Dirk Lehnick

Dr. Dirk Lehnick

University of Lucerne
orcid

Research Focus & Metrics

Academic Career Length

31Years (1996-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 April 1998 in Gut
Verified
Journal Article
Open access
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PLP G Lankisch
P G Lankisch
ISI Schmidt
I Schmidt
HKH König
H König
DLDirk Lehnick
Dirk Lehnick
RKR Knollmann
R Knollmann
SLS Liebe
S Liebe
Background/Aim—The suggestion that estimation of faecal elastase 1 is a valuable new tubeless pancreatic function test was evaluated by comparing it with faecal chymotrypsin estimation in patients categorised according to grades of exocrine pancreatic insufficiency (EPI) based on the gold standard tests, the secretin-pancreozymin test (SPT) and faecal fat analysis. Methods—In 64 patients in whom EPI was suspected, the following tests were performed: SPT, faecal fat analysis, faecal chymotrypsin estimation, faecal elastase 1 estimation. EPI was graded according to the results of the SPT and faecal fat analysis as absent, mild, moderate, or severe. The upper limit of normal for faecal elastase 1 was taken as 200 μg/g, and for faecal chymotrypsin 3 U/g stool. Levels between 3 and 6 U/g stool for faecal chymotrypsin are usually considered to be suspicious for EPI. In this study, both 3 and 6 U/g stool were evaluated as the upper limit of normal. Results—Exocrine pancreatic function was normal in 34 patients, of whom 94, 91, and 79% had normal faecal elastase 1 and faecal chymotrypsin levels (<3 U/g and <6 U/g) respectively. Thirty patients had EPI, of whom 53, 37, and 57% had abnormal faecal enzyme levels (differences not significant). When EPI was graded as mild, moderate, or severe, 63% of patients had mild to moderate EPI, and 37% had severe EPI. In the latter group, between 73 and 91% of patients had abnormal faecal enzymes. In the group with mild to moderate EPI, abnormal test results were obtained for both faecal enzymes in less than 50% of the patients (differences not significant). Some 40% of the patients had pancreatic calcifications. There were no significant differences for either faecal enzyme between the two groups with and without pancreatic calcifications. In 62% of the patients who underwent an endoscopic retrograde cholangiopancreatography (ERCP), abnormal duct changes were found. Again, there were no significant differences for either faecal enzyme between the two groups with abnormal and normal ERCP. Conclusion—Estimation of faecal elastase 1 is not distinctly superior to the traditional faecal chymotrypsin estimation. The former is particularly helpful only in detecting severe EPI, but not the mild to moderate form, which poses the more frequent and difficult clinical problem and does not correlate significantly with the severe morphological changes seen in chronic pancreatitis.

1 April 1999 in Gut
Verified
Journal Article
Open access
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PLP G Lankisch
P G Lankisch
SBS Burchard-Reckert
S Burchard-Reckert
DLDirk Lehnick
Dirk Lehnick
BACKGROUND In most treatment studies on acute pancreatitis, pancreatologists base their diagnosis on amylase/lipase levels more than three times above the upper limit of normal (>3n) and thus exclude patients with smaller enzyme level increases. The recommendations derived from the results of treatment studies do not take into account such patients. Non-pancreatologists frequently believe that only patients with high enzyme levels have a serious prognosis. AIMS To question the assumption that high enzyme levels indicate severe, and conversely low enzyme levels indicate mild, acute pancreatitis. PATIENTS/METHODS This retrospective study includes 284 consecutive patients with a first attack of acute pancreatitis. The cause was biliary in 114 (40%) patients, alcoholism in 83 (29%), other in 21 (7%), and unknown in 66 (23%). Patients were divided into two groups according to their serum enzyme levels (amylase: ⩽3n, n = 88; >3n, n = 196; lipase: ⩽3n, n = 51; >3n, n = 233). Renal impairment, indication for dialysis and artificial ventilation, development of pseudocysts, necessity for surgery, and mortality were taken as parameters of severity. RESULTS The incidence of severity was the same for both the ⩽3n and >3n groups. CONCLUSIONS The severity of acute pancreatitis is independent of the elevation in serum amylase/lipase level (⩽3n or >3n) on admission. Patients with only a slight increase can also have or develop severe acute pancreatitis. Patients with ⩽3n elevated enzyme levels on admission represent a substantial group that treatment studies have frequently overlooked. This is especially true for patients with alcohol induced acute pancreatitis whose amylase levels are lower than in other aetiological groups.

3 September 2020 in Clinical Infectious Diseases
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Journal Article
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MSMartin Stocker
Martin Stocker
WHWendy van Herk
Wendy van Herk
SHSalhab el Helou
Salhab el Helou
SDSourabh Dutta
Sourabh Dutta
FSFrank A B A Schuerman
Frank A B A Schuerman
ARAnnemarie M C van Rossum
Annemarie M C van Rossum
Background: Neonatal early-onset sepsis (EOS) is one of the main causes of global neonatal mortality and morbidity, and initiation of early antibiotic treatment is key. However, antibiotics may be harmful. Methods: We performed a secondary analysis of results from the Neonatal Procalcitonin Intervention Study, a prospective, multicenter, randomized, controlled intervention study. The primary outcome was the diagnostic accuracy of serial measurements of C-reactive protein (CRP), procalcitonin (PCT), and white blood count (WBC) within different time windows to rule out culture-positive EOS (proven sepsis). Results: We analyzed 1678 neonates with 10 899 biomarker measurements (4654 CRP, 2047 PCT, and 4198 WBC) obtained within the first 48 hours after the start of antibiotic therapy due to suspected EOS. The areas under the curve (AUC) comparing no sepsis vs proven sepsis for maximum values of CRP, PCT, and WBC within 36 hours were 0.986, 0.921, and 0.360, respectively. The AUCs for CRP and PCT increased with extended time frames up to 36 hours, but there was no further difference between start to 36 hours vs start to 48 hours. Cutoff values at 16 mg/L for CRP and 2.8 ng/L for PCT provided a sensitivity of 100% for discriminating no sepsis vs proven sepsis. Conclusions: Normal serial CRP and PCT measurements within 36 hours after the start of empiric antibiotic therapy can exclude the presence of neonatal EOS with a high probability. The negative predictive values of CRP and PCT do not increase after 36 hours.

14 May 2010 in Climacteric
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MEM. Eugster-Hausmann
M. Eugster-Hausmann
JWJ. Waitzinger
J. Waitzinger
DLDirk Lehnick
Dirk Lehnick
Objective To investigate the pharmacokinetics of 10 μg and 25 μg 17β-estradiol (E2) vaginal tablets in postmenopausal women with vaginal atrophy. Methods Fifty-eight women received either 10 μg or 25 μg estradiol vaginal tablets, administered once daily for 2 weeks, followed by twice-weekly dosing for 10 weeks. Blood samples were taken over 24 h at baseline (day -1) and days 1, 14, 82 and 83. Estradiol (E2), estrone (E1) and estrone sulfate (E1S) levels were quantified by gas chromatography–mass spectrometry (GCMS) and assessed by the average plasma concentration from time 0 to 24 h (Cave) derived from the area under the curve within 24 h (AUC(0-24)) divided by 24 h. Results Mean Cave values were 9.39 and 19.84 pg/ml on day 1, 6.56 and 18.29 pg/ml on day 14, and 4.64 and 9.41 pg/ml on day 83 for the 10 μg and 25 μg doses, respectively. After 12 weeks, E1 and E1S levels were slightly higher with the 25 μg dose and in the same range with the 10 μg dose, as compared to baseline. Conclusions During 12 weeks' administration, 10 μg vaginal tablets resulted in at least 50% lower mean estradiol concentrations than with the 25 μg dose within 24 h after dosing. Administering the 25 μg dose, mean E2 levels during the first 2 weeks exceeded the published reference range for postmenopausal women using the GCMS method, while, with the 10 μg dose, mean E2 levels remained in that range from the beginning, indicating minimized estradiol absorption.

1 January 2001 in Journal of Internal Medicine
Verified
Journal Article
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PLP. G. Lankisch
P. G. Lankisch
MGM. Gerzmann
M. Gerzmann
JGJ.‐F. Gerzmann
J.‐F. Gerzmann
DLDirk Lehnick
Dirk Lehnick
Lankisch PG, Gerzmann M, Gerzmann J‐F, Lehnick D (Municipal Clinic of Lüneburg, Lüneburg, and University of Göttingen, Göttingen, Germany). Unintentional weight loss: diagnosis and prognosis. The first prospective follow‐up study from a secondary referral centre. J Intern Med 2001; 249: 41–46.Objectives. To establish the incidence and causes of unintentional weight loss and to compare prognoses.Design. Prospective.Setting. Secondary referral centre.Subjects. 158 patients (89 female, 56%; 69 male, 44%) referred by general physicians for unexplained weight loss or for other reasons. In the latter case, weight loss was established after admission to hospital. Follow‐up lasted for up to 3 years.Main outcome measure. Determining the course of weight loss in patients with diagnosed and undiagnosed causes.Results. The cause of weight loss was established in 132 (84%) patients and remained unclear in 26 (16%). Reasons were non‐malignant (60% of patients) and malignant (24%) diseases. Psychological disorders represented 11% of the non‐malignant group. A gastrointestinal disease caused weight loss in 50 (30%) patients. Of malignant disorders, 53% (20 of 38 patients) were gastrointestinal. Amongst the non‐malignant group, 39% (30 of 77 patients) had somatic disorders. The prognosis for unknown causes of weight loss was the same as for non‐malignant causes.Conclusion. Contrary to common belief, weight loss is not usually due to a malignant disease. A gastrointestinal tract disorder accounts for weight loss in every third patient. If minimal diagnostic procedures cannot establish a diagnosis, then endoscopic investigation of the upper and lower gastrointestinal tract and function tests should be performed to exclude malabsorption.

1 November 2001 in Digestive Diseases and Sciences
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PLPaul Georg Lankisch
Paul Georg Lankisch
CAChristine Assmus
Christine Assmus
DLDirk Lehnick
Dirk Lehnick
PMPatrick Maisonneuve
Patrick Maisonneuve
ALAlbert B. Lowenfels
Albert B. Lowenfels