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Biomedical subjects

J Mössner

Publications and source records attributed to J Mössner.

At least 91 records · Page 5Linked to original sources

[Changes in incidence and prevalence of acute and chronic pancreatitis in Germany].

It is difficult to provide valid data with regard to changes in incidence and prevalence of acute pancreatitis in Germany. The lack of information is due to strict legal regulations to protect personal data, a certain lack of interest in epidemiological research and the lack of exact statistics of diseases treated in hospitals. The incidence of acute pancreatitis in other industrialized Western countries is about 10 new cases per year and 100,000 inhabitants. The increase of alcohol consumption over the last 30 years is associated with an increase of ethanol-induced pancreatitis. One may speculate that due to improved diagnostic possibilities, such as CT scan, cases where acute pancreatitis is diagnosed at autopsy are rare. Due to the increase in alcohol consumption it can be assume that the incidence and prevalence of chronic pancreatitis have increased in Germany similar to well-documented data from Denmark. Since alcohol consumption is slightly decreasing in Germany it is likely that the present incidence of about 10 cases of chronic pancreatitis per 100,000 inhabitants will also decrease.

Acute Disease↗

Nuclear factor-kappaB mediates simultaneous induction of inducible nitric-oxide synthase and Up-regulation of the cationic amino acid transporter CAT-2B in rat alveolar macrophages.

The connection between the regulation of L-arginine transport and nitric oxide (NO) synthesis was studied in rat alveolar macrophages. Lipopolysaccharides (LPSs) and interferon-gamma stimulated in the same concentration- and time-dependent manner NO synthesis (measured by nitrite accumulation) and L-[(3)H]arginine uptake. This correlated with an increased mRNA expression for iNOS and the cationic amino acid transporter CAT-2B (analyzed by reverse transcription-polymerase chain reaction), with the same kinetics observed for the up-regulation of both mRNAs. Because nuclear factor-kappaB (NF-kappaB) is essential for induction of iNOS its role for the regulation of CAT-2B expression and L-arginine transport was investigated. The NF-kappaB inhibitors pyrrolidine dithiocarbamate and N(alpha)-p-tosyl-L-lysine chloromethyl ketone abrogated LPS- and interferon-gamma-induced increase of nitrite accumulation and L-[(3)H]arginine uptake as well as up-regulation of iNOS and CAT-2B mRNA. LPS-induced increase in iNOS and CAT-2B mRNA was also suppressed by specific NF-kappaB decoy oligodesoxynucleotides, confirming the essential role of NF-kappaB for iNOS and CAT-2B expression. Dexamethasone did not affect the initial (5 h) LPS-induced increase of iNOS and CAT-2B mRNA, but down-regulated both mRNAs after prolonged (20 h) exposure and this was accompanied by partial inhibition of LPS-stimulated nitrite accumulation and L-[(3)H]arginine uptake. These findings demonstrate parallel regulation of the expression of iNOS and CAT-2B, and of NO synthesis and L-arginine uptake in rat alveolar macrophages. NF-kappaB is an essential transcription factor not only for the induction of iNOS, but also for the up-regulation of CAT-2B. The simultaneous up-regulation of CAT-2B with iNOS is considered as a mechanism to ensure a high substrate supply for iNOS.

Amino Acid Transport Systems, Basic↗

Cyclooxygenase-2 transcription is stimulated and amylase secretion is inhibited in pancreatic acinar cells after induction of acute pancreatitis.

Cyclooxygenases as the key enzymes of prostaglandin synthesis have an important role in regulation of inflammation. We describe that Cox-1 and Cox-2 are synthesized in rat pancreatic acinar cells. Upon induction of pancreatitis, Cox-2 mRNA increases while Cox-1 expression remains constant. However, the cyclooxygenase inhibitor indomethacin has no influence by a feed-back mechanism on the expression of the two isoforms. We have previously shown that prostaglandins of the E-type inhibit cholecytoskinin-stimulated amylase secretion. Consistent with this observation, we find here that pancreatitis inhibits CCK-stimulated amylase secretion from isolated acini. In agreement with this result, the effect is neutralized by indomethacin inhibition of prostaglandin synthesis. In summary, we have found that both cyclooxygenases are synthesized in pancreatic acinar cells and that their expression is differentially regulated which in turn influences amylase secretion.

Acute Disease↗

Expression of p73 and its relation to histopathology and prognosis in hepatocellular carcinoma.

BACKGROUND: The protein p73, the first identified homologue of the tumor suppressor gene p53 (also known as TP53), has been shown to induce apoptosis (programmed cell death), but its function in tumor development has not been established. This study was undertaken to investigate the expression of p73 in liver tissue of patients with hepatocellular carcinoma (HCC) and to determine whether this expression has any impact on prognosis. METHODS: In situ hybridization and immunohistochemistry for the detection of p73 RNA transcripts and protein, respectively, were performed in tissues from 193 patients with curatively (R0-) resected HCC. Patients receiving liver transplantation were excluded. The results obtained were analyzed with respect to their association with pathohistologic stage, Edmondson grade, p53 expression status and several histopathologic factors of possible prognostic value, and, finally, with patient survival. RESULTS: RNA transcripts encoding p73 were detected by in situ hybridization in tumor cells but not in stromal, endothelial, or inflammatory cells or in cholangiocytes. Transcripts were also found occasionally in non-neoplastic hepatocytes. By immunohistochemistry, we detected p73 protein in 61 (32%) of the 193 carcinomas examined. Positive immunohistochemical staining was confined to the cell nucleus. Univariate survival analysis showed that p73 expression status was statistically significantly related to prognosis (two-sided P<.0001). Patients with p73-positive tumors had a poorer prognosis than those with p73-negative carcinomas. Multivariate Cox survival analysis identified the age of the patient, p73 expression status, co-existing cirrhosis, and Edmondson grade as independent prognostic factors. CONCLUSION: The protein p73 is overexpressed by a subset of HCCs and could serve as a useful indicator of prognosis in patients with this disease.

Apoptosis↗

[Pyoderma gangrenosum and portal vein thrombosis in a 33-year-old female patient].

HISTORY AND CLINICAL FINDINGS: The diagnosis of pyoderma gangraenosum (PG) was made in a 33-year-old woman with ulcerative (palm-sized) skin changes and pain of the lower leg that had developed over two weeks and was accompanied by fever (39 degrees C). Treatment with prednisolone and azathioprine was initiated. As soon as the medication was reduced new skin changes developed. Two months after onset of the illness she had to be hospitalized because of fever, epigastric pain on pressure and deteriorating general condition. Physical examination provided no significant further information. LABORATORY RESULTS: The differential count demonstrated leucocytosis (15.5 Gpt/l) with a marked monocytosis (25%) as well as anaemia (haemoglobin concentration 5.2 mmol/l). C-reactive protein was elevated (120.20 mg/l). Thromboplastin time was 60%, D-dimer 1000 micrograms/l, thrombin-antithrombin-III complex 9.7 micrograms/l. ADDITIONAL INVESTIGATIONS: Sonography and computed tomography of the upper abdomen revealed splenomegaly, ascites, thrombosis of the portal, splenic and superior mesenteric veins. Bone marrow puncture showed marked increase in blasts (14%) and monocytes (10%). TREATMENT AND COURSE: The findings indicated chronic myelomonocytic leukaemia with PG and the described venous thromboses. The cutaneous changes completely receded on administration of hydroxyurea (1.0 g/d). Other causes of the skin eruption were excluded. Phenprocoumon (INR between 2 and 3) was given in treatment of the thromboses. CONCLUSION: When PG is diagnosed, intensive search for an underlying cause must be undertaken, because of its frequent association with serious systemic disease. Only early specific treatment will improve the skin condition.

Adult↗

Palliation of pain in chronic pancreatitis. Use of enzymes.

According to the concept of negative feedback regulation of pancreatic enzyme secretion by proteases, treatment with pancreatic extracts has been proposed to lower pain in chronic pancreatitis by decreasing pancreatic duct pressure. The author, however, has demonstrated in healthy volunteers that intraduodenal application of porcine pancreatic extracts does not inhibit but rather stimulates pancreatic enzyme secretion. This is probably because of the high-protein content of porcine pancreatic extracts that may overwhelm a potential inhibitory effect of proteases. In a prospective placebo-controlled, double-blind multicenter study to investigate the effect of acid-protected porcine pancreatic extracts on pain in 43 patients with chronic pancreatitis, pain improved in most patients regardless of whether they started with placebo or verum. There was no significant difference between both treatment arms. In a meta-analysis, which included the author's study, six randomized, double-blind, placebo-controlled studies were evaluated. Statistical analysis demonstrated no benefit of the application of porcine pancreatic extracts to relieve pain in chronic pancreatitis. The author concluded that pancreatic extracts neither inhibit pancreatic enzyme secretion nor are they efficient in lowering pain in chronic pancreatitis.

Animals↗

Expression of p73, a novel protein related to the p53 tumour suppressor p53, and apoptosis in cholangiocellular carcinoma of the liver.

p73, the first homologue of the tumour suppressor protein p53, was recently discovered on chromosome 1p36 and has been shown to induce apoptosis in a p53-like manner. The present study was performed with the aim of investigating the expression of p53, its new homologue p73 and the occurrence of apoptosis in cholangiocellular carcinoma. Protein levels of p73 were examined in 41 patients with curatively (R0-) resected cholangiocellular carcinomas with an antiserum, raised against a peptide in the N-terminal domain of p73. The incidence of mutations in the p53 gene was analysed by direct sequencing and also immunohistochemically. Apoptotic cell death was assessed using in-situ end-labelling (ISEL) technique in combination with morphological criteria. The results obtained were correlated with patient survival. Immunostaining of p73 protein was detected in 17/41 carcinomas examined (41%). The immunoreactivity was confined to the cell nucleus. In 15/41 patients (37%), mutations of the p53 gene were observed. Eleven out of these 15 patients stained also positive for p73. In contrast, out of 26 patients without any detectable p53 mutation, only six exhibited p73 immunostaining. We failed to observe a correlation between p73 expression or p53 and apoptosis within a given tumour. Survival analysis including the parameters stage and grade of disease, p73 and p53, and also apoptosis, showed that tumour stage and grade as well as p53 and p73 were significantly related to prognosis. In Cox regression survival analysis, however, only extent of primary tumour and lymph node status had an independent prognostic impact. Our results with a high prevalence of p73 within tumours harbouring mutated p53 gene suggest that p73 could compensate for p53 function. We failed to establish p73 or p53 as independent prognostic factors in cholangiocellular carcinoma of the liver.

Apoptosis↗

A double-blind, randomized, multicentre, crossover study to prove equivalence of pancreatin minimicrospheres versus microspheres in exocrine pancreatic insufficiency.

BACKGROUND: Modern pancreatin preparations consist of enteric-coated microspheres to protect the enzymes from gastric acid. There are, however, no clinical trials comparing different sizes of pancreatin microspheres with regard to fat excretion and fat intake. AIM: To prove both equivalent efficacy and safety of conventional pancreatin microspheres and smaller pancreatin minimicrospheres in patients with exocrine insufficiency due to chronic pancreatitis. METHODS: In this prospective, randomized, double-blind, multicentre, crossover trial, patients with a stool fat excretion of > 7.5 g/day during a placebo period were randomly assigned either to the minimicrosphere/microsphere treatment sequence or vice versa. The primary end-point was the coefficient of fat absorption, which was calculated from fat excretion and fat intake during the course of a standardized diet. Stool weight, clinical symptoms and the safety of the preparations were also evaluated. RESULTS: Thirty-seven patients entered the study, of whom 23 fulfilled the criteria for the crossover period. In the per protocol analysis (n=18), the 90% confidence intervals for the coefficient of fat absorption of both crossover periods lay entirely within the equivalence range (P=0.02). The intention-to-treat analysis revealed similar results, but the equivalence range was slightly missed (P=0.07). Similar results were obtained for the secondary parameters and the reported adverse events. CONCLUSIONS: Pancreatin minimicrospheres have been shown to be equally effective as microspheres in improving the coefficient of fat absorption in patients with exocrine insufficiency due to chronic pancreatitis.

Adult↗

The pancreatitis-associated protein in hereditary and chronic alcoholic pancreatitis.

The pancreatitis-associated protein (PAP) was investigated in patients with hereditary and chronic alcoholic pancreatitis. Blood levels of pancreatic enzymes and PAP were measured in nine families with hereditary pancreatitis; in three of them, the mutation N21I, and in six, the R117H variant of the cationic trypsinogen were present. In all family members, similar to controls, only normal values of the PAP were found. There was no evidence for polymorphism of the PAP gene in patients with hereditary or alcoholic pancreatitis. Immunohistochemically PAP was detected in the apical parts of the acinar cells but not in ducts, interstitial tissue, islets, or blood vessels. Intensity of PAP labeling was directly related to the deterioration of the acinar units, and its concentration was inversely related to chymotrypsinogen immunoreactivity in the same tissue. Similar immunohistochemical findings were present in chronic alcoholic and hereditary pancreatitis. We conclude that there is a lack of PAP polymorphism in hereditary and alcoholic pancreatitis and that expression of the PAP in both groups of patients is related to the degree of cellular damage of the pancreas.

Acute-Phase Proteins↗

Screening for mutations of the cationic trypsinogen gene: are they of relevance in chronic alcoholic pancreatitis?

BACKGROUND: In hereditary pancreatitis mutations of exons 2 (N21I) and 3 (R117H) of the cationic trypsinogen gene have been described. AIMS: To investigate whether the same mutations can also be found in patients with chronic alcoholic pancreatitis. METHODS: Leucocyte DNA was prepared from 23 patients with chronic alcoholic pancreatitis, 21 with alcoholic liver cirrhosis, 34 individuals from seven independent families with hereditary pancreatitis, and 15 healthy controls. DNA was also obtained from pancreatic tissue (n=7) and from pancreatic juice (n=5) of patients suffering from chronic alcoholic pancreatitis. R117H was detected by restriction digestion with Afl III. N21I was identified by an allele specific polymerase chain reaction (PCR). RESULTS: R117H was detected in four families with hereditary pancreatitis. The N21I mutation was identified in three families. All mutations were confirmed by sequencing of the corresponding DNAs. In patients with chronic alcoholic pancreatitis neither the exon 2 nor exon 3 mutations were present in blood leucocytes, pancreatic juice, or pancreatic tissue. DNA of the patients with alcoholic liver cirrhosis as well as all controls was of wild type. CONCLUSIONS: The allele specific PCR may be used to screen for the N21I mutation of cationic trypsinogen. Both trypsinogen mutations were found in hereditary pancreatitis but do not seem to be major pathogenic factors in chronic alcoholic pancreatitis.

Adult↗

Cationic proteins inhibit L-arginine uptake in rat alveolar macrophages and tracheal epithelial cells. Implications for nitric oxide synthesis.

Eosinophil-derived cationic proteins play an essential role in the pathogenesis of bronchial asthma. We tested whether cationic proteins interfere with the cationic amino-acid transport in alveolar macrophages (AMPhi) and tracheal epithelial cells, and whether L-arginine-dependent pathways were affected. The effect of cationic polypeptides on cellular uptake of [(3)H]-L-arginine, nitrite accumulation, and the turnover of [(3)H]-L-arginine by nitric oxide (NO) synthase and arginase (formation of [(3)H]-L-citrulline and [(3)H]-L-ornithine, respectively) were studied. Poly-L-arginine reduced [(3)H]-L-arginine uptake in rat AMPhi and tracheal epithelial cells in a concentration-dependent manner (at 300 microgram/ml by 70%). Poly-L-lysine, protamine, and major basic protein (each up to 300 microgram/ml) tested in rat AMPhi inhibited [(3)H]-L-arginine uptake by 35 to 50%. During 6 h incubation in amino acid-free Krebs solution, rat AMPhi, precultured in the absence or presence of LPS (1 microgram/ml), accumulated 1.4 and 3.5 nmol/10(6) cells nitrite, respectively. Addition of 100 microM L-arginine increased nitrite accumulation by 70 and 400% in control and lipopolysaccharide-treated AMPhi, respectively. Nitrite accumulation in the presence of L-arginine was reduced by poly-L-arginine and poly-L-lysine (100 and 300 microgram/ml) by 60 to 85% and 20 to 30%, respectively. Poly-L-arginine, but not poly-L-lysine, inhibited nitrite accumulation already in the absence of extracellular L-arginine. Poly-L-arginine (300 microgram/ml) inhibited [(3)H]-L-citrulline formation by AMPhi stronger than that of [(3)H]-L-ornithine. We conclude that cationic proteins can inhibit cellular transport of L-arginine and this can limit NO synthesis. Poly-L-arginine inhibits L-arginine uptake more effectively than other cationic proteins and exerts additional direct inhibitory effects on NO synthesis.

Animals↗

Relative versus absolute carbohydrate-deficient transferrin as a marker of alcohol consumption in patients with acute alcoholic hepatitis.

BACKGROUND: Carbohydrate-deficient transferrin has been described as a sensitive and specific marker for alcohol consumption. This study investigated the usefulness of carbohydrate-deficient transferrin as a marker of alcohol consumption in acute alcoholic hepatitis. METHODS: Absolute concentrations (U/I) and relative values (%) of carbohydrate-deficient transferrin determined in serum with commercial assays, as well as conventional markers for alcohol consumption, were compared with the alcohol consumption (as estimated by a questionnaire) in patients with acute alcoholic hepatitis (n = 19), alcoholic liver cirrhosis (n = 37), and nonalcoholic liver diseases (n = 16). RESULTS: The concentration of carbohydrate-deficient transferrin was increased (p < 0.001) in nonabstaining patients (median intake 80 g alcohol/day) with alcoholic liver cirrhosis (45.7 +/- 30 U/l), but not in patients with acute alcoholic hepatitis (20.0 +/- 7.8 U/l) despite higher alcohol consumption (median 130 g/d), nor in abstainers with alcoholic liver cirrhosis (19.4 +/- 6.0 U/l) or nonalcoholic liver disease (18.5 +/- 6.7 U/l). However, the relative values of carbohydrate-deficient transferrin were increased both in acute alcoholic hepatitis (7.9 +/- 2.1%) and nonabstainers with alcoholic liver cirrhosis (7.4 +/- 2.8%), but not in abstainers with alcoholic liver cirrhosis (4.6 +/- 3.5%) or nonalcoholic liver disease (3.8 +/- 0.9%) (p < 0.001). In acute alcoholic hepatitis, the sensitivity and specificity were only 32% and 87% for absolute concentrations, respectively, but 79% and 97% for relative values of carbohydrate-deficient transferrin. The concentrations of carbohydrate-deficient and total transferrin in serum were strongly correlated (r = 0.60; p = 0.008). CONCLUSIONS: The relative value (% of total), but not the absolute concentration, of carbohydrate-deficient transferrin in serum is a useful marker of alcohol consumption in acute alcoholic hepatitis.

Adult↗

A phase II pilot trial of 13-cis retinoic acid and interferon-alpha in patients with advanced pancreatic carcinoma.

BACKGROUND: Advanced unresectable pancreatic adenocarcinoma has a dismal prognosis. The authors previously have shown that retinoic acid (RA) and interferon-alpha (IFN-alpha) inhibit growth and induce differentiation in human pancreatic carcinoma cells in vitro and in vivo. The purpose of this trial was to examine the feasibility and tolerability of a combination therapy of 13-cis RA and IFN-alpha in patients with advanced unresectable pancreatic carcinoma. METHODS: Twenty-two patients (median age, 62 years) with histologically confirmed, unresectable pancreatic adenocarcinoma classified as International Union Against Cancer Stage III (5 patients) or IV (17 patients) were included. Patients received 1 mg/kg body weight 13-cis RA orally and 6 million IU IFN-alpha subcutaneously daily. Restaging by ultrasound, computed tomography scan, and chest X-ray was performed every 2 months. RESULTS: No complete remission and 1 partial remission (PR) (4.5%) were observed. Fourteen patients (63.6%) demonstrated stable disease with a median duration of 5.0 months (range, 2.3-17.7+ months). Toxicity mainly was related to IFN-alpha and predominantly was hematologic (no toxicity was World Health Organization [WHO] Grade 4 and 13.6% were WHO Grade 3). Nonhematologic toxicities did not exceed Grade 2 (skin and oral mucosa) and mainly were related to 13-cis RA. The median survival of the patients with Stage III disease was 8.7 months (range, 6.8-23.9+ months) and was 7.4 months for patients with Stage IV disease (range, 0.9-19.2+ months), resulting in a median overall survival of 7.7 months (range, 0.9-23.9+ months). CONCLUSIONS: Combination therapy with 13-cis RA and IFN-alpha is feasible and well tolerated in patients with advanced pancreatic carcinoma. Based on the median survival rates observed in this study this combination should be investigated further in Phase III trials.

Adenocarcinoma↗

[Chronic pancreatitis: nutrition and pain therapy].

Therapy of chronic pancreatitis rests on five arms: Avoidance of alcohol, treatment of pain, replacement therapy for exocrine and endocrine insufficiency and adequate nutrition. Alcohol withdrawal improves pain and the patient's compliance. It also seems to retard the chronic inflammatory process. Therapy of pain depends on the pathomechanism of pain. There is a lack of prospective, controlled studies comparing various treatment regimens. Thus, treatment options are partly dependent on the experience of the physician taking care of the patient and include i.e. for pseudocysts: surgical vs percutaneous or endoscopic drainage; for stenosis of the main pancreatic duct close to the papilla: surgical vs endoscopic drainage (stents); for distal bile duct stenosis: endoscopic stents vs biliodigestive anastomosis vs pancreatic head resection; for pancreatic stones: extracorporal shock wave lithotripsy followed by endoscopic stone extraction vs surgery (pancreaticojejunostomy), finally for inflammatory tumor of the pancreatic head combined with pain with or without compression of the distal bile duct or duodenum: duodenum-preserving pancreatic head resection vs Whipple resection. Patients with pain resistant to medical treatment may be candidates for a transcutaneous blockade of the plexus coeliacus or for epidural nerve blockade before one choses a surgical procedure. Application of pancreatic enzymes does not seem to have a major beneficial effect on pancreatic pain. Modification of nutrition has become less restrictive. Thanks to improved substitution with acid resistant porcine pancreatic extracts with high lipase activity, fat restriction is no longer of paramount importance. However, supply with sufficient calories is still difficult due to pain, inadequate compliance and hypermetabolism.

Chronic Disease↗

Activation of L-arginine transport by protein kinase C in rabbit, rat and mouse alveolar macrophages.

1. The role of protein kinase C in controlling L-arginine transport in alveolar macrophages was investigated. 2. L-[3H]Arginine uptake in rabbit alveolar macrophages declined by 80 % after 20 h in culture. 4beta-Phorbol 12-myristate 13-acetate (PMA), but not 4alpha-phorbol 12-myristate 13-acetate (alpha-PMA), present during 20 h culture, enhanced L-[3H]arginine uptake more than 10-fold. Staurosporine and chelerythrine opposed this effect. 3. L-[3H]Arginine uptake was saturable and blockable by L-lysine. After PMA treatment Vmax was increased more than 5-fold and Km was reduced from 0.65 to 0.32 mM. 4. Time course experiments showed that PMA increased L-[3H]arginine uptake almost maximally within 2 h. This short-term effect was not affected by cycloheximide or actinomycin D. 5. L-[3H]Arginine uptake and its stimulation by PMA was also observed in sodium-free medium. 6. L-Leucine (0.1 mM) inhibited L-[3H]arginine uptake by 50 % in sodium-containing medium, but not in sodium-free medium. At 1 mM, L-leucine caused significant inhibition in sodium-free medium also. L-Leucine showed similar effects on PMA-treated cells. 7. N-Ethylmaleimide (200 microM, 10 min) reduced L-[3H]arginine uptake by 70 % in control cells, but had no effect on PMA-treated (20 or 2 h) cells. 8. In alveolar macrophages, multiple transport systems are involved in L-arginine uptake, which is markedly stimulated by protein kinase C, probably by modulation of the activity of already expressed cationic amino acid transporters.

Amino Acid Transport Systems, Basic↗

[Vulvar involvement as a rare extra-intestinal manifestation of Crohn disease].

BACKGROUND: Crohn's disease may involve all parts of the gastrointestinal tract. Extraintestinal manifestations with and without continuity to the intestine are described. The most common complications are the involvement of bone (articulations), liver and eyes. Crohn's disease of the vulva is rare and only a few cases have been reported in the literature. CASE REPORT: The 45-year-old woman has a 15-year history of a marked chronic-inflammatory bowel disease. The diagnosis of Crohn's disease was never confirmed histologically. In 1984, she developed a painful vulvar swelling and erythema. A fungal infection was suspected and she was treated with topical antimycotic medication, but there wasn't any improvement. In July 1995, biopsies of the vulva showed a granulomatous inflammation consistent with Crohn's disease. Oral metronidazol therapy (20 mg/kg/day) was started. After 2 months, the erythema had healed completely but the vulvar swelling remained. CONCLUSIONS: The treatment of this extraintestinal manifestation is very difficult. Systemic or topical application of steroids is without response in most cases. Surgical excision showed good results in a few cases. A long-term treatment with oral metronidazol 20 mg/kg/day could be a chance for healing without adverse effects.

Administration, Oral↗