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Rahel Hirsch, whose 150th birthday was celebrated on 15 September 2020, is one of the female pioneers of medicine in Germany. Since it was not yet possible for women to study medicine in Germany at the end of the 19th century, she initially worked as a teacher. In 1898 she went to Switzerland to study medicine, graduating in Strasbourg in 1903. From 1903 to 1919 she worked in the 2nd Medical Clinic of the Berlin Charite hospital. Due to her scientific achievements, she was the first female medical doctor in Prussia to be awarded the title of professor in 1913. Her early investigations into the permeability of the intestinal mucosa for large corpuscular particles and their renal elimination were initially met with rejection and ignorance. It took more than half a century until the phenomena she discovered found their way into the specialist literature as the "Hirsch effect". After the First World War, Rahel Hirsch worked mainly in her own practice. As a Jew during the dictatorship of the National Socialists, she was marginalised and increasingly endangered, and emigrated to England in 1938. There she lived in modest circumstances and died in London in 1953. Rahel Hirsch, who asserted herself in a male-dominated environment both as a doctor and as a scientist, is a suitable role model for those who work for more gender equality in medicine and society today.

Rahel Hirsch, whose 150

Zahlreiche historische Mitteilungen uber Krankheitsverlaufe und klinisch-pathologische Befunde legen es nahe, dass Colitis ulcerosa und der Morbus Crohn bereits in fruheren Jahrhunderten auftraten. Als Entitat wurde die Colitis ulcerosa am Ende des 19. Jahrhunderts von anderen Darmerkrankungen abgegrenzt. 1932 wurde ein eigenstandiges Krankheitsbild beschrieben, das das Eponym Morbus Crohn erhielt. Seit den 1950er Jahren haben sich die Kenntnisse zur moglichen Pathogenese sowie zur Phanomenologie beider Erkrankungen parallel zur wissenschaftlich-technischen Entwicklung mit groser Dynamik vermehrt; das Gleiche gilt fur die differenzierte medikamentose und chirurgische Therapie. Der Beitrag vermittelt eine Ubersicht von der Erstbeschreibung beider Krankheiten bis zur heutigen modernen gezielten Behandlung mit Antikorpern.

Pancreatitis as an extraintestinal manifestation of Crohn's disease (CD) is controversial. We review the episodes of acute pancreatitis in patients with CD. Of 852 patients, 12 developed clinically overt pancreatitis, representing a frequency of 1.4% in a follow-up period of 10 years. In 10 patients, common causes of pancreatitis were excluded. In 2 patients, drug-induced disease (azathioprine, sulfasalazine) could not be ruled out. Recurrence of pancreatitis was observed in only 2 patients. Younger patients and those with active disease seemed more at risk for development of pancreatitis. If prednisolone was needed for treatment of active CD, no adverse effect was observed for the pancreatitis. Along with the clinical features, we studied autoantibodies against exocrine pancreas; the incidence of autoantibodies in patients with pancreatitis was the same as in the controls who did not develop pancreatic abnormalities. This does not support the hypothesis that acute pancreatitis in CD is associated with the formation of pancreatic autoantibodies.

We report four new cases of oral manifestation in Crohn's disease (CD) and evaluate 75 reported cases for morphology and site of oral and intestinal manifestations of CD, clinical manifestation, and treatment. Oral CD was the presenting symptom in 43 of 72 (60%) patients and relapsed in 34 of 60 (57%). Median age at presentation was 22 (range 6-57) years, and males were affected more often (1.85:1, male:female ratio). From a total of 228 oral lesions in 79 patients, lips (57 lesions), gingiva (40 lesions), vestibular sulci (31 lesions), and buccal mucosa (25 lesions) were the sites most frequently affected. Edema (62 lesions), ulcers (57 lesions), and polypoid papulous hyperplastic mucosa (45 lesions) were the most common type of lesions. The rate of granuloma detection was high in oral (67-77%) and intestinal lesions (45-71%). A total of 66 courses of drug therapy in 51 patients were analyzed. Complete remission of oral symptoms was achieved by systemic steroids and/or azathioprine in 13 of 26 (50%) patients, whereas strictly topical treatment with steroids resulted in complete remission of oral symptoms in 7 of 12 (58%). We conclude that oral CD exhibits a characteristic morphologic appearance, as often as not preceding intestinal symptoms in adolescents and young adults. Thus, patients with orofacial granulomatosis CD should be vigorously searched for by complete gastrointestinal endoscopic investigation. Oral CD may cause disabling pain and facial distortion, and results of treatment remain unrewarding. In the absence of data from controlled therapeutic trials, systemic steroids and/or azathioprine are recommended if topical treatment has failed to control symptoms.

Pancreatic autoantibodies (PABs) are found in 31% of patients with Crohn's disease (CD), but they do not correlate with the activity of intestinal disease or the incidence of acute pancreatitis. Exocrine pancreatic insufficiency has been observed in patients with CD. The aim of our study was to correlate the occurrence of PABs with exocrine pancreatic function to explore the clinical significance of these antibodies. Serum samples of 64 patients with CD were tested for PABs by indirect immunofluorescence. In addition, all patients were tested for exocrine pancreatic insufficiency by a fluorescein dilaurate test. PABs were detected in 26 of 64 patients (40%). The PAB-positive and -negative groups did not differ in clinical characteristics, such as age, sex, involvement of intestine, previous surgical interventions, drug therapy, and disease activity. Seven of the antibody-positive patients (27%) had impaired pancreatic function, in contrast to three of 38 PAB-negative patients (8%) (p < 0.05). In conclusion, exocrine pancreatic function is impaired significantly more often in PAB-positive than in PAB-negative patients. A prospective follow-up is required to determine whether PAB-positive patients are more likely to develop pancreatic insufficiency later in their course of disease.

To assess the association between symptomatic relapse of inflammatory bowel disease (IBD) and superinfection with enteropathogenic microorganisms, we determined prospectively the incidence of infections with enteropathogenic bacteria, protozoa, and helminths in patients with confirmed longstanding IBD. Sixty-four patients with IBD (49 with Crohn's disease [CD] and 15 with ulcerative colitis [UC]) were consecutively enrolled in the study when relapse occurred. Multiple biopsies for histological and microbiological investigations were taken from all patients who were evaluated by colonoscopy. Parallel stool specimens were investigated for the presence of enteropathogenic bacteria, protozoa, and helminths. In six patients, we detected Clostridium difficile or toxin B (five CD, one UC), in one patient Campylobacter jejuni (CD), and in another patient Salmonella typhimurium (UC). Enteropathogenic Escherichia coli were isolated from three patients. Investigation of biopsies for Mycobacteria, microscopic examination of stool samples for helminths, and immunofluorescence for chlamydia were negative in all patients. In summary, as we found enteropathogenic microorganisms so infrequently in patients with relapse of IBD, despite intensive microbiological screening by tissue sampling for detection of gut adherent bacteria, we believe that microorganisms play only a minor role in the exacerbation of IBD.

With its mucosal surface thought to be 200 times the body surface area, the gastrointestinal tract is a major route of exposure to pathogenic organisms and environmental chemicals. Food- and water-borne chemicals enter the body via the gastrointestinal tract. Most agents are ingested; however, some inhaled substances are swallowed after being trapped in the mucus of the respiratory tract. Thus, apart from its classic role of nutrient absorption, the gastrointestinal tract must also protect the body from environmental assault (83, 89, 109, 137, 166).