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H Mönig

Publications and source records attributed to H Mönig.

At least 19 recordsLinked to original sources
PubMed2006

Absence of exercise-induced leptin suppression associated with insufficient epinephrine reserve in patients with classic congenital adrenal hyperplasia due to 21-hydroxylase deficiency.

OBJECTIVE: Patients with congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency suffer from glucocorticoid and mineralocorticoid deficiency. They have insufficient epinephrine reserves and increased basal leptin levels and are often insulin resistant. In healthy subjects, an inhibitory effect of acute catecholamine elevation on the leptin plasma concentrations has been reported. However, it is not yet known how leptin levels respond to exercise in CAH patients. METHODS: We performed a cycle ergometer test in six CAH patients to measure the response of plasma leptin, glucose and the catecholamines, epinephrine (E) and norepinephrine (N), as well as their respective metabolites, metanephrine (M) and normetanephrine (NM), to intense exercise. RESULTS: Baseline leptin concentrations in CAH patients were not different from those of controls. Leptin levels decreased significantly with exercise in healthy controls, whereas they remained unchanged in CAH patients. In contrast to controls, CAH patients showed no rise of plasma glucose. Basal and stimulated E and M levels were significantly lower in CAH patients compared to controls. Baseline and stimulated N and NM levels were comparable, showing a significant rise after exercise. Peak systolic blood pressure and peak heart rate in both groups were comparable. CONCLUSION: CAH patients do not manifest exercise-induced leptin suppression. The most probable reason for this is their severely impaired epinephrine stress response. In addition, epinephrine deficiency is leading to secondary changes in various catecholamine dependent metabolic pathways, e. g., energy balance. Although obvious clinical sequelae are so far unknown, the catecholamine-deficient state and the resulting hyperleptinemia might contribute to the severity of the disease in CAH.

Adolescent↗
PubMed2006

Expression and distribution of prolactin receptor in normal, fibrotic, and cirrhotic human liver.

Liver cirrhosis is often associated with elevated levels of prolactin (PRL). This is commonly attributed to impaired hepatic metabolism of estrogens. However, there is evidence suggesting that PRL may be an important factor in hepatic tissue regeneration. To investigate the role of PRL in the pathogenesis of liver cirrhosis, we used RT-PCR and immunhistochemical staining to analyze changes in the expression and the histological distribution of the prolactin receptor (PRLR) in normal, fibrotic and cirrhotic hepatic tissue. Liver tissue was obtained from 29 surgically explanted human livers. The histological examination demonstrated normal liver tissue (n=9) as well as different grades of fibrosis (n=10) and cirrhosis (n=10). In liver cirrhosis and fibrosis, PRLR-mRNA was expressed at a higher level compared to normal liver specimens. Immunohistochemical staining of normal liver tissue demonstrated homogeneous distribution of the PRLR in the hepatocytes and in the epithelial cells of the bile ducts. This pattern of distribution was lost in fibrosis, where an accumulation of the PRLR was observed in the damaged hepatocytes. As no PRL-mRNA was detectable in normal, fibrotic or cirrhotic tissue, PRL does not act through autocrine or paracrine mechanisms. These data confirm previous results, which we obtained using an animal model for experimental liver cirrhosis in rats suggesting a metabolic function of PRL in normal liver and a regenerative function in fibrotic and cirrhotic liver. In conclusion, PRL might be involved in the pathogenesis of liver cirrhosis.

DNA Primers↗
PubMed2004

Expression of leptin and leptin receptor during the development of liver fibrosis and cirrhosis.

Leptin is involved in the regulation of food intake and is mainly secreted by adipocytes. Major secretagogues are cytokines such as TNF-alpha or IL-1. Leptin in turn upregulates inflammatory immune responses. Elevated leptin serum levels have been detected in patients with liver cirrhosis, a disease frequently associated with elevated levels of circulating cytokines as well as hypermetabolism and altered body weight. Recently, leptin has been detected in activated hepatic stellate cells in vitro and an involvement of leptin in liver fibrogenisis has been suggested. The current study was designed to further clarify the role of leptin in liver disease by characterizing leptin and leptin receptor expression in the development and onset of experimental liver fibrosis. Liver fibrosis and cirrhosis was induced in rats by use of phenobarbitone and increasing doses of CCl (4). Leptin and leptin receptor mRNA expression was determined by semiquantitative RT-PCR, protein expression by Western blot analysis and localization of leptin and its receptor by immunohistochemistry. Normal liver tissue does not express leptin, but leptin receptor mRNA. Increasing levels of leptin mRNA were detected in fibrotic and cirrhotic livers correlated to the degree of fibrosis. Leptin receptor mRNA expression was not significantly altered in damaged livers. Increasing levels of leptin were detected in fibrotic and cirrhotic livers, whereas protein expression of the receptor remained unchanged. Throughout different stages of liver fibrosis, leptin immunoreactivity was localized in activated hepatic stellate cells only, whereas immunoreactivity for the receptor was mainly seen on hepatocytes. In conclusion, leptin is expressed at increasing levels in activated hepatic stellate cells in vivo, which may therefore be a source of increased leptin tissue and serum levels contributing to the pathophysiology and morphological changes of chronic liver disease.

Animals↗
PubMed2004

Congenital adrenal hyperplasia - how to improve the transition from adolescence to adult life.

Congenital adrenal hyperplasia (CAH) is caused by a defect in the biosynthesis of cortisol that results in maximal activity of the hypothalamic-pituitary adrenal axis with hyperplasia of the adrenals and hyperandrogenism due to the accumulation of androgen precursors. In the salt-wasting subtype of the disorder, which accounts for appr. 75 % of patients with classical CAH, patients are unable to synthesise sufficient amounts of aldosterone and are prone to life-threatening salt-losing crises, whereas the simple virilising form is predominantly characterized by clitoris hypertrophy and posterior labial fusion. In addition, a non-classical variant can be discerned which in most cases is diagnosed at the time of puberty or early adolescence when hirsutism and menstrual irregularities may occur. The vast majority of CAH patients have 21-hydroxylase deficiency (90 - 95 %). Less common forms, such as 11beta-hydroxylase deficiency, will not be discussed in this review. Unfortunately, a considerable number of CAH patients is lost to regular and competent follow-up once they move out of paediatric care. This is most probably the result of insufficient co-operation between paediatric and adult endocrinologists at the time of transition from adolescence to adulthood. Furthermore, there is a lack of clinical guidance regarding psychosexual development in these patients. In this overview we will focus on special aspects of CAH treatment in adolescence and adulthood, and report on our 10-year experience with a transfer system for endocrine patients from paediatric to internal medical care, known as the "Kieler Modell". For practical purposes, we here provide charts for follow-up of CAH patients that can be adapted for use in any endocrine outpatient clinic.

Adolescent↗
PubMed2002

Limited value of elevated erythrocyte sedimentation rate as an indicator of malignancy.

BACKGROUND: Patients with an elevated erythrocyte sedimentation rate (ESR) are often suspected of having malignant disease and are subjected to extensive investigations. Thus, the finding of an elevated ESR can result in considerable costs and might even be dangerous for the patient if invasive studies are ordered. OBJECTIVES: Our aims were to establish (i) the prevalence of malignant diseases in hospitalized patients and out-patients with elevated ESR; and (ii) the long-term incidence of malignant diseases in patients during 5 years after unsuccessful investigation for elevated ESR. METHODS: A cross-sectional survey was carried out in 128 patients admitted to the Department of General Internal Medicine, University of Kiel and in 94 out-patients under the care of a GP. A retrospective cohort study of 50 patients was also carried out by contacting GPs of patients discharged from hospital after unsuccessful investigation. RESULTS: In the hospitalized patients, the ESR was elevated in 53.1% (68/128) and was normal in 46.9% (60/128). Malignancy was found in 25.0% (17/68) of patients with elevated ESR and in 15% (9/60) of patients with normal ESR (P = 0.16). Of the out-patients, 94 patients with elevated ESR were investigated, of whom 8.5% (8/94) had malignancies (P = 0.004 compared with hospitalized patients). In the follow-up study of 50 patients who had been discharged with the diagnosis "elevated ESR of unknown origin", follow-up information was available from 38 individuals. Of these, 71.0% (27/38) had not developed signs or symptoms of any disease at the time of investigation. Malignant disease had developed in only 5.3% (2/38). CONCLUSION: The prevalence of malignancy in patients with elevated ESR is low, in both the clinical and the general practice setting. Elevation of ESR is not an early sign of malignant disease and does not justify extensive investigation in a patient who has no symptoms which are suggestive of a tumour.

Blood Sedimentation↗
PubMed2001

Expression and distribution of the prolactin receptor in normal rat liver and in experimental liver cirrhosis.

Recent results have suggested a role for prolactin (PRL) as a regeneration factor in the liver. In order to investigate the involvement of prolactin in the pathogenesis of liver cirrhosis, we studied the expression of the prolactin receptor (PRLR) and PRL during the development of cirrhosis in an animal model. 30 male rats were exposed to CCl4 by inhalation. Phenobarbitone was added to the drinking water to accelerate the formation of toxic metabolites by enzyme induction. Two control groups of 30 animals each were treated with phenobarbitone only or received no treatment. 10 animals of each group were sacrificed 35, 55, and 70 days after initiation of treatment. Liver tissue was subjected to histological examination, which demonstrated fibrosis of different grades and cirrhosis in the CCl4-treated rats. Expression of PRLR mRNA was investigated by mRNA extraction, RT-PCR and computer-supported densitometric evaluation. Compared to control liver, PRLR mRNA was expressed at a higher level in fibrotic and cirrhotic liver specimens. In normal tissue, immunohistochemical staining showed a high concentration of PRLR around the central vein and in the epithelium of the bile ducts. This pattern of distribution was lost in fibrosis and cirrhosis. An accumulation of PRLR was demonstrated within the damaged cells. Neither PRL nor PRL mRNA was detectable in normal, fibrotic, or cirrhotic liver. We conclude that PRLR is distributed in normal rat liver in a typical pattern which is lost with increasing fibrosis. PRL is not produced by rat liver, indicating that PRL does not act through autocrine or paracrine mechanisms.

Animals↗
PubMed2001

Longitudinal imaging reveals pituitary enlargement preceding hypoplasia in two brothers with combined pituitary hormone deficiency attributable to PROP1 mutation.

Mutations of the PROP-1 gene cause combined pituitary hormone deficiency. Progressive ACTH/cortisol insufficiency is found in a few patients. Congenital hypoplasia of the anterior pituitary gland is the most common magnetic resonance imaging finding in patients with PROP-1 mutations. We present two brothers with compound heterozygosity for the two mutations 150delA and 301-302delAG of the PROP-1 gene. Both showed combined pituitary hormone deficiency of GH, TSH, PRL, and gonadotropins, as is typical for PROP-1 deficiency. We observed a developing insufficiency of ACTH and cortisol secretory capacity in both patients. Computed tomography revealed an enlarged pituitary in the older brother at 3.5 yr of age. Repeated magnetic resonance imaging after 12 yr showed a constant hypoplasia of the anterior pituitary lobe. Similarly, magnetic resonance imaging of the younger brother showed a constant enlargement of the anterior pituitary gland until 10 yr. At the age of 11 yr, the anterior pituitary was hypoplastic. The reason for pituitary enlargement in early childhood with subsequent decrease in pituitary size is not known. We speculate that altered expression of early transcription factors could be involved. Because both patients have the same PROP-1 mutations and an identical pattern of combined pituitary hormone deficiency, we suggest that early pituitary enlargement may be the typical course in such patients in whom pituitary surgery is not indicated.

Child↗
PubMed2000

Gallstones, the choledochoduodenal junction and initiation of acute pancreatitis: are two stones the culprits rather than one stone?

Reflux of biliary secretions into the pancreatic duct following gallstone obstruction of the common biliary pancreatic ampulla has been implicated as a cause of acute pancreatitis. However, the pancreatic duct pressure is higher than the biliary pressure and, therefore, the simple obstruction of the choledochoduodenal junction by one gallstone does not result in biliary pancreatic reflux. We propose a mechanism whereby simultaneous migration and sequential impaction above and below the common biliary pancreatic ampulla of two gallstones allows for the creation of a toxic bile-pancreatic juice mixture in the common bile duct, subsequent reversal of the pressure gradient and reflux of the toxic secretions into the pancreatic duct.

Acute Disease↗
PubMed1999

Activation of the hypothalamo-pituitary-adrenal axis in response to septic or non-septic diseases--implications for the euthyroid sick syndrome.

OBJECTIVE: To determine whether cytokine release or activation of the hypothalamo-pituitary-adrenal (HPA) axis is predominantly involved in the development of the euthyroid sick syndrome (ESS). DESIGN: Prospective observational study. SETTING: Intensive care unit at a tertiary care medical center in Germany. PATIENTS: Nine patients with sepsis of different causes and eight patients with acute myocardial infarction. INTERVENTIONS: None. MEASUREMENTS AND RESULTS: Immediately on admission and on day 7 the following parameters were determined: total thyroxine (T4), free thyroxine (FT4), total triiodothyronine (T3), thyrotropin (TSH), interleukin-1 beta (IL-1 beta), interleukin-2 (IL-2), soluble interleukin-2 receptor (sIL-2R), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-alpha), serum cortisol and plasma adrenocorticotropin (ACTH). On admission, concentrations of all thyroid hormones and TSH were significantly lower in septic patients compared to non-septic patients, whereas all cytokines except IL-2 were significantly elevated in the sepsis group. By contrast, there was no difference in serum cortisol and plasma ACTH levels between the two groups. On day 7, T4 and T3 were still lower in the septic group, whereas IL-1 beta, sIL-2R and IL-6 were still elevated. Again, no differences were found with regard to cortisol and ACTH levels. CONCLUSIONS: Euthyroid sick syndrome occurs very early during the course of septic diseases. Significantly decreased levels of total T4, FT4, T3 and TSH in septic patients suggest central suppression of TSH as well as inhibition of thyroid hormone release in ESS. The HPA axis is activated in septic patients and in non-septic patients and does not contribute to the development of ESS.

Adult↗
PubMed1999

Iodine absorption in patients undergoing ERCP compared with coronary angiography.

BACKGROUND: Systemic absorption of iodinated contrast material occurs during endoscopic retrograde cholangiopancreatography (ERCP), the clinical significance of which has not yet been determined. METHODS: Urinary iodine excretion was measured before and after coronary angiography (n = 20) and ERCP (n = 12). Thyroid hormone levels were determined before iodine load and after 6 and 24 weeks. RESULTS: Before coronary angiography, iodine excretion was 101 +/- 38.3 micromol/mol creatinine and increased to 865. 10(5) +/- 721. 10(5) micromol/mol on the next day (p </= 0.001). After 6 weeks, it was still elevated (167 +/- 88.8 micromol/mol, p < 0.01). Before ERCP, iodine excretion was 115 +/- 60.3 micromol/mol and reached a peak of 5.3. 10(5) +/- 4.9. 10(5) micromol/mol (p < 0.001). Six weeks later, it had returned to baseline. Two patients in the coronary angiography group but none in the ERCP group had suppressed thyrotropin after 6 weeks. CONCLUSIONS: The systemic iodine load during ERCP is approximately 0.6% of the iodine load during coronary angiography. Therefore routine measurement of thyroid hormones before ERCP is not recommended.

Absorption↗
PubMed1999

Comèl-Netherton syndrome complicated by papillomatous skin lesions containing human papillomaviruses 51 and 52 and plane warts containing human papillomavirus 16.

We describe a 28-year-old woman with characteristic clinical signs of Comèl-Netherton syndrome (CNS) who showed numerous plane warts on her face and forearms and papillomatous skin tumours affecting her groins and genitoanal skin. Using human papillomavirus (HPV) type-specific primers for cutaneous and mucosal HPV types we identified HPV 16-specific sequences in plane warts and HPV 51- and HPV 52-specific DNA in papillomatous skin from the patient's groins, suggesting a pathogenetic role (cofactor) for HPV in the development of verrucous skin lesions in patients with CNS. Whether the susceptibility to HPV infections is due to decreased cellular immunity or epidermal defence mechanisms remains to be seen.

Adult↗
PubMed1999

Predictive value of serum S100B for monitoring patients with metastatic melanoma during chemotherapy and/or immunotherapy.

In the immunohistology of malignant melanoma the use of polyclonal antibodies against protein S100 is well established. Recently, it was shown that S100B, a subunit of the S100 protein family, is detectable in the serum of melanoma patients and correlates with the stage of the disease in patients with metastatic melanoma. In the present study, the first evaluation of a large number of treatment observations (n = 77) in 64 different patients during chemotherapy and/or immunotherapy for advanced metastatic melanoma (stage IV) is presented. All patients received treatment according to standardized protocols comprising 8 weeks of treatment followed by routine staging procedures to evaluate therapeutic outcome. In 13 patients with tumour enlargement after first-line therapy, a second-line treatment was subsequently given. S100B immunoradiometric assay (IRMA) tests were performed before, during and after treatment at scheduled time points. In the interim analysis at 4 weeks 29 of 37 (78%) patients with tumour progression during treatment showed a raised S100B level. In the final analysis at 8 weeks, 31 of these 37 patients (84%) demonstrated rising S100B values (P < 0.001). Patients who responded to treatment (stable or regressing metastatic disease) showed constant or declining S100B levels in 38 of 40 patients (95%) at the interim analysis, at 8 weeks this was further increased to 39 of 40 patients (98%; P < 0.001). Thus, the use of S100B for monitoring treatment is adequate in the majority of cases. Our observations are of great interest for therapeutic trials of adjuvant and palliative therapies as the rise of S100B levels might indicate that re-staging and/or changes in therapy strategies should be chosen.

Adult↗
PubMed1999

Blunted nocturnal TSH surge does not indicate central hypothyroidism in patients after pituitary surgery.

The thyrotropin-releasing hormone stimulation test (TRH test) is commonly used as part of the endocrine evaluation after pituitary surgery. However, some patients with a normal thyrotropin (TSH) response to TRH after pituitary surgery develop central hypothyroidism during follow-up. On the other hand, hypothyroidism does not necessarily ensue in patients with a blunted TSH response. As TSH is secreted in a pulsatile fashion with maximum secretion in the early morning, we investigated whether measurement of the nocturnal TSH surge is useful for predicting development of thyrotropic function after pituitary surgery. Serum TSH concentrations were measured at hourly intervals from 16.00 h to 06.00 h in 13 healthy volunteers and in 10 patients within 2 weeks after pituitary surgery. A standard TRH test using i.v. injection of 200 microg synthetic TRH was performed the next morning. Three and six months later thyroid function was reassessed in all patients by measuring thyroid hormones and TSH. Healthy volunteers showed a clear nocturnal TSH surge from a nadir of 0.55 +/- 0.27 microIU/ml at 18.00 h to a peak concentration of 1.82 +/- 0.97 microU/ml at 06.00 h (p = 0.0015). DeltaTSH during TRH test was 6.31 +/- 2.27 microIU/ml. In contrast, following pituitary surgery, patients invariably showed a blunted nocturnal increase in TSH concentration, which was 0.27 +/- 0.20 microIU/ml at 18.00 h and 0.33 +/- 0.26 microIU/ml at 06.00 h (p = 0.044). DeltaTSH during TRH test was 1.99 +/- 2.51 microIU/ml and was subnormal in 8 out of 10 patients. Levothyroxine supplementation was initiated in two of these patients, because free T4 levels were also subnormal and clinical hypothyroidism was present. In the remaining patients with subnormal TRH response, no case of central hypothyroidism was identified at the follow-up visits after 3 and 6 months. We conclude from these data that both nocturnal TSH surge and TRH test are subnormal after pituitary surgery and do not indicate that central hypothyroidism will develop.

Adult↗
PubMed1999

Biliary pancreatic reflux-induced acute pancreatitis--myth or possibility?

OBJECTIVE: The mechanism whereby gallstone passage through the choledochoduodenal junction initiates acute pancreatitis is not known. We mimicked different patterns of stone impaction at the choledochoduodenal junction in a rabbit model and studied whether these result in biliary pancreatic reflux and the initiation of pancreatic inflammation. METHODS: In rabbits, catheters were introduced into the common bile duct (CBD) and the pancreatic duct. In five experiments, obstruction of these catheters at various time intervals mimicked different patterns of stone obstruction of both ducts prior to a stone impaction at the papilla of Vater: experiment I--no obstruction of the pancreatic duct and the CBD; experiment II--separate obstruction of the CBD and the pancreatic duct; experiment III--selective obstruction of the CBD; experiment IV--separate obstruction of the CBD and the pancreatic duct and subsequent decompression of the pancreatic duct; experiment V--obstruction pattern as in experiment IV associated with a bacterial infection of bile (10(8) E. coli/ml). Ductal pressures were recorded for 24 h. In order to study the effects of a subsequent impaction of the stone at the papilla of Vater, the catheters in the CBD and in the pancreatic duct were connected and mimicked a common channel behind a papillary stone. The flow direction of bile and pancreatic juice was directly observed. Pancreatic histology was analysed 24 h later. RESULTS: In experiments I-III, neither biliary pancreatic reflux nor acute pancreatitis was observed. In experiments IV and V, obstruction of the CBD caused an increase in the biliary pressure to 17 +/- 3 cm H2O, whereas the pancreatic duct pressure dropped to subnormal levels following obstruction and selective decompression (2 +/- 0.5 cm H2O). After the creation of a 'common channel', biliary pancreatic reflux was observed for 118 +/- 21 min. Flow of sterile bile into the pancreas was not harmful to the gland. Infected biliary pancreatic reflux initiated acute pancreatitis. CONCLUSIONS: 1. Bile flow into the pancreas may occur. 2. Biliary pancreatic reflux may initiate acute pancreatitis. 3. Bile reflux-induced acute pancreatitis requires previous biliary hypertension, temporary pancreatic duct obstruction, and the bacterial infection of choledochal secretions.

Acute Disease↗
PubMed1999

S100B protein detection in serum is a significant prognostic factor in metastatic melanoma.

The serum detection of S100B, a new melanoma marker, has shown clinical significance in early studies. The aim of our study of 1, 339 serum samples from 412 different melanoma patients and 107 control patients was to prove the prognostic value of serum S100B levels in melanoma patients at different stages of disease and at follow-up (median: 30 months). Using a cutoff level of 0.2 microgram/l S100B, 5 of 286 patients (1.7%) with primary tumors (stage I/II), 14/73 (19.2%) patients with locoregional metastasis (stage III) and 57/84 (67.9%) patients with advanced disease (stage IV) were S100B positive (statistically significant differences for stage I/II vs. III, I/II vs. IV, and III vs. IV, p < 0.001). The estimated overall survival time was significantly longer (p < 0.001) for patients with S100B values below 0.2 microgram/l compared to patients with elevated S100B levels (>/=0.2 microgram/l), which was independent of the stage of disease (I-IV). Regarding prognosis, we were furthermore able to distinguish different subgroups among stage III and IV patients using S100B serum levels (p < 0.01). Patients with different cutaneous non-melanoma diseases served as S100B-negative controls. S100B serum evaluations using the Sangtec(R)100 IRMA are highly specific and sensitive for the detection of metastatic melanoma. S100B has been shown to be a relevant prognostic factor for survival in a study with a large sample size of melanoma patients including close follow-up evaluations.

Adult↗
PubMed1998

[Cabergoline].

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Antiparkinson Agents↗