Search PubMed⌕ Search

Biomedical subjects

E Jungmann

Publications and source records attributed to E Jungmann.

At least 37 records · Page 2Linked to original sources

Hormonal modifications in patients admitted to an internal intensive care unit for acute hypoxaemic respiratory failure.

To clarify which endocrine modifications can be observed in acute hypoxaemic respiratory failure, 15 severely ill male patients [PAT; median age: 61 (range: 48 years); median height: 173 (range: 12) cm; median mass: 73 (range 31) kg] were investigated immediately upon admission to an intensive care unit (ICU) for this clinical disorder. Before starting treatment, the blood gases were measured and a number of selected hormones with special relevance for an ICU setting were determined. These are known to be modified by acute hypoxaemia in healthy subjects and to possess glucoregulatory properties, or an influence upon cardiocirculation or the vascular volume regulation: insulin, cortisol, adrenaline, noradrenaline, atrial natriuretic peptide, renin, aldosterone, angiotensin converting enzyme, and endothelin-I (ET). To elucidate whether potential endocrine changes resulted from acute hypoxaemia alone, the underlying disease, or unspecific influences connected with the ICU setting, all measurements were compared to those of a completely healthy reference group (REF) with comparable acute experimental hypoxaemia. The latter state was achieved by having the REF breathe a gas mixture with the oxygen content reduced to 14% (H). In the REF, neither the medians nor the distribution of endocrinologic measurements were modified significantly by acute hypoxaemia. In the PAT, the medians were increased considerably, yet with a slight diminution of ET. The distribution of individual values was considerably broader than in the REF with H. In conclusion, considerable increases in the means of the above hormones, with the exception of ET, can be registered in severely ill patients admitted to ICUs with acute hypoxaemic failure. However, such modifications cannot be considered attributable exclusively to acute arterial hypoxaemia. The underlying clinical disorders, such as septicaemia or an unspecific endocrine epiphenomenon, including severe and not only hypoxaemic stress, seem to be predominant.

Acute Disease↗

Chemoprophylaxis of diabetic nephropathy in the elderly.

Renal disease in elderly diabetic patients is costly in terms of morbidity, mortality and medical payments. Therefore, prevention of diabetic nephropathy has become a prominent goal in the treatment of diabetic patients. Preventive treatment should begin not later than at the stage of persistent microalbuminuria, and regular screening for microalbuminuria is recommended for both elderly and younger diabetic patients. Improved metabolic control, through diet and hypoglycaemic therapy, has been demonstrated to lower urinary albumin excretion. The target level of glycated haemoglobin is < 8%, or < 2% higher than the upper limit of normal in nondiabetic people. Insulin therapy has no adverse effects on renal indices, unless it increases bodyweight and consequently raises blood pressure. To preserve renal function in elderly diabetic patients, blood pressure should be kept well below 140/90 mm Hg. Treatment with ACE inhibitors may be the 'gold standard' intervention, and should be initiated at the lowest possible dosage and then titrated until the maximum tolerated dosage has been reached. Nonchronotropic calcium antagonists have been shown to be as effective as ACE inhibitors with regard to their effects on blood pressure, renal haemodynamics and urinary albumin excretion. Most dihydropyridines have been found to increase or to have no effect on urinary albumin excretion despite significant blood pressure reduction. A renoprotective action of diuretics is generally unlikely, with the possible exception of indapamide. Although beta-blockers are effective antihypertensive agents, they may not adequately preserve kidney function in diabetic patients. Because beta-blocker treatment may mask the symptoms of hypoglycaemia, they should be reserved for patients with coronary artery disease or arrhythmias.

Aged↗

[Urinary albumin excretion by patients with type 2 diabetes mellitus. Effect of blood pressure and metabolic regulation].

BACKGROUND: There is still controversy as to whether increased urinary albumin excretion (UAE) in patients with type 2 diabetes mellitus may have similar pathognomonic relevance as in type 1 diabetes and whether improved metabolic control may beneficially influence increased UAE in type 2 diabetic patients to the same extent as in type 1 diabetic patients. PATIENTS AND METHODS: In a cross-sectional study in 234 patients with type 2 diabetes (age, 64 +/- 1 years, known duration of diabetes, 14 +/- 1 years) UAE, haemoglobin A1, blood pressure, cholesterol, triglyceride and creatinine levels were measured and signs of retinopathy were evaluated. Results were compared with the findings in 247 patients with type 1 diabetes (age, 39 +/- 1 years, duration of diabetes, 15 +/- 1 years). In a longitudinal study, UAE, haemoglobin A1, blood pressure, cholesterol, triglyceride and creatinine levels were measured in 41 patients with type 2 diabetes and secondary failure of oral hypoglycemic treatment (age, 62 +/- 1 years, known duration of diabetes, 11 +/- 1 years) before and after 2-year insulin treatment. RESULTS: In the cross-sectional study, 39% of the type 2 diabetic patients had increased UAE, 27% had microalbuminuria, in contrast to 21% and 14%, respectively, of the type 1 diabetic patients (p < 0.01). In type 2 diabetes, macroalbuminuria was detected after an average of 15 +/- 2 years in contrast to 25 +/- 2 years in type 1 diabetes (p < 0.01). In comparison to macroalbuminuric type 1 diabetic patients, macroalbuminuric type 2 diabetes patients exhibited a lower prevalence of renal insufficiency (30 vs. 53%, p < 0.05) as well as of retinopathy (59 vs. 88%, p < 0.05), but a higher prevalence of hypertension (93 vs. 65%, p < 0.05) as well as of hyperlipidaemia (p < 0.01). There was a significant relation between UAE and haemoglobin A1 in patients with type 1 diabetes (p < 0.01) which could not be demonstrated in type 2 diabetic patients. In the longitudinal study, UAE fell from 86 +/- 28 to 51 +/- 16 mg/24 hours (p < 0.05) and the prevalence of UAE of more than 30 mg/24 hours decreased from 45 to 25% (p < 0.05) after 2-year insulin treatment, while blood pressure remained constant and haemoglobin A1 fell from 12.3 +/- 0.4 to 8.8 +/- 0.3% (p < 0.01). In comparison to patients with normal or normalized UAE after 2 years, patients with persistently elevated UAE had more advanced kidney disease (p < 0.05), more pronounced insulin resistance and a higher prevalence of calculated mean arterial blood pressure above 103 mm Hg and of haemoglobin A1 higher than 9% (normal, < 7%) in the course of the study (p < 0.05). CONCLUSION: In patients with both type 2 and type 1 diabetes mellitus, increased UAE is a marker for the nephropathy-related sequelae of long-term hyperglycaemia. In type 2 diabetic patients, however, the frequently pre-existing hypertension as well as other disease mechanism of the "metabolic syndrome" ("syndrome X") may additionally determine course and progression of diabetic kidney disease.

Aged↗

Chronic angiotensin-converting enzyme inhibition may improve sodium excretion in cardiac transplant hypertension.

Cyclosporine-associated hypertension (CAH) may be mediated in part by sodium and volume retention. To investigate this issue, we studied the effects of a calcium antagonist, nitrendipine (NIT, 10-20 mg b.i.d.), and a converting enzyme inhibitor, lisinopril (LIS, 10-20 mg o.d.), on blood pressure (office BP, 24 hr ambulatory BP), excretion of an acute sodium load (200 mmol/2 hr i.v.), glomerular filtration rate (insulin clearance), cumulative dopamine excretion, plasma atrial natriuretic peptide (ANP), and endothelin excretion in 8 patients with CAH after cardiac transplantation in a double-blind, randomized, crossover trial for 6 weeks. Five patients received a diuretic during the trial at a constant dose. Office diastolic BP (DBP) decreased significantly with LIS from 97 +/- 6 to 87 +/- 9 mmHg and with NIT from 96 +/- 7 to 92 +/- 12 mmHg. Ambulatory 24 hr DBP decreased significantly from 96 +/- 7 mmHg to 86 +/- 10 mmHg (LIS) and to 84 +/- 11 mmHg (NIT). Ambulatory DBP during the day was lowered significantly from 98 +/- 11 mmHg to 87 +/- 10 mmHg (LIS) and to 88 +/- 9 mmHg (NIT) and during the night from 95 +/- 9 mmHg to 86 +/- 8 mmHg (LIS) and to 79 +/- 7 mmHg (NIT). Cumulative sodium excretion 6 hr after an acute sodium load increased to 52 +/- 39 mmol (placebo), 96 +/- 44 mmol (LIS, P < 0.05 vs. placebo), and 71 +/- 34 mmol (NIT). Glomerular filtration rate, cumulative dopamine excretion, ANP, and endothelin excretion did not differ between either treatment group. We conclude, that: (1) both drugs were similar in lowering office BP and during the day, but NIT tended to be more effective during the night; and (2) cumulative sodium excretion during LIS was significantly increased compared with placebo. There was a similar trend during NIT also. Therefore, it is possible that chronic angiotensin-converting enzyme inhibition and possibly calcium antagonists might improve the sodium-retaining state in CAH independent of differences in blood pressure, ANP, dopamine, or renal function.

Angiotensin-Converting Enzyme Inhibitors↗

Modification of the responses of endothelin-1 to exhaustive physical exercise under simulated high-altitude conditions with acute hypoxia.

To assess whether acute alveolar hypoxia leads to the release of endothelin-1 (ET) in vivo, ET, cortisol (CORT), and lactate (LA) levels were determined in 15 healthy subjects at rest and during exhaustive incremental cycle ergometry on two separate test days. The subjects were to breathe a gas mixture with reduced O2 content ([H] fraction of inspired O2, 0.14) on one day and normal air on the other (N). Modified responses of LA and CORT to exhaustive incremental cycle ergometry on the H day indicated elevated anaerobic tissue metabolism and increased physical stress. With acute alveolar hypoxia, the response of ET to exhaustive physical labor was found to be augmented.

Acute Disease↗

Increase of serum insulin and stable c-peptide concentrations with exhaustive incremental graded exercise during acute hypoxia in sedentary subjects.

Hypoxia was shown to reduce insulin concentrations at rest and during exercise. However, some studies have also demonstrated increases in the hormone associated with arterial desaturation. This study was conducted in order to decide [1] whether acute alveolar hypoxia increased or decreased the circulating insulin levels, and [2] to elucidate whether interactions of insulin with other hormones were of relevance in this respect. Glucose (GLU), insulin (INS), c-peptide (CP), adrenaline and noradrenaline (CATs), atrial natriuretic peptide (ANP) and cortisol (CORT) as well as the capillary blood gases were determined in 15 healthy fasting male volunteers (age: 26.2 +/- 2.8 years, body mass index: 22.4 +/- 2.7 kg.m-2). On two separate test days the subjects breathed, in random order, either normal air (N) or a gas mixture with reduced oxygen content (H; FIO2: 0.14). Measurements were made at rest as well as during an incremental cycle exercise in a supine position (increments of 6 min and 50 W) at 100 W and 150 W, at volitional exhaustion (N: 227 +/- 36 W; H: 200 +/- 32 W) as well as in the 5th min of recovery. Arterial desaturation was seen throughout on H-day. At rest all hormones and GLU were normal and showed no influence of H. During exercise INS remained constant on N-day, increased on H-day and was significantly higher with H than with N, most pronounced at 150 W and at volitional exhaustion with 20%, respectively. For CP and GLU no significant exercise-induced changes were seen on either test day and no influence of H was detected.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗

[The status of the gonadotropin releasing hormone test in differential diagnosis of delayed puberty in adolescents over 14 years of age].

BACKGROUND: In patients with delayed puberty with a bone age less than 11 years in girls or 12 years in boys, the clinical and endocrinological examination allows the differentiation of patients with the various forms of hypergonadotropic hypogonadism, but not of patients with hypogonadotropic hypogonadism from more prevalent constitutional delay in puberty. Therefore, watchful waiting is generally recommended for differential diagnosis in patients with delayed puberty. On the other hand, the late onset of sexual hormone replacement in patients with hypogonadism will worsen their outcome. PATIENTS AND METHOD: Therefore, we decided to carry out a retrospective study in 105 adolescents who were examined because of short stature or delayed puberty, who were aged 14 to 22 years at first visit and in whom the differential diagnosis of delayed puberty was documented after an at least one-year follow-up in order to find out which endocrinological parameters could have effectively predicted the final diagnosis already at the first visit. RESULTS: Patients with hypogonadotropic hypogonadism differed from patients with constitutional delay in puberty by lower responses of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) levels to gonadotropin-releasing hormone stimulation (GnRH, 100 micrograms iv) (p < 0.01) as well as by smaller testicular volume (p < 0.05) and by lower testosterone levels (p < 0.01). Stimulated LH < 10 mU/ml differentiated patients with hypogonadotropic hypogonadism from constitutional delay in puberty with a sensitivity of 82% and a specificity of 98%. CONCLUSION: In patients with delayed puberty aged 14 years and older bone age usually exceeds 11 years in girls or 12 years in boys. It thus is in the range, in which normal adult responses of LH to GnRH can be expected. In contrast to patients aged less than 14 years, therefore, measuring GnRH-stimulated LH levels in these patients allows the rapid and effective differential diagnosis of delayed puberty.

Adolescent↗

[The nephroprotective effect of ramipril. Effect on blood pressure and metabolic control in insulin-treated patients with type-2 diabetes mellitus].

AIM: Investigation of the impact of blood pressure and metabolic control on the nephroprotective effect of ramipril in insulin-dependent diabetics. METHOD: Within the framework of an open prospective therapeutic trial, 18 hypertensive, insulin-treated diabetics received ramipril, 5 mg/day, for an average period of 11 months. All the patients had previously received various forms of antihypertensive medication, and had microalbuminuria. RESULTS: Urinary excretion of albumin and N-acetyl-beta-D-glucosaminidase decreased in 13 patients (group 1), but increased in the remaining five patients (group 2). Blood pressure clearly decreased in group 1, but remained constant in group 2. In terms of clinical and biochemical data, the group 2 patients differed from those in group 1, having a lower age, a shorter history of diabetes and higher hemoglobin A1c levels despite higher doses of insulin. CONCLUSIONS: The present observations show that inadequate metabolic control and refractory hypertension in type 2 diabetics accelerate progression of diabetic nephropathy, and may thus negate the nephroprotective effect of the converting enzyme inhibitor, ramipril.

Aged↗

Elevated endothelin levels in patients with hyperlipoproteinemia.

We determined lipoproteins, apolipoproteins, and endothelin in 98 patients (58 female and 40 male, age 18-72 years) with hyperlipidemia (plasma cholesterol > 2.5 g/l and/or triglycerides > 2.0 g/l) and in 50 healthy subjects (20 female, 30 male, age 19-68 years). In patients with hyperlipidemia endothelin levels were elevated compared to healthy controls. Patients with plasma cholesterol above 2.5 g/l had higher endothelin and lipoprotein(a) concentrations than patients with plasma cholesterol levels less than 2.5 g/l. A positive correlation was found between the concentrations of endothelin and apolipoprotein B (r = 0.2137; P < 0.013). Smoking patients with lipoprotein (a) above 300 mg/l had higher endothelin levels than both nonsmoking patients with lipoprotein (a) above 300 mg/l and smokers with normal lipoprotein(a). In smokers endothelin correlated positively with Lp(a) (r = 0.709; P < 0.01). No correlation was found between endothelin and triglycerides nor between endothelin and age or sex. The results suggest that the vasoconstrictor endothelin contributes to the increased vasal tone in hyperlipidemia. Because endothelin also has mitogenic properties, it may play a relevant role in the development of premature atherosclerosis in patients with hyperlipidemia.

Adolescent↗

Elevated endothelin-1 levels after cigarette smoking.

The effect of short-term nicotine consumption on endothelin-1 (ET-1) levels was studied in 10 male healthy smokers. Volunteers smoked in random order on 3 separate days a low-tar cigarette or a high-tar cigarette, or were studied without having smoked (no-cigarette experiment). ET-1, corticotropin, and cortisol levels, heart rate, and blood pressure were determined before and 1, 3, 5, 10, 20, and 30 minutes after smoking. In contrast to results obtained after smoking a low-tar cigarette or not smoking, smoking a high-tar cigarette resulted in a significant increase in ET-1 levels within 10 minutes, followed by an increase in corticotropin levels within 20 minutes after smoking. Thirty minutes after smoking, cortisol levels were higher after a high-tar cigarette compared with a low-tar cigarette or no smoking. Increases in heart rate and systolic blood pressure were likewise higher after smoking a high-tar cigarette than after smoking a low-tar cigarette. In conclusion, it is tempting to speculate that ET-1 may indeed act as the long-searched-for link between vasopressin and corticotropin-releasing hormone (CRH) and thus play an essential role in the stimulation of the hypothalamic-pituitary-adrenal axis. In addition, these results suggest that the increase in the level of ET-1, a powerful vasoconstrictor and mitogen, may play an important part in the disease mechanisms of atherosclerosis arising from smoking.

Adrenocorticotropic Hormone↗