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Biomedical subjects

C C Sieber

Publications and source records attributed to C C Sieber.

At least 19 recordsLinked to original sources
PubMed2006

[Diagnosing malnutrition in the elderly].

The concept of malnutrition in the geriatric population describes a deficient state of energy and nutrient intake with harmful clinical consequences. Despite of having a significant effect on morbidity and mortality, there are no generally accepted criteria for diagnosing malnutrition in the elderly. With increasing age the general recognition of the nutritional status becomes more important for the diagnosis of malnutrition than isolated parameters. Recording a patient"s history must include any weight loss and changes in appetite. Reasons for a diminished nutritional intake must be explored systematically as well. As part of physical examination one has to pay attention to clinical signs of malnutrition (general muscular atrophy, loss of subcutaneous fat) and to signs of micronutrient deficiencies. The documentation of oral intake can supply important evidence for deficient intake of energy and nutrients. Of special relevance among anthropometric values are a BMI of less than 20 kg/m and calf circumference of less than 31 cm. Individual follow-up data are superior to isolated measurements Laboratory diagnostic tests (for example albumin) are of minor importance for the diagnosis of malnutrition because of their low specificity. As a consequence of unsolved methodical problems, bioelectrical impedance analysis can currently be recommended only to those who are experienced with this method and its limitations. Screening and assessment tools like Mini Nutritional Assessment (MNA) and Nutritional Risk Screening(NRS) are helpful for a quick and simple identification of malnourished patients and those who are at risk. The MNA is especially applicable for people who live independently and for cooperative residents of nursing homes. The NRS is a valuable alternative for hospital patients and those unable to cooperate. Screening for malnutrition should be routine practice in the elderly population, especially for those at high risk for it like in hospitals and in nursing homes.

Aged↗
PubMed2006

[Drug administration and dosage forms in geriatric patients].

The demographic shift demands more and more customized medical supplies and management structures for geriatric patients. The elderly patient with age-related functional restrictions and multi-morbidity is at special risk for an ill-adapted pharmacotherapy. In addition the frail elderly person is dependent on general-practitioner assistance. The prescription of a suitable drug and a safe and workable (galenic) application form is key to therapeutic success. Age-based intake regulations, repeated education, and intake training are crucial tasks for the general-practitioner when caring for a fast growing elderly patient population.

Aged↗
PubMed2005

Comparison of the Mini Nutritional Assessment, Subjective Global Assessment, and Nutritional Risk Screening (NRS 2002) for nutritional screening and assessment in geriatric hospital patients.

The Mini Nutritional Assessment (MNA), the Subjective Global Assessment (SGA) and the Nutritional Risk Screening (NRS) are screening and assessment tools aimed at detecting malnourished individuals and those at risk for malnutrition. In our study we tested their applicability in geriatric hospital patients and compared the results of the three tools. We examined prospectively all patients of two acute geriatric wards by the MNA, the SGA and the NRS. 121 patients were included in the study. The MNA could be completed in 66.1% of all patients, the SGA in 99.2% and the NRS in 98.3%. There was a significant association of all three tools with the BMI (p<0.01). With regard to serum albumin and to length of hospital stay (p<0.05), only a significant association could be shown for the MNA (p<0.05). Although the categories of the results were not completely identical for the three tools there were more patients at risk or malnourished according to the MNA (70%) than according to the SGA (45%) or the NRS (40.3%). The direct comparison of the NRS with the MNA and the SGA demonstrated significant differences, especially for the latter (p<0.001). In a relevant percentage of those tested, MNA, SGA, and NRS identify different individuals as malnourished or at risk for malnutrition. Because of its association with relevant prognostic parameters, the MNA is still the first choice for geriatric hospital patients. For those patients to whom the MNA cannot be applied, the NRS is recommended.

Aged↗
PubMed2005

[The concept of frailty--from phenomenology to therapeutic approaches].

Frailty--the weakness of many (oldest) old persons--induces a lot of human sorrow with functional disabilities as well as health-economic costs. Sarcopenia (loss of muscle mass) is also a form of frailty and a co-factor of two of the "geriatric Is"--immobility and instability. Pathophysiologically, both phenomena show signs of an inflammatory state. Physical activity and a healthy diet can partially reverse these health problems. Therefore, therapeutic strategies emerge to treat these frequent and clinically relevant phenomena.

Aged↗
PubMed2001

In vivo angiogenesis in normal and portal hypertensive rats: role of basic fibroblast growth factor and nitric oxide.

BACKGROUND: Angiogenesis plays a pivotal role in many processes. Here, we studied whether angiogenesis to basic fibroblast growth factor (bFGF) in normal and portal hypertensive rats requires nitric oxide (NO). METHODS: To measure angiogenesis in vivo, two Teflon rings filled with collagen I (Vitrogen 100) were fixed in the mesenteric cavity at day 0, with one supplemented with bFGF (100 ng). Portal hypertension was induced by partial portal vein ligation (PVL). Sham-operated rats served as controls (CON). The role of NO was tested by adding the NO formation antagonist N(omega)-nitro-L-arginine (NNA; 3.3 mg/kg per day) to the drinking water. After 16 days, rings were explanted and embedded, and vessels were morphometrically counted. RESULTS: bFGF significantly stimulated vessel formation per implant in CON rats (from 624 +/- 97 without stimulation to 1123 +/- 171, n = 11, P < 0.01), but not in PVL rats (from 1106 +/- 174 without stimulation to 1046 +/- 202, n = 9). Without stimulation, numbers of ingrown vessels were significantly (P < 0.05) higher in PVL compared to CON rats. NNA substantially inhibited angiogenesis in both groups (P < 0.01). Vessel numbers were 202 +/- 124 for PVL (n = 5) and 197 +/- 14 for CON (n = 5) animals. bFGF did not reverse angiogenesis prevented by NNA (373 +/- 98 for PVL, 265 +/- 26 for CON, n = 5 per group, NS). CONCLUSIONS: NO formation inhibition diminishes both unstimulated and bFGF-stimulated angiogenesis in CON rats. Moreover, bFGF cannot rescue NNA-inhibited angiogenesis in PVL rats.

Animals↗
PubMed2001

Role of gender upon basal and postprandial systemic and splanchnic haemodynamics in humans.

BACKGROUND: Food intake, accompanied by systemic and splanchnic haemodynamic changes, has only been studied in males. The extent to which splanchnic postprandial hyperaemia shows gender differences is unknown. METHODS: We tested 1) the splanchnic hyperaemic response to food in females and 2) whether postprandial haemodynamic changes show gender differences. Twenty-four healthy women (aged 20-35 years) and 20 healthy men (aged 21-34 years) participated in the study. A liquid test meal (Ensure plus, 1.5 kcal/ml) was perfused intraduodenally for 75 min through an enteral feeding tube at a rate of 3 ml/min after a 45-min basal period. Blood flow parameters were measured using Echo-Doppler technology. RESULTS: Basal diastolic arterial blood pressure was significantly (P < 0.05) lower in females (66+/-2 versus 72+/-2 mmHg), whereas heart rate was the same (58+/-2 b/min, ns). Postprandially, diastolic blood pressure fell, but reached significance only in males (-10+/-3 mmHg; P < 0.05). Mean velocity in the superior mesenteric artery (SMA) was significantly (P < 0.05) higher in females compared to males at baseline (47+/-3 versus 39+/-2 cm/s), whereas maximal postprandial changes were similar (64+/-6 versus 56+/-6 cm/s, ns). Volume flow in the portal vein (PV) at baseline was 656+/-29 and 716+/-35 ml/min females and males, respectively (ns between gender). Maximal postprandial changes amounted to 808+/-86 and 884+/-107 ml/min, respectively (ns). CONCLUSIONS: 1) Perfusion of a liquid test meal induces significant increases in flow parameters in the SMA and PV in both genders. 2) These changes are partly paralleled by alterations in systemic haemodynamics. 3) Postprandial splanchnic flow parameters are qualitatively and quantitatively not different between genders.

Adult↗
PubMed1999

Increased angiogenesis in portal hypertensive rats: role of nitric oxide.

Systemic and especially splanchnic arterial vasodilation accompany chronic portal hypertension. Different soluble mediators causing this vasodilation have been proposed, the strongest evidence being for nitric oxide (NO). No data exist if structural vascular changes may partly account for this vasodilatory state. Here, we developed a new in vivo quantitative angiogenesis assay in the abdominal cavity and determined if: 1) portal hypertensive rats show increased angiogenesis; and 2) angiogenesis is altered by inhibiting NO formation. Portal hypertension was induced by partial portal vein ligation (PVL). Sham-operated rats served as controls (CON). During the index operation (day 0), a teflon ring filled with collagen I (Vitrogen 100) was sutured in the mesenteric cavity. After 16 days, rings were explanted, embedded in paraffin, and ingrown vessels counted using a morphometry system. The role of NO was tested by adding an antagonist of NO formation (Nomega-nitro-L-arginine [NNA], 3.3 mg/kg/d) into the drinking water. The mean number of ingrown vessels per implant was significantly higher in PVL rats compared with CON rats, i.e., 1,453 +/- 187 versus 888 +/- 116, respectively (P <.05; N = 5 per group). NNA significantly (P <.01) inhibited angiogenesis in PVL (202 +/- 124; N = 5) and in CON (174 +/- 25; N = 6) rats, respectively. In contrast, the beta-adrenergic blocker, propranolol, did not prevent angiogenesis either in PVL or CON rats in a separate set of experiments (data not shown). The conclusions drawn from this study are that: 1) rats with portal hypertension show increased angiogenesis; and 2) inhibition of NO formation significantly prevents angiogenesis in both PVL and CON rats. Therefore, splanchnic vasodilation in chronic portal hypertension may also be a result of structural changes.

Adrenergic beta-Antagonists↗
PubMed1999

Dose-dependent gastrointestinal effects of the somatostatin analog lanreotide in healthy volunteers.

OBJECTIVE: To investigate the gastrointestinal effects of intravenous lanreotide. METHODS: Twenty healthy male subjects participated in 2 subsequent placebo-controlled, double-blind crossover studies. The effects of 3 doses of lanreotide (50, 100, and 200 microg/h) were investigated on 24-hour intragastric acidity (study I), food-stimulated gallbladder contraction, and plasma cholecystokinin release (study II). RESULTS: Lanreotide showed linear pharmacokinetics. It raised median intragastric pH significantly and in a dose-dependent manner: from 1.4+/-0.2 (placebo) to 2.5+/-0.8 (P < .002) during administration of 50 microg/h lanreotide, to 3.2+/-0.7 (P < .001) during 100 microg/h lanreotide, and to 4.3+/-0.7 (P < .001) during 200 microg/h lanreotide. However, no significant inhibition of gastrin secretion could be established. All doses completely inhibited postprandial gallbladder contraction. CONCLUSION: Intravenous administration of lanreotide at rates applied in this study was able to significantly inhibit intragastric acid secretion and postprandial gallbladder contraction; under these conditions few untoward effects were noted.

Adult↗
PubMed1998

Hemodynamic effects of the somatostatin analog lanreotide in humans: placebo-controlled, cross-over dose-ranging Echo-Doppler study.

Because of their vasoactive effects, somatostatin and its analogs are increasingly used in the management of complications of chronic liver diseases such as variceal bleeding. Postprandial hyperemia augments splanchnic blood flow, subsequently increasing portal pressure. The aim of this study was to explore effects of the somatostatin analog, lanreotide, on food-stimulated hemodynamic parameters in healthy human subjects. A dose-response curve was constructed in eight healthy male subjects in a placebo-controlled cross-over study. On 4 different days, either 0 (placebo), 50, 100, or 200 microg/h of lanreotide was infused intravenously in random order, starting at 45 minutes for 7 hours. On each day, a liquid test meal (Ensure plus, 1.5 kcal/mL) was perfused intraduodenally at a rate of 3 mL/min over 7 hours after a 45-minute basal period. Diastolic arterial pressure (dBP), heart rate (HR), superior mesenteric arterial (SMA) average flow velocity (SMA-V), SMA pulsatility index (SMA-PI), portal venous volume flow (PV-F), and renal artery (RA) resistance index (RA-RI) were measured on regular intervals (flows using Echo-Doppler technology). Lanreotide at all doses abolished food-stimulated splanchnic hyperemia both in the SMA and PV over 7 hours. The fall in dBP and increase in HR after food perfusion were blunted under lanreotide. Food as well as lanreotide did not modify RA-RI. In summary: 1) lanreotide inhibits food-induced splanchnic hyperemia in normal subjects; 2) in parallel, systemic hemodynamic alterations to food stimulation are abolished with lanreotide; and 3) renal vascular resistance is unchanged. Because of its persistent splanchnic vasoconstrictive effect, lanreotide should be tested in patients with portal hypertension.

Adult↗
PubMed1998

Neurally-mediated vasodilatation in normal and portal hypertensive rats: role of nitric oxide and calcitonin gene-related peptide.

BACKGROUND/AIMS: Portal hypertension is associated with systemic vasodilatation and vascular hyporeactivity, and is reversed by inhibiting nitric oxide biosynthesis. Nitric oxide and calcitonin gene-related peptide are neurotransmitters of non-adrenergic non-cholinergic nerves. The role of nitric oxide and calcitonin gene-related peptide in nerve-stimulated vasodilatation in portal hypertension is unknown. METHODS: We tested (i) if in vitro perfused superior mesenteric arterial vascular beds of portal hypertensive rats (induced by partial portal vein ligation) showed an increased vasodilatation to periarterial nerve stimulation compared to normal controls, and (ii) if this vasodilatation was modulated by nitric oxide and calcitonin gene-related peptide antagonism. RESULTS: Vasodilatatory responses to periarterial nerve stimulation (10 V, 1 ms) with increasing frequencies (Hertz, 2-12) in preconstricted vessels (methoxamine and guanethidine) were significantly smaller in vessel preparations of control (n=8) compared to portal hypertensive (n=7) rats, values with 8 Hertz being 32.3+/-3.6% and 44.9+/-3.6%, respectively (p<0.05). This difference was reversed by inhibiting nitric oxide and calcitonin gene-related peptide action with the nitric oxide-biosynthesis inhibitor N(omega)-Nitro-L-arginine, values for 8 Hertz being 28.7+/-4.8% (controls) and 37.8+/-3.3% (portal hypertensive, ns) or with the calcitonin gene-related peptide antagonist CGRP8-37, values being 25.2+/-2.8% (controls) and 27.8+/-4.2% (portal hypertensive, ns), respectively (n=4-6 per group). Vasodilatation to the beta-agonist isoproterenol was not significantly different between groups with and without calcitonin gene-related peptide and nitric oxide antagonism. CONCLUSION: Portal hypertensive rats display a significantly enhanced vasodilatation to periarterial nerve stimulation, which is reversed by inhibiting the non-adrenergic non-cholinergic neurotransmitters nitric oxide and especially calcitonin gene-related peptide.

Animals↗
PubMed1997

Hyposensitivity to nerve stimulation in portal hypertensive rats: role of nitric oxide.

Portal hypertension goes along with vascular hyporeactivity, partly mediated by nitric oxide (NO). Interactions between the adrenergic nervous system and NO in portal hypertension are undetermined. We tested (1) whether superior mesenteric arterial beds of portal hypertensive rats have an altered sensitivity to periarterial nerve stimulation (PNS) and (2) the role of NO in modulating nerve-stimulated responses. Vasopressor responses to PNS (Hz, 2-32) were similar in preparations of partial portal vein-ligated (PVL, n = 12) and control (CON, n = 12) rats (60.0 +/- 6.7 and 47.8 +/- 6.1 CmH2O respectively) for 24 Hz (NS), but sensitivity of vessels of portal hypertensive animals displayed a significant rightward shift [Hz needed for 50% of maximal response (HZ50) being 15.5 +/- 0.4 and 12.9 +/- 0.6 for PVL and CON respectively, P < 0.001]. NO formation inhibition by N omega-nitro-L-arginine (10(-4) mol L-1) significantly increased responses to PNS (P < 0.05), the absolute values for 24 Hz being 101.4 +/- 11.7 cmH2O for PVL (n = 8) and 86.4 +/- 11.4 cmH2O for CON (n = 7) (NS). NO formation inhibition reversed the hyposensitivity in preparations of PVL, Hz50 being 13.9 +/- 0.5 and 13.2 +/- 0.2 for PVL and CON respectively (NS). Adrenergic receptor antagonism with prazosin (10(-7) mol L-1) and yohimbine (10(-6) mol L-1) inhibited PNS-mediated vasopressor reactivity (n = 6 per group, P < 0.001), confirming the nervous origin of vasoconstrictor responses. It is concluded that (1) portal hypertension goes along with a significant hyposensitivity to PNS and (2) this hyposensitivity is reversed by NO-formation inhibition

Animals↗
PubMed1997

[Portal hypertension].

Portal hypertension is a frequent and clinically important complication of chronic liver diseases. Beside bleeding episodes from oesophageal and gastric varices, ascites formation and hepatic encephalopathy are sequelae of the haemodynamic changes seen under chronic portal hypertensive conditions. These are characterized by a systemic vasodilatation and a subsequent hyperdynamic circulation, leading to an increased arterial inflow into the splanchnic vascular bed. This so-called "arterial vasodilatation theory" is crucial for the persistence of portal hypertension even after the opening of decompressing collaterals. Furthermore, these changes are pathophysiologically linked to ascites formation and the development of hepatic encephalopathy. This article briefly discusses the diagnostic and therapeutic procedures in patients with ascites and hepatic encephalopathy. With regard to the diagnosis and treatment of varices and their bleeding, the reader is referred to the article of Eberhard Renner in the same issue of this journal.

Antihypertensive Agents↗
PubMed1996

Long-term octreotide treatment prevents vascular hyporeactivity in portal-hypertensive rats.

Chronically portal-hypertensive rats show in vitro vascular hyporeactivity in large part mediated by the endothelium-derived vasodilator nitric oxide. We tested whether long-term octreotide treatment (15 micrograms/kg subcutaneously in 5% D/W, 8-hourly) corrects the in vitro vascular hyporeactivity. Increases in perfusion pressures (delta mm Hg) to potassium chloride (30-300 mmol/L) of in vitro perfused superior mesenteric arterial vascular beds of partial portal vein-ligated (PVL) rats were significantly (P < .05) higher in octreotide (n = 9) compared with placebo (n = 10, 5% D/W) treated animals. Octreotide significantly (P < .05) increased mean arterial pressure compared with placebo, the values being 129 +/- 3 and 117 +/- 4 mm Hg, respectively. Furthermore, a significant (P < .001) correlation was observed between in vitro vascular reactivity and mean arterial pressure. Incubation of separate vascular beds (n = 7 for both PVL and sham-operated rats) with octreotide (10(-6) mol/L) did not enhance pressure responses to 125 mmol/L potassium chloride, and failed to increase perfusion pressures in preconstricted vessel preparations (n = 6), excluding a direct inhibitory effect on NO. In summary, long-term octreotide treatment prevents in vitro vascular hyporeactivity in prehepatic portal-hypertensive rats, and octreotide does not exert its action through direct effects on endothelium-derived NO.

Animals↗
PubMed1996

Concomitant active Crohn's disease and the acquired immunodeficiency syndrome.

Symptomatic human immunodeficiency virus (HIV) infection is accompanied by depressed CD4+ T-lymphocyte counts. These cells seem to play a role in the inflammatory processes in Crohn's disease. It has even been speculated that depression of CD4+ T-lymphocytes in HIV infection may cure Crohn's disease. Here we describe a 41-year-old drug-addicted man with a 9-year history of Crohn's disease. HIV infection was diagnosed 8 years ago. At present he has stage-C3 HIV infection. He was admitted because of weight loss and chronic diarrhea with rectal blood and mucus discharge. Crohn's disease was confirmed endoscopically and histologically. Infectious diarrhea known to mimic Crohn's disease in patients with acquired immunodeficiency syndrome (AIDS) was excluded. In summary, we describe a patient with AIDS (CD4 count, 84/microliter) and active Crohn's disease, showing that both illnesses can occur simultaneously.

Acquired Immunodeficiency Syndrome↗