Postmortem determination of concentrations of stress hormones in various body fluids--is there a dependency between adrenaline/noradrenaline quotient, cause of death and agony time?

To find out whether a certain cause of death or a certain length of an agonal period shows specific adrenaline or noradrenaline profiles, heart blood, femoral vein blood, liquor, urine and vitreous humour were taken from corpses (n = 98) at the Medical School Hannover, and noradrenaline and adrenaline were determined using high-performance liquid chromatography (HPLC). Corpses were classified according to the following five categories: short agony, long agony, state after hanging, state after asphyxiation and state after CPR with documented administration of epinephrine. Once results were collected the adrenaline/noradrenaline quotient was determined. It became clear that there were no significant differences regarding the concentration of adrenaline and noradrenaline in the various body fluids in relation to the above-mentioned categories. The means adrenaline/noradrenaline quotients in femoral vein blood were 0.21 +/- 0.29 for hanged persons, 0.38 +/- 0.47 for asphyxiated persons, 0.17 +/- 0.19 for those with short agony and 0.42 +/- 0.43 for those with long agony, significantly below 1 (p < 0.001; p = 0.001; p = 0.003). For condition after CPR we found an adrenaline/noradrenaline quotient of 2.81 +/- 5.8. In liquor the adrenaline/noradrenaline quotients for short agony was 0.17 +/- 0.17, for hanged persons 0.18 +/- 0.19 and for asphyxiated ones 0.30 +/- 0.38, significantly lower than 1 (p < 0.001). In urine the adrenaline/noradrenaline quotients for all categories are lower than 1 (p < 0.001); short agony (0.13 +/- 0.09), long agony (0.21 +/- 0.16), hanged (0.15 +/- 0.16), asphyxiated (0.14 +/- 0.08) and CPR (0.14 +/- 0.06). In vitreous humour the quotients for short agony (0.14 +/- 0.28), long agony (0.13 +/- 0.12), hanged (0.07 +/- 0.09) and asphyxiated (0.09 +/- 0.11) are lower than 1 (p < 0.001). The spread of data for the adrenaline/noradrenaline quotient did not allow for any conclusions about cause of death and length of agony in individual cases.

[Glutamic acid decarboxylase autoantibody concentration and glucose tolerance in late pregnancy]. / Glutamat-Azetat-Dekarboxylase-Autoantikörper-Konzentration und Glukosetoleranz in der Spätschwangerschaft.

Genetic and immunological factors may play a role as possible causes for gestational diabetes. Autoantibodies to glutamic acid decarboxylase (GADA) are frequently found in patients with insulin dependent diabetes, but have only rarely been analyzed with regard to the carbohydrate tolerance in pregnancy. An oral glucose tolerance test (oGTT) with 75 g glucose was performed in 110 pregnant patients during the third trimenon. Glucose (glucose dehydrogenase method) and insulin (RIA) concentrations were measured after 0, 30, 60, 120, and 180 minutes. Patients were divided into five groups of increasing glucose intolerance based on the highest glucose concentration reached during the oGTT. GADA were measured using a quantitative enzyme-immunoassay. Only a single patient showed pathologically elevated GADA, and her oGTT results were within the normal range. GADA in subjects with normal pathological glucose tolerance showed no significant difference (276.6 +/- 151.6 and 263.0 +/- 107.1 mU/ml respectively). There was a tendency of positive correlations between high GADA-levels and higher concentrations of insulin as well as an increased insulin-glucose-index. These findings suggest that pregnant patients with higher GADA-levels may have an increased insulin resistance. In conclusion, the concentration of GADA was not found to be helpful in evaluating the current metabolic situation in gestational diabetes. It remains unclear whether elevated GADA during pregnancy have a prognostic value regarding the manifestation of overt diabetes mellitus later in life.

[Autoimmune encephalopathy in Hashimoto's thyroiditis. A differential diagnosis in progressive dementia syndrome]. / Autoimmunenzephalopathie bei Hashimoto-Thyreoiditis. Eine Differentialdiagnose bei progressivem Demenzsyndrom.

HISTORY AND CLINICAL FINDINGS: A 58-year-old woman, known for 10 years to have Hashimoto's thyroiditis, was admitted from another hospital where, after an initial period of unconsciousness, she had developed progressive severe dementia, abnormal arousal and generalized myoclonia. Jakob-Creutzfeldt disease (JCD) was suspected. INVESTIGATIONS: The electroencephalogram (EEG) showed marked slowing of the basic activity and episodes of triphasic waves. The titres of thyroid antibodies (TPO 764 kU/l, TgAk 398 kU/l) and of the antinuclear antibodies (ANA 1:1280) were raised, as was the erythrocyte sedimentation rate (80/120 mm and the cerebrospinal fluid albumin concentration (1 g/l). TREATMENT AND COURSE: The history and findings suggested autoimmune encephalitis (AIE) and treatment with prednisolone, 2 mg/kg body weight daily, was initiated, achieving lasting improvement of arousal within two days. 6 weeks later the EEG merely showed mild alteration of basic activity. The thyroid antibody titres were now within normal limits and the signs of inflammation were regressing. CONCLUSION: In case of rapidly progressive dementia autoimmune antibodies should be looked for in the differential diagnosis, because autoimmune disease may be the treatable cause.

Urodilatin is involved in sodium homeostasis and exerts sodium-state-dependent natriuretic and diuretic effects.

Urodilatin is involved in sodium homeostasis exerts sodium-state-dependent natriuretic and diuretic cts. Eight male volunteers participated in a study consisting of three consecutive phases of 7 days each. The volunteers a sodium diet with 52, 172.6, and 347.8 mmol um/day. Sodium excretion increased from 57.4 +/- 3.7 via .8 +/- 4.6 (P < 0.001) to 322.5 +/- 10.2 mmol/24 h (P < 0.001) at the end of each sodium diet. Urinary urodilatin excretion increased from 24.8 +/- 3.0 via 35.5 +/- 9.0 (P = 0.07) to 49.0 = mol/min (P < 0.01). At the end of each diet, urodilatin was infused for 2 h at 20 ng.kg body wt-1.min-1. Natriuresis increased after low- (4.1 to 52.9 mmol/h, P < 0.001), normal (6.9 to 44.9 mmol/h, P < 0.05), and high-sodium diet (20.1 to 102.9 mmol/h, P < 0.001). Diuresis increased from 174 to 709 (P < 0.001), 395 to 1,026 (P < 0.05), and 266 to 1,339 ml/h < 0.001). The present results indicate that endogenous urodilatin plays an important role in sodium homeostasis and that renal response to exogenous urodilatin is modulated by sodium balance.