A Previously Healthy Adolescent With Acute Psychosis and Severe Hyperhidrosis.

A previously healthy 15-year-old boy presented with 3 months of progressive psychosis, insomnia, back and groin pain, and hyperhidrosis. On examination, the patient was disheveled, agitated, and soaked with sweat, with systolic blood pressure in the 160s and heart rate in the 130s. Aside from occasional auditory and visual hallucinations, his neurologic examination was normal. The patient was admitted for an extensive workup, including MRI of the brain and spine and lumbar puncture, which were normal. Through collaboration with various pediatric specialists, including psychiatry and neurology, a rare diagnosis was ultimately unveiled.

Elevated social stress levels and depressive symptoms in primary hyperhidrosis.

Primary hyperhidrosis is defined as excessive sweating of certain body areas without physiological reasons. Hyperhidrotic individuals report a high psychological strain and an impairment of their quality of life. Thus, the aim of the study is to investigate the relation between hyperhidrosis and different psychological as well as physiological aspects of chronic stress as a co-factor for the etiology of depression. In this study, forty hyperhidrotic subjects were compared to forty age- and sex-matched healthy control subjects. The Trier Inventory of Chronic Stress ('Trierer Inventar zum chronischen Stress': TICS), the Beck Depression Inventory (BDI-II) and the Screening for Somatoform Disorders (SOMS-2) were used to examine the correlation between primary hyperhidrosis and stress as well as accompanying depressive and somatic symptoms. The cortisol awakening response of each subject was analyzed as a physiological stress correlate. In hyperhidrotics, we found a significant lack of social recognition as well as significantly more depressive symptoms compared to the control subjects. A subgroup of patients with axillary hyperhidrosis had the highest impact on these increased issues of chronic stress, pointing to a higher embarrassment in these subjects. Especially in social situations, hyperhidrotics showed higher stress levels, whereby a vicious circle of stress and sweating is triggered. However, the cortisol awakening response did not significantly differ between hyperhidrotics and controls. Moreover, affected persons suffer from more depressive symptoms, which may be caused by feelings of shame and a lack of self-confidence. This initial study provides an impetus for further investigation to reveal a causative relationship between hyperhidrosis and its psychological concomitants.

Evaluation of trace elements, calcium, and magnesium levels in the plasma and erythrocytes of patients with essential hyperhidrosis.

BACKGROUND: Essential hyperhidrosis is a disease that expresses itself with excessive sweating in palmar, plantar, axillary, and craniofacial regions. The etiopathogenesis of the disease, which has particular importance because of leading to psychosocial morbidity, could have not been completely elucidated. In previous studies, it has been shown that oxidative stress might play a role in the pathogenesis. AIMS: Assessing the levels of trace elements such as Se, Zn, Cu, Fe, and Mg that have an important role in oxidative stress, as well as Ca and Mg that have an important role in membrane physiology, in patients with essential hyperhidrosis. MATERIALS AND METHODS: Blood samples taken from the patient group with essential hyperhidrosis (42) and the control group (37) were separated into plasma and erythrocytes, and the levels of the bioelements were measured by use of ICP-OES device. RESULTS: Erythrocyte levels of Se, Fe, Cu, Zn, Ca, and Mg were detected significantly higher in patients with essential hyperhidrosis. Furthermore, plasma levels of Cu, Ca, and Mg were significantly lower in patients with essential hyperhidrosis. Plasma levels of Se, Fe, and Zn showed no statistical difference between two groups. DISCUSSION: It was thought that the high levels of Cu and Fe in erythrocytes may play a role in increased intracellular oxidative stress, whereas the increase in Se and Zn levels may be secondary to increased oxidative stress. Low extracellular concentrations of Ca and Mg raise the thought that they play a role either enhancing the membrane excitability of eccrine sweat glands or influencing the autonomic nerve system. CONCLUSION: The levels of trace elements, which were determined to be different from the control group, may play a role in the pathogenesis of essential hyperhidrosis either in direct relation with or without oxidative mechanisms.

Spontaneous endogenous hypermelatoninemia: a new disease?

Melatonin, a major photoperiod-dependent hormone, regulates circadian rhythms and biological rhythms and acts as a prominent sleep promoter. Symptoms related to hypermelatoninemia have been reported in individuals supplemented with melatonin. However, spontaneous endogenous hypermelatoninemia has not been reported previously. A 6-year-old girl previously diagnosed with Shapiro's syndrome was admitted to our hospital on several occasions during a 1-year period with complaints of altered consciousness, syncope, hypothermia and episodes of sweating. The episodes occurred daily and during sleep and lasted for 1-6 h. During these episodes, she sweated profusely and felt faint and her skin was pale and cool. Other complaints included recurrent abdominal pain, urge incontinence and myopia. She was shown to have hypermelatoninemia (>1,000 pg/ml, normal range 0-150 pg/ml) during these episodes. The duration of her attacks decreased with phototherapy and she was successfully treated with propranolol. To our knowledge, this is the first case of hypermelatoninemia without any detectable organic pathology. We did not determine the exact mechanism of hypermelatoninemia in this patient; however, it might have been related to irregular control of pinealocytes by the suprachiasmatic nucleus or related pathways. Hypermelatoninemia should be considered in patients with spontaneous periodic hypothermia and hyperhidrosis, and also in patients with Shapiro's syndrome.

[When eating becomes dangerous...]. / Von der Frau, der das Essen nicht bekam.

We report the case of a 59-year-old women with idiopathic insulin auto-immune syndrome, a rare cause of endogenous hyperinsulinemic hypoglycemia. It is characterized by extremely high levels of insulin in the presence of high titers of insulin antibodies despite the absence of previous insulin injections. Early postprandial increase in glucose concentrations due to impaired insulin action resulting from the buffering effect of the antibodies and late postprandial hypoglycemia as a consequence of the dissociation of insulin from the antibodies was observed. A correct diagnosis is important to avoid unnecessary investigations and surgery in these patients who are best treated conservatively - with a good prognosis - by fractionating carbohydrate intake during the day.

Is nitric oxide involved in the pathophysiology of essential hyperhidrosis?

BACKGROUND: Essential hyperhidrosis (EH) is a disorder of excessive, bilateral, and relatively symmetric sweating occurring in the axillae, palms, soles, or craniofacial region without obvious etiology. The expression of endothelial nitric oxide synthase (eNOS) in eccrine clear cells, reported by an immunohistochemical technique, has suggested that nitric oxide (NO) may play a role in the physiology of production and/or excretion of sweat in the human skin eccrine gland. AIM: To determine plasma NO levels in patients with EH and healthy controls. METHODS: We assessed the levels of plasma NO in patients with EH (n = 31) in comparison with those in age- and sex-matched healthy controls (n = 28). Total nitrite (nitrite + nitrate) was measured by a spectrophotometer at 545 nm after the conversion of nitrate to nitrite by copperized cadmium granules. RESULTS: Plasma NO levels were found to be significantly increased in EH patients in comparison with the control group (P = 0.0001). CONCLUSIONS: These findings indicate a possible role of increased plasma NO levels in the pathophysiology of EH.

Effect of endoscopic transthoracic sympathicotomy on plasma natriuretic peptide concentrations in humans.

BACKGROUND: The effects of endoscopic transthoracic sympathicotomy (ETS) on plasma natriuretic peptides concentrations in humans were examined in order to elucidate the role of the sympathetic nervous system in their regulation. METHODS AND RESULTS: Thirty-seven patients with palmar hyperhidrosis underwent ETS. Cardiac functional indices were assessed by echocardiography, and plasma atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) concentrations were measured before and after ETS. ETS caused decreases in heart rate, mean arterial pressure, systemic vascular resistance, and increases in left ventricular (LV) end-diastolic volume, stroke index, ejection fraction, and left atrial diameter. LV end-systolic volume and cardiac index remained unchanged. Following ETS, ANP increased from 10.7+/-5.9 to 24.7+/-16.8 pg/ml (p < 0.01), and BNP increased from 5.1+/-4.2 to 19.7+/-21.5 pg/ml (p < 0.01). From the multivariate regression analysis, ETS, age and gender were determined to be significant predictors of changes in the ANP and BNP concentrations. None of the hemodynamic parameters were useful as independent predictors. CONCLUSION: The plasma concentrations of ANP and BNP increased after ETS, independent of hemodynamic changes, and apparently because of the release of the inhibitory effects of the cardiac sympathetic nerves on natriuretic peptide secretion.

Relation between hemodynamic changes after endoscopic transthoracic sympathicotomy and the number of sympathetic segments operated.

We examined the relation between hemodynamic changes after endoscopic transthoracic sympathicotomy (ETS) and the number of sympathetic segment operated. Cardiac functional indices using echocardiography and plasma noradrenaline concentration (NOR) were measured before and after ETS in 25 patients with palmar hyperhidrosis. Patients were divided into 2 groups. Group Th2-3 consisted of 16 patients (mean age 28 +/- 8 years),who underwent Th2-3 ETS. Group Th2-4 consisted of 6 patients (mean age 29 +/- 9 years), who underwent Th2-4 ETS. Before ETS, all hemodynamic parameters and NOR were similar between the 2 groups. After ETS, heart rate, systolic, diastolic, and mean blood pressures, rate-pressure product, and NOR decreased,whereas left ventricular end-systolic volume index, cardiac index, and ejection fraction did not change in the 2 groups. Systemic vascular resistance decreased in group Th2-4, whereas it did not change in group Th2-3. Left ventricular end-diastolic volume index and stroke index increased in group Th2-3, whereas it did not change in group Th2-4. After ETS, rate-pressure product, systolic, diastolic, and mean blood pressures in group Th2-4 were smaller than those in group Th2-3, whereas other parameters were similar between the 2 groups. Among percent changes in all hemodynamic parameters and NOR occurring after ETS, only the percent decrease in systolic blood pressure in group Th2-4 was larger than that in group Th2-3 (-15 +/- 12 % vs.-4+/-8%, respectively, p < 0.05). These findings suggest that only the change in blood pressure is related to the difference in the number of sympathetic segment operated.

Sweat secretion rates in growth hormone disorders.

BACKGROUND: While increased sweating is a prominent symptom in patients with active acromegaly, reduced sweating is gaining status as part of the growth hormone deficiency (GHD) syndrome. DESIGN AND SUBJECTS: Sweat secretion rate (SSR), as measured by pilocarpine iontophoresis represents the maximal capacity for stimulated sweat secretion in a localized skin area. SSR was studied in 37 patients with a history of acromegaly, 20 adult patients with GHD before and during long-term GH substitution of GHD adults, and 58 control subjects. RESULTS: Acromegaly: Patients with acromegaly had significantly higher SSR than healthy controls (Z-score + 1.9 (+/- 1.1) mean (+/- SD) (P < 0.001)). SSR was increased irrespective of current clinical disease activity. Thus, the SSR Z-scores in 16 clinically inactive patients were + 2.1 (+/- 1.2), in 10 slightly or doubtfully active patients + 1.5 (+/- 0.7) and in 11 active patients + 1.8 (+/- 1.3). There was no correlation between SSR and IGF-I. GHD: Twenty adult patients participated in an 18-month randomised, placebo controlled, double blinded study of physiological dose GH substitution, followed by 18 months of open GH treatment. SSR at baseline was reduced in male but not in female GHD patients. Mean SSR (95% confidence interval) for 11 male patients was 89.0 mg/30 minutes (51.9-126.1) as compared to 133.5 mg/30 minutes (59.2-259.9) (P = 0.01) in 24 male controls, and for 11 female patients 48.2 mg/30 minutes (25.9-70.6) as compared to 49.2 mg/30 minutes (12.6-93. 9) in 34 female controls. GH treatment in physiological substitution doses for up to 36 months had no effect on SSR. CONCLUSION: We have demonstrated that longstanding GH hypersecretion in patients with acromegaly induces irreversible changes of sweat gland function, with persistently elevated SSR despite treatment and clinical cure. In GHD patients, SSR was reduced in males but not in females, which together with the established gender difference in normal controls emphasises the role of androgen deficiency as a cofactor for reduced sweating in hypopituitary patients. Sweat gland development seems to be more susceptible to lack of hormones in childhood and adolescence than in adulthood, whereas growth hormone excess can modify sweat function later in life.

Plasma catecholamine concentrations in essential hyperhidrosis and effects of thoracoscopic D2-D3 sympathicolysis.

Essential hyperhidrosis (EH) is caused by a poorly understood overactivity of the sympathetic fibres passing through the upper dorsal sympathetic ganglia D2 and D3. These ganglia are also in the pathway of the sympathetic innervation of the heart and lungs. Therefore, although the predominant sympathetic neurotransmitter at the eccrine sweat glands is acetylcholine, the plasma concentration of noradrenaline (NA) (which is the main sympathetic neurotransmitter at the end organs including the heart and the lungs) may be elevated. Furthermore, as there are some indications for generalized sympathetic overactivity in EH, the plasma concentration of adrenaline (A) may also be elevated. Plasma levels of NA and A were therefore determined in 13 EH patients before and after thoracoscopic D2-D3 sympathicolysis (TS). Preoperative NA and A plasma levels were all within the normal limits used in our laboratory. After TS, mean NA plasma levels are significantly decreased, whereas mean A are unchanged. We conclude that sympathetic overactivity in EH is limited to the upper dorsal sympathetic ganglia and that some of the cardiovascular and pulmonary effects that are observed after TS may be associated with the decrease in NA.

Idiopathic hypocalcemia in foals.

Five thoroughbred foals (4 fillies and 1 colt), all in good to excellent body condition, ranging in age from 4 days to 5 weeks at the time of onset of signs, were presented to 2 Kentucky equine hospitals from 1992 through 1996. All 5 foals presented with tachycardia, hyperhidrosis, diarrhea or a recent history of diarrhea, and muscle rigidity or stiff gait. Four of the 5 foals presented for recumbency, seizure-like activity with opisthotonos, or pronounced extensor muscle rigidity. All 5 foals were hypocalcemic. All foals either died or had euthanasia performed. None responded to oral calcium supplementation. The cause of the hypocalcemia was unknown. Different idiopathic hypocalcemia syndromes may exist in foals.

Sequential cerebrospinal fluid and plasma sampling in humans: 24-hour melatonin measurements in normal subjects and after peripheral sympathectomy.

Simultaneous measurements of plasma and cerebrospinal fluid (CSF) melatonin and urinary excretion of 6-hydroxymelatonin were performed in four normal volunteers and one patient before and after upper thoracic sympathectomy for the control of essential hyperhidrosis. For normal individuals, hourly 24-h melatonin concentrations in plasma and CSF exhibited similar profiles, with low levels during the day and high levels at night. Peak plasma levels varied from 122-660 pmol/L, and the peak CSF levels from 94-355 pmol/L. The onset of the nocturnal increase in melatonin did not occur at the same time for each individual. Urinary 6-hydroxymelatonin levels also exhibited a daily rhythm, with peak excretion at night. The individual with the lowest nocturnal levels of circulating melatonin also had the lowest excretion of 6-hydroxymelatonin. In the patient with hyperhidrosis, a prominent melatonin rhythm was observed preoperatively in the CSF and plasma. After bilateral T1-T2 ganglionectomy, however, melatonin levels were markedly reduced, and the diurnal rhythm was abolished. These results provide direct evidence in humans for a diurnal melatonin rhythm in CSF and plasma as well as regulation of this rhythm by sympathetic innervation.