Biomedical subjects

J Gustafsson

Publications and source records attributed to J Gustafsson.

At least 19 recordsLinked to original sources

PubMed2006

Increased lipolysis in LCHAD deficiency.

An increasing number of fatty acid oxidation defects are being detected owing to diagnostic improvements and a greater awareness among clinicians. The metabolic block leads to energy disruption, fatty infiltration, and toxic effects on organ functions exerted by beta-oxidation metabolites. This investigation was undertaken to assess the influence of long-chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD) deficiency on lipolysis and energy turnover. We addressed the question whether the lipolysis and glucose production rates would be altered in the fasting state in a child with this disease. Lipolysis, glucose production and resting energy expenditure (REE) were studied in a 17-month-old girl with LCHAD deficiency and her healthy twin sister. Lipolysis and glucose production were determined after a 4-6 h fast by constant-rate infusion of [1,1,2,3,3-(2)H(5)]glycerol and [6,6-(2)H(2)]glucose and analysis by gas chromatography-mass spectrometry. REE was estimated by indirect calorimetry. The affected girl showed 50% higher lipolysis than did her sister, whereas the glucose production rates were similar. Plasma levels of dicarboxylic acids of 6-12 carbon atoms chain length, 3-hydroxy fatty acids of 6-18 carbon atoms chain length, total free fatty acids, and acylcarnitines were increased in the patient, as was REE. Since glucose production rates and plasma glucose levels were similar in the two girls, the increased lipolysis observed in the patient probably represents a compensatory mechanism for energy generation. This is achieved at the price of an augmented risk for fatty acid infiltration and toxic effects of beta-oxidation intermediates. This highlights the importance of avoiding fasting in these patients.

Acyl-CoA Dehydrogenase, Long-Chain↗

PubMed2006

Decreased maternal lipolysis in intrauterine growth restriction in the third trimester.

OBJECTIVE: Intrauterine growth restriction (IUGR) is a common complication of pregnancy. There are many possible aetiologic factors of maternal, placental and/or fetal origin. Often there is no known explanation. The aim of this study was to investigate whether a reduction in maternal energy substrate production could be one of the factors involved in IUGR. DESIGN: Measurement of maternal energy substrate production and glucoregulatory hormones in women with growth-restricted fetuses. SETTINGS: University Hospital, Uppsala, Sweden. POPULATION: Ten healthy pregnant women with IUGR were compared with eight recently reported healthy women with normal pregnancies. The women were studied at 35.4+/-1.6 weeks of gestation after an overnight fast. METHODS: Rates of glycerol and glucose production were analysed by gas chromatography/mass spectrometry following constant-rate infusion of [1,1,2,3,3-(2)H5]glycerol and [6,6-(2)H2]glucose. MAIN OUTCOME MEASURE: Third trimester glycerol and glucose production. RESULTS: Glycerol production, reflecting lipolysis, was lower in the women with IUGR than in those with normal pregnancies, 2.36+/-0.58 versus 3.06+/-0.66 micromol kg-1 minute-1 (P=0.033), whereas there was no difference in rate of glucose production (glucose production rate [GPR]), 12.1+/-1.5 versus 13.2+/-1.5 micromol kg-1 minute-1 (P=0.23). Plasma glycerol levels were increased in the women with IUGR (P=0.008). CONCLUSIONS: Lipolysis is lower in pregnancies complicated by IUGR as compared with normal pregnancies. Increased lipolysis during pregnancy provides substrate for maternal energy metabolism, which spares glucose for the fetus. A reduced maternal production of energy substrate could be one of several factors underlying IUGR. A lack of relationship between insulin levels and either lipolysis or GPR suggests defective regulation of energy substrate production in this group of pregnant women.

Adult↗

PubMed2004

Pubertal development and final height after autologous bone marrow transplantation for acute lymphoblastic leukemia.

We describe pubertal development and growth in 17 children who underwent bone marrow transplantation (BMT), including total body irradiation (TBI) for ALL. Seven children also received cranial irradiation (CI) and five boys testicular irradiation. All underwent transplantation before (n=15) or at the beginning of (n=2) puberty and reached a final height (FH). Puberty started spontaneously in all boys not given testicular irradiation. All boys who received testicular irradiation developed hypergonadotrophic hypogonadism. Puberty started spontaneously in two girls and was induced with increasing doses of ethinylestradiol in two girls. In two girls, a low dose of ethinylestradiol was given until menarche. In one girl with early onset of puberty and short stature, puberty was blocked with a GnRH analogue. The standard deviation score for height decreased significantly from BMT to FH, both in the children who received TBI only (-1.1, P=0.005) as well as in those given additional CI (-1.7, P=0.027). Most of the loss occurred during puberty. In all, 10 children received growth hormone (GH) treatment. CI, young age at BMT, and short duration of GH treatment were predictors of height loss after BMT. Although limited by the small and heterogeneous sample, our study supports the use of early GH treatment in children with decelerating growth rate and low GH levels.

Adolescent↗

PubMed2004

Final height after combined growth hormone and GnRH analogue treatment in adopted girls with early puberty.

BACKGROUND: Girls adopted from developing countries often have early or precocious puberty, requiring treatment with gonadotrophin-releasing hormone (GnRH) analogues. During such treatment, decreased growth velocity is frequent. AIM: To study whether the addition of growth hormone (GH) to GnRH analogue treatment improves final height in girls with early or precocious puberty. METHODS: Forty-six girls with early or precocious puberty (age < or =9.5 y) adopted from developing countries were randomized for treatment for 2-4 y with GnRH analogue, or with a combination of GH and GnRH analogue. RESULTS: During treatment, the mean growth velocity in the GH/GnRH analogue group was significantly higher compared to the control group. Combined GH/GnRH analogue treatment resulted in a higher final height: 158.9 cm compared to 155.8 cm in the GnRH analogue-treated group. Three out of 24 girls (13%) in the combined group and nine of the 22 girls (41%) treated with GnRH analogue alone attained a final height below -2 standard deviation scores (SDS). CONCLUSION: The difference between the two groups is statistically significant, and possibly of clinical importance. A future challenge is to identify a subgroup with clinically significant advantage of GH addition to GnRH analogue treatment. Being very short on arrival in Sweden and being short and young at start of treatment are possible indicators.

Adoption↗

PubMed2004

Endogenous glucose production and lipolysis in anorexia nervosa--a study using stable isotope-labelled compounds.

UNLABELLED: Glucose production and lipolysis were investigated in teenage girls with anorexia nervosa using glucose and glycerol labelled with stable isotopes. The production of energy substrates were also maintained in the very underweight patients who showed higher relative rates of substrate mobilization compared to those who had gained some weight. CONCLUSION: The investigation shows that glucose production, necessary to provide fuel for the central nervous system, is also maintained in starving patients with anorexia nervosa.

Adolescent↗

PubMed2004

A novel nonsense mutation of the mineralocorticoid receptor gene in a Swedish family with pseudohypoaldosteronism type I (PHA1).

Pseudohypoaldosteronism type I (PHA1) is a condition associated with salt wasting leading to dehydration, hypotension, hyperkalemia, and metabolic acidosis. Sporadic cases and two familial forms, one autosomal dominant and one autosomal recessive form, have been described. The autosomal dominant or sporadic form manifests milder salt wasting that remits with age. Mutations in the gene encoding the mineralocorticoid receptor (MR) have been identified in patients with the autosomal dominant inheritance. However, recent studies suggest that the autosomal dominant and sporadic forms are genetically heterogeneous and that additional genes might be involved. We report on the study of 15 members of a Swedish five-generation family with the autosomal dominant form of PHA1. Interestingly, neuropathy was found in two of five affected individuals. A novel heterozygous nonsense mutation C436X in exon 2 was identified in the index patient by linkage analysis, PCR, and direct sequencing of the MR gene. Analysis of the family demonstrated that the mutation segregated with PHA1 in the family. It is unclear whether the neuropathy is associated with the mutation found. Our results together with previously published data suggest that loss-of-function mutations of the MR gene located at 4q31.1, commonly are associated with the autosomal dominant form of PHA1.

Adult↗

PubMed2002

Insulin sensitivity and lipolysis in adolescent girls with poorly controlled type 1 diabetes: effect of anticholinergic treatment.

OBJECTIVES: Increased GH secretion could be one factor behind the impaired glycaemic control often seen in adolescent girls with type 1 diabetes. Because GH induces insulin resistance, treatment with anticholinergic agents, such as pirenzepine (PZP), has been used to reduce GH secretion. However, in a previous study of adolescent girls with type 1 diabetes, we observed an improvement in glycaemic control during 12 weeks of PZP therapy despite unchanged excretion of GH in urine. Considering the complex mechanisms behind urinary GH excretion, the effects of PZP on pituitary GH secretion or secretory pattern cannot be excluded. Thus, to assess the effect of anticholinergic treatment on metabolic control in adolescent girls with diabetes, we have investigated GH secretion, insulin sensitivity and lipolysis before and during treatment with PZP. PATIENTS: Eleven adolescent girls with type 1 diabetes and poor metabolic control were investigated before and after treatment with PZP, 100 mg orally, twice a day for 3 weeks. DESIGN: Serum samples for analysis of haemoglobin A1c and IGF-I were obtained in addition to serum profiles of GH, insulin and IGFBP-1 before and after 3 weeks of PZP treatment. Effects on insulin sensitivity and lipolysis were also assessed. MEASUREMENTS: IGFBP-1 was measured every hour, whereas serum GH and insulin were measured every 20 min for 24 h. Insulin sensitivity was analysed with the hyperinsulinaemic euglycaemic clamp technique. The rate of lipolysis was assessed under basal conditions following a constant rate infusion of [1,1,2,3,3-2H5]-glycerol. In five girls, lipolysis was also estimated during the hyperinsulinaemic euglycaemic clamp. RESULTS: There was a significant reduction in haemoglobin A1c levels (9.9 +/- 0.2%vs. 9.1 +/- 0.2; P < 0.0001) during 3 weeks of PZP treatment. In additional, the glucose requirement during the euglycaemic hyperinsulinaemic clamp increased by more than 30% (72.5 +/- 4.9 vs. 96.8 +/- 8.5 mg/m2/min; P = 0.003). However, we could not demonstrate any significant changes in GH secretion (area under the curve, basal levels or peak amplitude) or in the GH secretory pattern (peak height, peak length or interpeak interval). Concordantly, the IGF-I levels were statistically unchanged, as were IGFBP-1 concentrations. The rate of lipolysis did not change under basal conditions (3.40 +/- 0.53 vs. 3.04 +/- 0.54 micro mol/kg/min, n = 11, P = 0.54) or during the hyperinsulinaemic euglycaemic clamp (1.58 +/- 0.21 vs. 2.08 +/- 0.26 micro mol/kg/min; n = 5, P = 0.32). CONCLUSIONS: Our observations of an increased glucose requirement during the clamp as well as a decrease in haemoglobin A1c demonstrate improved insulin sensitivity in the adolescent girls with diabetes following pirenzepine therapy. The mechanism behind the improvement is not clear, as neither secretion nor the secretory pattern of GH changed significantly. The persistently high levels of GH might explain the unaltered rate of lipolysis despite the improved insulin sensitivity. The observed improvement in glycaemic control in adolescent girls with type 1 diabetes following pirenzepine therapy is promising, although more studies on this topic are needed.

Adolescent↗

PubMed2002

Growth charts for Down's syndrome from birth to 18 years of age.

BACKGROUND: Growth in children with Down's syndrome (DS) differs markedly from that of normal children. The use of DS specific growth charts is important for diagnosis of associated diseases, such as coeliac disease and hypothyroidism, which may further impair growth. AIMS: To present Swedish DS specific growth charts. METHODS: The growth charts are based on a combination of longitudinal and cross sectional data from 4832 examinations of 354 individuals with DS (203 males, 151 females), born in 1970-97. RESULTS: Mean birth length was 48 cm in both sexes. Final height, 161.5 cm for males and 147.5 cm for females, was reached at relatively young ages, 16 and 15 years, respectively. Mean birth weight was 3.0 kg for boys and 2.9 kg for girls. A body mass index (BMI) >25 kg/m(2) at 18 years of age was observed in 31% of the males and 36% of the females. Head growth was impaired, resulting in a SDS for head circumference of -0.5 (Swedish standard) at birth decreasing to -2.0 at 4 years of age. CONCLUSION: Despite growth retardation the difference in height between the sexes is the same as that found in healthy individuals. Even though puberty appears somewhat early, the charts show that DS individuals have a decreased pubertal growth rate. Our growth charts show that European boys with DS are taller than corresponding American boys, whereas European girls with DS, although being lighter, have similar height to corresponding American girls.

Adolescent↗

PubMed2001

The transcription factors SOX9 and SOX10 are vitiligo autoantigens in autoimmune polyendocrine syndrome type I.

Vitiligo is common in the hereditary disorder autoimmune polyendocrine syndrome type I (APS I). Patients with APS I are known to have high titer autoantibodies directed against various tissue-specific antigens. Using sera from APS I patients for immunoscreening of a cDNA library from human scalp, we identified the transcription factors SOX9 and SOX10 as novel autoantigens related to this syndrome. Immunoreactivity against SOX9 was found in 14 (15%) and against SOX10 in 20 (22%) of the 91 APS I sera studied. All patients reacting with SOX9 displayed reactivity against SOX10, suggesting shared epitopes. Among the 19 patients with vitiligo, 12 (63%) were positive for SOX10 (p < 0.0001). Furthermore, three of 93 sera from patients with vitiligo unrelated to APS I showed strong reactivity against SOX10, which may indicate a more general role of SOX10 as an autoantigen in vitiligo.

Autoantigens↗

PubMed2001

Diabetes control deteriorates in girls at cessation of growth: relationship with body mass index.

AIM: Diabetic patients, particularly girls, often experience poor metabolic control during puberty and adolescence. The aim of this study was to investigate metabolic control during adolescence, especially in relation to pubertal stages, growth, insulin treatment and body mass index (BMI). METHODS: We studied the records of 38 (consecutive) girls with prepubertal onset of Type 1 diabetes mellitus. Data from the age of 10 to 18-20 years were obtained with regard to glycaemic control, growth, age at menarche, final height and BMI, and analysed in relation to both chronological age and age at menarche. RESULTS: HbA1c was lowest 3 years before menarche; mean (+/- sd) 7.6 (+/- 1.2). After the pubertal growth spurt, there was a marked impairment of metabolic control, the highest level of HbA1c occurring 3 years after menarche. Mean age at menarche was 13.3 (+/- 1.1) years and mean linear growth after menarche only 4.7 cm, giving a final height of 164.9 (+/- 5.3) cm which is 2.7 cm below the Swedish mean. During adolescence the degree of correlation between BMI and HbA1c continuously increased, pointing out the effect of body fat on metabolic control in this age group. The level of HbA1c at 10 years of age could not predict the metabolic control after cessation of puberty, but prepubertal BMI appears to be a risk factor for both obesity and poor glycaemic control in late adolescence. CONCLUSIONS: The highest HbA1c was found after cessation of growth. Prepubertal BMI is a possible predictor of metabolic control in adolescent diabetic girls.

Adolescent↗

PubMed2001

Peripheral astigmatism in emmetropic eyes.

The long-term aim of the work introduced here is to investigate the influence of off-axis aberrations on human vision, especially for subjects with a large central scotoma. The latter use their peripheral vision in spite of its poor off-axis optical quality, and a correction of the off-axis aberrations might be of great assistance. The eccentric fixation angles used by these subjects can be up to 20-30 degrees. In this initial study we have measured oblique astigmatism, the major off-axis aberration, in 20 emmetropic eyes in 10 degrees steps out to 60 degrees nasally and temporally using a 'double pass' setup. The results show very large individual differences and the oblique astigmatism also varies from nasal to temporal side. In an off-axis measurement angle of 30 degrees the astigmatism varied between subjects from 1 to 7-D, with a mean astigmatism of about 4-D on the nasal side and about 1.5-D lower on the temporal side. At 60 degrees temporally, the mean astigmatism was 7-D. At 60 degrees nasally, all subjects had astigmatism larger than 8-D and the mean astigmatism was 11-D. The results indicate that any attempt to correct the off axis astigmatism in an eye with central scotoma cannot be based on central refraction; instead, individual measurements are necessary.

Adult↗

PubMed2001

Errors in estimating neonatal production of glucose with stable isotopes during "approximate steady state".

In studies of glucose metabolism in neonates, a commonly used approach is based on constant rate infusion of glucose labelled with a stable isotope in order to reach an approximate steady state with regard to isotopic enrichment in plasma. Under presumed conditions of a glucose steady state, the rates of appearance and disappearance of glucose can, in principle, be calculated with use of a simple steady-state formula. However, in the neonate, steady-state conditions do not generally prevail and results derived on such assumptions are questionable. In the present study, we have taken a pragmatic approach and compared estimates obtained from the conventional formula with values calculated with Steele's non-steady-state method. The results show that the estimated glucose appearance and disappearance rates change more or less over the observed time period in all the typical cases studied, and that "steady-state estimates" may differ from the corresponding non-steady-state values by up to 37%. In a sensitivity analysis, the value of the distribution volume factor was found to be non-critical, a circumstance that supports the use of Steele's method. Thus, even though the classical Steele pool-fraction method for computation of rates of appearance and disappearance under non-steady-state conditions has been criticized, it is still the most realistic alternative to the frequently used simple steady-state formula in applications to newborns.

Deuterium↗

PubMed2001

Estrogen receptor beta regulates sexually dimorphic neural responses to estradiol.

Estrogen receptors (ERs) mediate many sexual dimorphisms in the neuroendocrine system and in behavior. We examined the consequences of the loss of functional estrogen receptor beta (ERbeta) on two sexually differentiated neural responses to estrogen. In wild type (WT) male mice, but not in females, estradiol (E(2)) treatment decreased estrogen receptor alpha immunoreactive (ERalpha-ir) cell numbers in the arcuate nucleus (ARC), the preoptic area (POA), and the ventromedial nucleus (VMN). These sex differences were reversed in ERbeta knockout (ERbetaKO) mice. Castrated ERbetaKOs did not show any change in ERalpha-ir cell number after E(2) treatment. Yet, E(2) decreased ERalpha-ir cell number in ovariectomized ERbetaKOs. Estradiol treatment increased progesterone receptor immunoreactive (PR-ir) cell number in WT female VMN and POA, but no change was noted in brains of WT castrates. In ERbetaKO mice the opposite relationship was found, E(2) treatment increased PR-ir cell number in male, but not in female, brains. Our results show that ERbeta influences several sexually dimorphic neural responses to estrogen. Moreover the data clearly show that ERbeta can modulate neural expression of ERalpha.

Animals↗

PubMed2001

Quantitative analysis of estrogen receptor proteins in rat mammary gland.

Estrogen receptor alpha and beta proteins (ERalpha and ERbeta) at various stages of development of the rat mammary gland were quantified by Western blotting. ERalpha and ERbeta recombinant proteins were used as standards, and their molar concentrations were measured by ligand binding assays. In 3-week-old pregnant, lactating, and postlactating rats the ERalpha content ranged from 0.30-1.55 fmol/microg total protein (mean values). The ERbeta content of the same samples ranged between 1.06-7.50 fmol/microg total protein. At every developmental stage, the ERbeta content of the mammary gland was higher than that of ERalpha. When receptor levels were normalized against beta-actin, it was evident that ER expression changed during development, with maximum expression of both receptors during the lactation period. With an antibody raised against the 18-amino acid insert of the ERbeta variant, originally called ERbeta2 but named ERbetains in this paper, Western blots revealed that ERbetains protein was up-regulated during the lactation period. RT-PCR showed that the levels of messenger RNA of ERbetains paralleled those of the protein. Double immunohistochemical staining with anti-ERalpha and anti-ERbetains antibodies revealed that ERbetains protein colocalized with ERalpha in 70-80% of the ERalpha-expressing epithelial cells during lactation and with 30% of these cells during pregnancy. These observations indicate that expression of ERbetains is regulated not only quantitatively, but also with regard to its cellular distribution. As ERbetains acts as the dominant repressor of ERalpha, we suggest that its coexpression with ERalpha quenches ERalpha function and may be one of the factors that contribute to the previously described insensitivity of the mammary gland to estrogens during lactation.

Actins↗

PubMed2001

Immunocytochemical demonstration of oestrogen receptor beta in blood vessels of the female rat.

The role of oestrogen receptor (ER) beta in vascular function remains unclear. With the use of a specific ERbeta antibody we have now, using immunocytochemistry, visualized ERbeta in different parts of the vascular tree. In about 70% of medial smooth muscle cells of female rat aorta, tail artery and uterine artery, nuclear immunoreactivity to ERbeta was observed. In these vessels endothelial cells also expressed ERbeta. Vascular expression of the ERalpha subtype was lower than that of ERbeta. In aorta and tail artery, no immunoreactivity towards ERalpha was observed, while in uterine vessels occasional medial smooth muscle and endothelial cells expressed this ER subtype. ERbeta and alpha expression in uterine vessels was independent of the stage of the oestrous cycle, suggesting that variations in uterine blood flow occurring during the cycle are independent of ER density. The regional distribution of ERalpha, as determined by immunocytochemistry, was supported by measurements of ERalpha levels by enzyme immunoassay. In the uterine artery, the level of ERalpha was several times higher (P<0.001) than that of aorta and tail artery (10.1+/-1.7 fmol/mg protein in the uterine artery vs 3.3+/-1.0 and 0.5+/-0.5 fmol/mg protein in aorta and tail artery respectively). Thus, a prominent nuclear expression of ERbeta was observed in the vascular wall of several parts of the vascular tree, while ERalpha predominantly was expressed in uterine vessels, suggesting that ERbeta and alpha may have different roles in vascular function.

Analysis of Variance↗

PubMed2001

Anticholinergic treatment improves glycaemic control in adolescent girls with insulin-dependent diabetes mellitus.

UNLABELLED: Metabolic control often deteriorates during puberty in girls with insulin-dependent diabetes. It is well accepted that there is an abnormality in the growth hormone (GH)-insulin-like growth factor-I (lGF-I) axis in these girls, resulting in reduced IGF-I levels and elevated GH. As GH antagonizes insulin, attempts have previously been made to reduce excess GH secretion through anticholinergic treatment. However, most of these studies have been performed on adult patients. The aim of the present study was to evaluate the effects of 12 wk of oral anticholinergic treatment with Pirenzepine, 100 mg twice daily, in 16 adolescent girls with diabetes. Serum samples of IGF-I, glycated haemoglobin and fasting IGF-binding protein 1 were analysed at initiation and after 3, 8 and 12 wk of Pirenzepine therapy. Nocturnal urinary GH excretion was also examined. Glycated haemoglobin declined significantly after 3 wk of Pirenzepine therapy (9.8 +/- 0.18 vs 9.2 +/- 0.17; p < 0.001) and was still improved at the end of the study. Unexpectedly, nocturnal urinary GH excretion did not change. Serum IGF-I continuously increased during the study, while IGF-binding protein 1 levels were not significantly altered. CONCLUSION: Anticholinergic treatment with Pirenzepine improves glycaemic control in adolescent girls with diabetes. Although nocturnal urinary GH excretion was unchanged there may still be changes in pituitary GH secretion to explain the improvement. Effects of Pirenzepine on gastrointestinal motility can represent other possible mechanisms behind the improved metabolic control.

Adolescent↗

PubMed2000

Novel effects of estradiol and estrogen receptor alpha and beta on cognitive function.

Estrogen influences the development of memory function in humans and rodents and can modulate memory in adults. In these studies we examined the role of the estrogen receptors alpha (ERalpha) and beta (ERbeta) in mediating performance on a hippocampal-dependent, hormone-sensitive task, inhibitory avoidance (IA). Ovariectomized (OVX) estrogen receptor-alpha-knockout (ERalphaKO) mice displayed impaired performance on the IA task and OVX heterozygotic (HET) mice exhibited performance that was intermediate between ERalphaKO and wild-type (WT) mice. Impaired performance by ERalphaKO mice was rescued by E(2) treatment. The ER antagonist, tamoxifen, did not block enhancement of retention by E(2) suggesting that E(2) mediated modulation of memory is not caused by known genomic receptor mechanisms. In contrast to ERalphaKO mice, IA performance by OVX estrogen receptor-beta-knockout (ERbetaKO) mice was not compromised. The results indicate an important role for ERalpha, relative to ERbeta, in the establishment of cognitive function and suggest that E(2) modulates memory function via a novel estrogenic mechanism.

Animals↗

PubMed2000

Identification of tyrosine hydroxylase as an autoantigen in autoimmune polyendocrine syndrome type I.

Patients with the autosomal recessively inherited autoimmune polyendocrine syndrome type I (APS I) have autoantibodies directed against several endocrine and nonendocrine organs. In this study a new autoantigen related to this syndrome, tyrosine hydroxylase, was identified in sera from patients with alopecia areata through immunoscreening of a scalp cDNA library. Immunoreactivity against in vitro expressed tyrosine hydroxylase was found in 41 (44%) of the 94 APS I patients studied and this reactivity correlated with the presence of alopecia areata (P = 0.02). These findings further stress the importance of enzymes involved in neurotransmitter biosynthesis as important immune targets in APS I.

Alopecia Areata↗