Biomedical subjects

Kristian Løvås

Publications and source records attributed to Kristian Løvås.

10 recordsLinked to original sources

PubMed2005

[Primary adrenal failure--causes, diagnostics and therapy].

BACKGROUND AND METHODS: An overview of primary adrenal failure with emphasis on replacement therapy is presented. The article is based on a review of recent literature and authors' personal experience. RESULTS AND CONCLUSIONS: Addison's disease is usually caused by an autoimmune destruction of the adrenal cortex. It is relatively rare (prevalence 14 per 100,000 inhabitants), but often considered as a differential diagnosis when evaluating fatigue, tiredness and loss of weight. Addison's disease is treated by repletion of glucocorticoids and mineralocorticoids. The recommended starting dose is 25 mg cortisone acetate per day divided into three (12.5 + 6.25 + 6.25 mg) or two doses (12,5 mg x 2). Mineralocorticoid replacement is given as fludrocortisone 0.05 - 0.2 mg in one dose per day. Treatment with 20 - 50 mg dehydroepiandrosterone has been studied in adrenal failure, but the evidence for positive effects is weak, and it can not be recommended as standard treatment in primary adrenal failure.

Addison Disease↗

PubMed2004

Retarded bone growth in thyroid hormone resistance. A clinical study of a large family with a novel thyroid hormone receptor mutation.

OBJECTIVE: Thyroid hormone resistance (RTH) is characterised by variable tissue hyporesponsiveness to thyroid hormone. The disorder is usually caused by mutations in the thyroid hormone receptor beta (TR beta). We describe a large family with this disorder. SUBJECTS AND MEASUREMENT: We identified 36 family members with RTH in four generations by screening relatives of patients with the diagnosis. The diagnosis was verified by identification of a mutation in the thyroid hormone receptor beta (TR beta) gene. Symptoms, clinical findings and laboratory tests of 29 affected individuals were compared with those of 16 first-degree relatives. RESULTS: Bone maturation in children with RTH was delayed. The height was lower both in children and in adults with RTH than in the controls. Children with RTH had lower birth weight than the controls, particularly when the condition was inherited from the father. We did not observe increased prevalence of neuropsychological symptoms associated with RTH in this family. Palpitations and increased pulse rate indicated mild cardiac hyperthyroidism. Direct sequence analysis of the TR beta gene revealed a novel point mutation, a heterozygous transition c.1031G>C in exon 9 theoretically substituting Gly344Ala. CONCLUSIONS: We found evidence of skeletal tissue hypothyroidism that resulted in permanent growth retardation from prenatal to adult life. We found substantial variations in thyroid hormone levels and clinical presentation, but most individuals were without symptoms of thyroid disorder.

Adolescent↗

PubMed2003

[Fooled by the diurnal rhythm].

BACKGROUND: Under ordinary circumstances, the daily secretion of cortisol displays a characteristic diurnal variation with a peak in the morning and a trough at night. It is important to understand the variation in cortisol secretion when analysing results of cortisol tests. PATIENT AND METHOD: We present a patient in whom work-up for acute headache revealed a pathologically low morning serum cortisol level. This led to further evaluation of adrenocortical function with an adrenocorticotropic hormone (ACTH) stimulation test and cortisol day profiles in serum and saliva. RESULTS AND INTERPRETATION: The analyses showed normal adrenocortical function and diurnal variation with normal amplitudes. The morning rise in cortisol secretion was, however, delayed by 7-8 hours due to a delayed sleep phase. This case illustrates the importance of the diurnal rhythm in the assessment of pituitary-adrenal function. There should be clinical suspicion of a disorder before a test is requested.

Adrenocorticotropic Hormone↗

PubMed2003

Replacement of dehydroepiandrosterone in adrenal failure: no benefit for subjective health status and sexuality in a 9-month, randomized, parallel group clinical trial.

The physiological role of dehydroepiandrosterone (DHEA) is not well understood, but studies suggest positive effects on subjective health and bone metabolism. We have conducted a clinical trial with DHEA replacement in adrenal failure with the primary aim of evaluating effects on subjective health status and sexuality. Thirty-nine women with adrenal failure were randomized to 9 months of treatment with 25 mg DHEA (n = 19) or placebo (n = 20). Treatment effects were assessed by validated questionnaires of subjective health and sexuality. DHEA replacement yielded a wide variation of effects on the subjective health scales, which were not different from the effects of placebo. Almost all patients receiving DHEA obtained normal androgen levels. Eighty-nine percent of the patients receiving DHEA experienced side-effects, in particular increased sweat odor and scalp itching. DHEA replacement did not significantly change the levels of blood lipids, IGF-I, and markers of bone metabolism. In conclusion, we do not find evidence of beneficial effects of DHEA on subjective health status and sexuality in adrenal failure. However, DHEA may be beneficial for subgroups of patients with adrenal failure, but these remain to be identified. Premenopausal androgen levels can be restored with 25 mg DHEA daily in most female patients, but side-effects are frequent.

Adrenal Gland Diseases↗

PubMed2003

Replacement therapy in Addison's disease.

Addison's disease or primary adrenal insufficiency is a rare disease, which is usually caused by autoimmune destruction of the adrenal cortex. The clinical picture is caused by deficiency of cortisol and aldosterone. These deficiencies are accompanied by adrenal androgen depletion of yet unknown significance. The current therapy is the replacement of glucocorticoids and mineralocorticoids, but the available drugs do not restore the normal diurnal variations in serum hormone levels. The clinical consequences of the grossly unphysiological replacement therapy are largely unknown. Many patients with Addison's disease on standard replacement therapy complain of fatigue, weariness, and reduced stress tolerance. One particular concern has been negative effects on both bone metabolism due to over-replacement of glucocorticoids and androgen depletion. This review discusses the evidence for the current drug and dosage recommendations. Current recommended daily starting dose for hydrocortisone and cortisone acetate are 20 and 25 mg, respectively, divided into two or preferably three doses. The mineralocorticoid depletion should be treated with fludrocortisone 0.05-2.0 mg/day [DOSAGE ERROR CORRECTED]. Replacement of dehydroepiandrosterone 20-50 mg has been advocated in adrenal failure, but the evidence for benefit is weak.

Addison Disease↗

PubMed2003

Sleep disturbances in patients with Addison's disease.

OBJECTIVE: The standard replacement therapy in Addison's disease does not restore normal nocturnal levels of the hormones of the hypothalamic-pituitary-adrenal axis. The aim of the study was to describe the prevalence and characteristics of sleep disturbances in patients with Addison's disease. METHODS: Sixty patients completed a self-administered sleep questionnaire and the Epworth Sleepiness Scale (ESS) questionnaire. Activity-based monitoring (actigraph recordings) and sleep diaries were obtained from eight patients. RESULTS: Thirty-four percent reported weekly sleep disturbances (difficulties falling asleep in 13%; repeated awakenings in 14%; early morning awakenings in 20%). The sleep need was 8.21 h (s.d. 1.34; range 6-14 h), and sleep onset latency was 29 min (s.d. 29, range 2-150 min). Forty percent of the patients were tired during daily activities more than once a week, but the scores of the ESS were 6.0 (s.d. 3.5), which is not higher than normal. The actigraph recordings showed higher sleep efficiency than the subjective recordings. CONCLUSION: We did not identify specific sleep disturbances which were characteristic for patients with Addison's disease. Patients with Addison's disease have increased daytime fatigue, but no more daytime sleepiness than normal.

Addison Disease↗

PubMed2002

Subjective health status in Norwegian patients with Addison's disease.

OBJECTIVE: Many patients with Addison's disease have complaints that might be related to the disease or to its treatment. However, only a few studies have addressed the subjective health status of patients with adrenocortical failure. The aim of the present study was to assess the subjective health status with special emphasis on fatigue among patients with Addison's disease. SUBJECTS, DESIGN AND MEASUREMENT: In a postal survey, 79 patients with confirmed primary adrenal failure (Addison's disease) completed the Short Form 36 (SF-36) and the Fatigue questionnaires. The subjective health status in Addison's disease was compared with normative data from the general population. RESULTS: General health and vitality perception were most consistently impaired in the patients with Addison's disease. The scores on physical functioning and role-physical were low in women. Social functioning and role-emotional scores were also lower than normal in the female patients, but this was confined to the patients with autoimmune polyendocrine syndromes. Patients with autoimmune polyendocrine syndromes tended to have lower scores than patients with solitary Addison's disease. The level of fatigue was higher than normal for both men and women. Working disability at ages 18-67 years was 26%, compared with 10% in the corresponding general Norwegian population. The high working disability increased with age and was higher in subgroups with concomitant endocrine diseases. Most subjective health parameters were lower among the disabled compared to the patients in work. CONCLUSIONS: Patients with Addison's disease under replacement therapy with cortisone acetate and fludrocortisone have reduced general health perception and vitality, and increased fatigue. Female patients reported reduced physical function, which might be due to adrenal androgen depletion. Mental health seems more influenced by concomitant endocrine diseases, but mental fatigue might be a specific feature in adrenal failure. The patient population is heterogeneous, with normal findings in a substantial proportion but markedly reduced subjective health status and working ability in many others. Thus, there might be potential for further refinement of replacement therapy.

Addison Disease↗

PubMed2002

High prevalence and increasing incidence of Addison's disease in western Norway.

OBJECTIVE: Estimates of the prevalence of Addison's disease in Caucasians have varied from 39 to 117 per million. We have carried out an epidemiological study to obtain a confident point prevalence estimate in the Norwegian population for the end of 1999, and to find out whether the incidence is changing. PATIENTS AND METHODS: The patients were identified by a search through registers of 10 hospitals and consultant endocrinologists serving a population of 916 000. The completeness of the list was tested by a survey of general practitioners in one district, and by the member list of the local Addison Association in another district. RESULTS: We identified 128 patients with Addison's disease (59 men and 69 women), yielding a prevalence of 140 per million. Recorded mean incidence in the past decade was 0.62 per 100,000 per year. Fifty-one patients (40%) had concomitant endocrine diseases. The aetiology was almost exclusively idiopathic or autoimmune. CONCLUSIONS: We found a higher prevalence of Addison's disease in western Norway than has previously been reported anywhere. Our findings support the hypothesis of a rising incidence of autoimmune adrenal insufficiency.

Addison Disease↗

PubMed2002

Autoimmune adrenocortical failure in Norway autoantibodies and human leukocyte antigen class II associations related to clinical features.

Autoimmune destruction of the adrenal cortex is the most common cause of primary adrenocortical insufficiency (Addison's disease) in industrialized countries. We have investigated a large Norwegian cohort of patients with Addison's disease in terms of clinical manifestations, autoantibodies, and human leukocyte antigen (HLA) class II haplotypes. The study comprised 94 patients (54 females) of ages 6-85 yr (mean 45 yr) with, either isolated Addison's disease or part of autoimmune polyendocrine syndrome type II. Among those diagnosed before the age of thirty, 53% were men, while among those diagnosed at 30 or above, 30% were men. Altogether 77 (82%) of the 94 patients had autoantibodies against 21-hydroxylase (21OH). Thirty-eight of the 40 patients with disease duration 5 yr or less had such autoantibodies. This frequency fell to 60% among patients with a disease duration greater than 35 yr. Five women had gonadal failure. This failure correlated with antibodies against side-chain cleavage enzyme (P = 0.03). Antibodies against glutamic acid decarboxylase and IA2 correlated with the presence of type 1 diabetes (P < 0.005 and P = 0.003, respectively). The frequency of the HLA DRB1*03-DQA1*05-DQB1*02 (DR3-DQ2) and DRB1*04-DQA1*03-DQB1*0302 (DR4-DQ8) haplotypes were positively correlated to Addison's disease, whereas the DRB1*01-DQA1*0101-DQB1*0501 (DR1-DQ5) haplotype was negatively correlated. In addition, the DRB1*04 subtype DRB1*0404 was increased among Addison patients relative to controls. We verify that autoimmunity is the main cause of Addison's disease in our cohort. In younger patients, the disease is equally common in men and women. Measurement of autoantibodies against 21OH is a valuable tool in establishing the etiological diagnosis, especially in patients with a short disease duration. Addison's disease is associated with the DR3-DQ2 and DR4 (0404)-DQ8 haplotypes. A particularly high risk for disease development is observed when these occur in a heterozygous combination (DR3-DQ2/DR4-DQ8).

Addison Disease↗

PubMedDate not supplied

Addison's disease.

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Addison Disease↗