol-binding protein and prealbumin, proteins commonly used to assess nutritional status, did not demonstrate important correlations with weight gain. Further studies are required to determine whether or not initial low IGF-I levels impede weight gain in AN patients and whether treatment with IGF-I (possibly in combination with growth hormone) may be of benefit in this disease process.

Adolescent↗
PubMed1992

The intellectual functioning of eating disorder patients.

This study investigated the intellectual functioning of a large group of eating disorder patients to examine two previously reported findings: (1) this population exhibits above-average general intellectual skills; and (2) a specific pattern of strength in verbal abilities. Standard intellectual testing of 100 consecutive inpatient females with eating disorder diagnoses was performed. Results indicate intellectual performance conforming to a normal distribution with no specific pattern of strengths or weaknesses.

Adolescent↗
PubMed1990

Osteoporosis in women with eating disorders: comparison of physical parameters, exercise, and menstrual status with SPA and DPA evaluation.

Osteoporosis has been reported in anorexia nervosa (AN), but not in other eating disorders. Thirty-three patients, 8 AN, 17 bulimia nervosa (BN), and 8 eating disorder not otherwise specified (EDNOS), were evaluated by bone densitometry (radius, spine, femur) to determine the prevalence and distribution of osteoporosis and the role of physical parameters, exercise and estrogen. All three diagnostic subgroups had evidence of decreased bone density, worst in the EDNOS subgroup and least in the BN subgroup. The most affected site was the femur, least the spine; the radius was intermediate. Age, body surface area, age of onset, and length of illness weakly correlated with the femur and spine density in the BN and EDNOS subgroups. Exercise was related to bone density in the AN subgroup in the femur, moderate exercise having a protective effect and strenuous exercise being detrimental. No significant correlation of bone density measurements with estradiol levels and/or history of amenorrhea was identified. Eating disorder patients are at risk for osteoporosis, which has multiple contributing factors including physical parameters and exercise. Estrogen deficiency by itself may not be a major causative factor.

Absorptiometry, Photon↗
PubMed1989

Risks of radioactive material transportation accidents in Oregon.

As a continuation of previous research on worst case transportation accidents involving radioactive material (Dodd and Humphries 1988a), and protective action guidance for radioactive material transportation accidents (Dodd and Humphries 1988b), this paper describes the risks from such accidents in Oregon. Radioactive material transportation risks are defined in terms of accident consequences multiplied by the accident probabilities and are expressed as latent cancer fatalities (LCFs). For each of 17 different shipment types, five dose contributions are summed and multiplied by the population density and accident probability. The five dose contributors considered are: inhalation, resuspension, cloudshine, groundshine and direct exposure. The variables over which each of these dose contributors are integrated include seven accident severity categories, three population density zones, five regions of the state, as well as many isopleth areas and radionuclides. Allowance is also made for the possible distribution of meteorological conditions in each area. The dose to the public, emergency responders, pedestrians and personnel in other traffic are all considered. It is concluded that the current level of risk is 1.2 X 10(-5) latent cancer fatalities per year in Oregon. This is equivalent to one LCF every 83,000 y. This compares to 1.2 non-radiological fatalities associated from the same shipments.

Accidents↗
PubMed1988

Protective action guide for radioactive material transportation accidents.

This paper briefly describes a report which has been developed to enable protective action guidance to be determined for transportation accidents involving radioactive material. The protective action guide uses data from on-scene observations as input to a series of simple flow charts leading to protective action recommendations. Where the necessary data is unavailable or unknown, the guide uses the assumptions and results found in the authors' worst case hazards analysis report.

Accidents↗
PubMed1988

Hazards assessment of worst case transportation accidents involving typical radioactive material shipments.

This paper reports the results of a study performed for the Oregon Department of Energy. The objectives of the study were to characterize the range of radioactive material shipments through the state and to determine the worst radiological hazards which might arise if these shipments were involved in transportation accidents. The direct and indirect radiological hazards were analyzed for worst case accidents involving a total of 10 typical shipments. The direct hazard primarily involved the gamma radiation from the material, while the indirect hazard considered the airborne release hazards of inhalation/ingestion, cloudshine and groundshine. The general and specific assumptions used in the study are given, and the results are tabulated, giving doses and dose rates as a function of distance. The data from the study are being incorporated into a protective action guide for use by state and local emergency responders. This guide bases the protective actions on the available, observable data and on flow charts which use the worst-case assumptions for unknown data.

Accidents↗
PubMed1987

Hyperamylasemia in patients with eating disorders.

Hyperamylasemia, which has been reported in patients with the eating disorders anorexia nervosa and bulimia, generally has been thought to result from pancreatitis. To evaluate the mechanisms of hyperamylasemia, we measured amylase, lipase, and isoamylase activity in 17 consecutive patients admitted to the eating disorder unit. Six patients had elevated amylase activity, and 5 of these 6 had isolated increases in salivary isoamylase activity. Six other patients had normal serum total amylase activity but modest elevations in the salivary isoamylase fraction. No patient developed clinical evidence of pancreatitis during hospitalization. Thus, the hyperamylasemia in patients with anorexia and bulimia often is caused by increased salivary-type amylase activity. The appropriate diagnostic test for hyperamylasemia in patients with anorexia or bulimia is the simple measurement of serum lipase or pancreatic isoamylase activity. If these levels are found to be normal, further tests to exclude pancreatitis are unnecessary.

Adolescent↗