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Biomedical subjects

Arnold E Andersen

Publications and source records attributed to Arnold E Andersen.

18 recordsLinked to original sources
PubMed2004

Unmasking a current medical pretender: anorexia nervosa in gastrointestinal practice.

Anorexia nervosa (AN) resembles the 'great pretenders' of medicine in the nineteenth century, syphilis and tuberculosis, by presenting occultly as a disorder of specific organs. Many physicians fail to identify the true primary cause, AN, which can mimic in its medical consequences gastrointestinal disorders, endocrine failure, pituitary tumors, or cancer. This is especially likely when the patients are older, have an established complex medical history, and challenge a specialist to find a medical cause and treatment, resulting in ordering more laboratory tests and medical instrumentation. Everyone suffers as a result, including the patient, the family, the frustrated physician, and the National Health Service, for whom the costs of medical care of these patients are enormous and out of proportion. Remembering that AN is as much a medical as a psychological disorder, assessing the patient with more time and expertise in history taking, and referring to a psychiatric consultant when National Institute for Clinical Excellence guidelines for identifying AN in non-mental health settings trigger suspicions, results in good outcome of the AN, cessation of ineffective gastrointestinal treatments, and substantial savings to the National Health Service.

Anorexia Nervosa↗
PubMed2003

Neuropsychological functioning pretreatment and posttreatment in an inpatient eating disorders program.

OBJECTIVE: This study was conducted to determine whether neuropsychological dysfunction associated with anorexia nervosa resolves with inpatient treatment. METHOD: Subjects were 28 women being treated for anorexia nervosa. Main study variables included body mass index (BMI), Beck Depression Inventory-II, and neuropsychological test scores. Subjects were tested at admission and discharge. RESULTS: Neuropsychological functioning improved across the course of treatment, with significant changes on tests of memory and psychomotor speed. This improvement was not significantly associated with change in BMI or with the other variables that were studied. DISCUSSION: Patients with anorexia nervosa exhibit subtle neuropsychological dysfunction, which resolves at least partially during treatment. This improvement does not appear to be associated with an increase in BMI. However, it is possible that BMI is not a sufficiently sensitive indicator of nutritional status or that longer-term follow-up is necessary to reveal the nutrition-cognition relationship that we were seeking.

Adult↗
PubMed2003

Brain tissue volume segmentation in patients with anorexia nervosa before and after weight normalization.

OBJECTIVE: To examine whether gray and white matter volumes are preferentially reduced and cerebral spinal fluid (CSF) increased with starvation in patients with anorexia nervosa compared with healthy controls and to determine what changes occur with weight normalization. METHOD: Whole intracranial volumes of patients and controls were segmented into gray matter, white matter, and CSF volumes and results compared. A subgroup of patients were rescanned after weight normalization. RESULTS: Total white matter and several regional white matter volumes were significantly reduced and total and regional CSF volumes were significantly increased in patients versus controls whereas gray matter was not significantly reduced. Total and regional CSF volumes were significantly decreased in patients upon weight normalization whereas white and gray matter volumes increased. DISCUSSION: These changes in brain tissue may be related to a variety of pathophysiologic mechanisms. We hypothesize that insulin-like growth factor-1 may be involved.

Adult↗
PubMed2003

Cognitive impairment in anorexia nervosa is not due to depressed mood.

OBJECTIVE: Previous research has revealed cognitive deficits in patients with anorexia nervosa. It is unclear whether these deficits are linked to co-morbid depression in this population. We examined the relationship between depressive symptoms and cognitive functioning. METHOD: A large sample of subjects (N = 98) was examined using a common measure of cognitive ability and two measures of depression. RESULTS: We confirmed that there is no relationship between depression and cognitive ability in this group. DISCUSSION: This suggests that alternative explanations be explored for cognitive deficits in patients with anorexia nervosa.

Adolescent↗
PubMed2002

Neuropsychological characteristics of patients in a hospital-based eating disorder program.

The existence of cognitive deficits associated with eating disorders has been debated for some time. The present study investigated cognitive impairments in a large sample of patients with anorexia nervosa from an inpatient treatment program. Fifty-nine women with anorexia nervosa were given a battery of neuropsychological tests assessing multiple cognitive domains. Over half of the patients had mild cognitive impairments in two or more neuropsychological tasks and approximately one-third failed two or more tasks. Depression level and body mass were not associated with cognitive impairment. Whether effective restoration of weight and resolution of core psychopathology contribute to reversal of cognitive deficits requires further research.

Adolescent↗
PubMed2002

Testosterone therapy in late-life major depression in males.

BACKGROUND: Major depression associated with aging in males may improve with anabolic/androgenic steroid therapy. The efficacy and safety of testosterone therapy in the treatment of depression in elderly hypogonadal males is inconclusive. The following study identifies a subgroup of elderly depressed males who may benefit from testosterone therapy. METHOD: Participants included 16 elderly eugonadal males with major depressive disorder (DSM-IV criteria) and a Hamilton Rating Scale for Depression (HAM-D) score > 18. Following a single-blind 2-week placebo lead-in, patients were randomly assigned to treatment with either a physiologic dose of testosterone cypionate (TC), 100 mg/week, or supraphysiologic dose of 200 mg/week IM for 6 weeks. Psychometric testing was carried out at entry into the study, at the TC injection baseline, and every 2 weeks thereafter. Tests included an objective measurement, the HAM-D, and the Buss-Durkee Hostility Inventory. RESULTS: One patient meeting inclusion criteria responded during the placebo lead-in; thus, 15 patients were randomly assigned to treatment (100 mg/week, N = 8; 200 mg/week, N = 7). There was a 42% decrease in the mean HAM-D scores from 20.1 to 11.9 (p <.0001). However, the majority of the change was due to improvement in the 10 late-onset (< or = 45 years old) depression patients, whose mean HAM-D score decreased from 19.8 to 9.3 (53%), versus the 5 early-onset depression patients, whose mean HAM-D score decreased from 20.8 to 17.0 (18%) (p =.0110). The TC dose did not affect the response. Similar HAM-D decreases of 43% and 41% occurred for the respective 100- and 200-mg/week doses. The HAM-D responder analysis found that none of 5 early-onset patients had HAM-D response, whereas 6 (60%) of 10 late-onset patients responded (p =.025). Similarly, none of the early-onset patients experienced a remission whereas 5 (50%) of the late-onset patients were categorized as remitters (p =.053). Correlations between the peak and mean total testosterone concentrations and HAM-D change scores suggested that only minimal TC doses were required to produce an antidepressant effect. CONCLUSION: These data suggest that testosterone therapy would best be limited to men with late-onset depression. The findings suggest that short-term therapy with TC is safe. Long-term treatment safety is unknown. Psychiatrists using testosterone therapy should ascertain that patients have been recently valuated for prostate cancer. If testosterone therapy is initiated, serial serum prostate-specific antigen sampling should be used for monitoring patients' prostate status.

Anabolic Agents↗