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PubMed2006

Quantitative studies of autonomic function.

Dysfunction of the peripheral and central autonomic nervous system is common in many neurological and general medical diseases. The quantitative assessment of sympathetic and parasympathetic function is essential to confirm the diagnosis of autonomic failure, to provide the basis for follow-up examinations, and potentially to monitor successful treatment. Various procedures have been described as useful tools to quantify autonomic dysfunction. The most important tests evaluate cardiovascular and sudomotor autonomic function. In this review, we therefore focus on standard tests of cardiovascular and sudomotor function such as heart-rate variability at rest and during deep breathing, active standing, and the Valsalva maneuver, and on the sympathetic skin response. These tests are widely used for routine clinical evaluation in patients with peripheral neuropathies. Refined methods of studying heart-rate variability, baroreflex testing, and detailed measures of sweat output are mostly used for research purposes. In this context, we describe the spectral analysis of slow modulation of heart rate or blood pressure, reflecting sympathetic and parasympathetic influences, and consider various approaches to baroreflex testing, the thermoregulatory sweat test, and the quantitative sudomotor axon reflex test. Finally, we discuss microneurography as a technique of direct recording of muscle sympathetic nerve activity.

Autonomic Nervous System↗
PubMed2005

Specific loss of connexin 26 expression in ductal sweat gland epithelium associated with the deletion mutation del(GJB6-D13S1830).

A whole array of cutaneous syndromes is associated with distinct dominant mutations in GJB2 encoding the gap junction protein connexin 26 (C x 26), including Vohwinkel's syndrome and keratitis-ichthyosis-deafness syndrome. In contrast, recessive GJB2 mutations occur in a large proportion of individuals with hearing loss but no obvious dermatological phenotype. Recently, a large deletion of approximately 342 kb, encompassing the coding region of GJB6 encoding C x 30, but not affecting GJB2, was shown to be associated with hearing loss. From analysis of patient skin, we provide immunohistochemical and bioinformatic data to show that the expression of C x 26 is affected by del(GJB6-D13S1830) in a cell-type-specific manner within the sweat gland. This putative regulatory element of C x 26 expression may be a key factor related to the severe or profound deafness associated with del(GJB6-D13S1830).

Chromosome Deletion↗
PubMed1990

Prenatal diagnosis of X-linked hypohidrotic ectodermal dysplasia by linkage analysis.

Prenatal diagnosis of X-linked hypohidrotic ectodermal dysplasia was previously performed by the direct histological analysis of fetal skin obtained by late second trimester fetoscopy. The recent gene mapping of the locus for the disorder to the region of Xq11-21.1 now permits the indirect prenatal diagnosis of the disorder by the method of linkage analysis, based on closely linked marker loci, during the first trimester of pregnancy. We report the prenatal diagnosis of a male fetus with a high probability of the disorder by a linkage analysis utilizing restriction fragment length polymorphisms at the DXS159, PGK1, and DXS72 loci, from a DNA sample obtained by a chorionic villus biopsy at 9 weeks gestation. After further counseling, the pregnancy was terminated but the diagnosis could not be confirmed by histological analysis, even though analysis of skin samples by light and electron microscopy showed lack of hair germs, primary dermal ridges, and sweat gland primordia, due to the early developmental stage of the fetus. The use of DNA-based linkage analysis now offers the opportunity for an earlier diagnosis of X-linked hypohidrotic ectodermal dysplasia by a method other than fetal skin sampling. However, families must also fully understand the present limitations of the method prior to undertaking the procedure.

Adult↗
PubMed2005

[Effectiveness and tolerance of pulsed estrogen therapy in the treatment of menopausal symptoms. Results of a Polish multicenter study].

OBJECTIVE: The main objective of the trial was to evaluate the efficacy and tolerance of a three-month pulsed estrogen therapy with intranasal 17 beta-estradiol in patients with menopausal symptoms. MATERIAL AND METHODS: Four-month, open, multicenter study (16 study centers in Poland). 309 patients with normal results of mammography and cytological examination who previously expressed informed consent for the participation in the trial were qualified to the study. Inclusion criterion was the diagnosis of at least moderate menopausal symptoms, defined as presence of night sweats disturbing sleep and hot flushes disturbing daily activity, and more than 30 points in the Green index. Exclusion criteria were: general estrogen-intake contraindications and contraindications for participation in the clinical trials. Patients included into the study were given intranasal 17 beta-estradiol 300 microg daily in continuous therapy and (patients with uterus) progestagen, according to the prescription. Main efficacy criterion was change of frequency and intensity of menopausal symptoms: night sweats and hot flushes. Additionally, Green index score was observed. Tolerance was assessed based on the adverse effects. Statistical analysis was performed using nonparametric Wilcoxon test and descriptive statistics. RESULTS: 273 patients completed the study. The night sweats were observed before the treatment in 90.5% patients with frequency of 8.8 per week. After 3 and 4 months of treatment the proportion of patients with night sweats decreased to 28.2% and 11.8% respectively, and the number of episodes to 2.7 and 2.2 per week (p < 0.0005). The hot flushes occurred before the treatment in average 12.1 times daily, after 3 months of treatment 1.3 times daily (p < 0.0005) and after 4 months of treatment 0.4 times daily (p < 0.0005). The Green index decreased from 35.6 points (before the treatment) to 11.6 points (after 3 months of treatment) (p < 0.0005) and 7.4 points (after 4 months of treatment) (p < 0.0005). During the treatment the adverse events were monitored--they occurred in 5.4% patients. The tolerance of the treatment after the end of the study was assessed by the physician as excellent or good in 96% patients. CONCLUSIONS: The results of the study give evidence for a high efficacy and very good tolerance to the treatment of menopausal symptoms using pulsed estrogen therapy with intranasal 17 beta-estradiol.

Administration, Intranasal↗
PubMed2003

CFTR genotypes in patients with normal or borderline sweat chloride levels.

In recent years, some patients bearing "atypical" forms of cystic fibrosis (CF) with normal sweat chloride concentrations have been described. To identify the spectrum of mutant combinations causing such atypical CF, we collected the results of CFTR (ABCC7) mutation analysis from 15 laboratories. Thirty patients with one or more typical symptoms of the disease associated with normal or borderline sweat chloride levels and bearing two CFTR mutations were selected. Phenotypes and genotypes of these 30 patients are described. A total of 18 different CFTR mutations were observed in the 60 chromosomes analysed. F508del was present in 31.6 % of the mutated chromosomes and 3849+10kbC>T in 13.3 %. R117H, D1152H, L206W, 3272-26A>G, S1235R, G149R, R1070W, S945L, and the poly-T tract variation commonly called IVS8-5T were also observed. The relative frequency of CFTR mutations clearly differed from that observed in typical CF patients or in CBAVD patients with the same ethnic origin. A mild genotype with one or two mild or variable mutations was observed in all the patients. These findings improve our understanding of the distribution of CFTR alleles in CF with normal or borderline sweat chloride concentrations and will facilitate the development of more sensitive CFTR mutation screening.

Adolescent↗
PubMed1996

The symptom structure of panic disorder: a trial using factor and cluster analysis.

Using cluster analysis of 207 patients with panic disorder (PD), we investigated the relationships between several panic symptoms at the time of panic attacks, which included anticipatory anxiety, agoraphobia, and 13 clinical symptoms based on the Diagnostic and Statistics Manual-III-Revised. Cluster analysis revealed three panic symptom clusters: cluster A (dyspnea, choking, sweating, nausea, flushes/chills); cluster B (dizziness, palpitations, trembling or shaking, depersonalization, agoraphobia, and anticipatory anxiety); and cluster C (fear of dying, fear of going crazy, paresthesias, and chest pain or discomfort). Generally, cluster A was comprised exclusively of physiological symptoms, among which respiratory symptoms were prominent, cluster B included both panic and non-panic symptoms such as agoraphobia and anticipatory anxiety, and cluster C was comprised chiefly of fear symptoms.

Adult↗
PubMed1995

Autologous stem cell transplantation for refractory and relapsed Hodgkin's disease: factors predictive of prolonged survival.

We analyzed patient, disease, and treatment related factors associated with long-term disease-free survival (DFS) in 62 patients with refractory or recurrent Hodgkin's disease treated with high-dose cyclophosphamide (6000 mg/m2), carmustine (BCNU; 300 mg/m2), and etoposide (900 mg/m2) (CBV) followed by autologous stem cell transplantation. There were no deaths resulting from toxicity of the preparative regimen, and all patients survived the peritransplant period. At 28 days post-transplant, the complete response (CR) rate was 76%. Patients who achieved a CR had a 50% estimated 3-year DFS (95% CI, 35-64%). Twenty-three (37%) patients remain in continuous clinical remission 1.3 to 7.7 years (median 3.8 years) after transplantation. In a univariate analysis, factors significantly associated with improved DFS included absence of B symptoms (fever, night sweats and unexplained weight loss) at transplant, response to pre-transplant salvage chemotherapy, less tumor bulk at time of transplant, and fewer prior treatment regimens. Stepwise multivariate analysis showed that the absence of B symptoms at time of transplant was independently and significantly associated with improved DFS after transplantation. CBV with autologous stem cell support can produce durable remissions with acceptable toxicity in a substantial proportion of patients who are asymptomatic at time of transplant. Earlier application of transplantation or development of additional effective antineoplastic modalities will be required to improve the results of transplantation for patients with advanced Hodgkin's disease.

Adolescent↗
PubMed1991

Symptoms of acute insulin-induced hypoglycemia in humans with and without IDDM. Factor-analysis approach.

OBJECTIVE: This study allocated the symptoms identified during acute hypoglycemia objectively to the autonomic or neuroglycopenic groups of symptoms by the use of factor analysis. RESEARCH DESIGN AND METHODS: Twenty-five nondiabetic subjects, 14 newly diagnosed insulin-dependent diabetic patients, and 16 insulin-dependent diabetic patients with diabetes greater than 4 yr duration were studied. Acute hypoglycemia was induced with insulin (2.5 mU.kg-1 body wt.min-1 i.v.), and symptoms of hypoglycemia were recorded with a seven-point scale at regular time points throughout the studies. Factor analysis of the symptom scores at the time of the acute autonomic reaction with principal component analysis followed by Varimax rotation was used to separate those symptoms that might belong to neuroglycopenic and autonomic groups. RESULTS: Hypoglycemia was induced to a mean +/- SE plasma glucose nadir of 1.3 +/- 0.1 mM in nondiabetic subjects, to 2.0 +/- 0.3 mM in newly diagnosed diabetic patients, and 1.4 +/- 0.2 mM in patients with diabetes of greater than 4 yr duration. The most frequently reported autonomic symptoms were sweating, trembling, and warmness, and the most frequently reported neuroglycopenic symptoms were inability to concentrate, weakness, and drowsiness. Neuroglycopenic symptoms were reported more commonly at the onset of hypoglycemia, which was identified by the development of symptoms. Factor analysis grouped trembling, anxiety, sweating, warmness, and nausea together, and this grouping was labeled an autonomic factor. A second factor was identified that included dizziness, confusion, tiredness, difficulty in speaking, shivering, drowsiness, and inability to concentrate, which was labeled a neuroglycopenic factor. CONCLUSIONS: This study demonstrated the high frequency with which neuroglycopenic symptoms occur at the onset of hypoglycemia and the symptoms that could be used by an individual patient as a warning of the development of acute hypoglycemia, although the rapid reduction of plasma glucose is faster than experienced by the ambulant diabetic patient. Factor analysis assisted with the allocation of symptoms to either the autonomic or neuroglycopenic groupings, but the allocation of some symptoms remained undefined, and care must be taken when assessing symptoms such as hunger, weakness, blurred vision, and drowsiness when comparing the frequency of autonomic versus neuroglycopenic symptoms. To reduce the confusion resulting from the use of different symptom questionnaires in studies of hypoglycemia, a sample questionnaire is presented, the development of which was assisted by our analysis.

Adult↗
PubMed2001

Thermoregulation and marathon running: biological and environmental influences.

The extreme physical endurance demands and varied environmental settings of marathon footraces have provided a unique opportunity to study the limits of human thermoregulation for more than a century. High post-race rectal temperatures (Tre) are commonly and consistently documented in marathon runners, yet a clear divergence of thought surrounds the cause for this observation. A close examination of the literature reveals that this phenomenon is commonly attributed to either biological (dehydration, metabolic rate, gender) or environmental factors. Marathon climatic conditions vary as much as their course topography and can change considerably from year to year and even from start to finish in the same race. The fact that climate can significantly limit temperature regulation and performance is evident from the direct relationship between heat casualties and Wet Bulb Globe Temperature (WBGT), as well as the inverse relationship between record setting race performances and ambient temperatures. However, the usual range of compensable racing environments actually appears to play more of an indirect role in predicting Tre by acting to modulate heat loss and fluid balance. The importance of fluid balance in thermoregulation is well established. Dehydration-mediated perturbations in blood volume and blood flow can compromise exercise heat loss and increase thermal strain. Although progressive dehydration reduces heat dissipation and increases Tre during exercise, the loss of plasma volume contributing to this effect is not always observed for prolonged running and may therefore complicate the predictive influence of dehydration on Tre for marathon running. Metabolic heat production consequent to muscle contraction creates an internal heat load proportional to exercise intensity. The correlation between running speed and Tre, especially over the final stages of a marathon event, is often significant but fails to reliably explain more than a fraction of the variability in post-marathon Tre. Additionally, the submaximal exercise intensities observed throughout 42 km races suggest the need for other synergistic factors or circumstances in explaining this occurrence. There is a paucity of research on women marathon runners. Some biological determinants of exercise thermoregulation, including body mass, surface area-to-mass ratio, sweat rate, and menstrual cycle phase are gender-discrete variables with the potential to alter the exercise-thermoregulatory response to different environments, fluid intake, and exercise metabolism. However, these gender differences appear to be more quantitative than qualitative for most marathon road racing environments.

Body Mass Index↗
PubMed2002

Syringoid eccrine carcinoma: report of a case with immunohistochemical analysis of cytokeratin expression.

Syringoid eccrine carcinoma is an extremely rare cutaneous malignant tumor, thought to be derived from eccrine sweat apparatus. We report a case of syringoid eccrine carcinoma occurring on the scalp of a 66-year-old woman and analyzed its cytokeratin expression immunohistochemically to clarify its histogenesis. The tumor consisted mainly of numerous small cords and nests extending from the reticular dermis to the subcutaneous tissue, which formed luminal or tubular structures mimicking the nests of syringoma. Immunohistochemical analysis revealed that most tumor cells expressed simple epithelial cytokeratins (CKs 7, 8, 18, 19) suggesting their sweat secretory differentiation, and that a small number of tumor cells showed an expression of stratified epithelial cytokeratins (CKs 5, 14) suggesting their ductal differentiation. We believe that the syringoid eccrine carcinoma of our case may differentiate mainly toward the sweat secretory cells rather than toward the dermal ductal cells.

Aged↗
PubMed1999

Immunohistochemical analysis of cytokeratin expression in apocrine cystadenoma or hidrocystoma.

Apocrine cystadenoma is a benign sweat gland tumor which consists of various histologic types of epithelium: epithelium with decapitation secretion, pseudostratified epithelium, and flattened epithelium. Immunophenotypes, especially the expression of cytokeratins, in 8 cases of this tumor were examined immunohistochemically, because the nature or differentiation of each epithelium is not well known. The following antibodies were used as primary antibodies: those against involucrin, smooth muscle actin, and human milk fat globulin respectively, and 15 kinds of monoclonal anti-cytokeratin antibodies. Although the staining pattern varied from case to case according to the proportion of each epithelium, these epithelia, except for the flattened epithelium, revealed invariable staining patterns. The staining pattern in the epithelium with decapitation secretion and the pseudostratified epithelium was similar to that in the secretory portion including myoepithelial cells and the junction of the excretory ductal portion with the secretory portion, respectively. However, the flattened epithelium, probably due to intraluminal pressure, showed various staining patterns similar to that in each portion of the apocrine gland. Based on the above observations, we confirmed that apocrine cystadenoma was a complex tumor differentiating into each portion of the apocrine gland, i.e. the dermal duct, the junction of the excretory ductal portion with the secretory portion, and the secretory portion.

Biomarkers, Tumor↗
PubMed2001

Effects of FK506 on nerve regeneration and reinnervation after graft or tube repair of long nerve gaps.

We compared the effects of FK506 administration on regeneration and reinnervation after sciatic nerve resection and repair with an autologous graft or with a silicone tube leaving a 6-mm gap in the mouse. Functional reinnervation was assessed by noninvasive methods to determine recovery of motor, sensory, and sweating functions in the hindpaw over 4 months after operation. Morphometric analysis of the regenerated nerves was performed at the end of follow-up. The nerve graft allowed for faster and higher levels of reinnervation in the four functions tested than silicone tube repair. Treatment with FK506 (for the first 9 weeks only) resulted in a slight, although not significant, improvement of the onset of reinnervation and of the maximal degree of recovery achieved after autografting. The recovery of pain sensibility and of the compound nerve action potentials in the digital nerves, which directly depend on axonal regeneration, showed better progression with FK506 than reinnervation of muscles and sweat glands, which require reestablishment of synaptic contacts with target cells. The myelinated fibers in the regenerated nerve showed a more mature appearance in the FK506-treated rats. However, FK506 showed a marginal effect in situations in which regeneration was limited, as in a silicone tube bridging a 6-mm gap in the mouse sciatic nerve. In conclusion, treatment with FK506 improved the rate of functional recovery after nerve resection and autograft repair.

Action Potentials↗
PubMed1987

Tissue culture of normal and cystic fibrosis sweat gland duct cells. I. Alterations in dome formation.

The elucidation of the underlying defect in fluid secretion by cystic fibrosis (CF) sweat glands is hindered by the unavailability of an experimental model for investigating this disease. As a potential model system, a serum-free growth medium was developed that supports the explant growth of epithelial cells from fragments of human skin. Immunohistochemical analysis demonstrated that these epithelial cell outgrowths originated from the duct of the sweat gland. By electron microscopy, the cells were demonstrated to possess keratinocyte-like morphology as noted by the presence of a multilayered outgrowth of cells containing well-defined keratin bundles. Identical outgrowths from skin biopsies of CF patients were compared to normal outgrowths and alterations were noted to occur in dome formation and in the number of intercellular spaces between cells. Doming alterations were also noted to occur in the CF heterozygous state. No differences in cell fine structure or in growth factor requirements for cell proliferation were noted between normal and CF cells. The potential use of this system as a model for CF research is discussed.

Culture Techniques↗
PubMed1997

Cystic fibrosis mutations in Romania.

UNLABELLED: We have investigated the genotype in 32 children with cystic fibrosis from Romania. The diagnosis of cystic fibrosis was made on the basis of typical clinical findings and sweat electrolyte levels using the pilocarpine iontophoresis method. CONCLUSION: Genetic analysis of 32 children with cystic fibrosis from Romania showed a 25% incidence of DeltaF508 mutation and a 64.5% incidence of unknown mutations, 5 other known mutations and 1 new mutation 1,717-2(A > G).

Blood Proteins↗