Introduction

Intestinal ultrasound (IUS) is a non-invasive method that is increasingly used to monitor disease activity in patients with inflammatory bowel disease.¹ There is currently no consensus on the appropriate implementation of IUS to assess post-surgical recurrence in Crohn’s disease (CD). ​

Aims & Methods

The aim of this study was to determine appropriate parameters for evaluating postoperative recurrence of CD using IUS after surgery. The modified RAND-University of California Los Angeles appropriateness method (RAM)² was implemented using an international panel of 16 experts, including gastroenterologists, surgeons, radiologists, and methodologists, to evaluate the appropriateness of statements related to using IUS for assessing postoperative recurrence of CD. This exercise specifically focused on assessing the anastomosis, neoterminal ileum after ileocecal resection, and primary anastomosis in CD. To inform statement generation for the RAM, a systematic review was performed to identify parameters described in the literature for the sonographic evaluation of postoperative disease recurrence in patients with CD. Statements were developed focusing on when, where, and how sonographic parameters should be assessed after surgery. Panellists voted anonymously in 2 rounds of surveys containing up to 122 statements, rating each statement for appropriateness on a 9-point Likert scale (1=highly inappropriate; 5=uncertain; 9=highly appropriate). Median appropriateness ratings were summarised, and interquartile ranges were calculated. The statement list and survey results were discussed in moderated videoconferences prior to voting. The panellists met in person to discuss the results and ratify the final statements.

Results

After 2 rounds of voting, 80% of the statements were rated as appropriate with agreement. IUS findings in the neoterminal ileum and the inlet of the neoterminal ileum were considered likely to reflect clinically meaningful disease. Recognising that immediate postoperative changes related to surgical healing may mimic CD, IUS should not be performed within 4 weeks of resection in the context of evaluating postoperative recurrence. Defining the entire component of the anastomosis as consisting of colonic blind side, ileal blind side, neoterminal inlet, and neoterminal ileum, if any were visible/present, was considered appropriate by the panellists. However, there was uncertainty with describing and measuring thickening within the blind loops and whether those segments represent postoperative recurrence. Use of bowel wall thickness, bowel wall stratification, bowel wall vascularity on Doppler, mesenteric inflammatory fat, lymphadenopathy, submucosal layer thickness, muscularis propria layer thickness, small bowel peristalsis, free fluid, abscess, inflammatory mass, fistula/sinus tract, anastomotic or neoterminal ileal stricture, luminal narrowing, pre-stenotic dilation, and stricture length were considered appropriate to assess postoperative CD recurrence, and parameters for each component were identified.

Conclusion

This first set of internationally guided recommendations (Table) for using IUS to assess postoperative recurrence of CD has been developed to facilitate standardisation of a non-invasive method of monitoring patients following surgical bowel resection.

References

¹ Dolinger MT, Kayal M. Intestinal ultrasound as a non-invasive tool to monitor inflammatory bowel disease activity and guide clinical decision making. World J Gastroenterol. 2023;29(15):2272-2282. Doi: 10.3748/wjg.v29.i15.2272
² Fitch K, Bernstein SJ, Aguilar MD, et al. The RAND/UCLA Appropriateness Method User’s Manual. Santa Monica, CA: RAND Corporation, 2001.

Disclosure

KLN has received consulting fees from AbbVie, Bristol Myers Squibb, Celltrion, Ferring, Fresenius Kabi, Janssen, McKesson, Pendopharm, Pfizer, and Takeda, with speaker's fees from AbbVie, Fresenius Kabi, Janssen, Pfizer and Takeda; and research support from Pfizer, and the Helmsley Trust.
SA has received speaker/honoraria fees from AbbVie, Fresenius Kabi, Janssen, Pfizer, and Takeda; and received research grants from A.I Vali and ATGen.
MA received consulting fee from Nikkiso Europe, Mundipharma, Janssen, AbbVie, Ferring, Galapagos, Alfasigma, Lilly, Sandoz, and Pfizer.
AdBvO has received speaker fees from Amgen, Takeda, and Janssen Pharmaceuticals.
PGK is a speaker and consultant for AbbVie, Celltrion, Johnson & Johnson, Pfizer and Takeda. He received scientific grants from Pfizer and Takeda, and is involved in clinical research for Ventyx, Roche, and Takeda.
CL has received advisory/consulting fees from AbbVie, Agomab, Celltrion, JnJ, Lilly, Pfizer, Takeda, Fresenius Kabi, Pendopharm, and Ferring.
CM received lecture and/or consulting fee from AbbVie, Alfasigma, Biocon Biologics, Bristol Myers Squibb, Ferring, Galapagos, Gilead, Lilly, J&J, Pfizer, and Takeda.
GM has received lectures or consulting fees from AbbVie, Janssen, Samsung, Galapagos, and Fresenius-Kabi.
RP reports being a Consultant for Abbott, AbbVie, Abbivax, Alimentiv Inc. (formerly Robarts), Amgen, Arena Pharmaceuticals, AstraZeneca, Biogen, Boehringer Ingelheim, Bristol-Myers Squibb, Celgene, Celltrion, Cosmos Pharmaceuticals, Eisai, Elan, Eli Lilly, Ferring, Galapagos, Fresenius Kabi, Genentech, Gilead Sciences, Glaxo-Smith Kline, JAMP Bio, Janssen, Merck, Mylan, Novartis, Oppilan Pharma, Organon, Pandion Pharma, Pendopharm, Pfizer, Progenity, Prometheus Biosciences, Protagonist Therapeutics, Roche, Sandoz, Satisfai Health, Shire, Sublimity Therapeutics, Takeda Pharmaceuticals, Theravance Biopharma, Trellus, Viatris, Ventyx, and UCB; reports Speaker’s Fees for: AbbVie, Amgen, Arena Pharmaceuticals, Bristol-Myers Squibb, Celgene, Eli Lilly, Ferring, Fresenius Kabi, Gilead Sciences, Janssen, Merck, Organon, Pfizer, Roche, Sandoz, Shire, and Takeda Pharmaceuticals; and reports Advisory Boards for: AbbVie, Alimentiv Inc. (formerly Robarts), Amgen, Arena Pharmaceuticals, AstraZeneca, Biogen, Boehringer Ingelheim, Bristol-Myers Squibb, Celgene, Eli Lilly, Ferring, Fresenius Kabi, Genentech, Gilead Sciences, Glaxo-Smith Kline, JAMP Bio, Janssen, Merck, Mylan, Novartis, Oppilan Pharma, Organon, Pandion Pharma, Pfizer, Progenity, Protagonist Therapeutics, Roche, Sandoz, Shire, Sublimity Therapeutics, Takeda Pharmaceuticals, and Ventyx.
MR reports receiving consulting/advisory fees from AbbVie, Janssen, UCB, Takeda, Pfizer, BMS, Organon, Amgen, Genentech, Gilead, Salix, Prometheus, Lilly, Celgene, Boehringer Ingelheim Pharmaceuticals Inc. (BIPI), Celltrion, and Roche.
JR has received lectures fees from AbbVie and Takeda; is or has been advisor for Gilead, Takeda, Agomab, Janssen, Boehringer Ingelheim, Lumen, Ferring, and Bracco; and has received consultant fees from Alimentiv Inc. He received scientific grants from Takeda and AbbVie.
AS has received consulting fees from Stryker and Johnson and Johnson.
SAT reports grant support from Takeda; consultancy with AstraZeneca; and shareholder of Motilent.
RW reports speaker or consultancy fees by Alimentiv Inc, Pfizer, Takeda, J&J, and Nautilus Scientific.
WAB reports no competing interests.
NKC reports being a Consultant for Samsung and Speaker for Bristol-Myers Squibb.
KBG has received grants from AbbVie, Pfizer Inc., Celltrion and Galapagos; consultancy fees from AbbVie, Eli Lilly, Galapagos, Gilead, Janssen Pharmaceuticals, Pfizer Inc., Samsung Bioepis, and Takeda; and speaker’s honoraria from AbbVie, Celltrion, Eli Lilly, Ferring, Janssen Pharmaceuticals, Pfizer Inc, Takeda, and Tillotts.
SA, SK, and LJC are employees of Alimentiv Inc.
CM has received consulting fees from AbbVie, Alimentiv Inc., Amgen, AVIR Pharma Inc, Bristol Myers Squibb, Celltrion, Ferring, Fresenius Kabi, Janssen, McKesson, Mylan, Pendopharm, Pfizer, Prometheus Biosciences Inc., Roche, Sanofi, Takeda, and Tillotts Pharma; speaker's fees from AbbVie, Amgen, AVIR Pharma Inc, Alimentiv Inc., Bristol Myers Squibb, Ferring, Fresenius Kabi, Janssen, Organon, Pendopharm, Pfizer, Sanofi, and Takeda; royalties from Springer Publishing; and research support from AbbVie, Ferring, and Pfizer.

Introduction

Primary thromboprophylaxis is used in the post-partum and the post-surgical period. 2014 Canadian Association of Gastroenterology guidelines and a 2021 Nature Reviews consensus recommend outpatient thromboprophylaxis only for those ambulatory inflammatory bowel disease (IBD) patients at high risk of thromboembolic events.

Aims & Methods

We aimed to analyse our inpatient burden and our rate of post-discharge thromboembolic (TEEs) in those with primary and secondary diagnoses pertaining to IBD. We also aimed to identify associated risk factors.
Our hospital inpatient and radiology databases were queried for discharges with primary and secondary diagnoses pertaining to IBD and scans pertaining to TEEs respectively.

Results

1,601 discharges pertaining to 954 individual patients were identified over the 13-years ended 2024. 54% (n=870) were female. Median age was 44 (IQR:32-59). 58% (n=932) pertained to Crohn’s disease.
Investigations for TEEs were performed during 117 admissions (7.3%). 10 patients had inpatient TEEs (0.6%). Age ≥ 50 years was significantly associated with inpatient TEE (Odds ratio [OR]: 1.89; 95% confidence intervals [CI]: 1.13-3.16; p=0.01). Male gender (OR: 0.92; 95% CI: 0.59-1.44; p=0.72), ulcerative colitis subtype (OR: 1.51; 95% CI: 0.95-2.41; p=0.08) and inpatient surgical intervention (OR: 1.39; 95% CIs: 0.89-2.17; p=0.15) were not significant associated factors.
63 discharges (3.9%) had imaging querying TEEs performed within 180 days. Six patients (0.4%) had TEEs within this time frame. No significant associations were identified for age ≥50 years (OR: 1.16; 95% CIs: 0.68-1.99; p=0.59), male gender (OR: 0.84; 95% CIs: 0.48-2.17; p=1.47, p=0.55), ulcerative colitis subtype (OR: 1.12; 95% CIs: 0.65-1.91; p=0.68), inpatient surgical intervention (OR: 1.37; 95% CIs: 0.79-2.35; p=0.26) or prior VTE (OR not calculable) in relation to post-discharge TEEs.

Conclusion

Our incidences of inpatient and post-discharge TEEs were low over 13-years. In agreement with international guidelines, we recommend against the need for routine primary prophylaxis in the post-discharge ambulatory period.

References

1. Nguyen GC, Bernstein CN, Bitton A, et al. Consensus statements on the risk, prevention, and treatment of venous thromboembolism in inflammatory bowel disease: Canadian Association of Gastroenterology. Gastroenterology. 2014;146(3):835-848.e6. doi:10.1053/j.gastro.2014.01.042
2. Olivera PA, Zuily S, Kotze PG, et al. International consensus on the prevention of venous and arterial thrombotic events in patients with inflammatory bowel disease. Nat Rev Gastroenterol Hepatol. 2021;18(12):857-873. doi:10.1038/s41575-021-00492-8

Introduction

Upadacitinib (UPA) has shown promising results in the pivotal trials, which require validation in clinical practice. Primary aim: To assess the durability of UPA treatment in patients with ulcerative colitis (UC). Secondary aims: To assess the short and long-term effectiveness, dose optimization and response to dosage adjustments, the impact of extraintestinal manifestations (EIM) and immunomediated diseases (IMIDs), and the tolerability of UPA in UC in a real-world setting.

Aims & Methods

Adult patients who started UPA for UC treatment at least 8 weeks prior to data collection and were part of the prospectively maintained ENEIDA registry of GETECCU were included. Patients on concomitant biologic agents or with a history of colectomy were excluded. Patients were followed-up from the first UPA dose until treatment discontinuation or the last visit. Effectiveness analysis was restricted to patients with active disease [Partial Mayo Score (PMS)>2] at UPA initiation. Clinical effectiveness was measured using PMS, and concomitant steroid use was assessed at each visit. Patients who discontinued UPA before their last visit were considered not in remission at subsequent time points (negative imputation).

Results

The study included 168 patients, 89% with active disease; 48% had been previously exposed to JAK inhibitors (JAKi), and 31% to all approved therapeutic targets. Mean time of follow-up was 5.6 months (interquartile range = 2.7-11 months). The proportion of patients under 45 mg/day of UPA was 77% at week 8 and 40% at week 16. A total of 29 patients discontinued treatment during a median follow-up time of 4.3 months. The incidence rate of UPA discontinuation was 27% per patient-year of follow-up, with no significant differences related to prior JAKi exposure (log-rank p-value > 0.05). The main reason for UPA discontinuation was loss of response (34%), with colectomy being the main subsequent treatment (21%). No predictive factors for UPA discontinuation were identified (including severity, number of previous advanced therapies, and prior JAKi exposure). Proportions of patients in steroid-free clinical remission (SFCR) were 67%, 71%, 65%, 60% and 75% at week 8, week 16, month 6, month 12 and month 18, respectively. In multivariate analysis, PMS at baseline [Odds ratio (OR) = 0.79, 95% confidence interval (CI) = 0.63-0.98] and previous exposure to JAKi (OR = 0.29, 95%CI = 0.14-0.61) were associated with lower probability of SFCR at week 8. Among 100 patients in SFCR at week 8, 13 (13%) lost response (31% per patient-year), and 10 (77%) of these had dose escalation, with 9 (90%) regaining SFCR. Of 31 patients (18%) with active EIM/IMIDs at the start of UPA, 15 (48%) showed improvement. Adverse events occurred in 45 patients (27%), with hypercholesterolemia being the most common, but no major cardiovascular or thromboembolic events were reported.

Conclusion

This study, the largest of its kind in clinical practice, confirms the short- and long-term benefits and the safety profile of UPA for UC. Although prior JAKi exposure reduced short-term effectiveness, it did not impact drug survival, indicating that UPA could be a viable option even for patients who have experienced JAKi failure.

Disclosure

María Chaparro has served as speaker, consultant or research or education funding from MSD, Abbvie, Hospira, Pfizer, Takeda, Janssen, Ferring, Shire Pharmaceuticals, Dr. Falk Pharma, Tillotts Pharma, Biogen, Gilead and Lilly.
Luisa de Castro has received grants for conference attendance from Abbvie, Johnsson and Johnsson, Takeda, Falk and Pfizer. She has received grants or participated as a speaker for Johnsson and Johnsson, Falk and Tillots.
Iago Rodríguez Lago has received financial support for traveling and educational activities from or has served as an advisory board member for Abbvie, Adacyte, Biogen, Celltrion, Chiesi, Faes Farma, Ferring, Fresenius Kabi, Galapagos, Janssen, Lilly, Mirum Pharmaceuticals, MSD, Pfizer, Roche, Takeda, and Tillotts Pharma. Research support from AbbVie. Iago Rodriguez Lago is supported by a research grant from Gobierno Vasco-Eusko Jaurlaritza [Grant No 2020111061].
Carla J. Gargallo-Puyuelo Conflicts with Abbvie, Takeda, Janssen, Ferring, Lilly.
Marisa Iborra reports grants and personal fees from MSD, Janssen, Abbvie, Takeda, Kern and Pfizer, during the conduct of the study.
Manuel Barreiro has served as a speaker, consultant and advisory member for or have received research funding from MSD, AbbVie, Janssen, Kern Pharma, Celltrion, Takeda, Gillead, Celgene, Pfizer, Sandoz, Biogen, Fresenius, Ferring, Faes Farma, Dr. Falk Pharma, Chiesi, Gebro Pharma, Adacyte, Vifor Pharma and Oncostellae.
Ruth de Francisco has received support for conference attendance, and research support from AbbVie, Faes Pharma, Ferring, Janssen, Pfizer, Takeda, and Galapagos.
R Pajares Villarroya has received financial support for educational activities from Takeda.
Trapero Martínez Ana María Conflict of interest; Abbvie, Jansen, Lilly, MSD.
Lara Arias García scientific advice, research support and/or training activities for Abbvie FAES Pharma, Kern Pharma, Ferring and MSD.
Raquel Camargo has received funding for different types of training activities from Johnson&Johnson, Avbbie, Pfizer, Ferring, Falk and Galapagos.
Margalida Calafat has served as a speaker or has received research or education funding or advisory fees from Takeda, Janssen, Faes Farma, Falk, Abbvie, Pfizer, Adacyte Therapeutics, Ferring, Gilead, Kern Pharma, and MSD.
MT Diz-Lois Palomares has received funding for training activities/congresses/lectures: Abbvie, Ferring, Johnson and Johnson, Lilly, Takeda.
F. Bermejo has been a speaker, consultant and advisory member or has received research funding from Abbvie, Takeda, Janssen, Pfizer, Lilly, MSD, Biogen, Amgen, Galapagos, Ferring, Faes Farma, Tillotts Pharma, Chiesi, Vifor Pharma.
Marta Calvo Moya has received support for conference attendance, speaker fees, research support, and consultancy fees from AbbVie, MSD, Takeda, Janssen, Pfizer, Lilly, Shire, Chiesi, DrFalk Pharma, Faes Pharma, Ferring, Kern Pharma, and Tillotts Pharma.
MJ Casanova, has received education funding from Pfizer, Takeda, Janssen, MSD, Dr. Falk, Shire, Ferring, Galápagos and Abbvie.
Francisco Mesonero has received funding for educational activities, conferences and scientific advice/consultations from MSD, AbbVie, Takeda, Janssen, Pfizer, Ferring, Kern Pharma, Dr. Falk Pharma, Celltrion Healthcare, Galapagos, Chiesi, Tillots Pharma and Faes Farma.
Yamile Zabana has received support for conference attendance, speaker fees, research support and consulting fees from: AbbVie, Adacyte, Alfa-Sigma, Almirall, Amgen, Boehringer Ingelheim, Dr Falk Pharma, FAES Pharma, Fresenius Kabi, Ferring, Galapagos, Janssen, J&J, Kern, Lilly, MSD, Otsuka, Pfizer, Sanofi, Shire, Takeda, Tillots.
Mónica Sierra has participated as a speaker and attended courses financed by MSD, Abbvie, Takeda, Pfizer, Lilly, Ferring, Sandoz.
B Caballol has received support for congress and conference attendance, speaker fees, research support or consulting fees from Abbvie, Ferring, Janssen, Pfizer, Takeda, Galapagos, Kern Pharma and Lilly.
Javier P. Gisbert has served as speaker, consultant, and advisory member for or has received research funding from MSD, Abbvie, Pfizer, Kern Pharma, Biogen, Mylan, Takeda, Janssen, Roche, Sandoz, Celgene/Bristol Myers, Gilead/Galapagos, Lilly, Ferring, Faes Farma, Shire Pharmaceuticals, Dr. Falk Pharma, Tillotts Pharma, Chiesi, Casen Fleet, Gebro Pharma, Otsuka Pharmaceutical, Norgine and Vifor Pharma.

Introduction

Total retocolectomy with ileal pouch anal anastomosis (IPAA) is the surgical procedure of choice for patients with ulcerative colitis (UC) refractory to clinical treatment and familial adenomatous polyposis (FAP) with many polyps in the rectum. Primary ileitis of the ileal pouch (IP) is one of the most common complications in UC, being rare in FAP. Previous studies have identified an increase in pro-inflammatory cytokines, as well as alterations in the apoptosis and macroautophagy pathways markers in the IP mucosa of UC patients, compared to those with FAP and normal distal ileum (controls). Since autophagy and apoptosis can be modulated by endoplasmic reticulum (ER) stress, we investigated this pathway in IP of UC compared to PAF and controls.

Aims & Methods

The aim was to evaluate the modulation of ER stress in the IP mucosa of UC and FAP patients who underwent IPAA, compared to controls. Thirty-two patients were included, ten in the UC group, twelve in FAP group and ten in the control group. Patients who had undergone ileostomy closure for less than one year and had clinical, histological, or endoscopic evidence of pouchitis were excluded. The patients underwent routine colonoscopy, and biopsies were performed from the IP. For the control group, biopsies were taken from the normal distal ileum. The local Ethics Committee approved the study. The biopsies were processed for RNA extraction and subsequent gene expression analysis using the quantitative PCR (qPCR) technique. The following transcripts were investigated: IRE1 (ERN), PERK (EIF2AK3), ATF6, GRP78 (HSPA5), GRP94 (HSP90B1), ATF3, STC2, DDIT3, DNAJC3, and CALR. Nonparametric tests were used for statistical analysis, with a significance level of p<0.05.

Results

The pouchitis disease activity index (PDAI) was applied to verify the absence of pouchitis, with all patients scoring lower than 7. There was no increase in the transcriptional level of the main ER stress pathway markers (ERE1, PERK, and ATF6) in the IP without pouchitis. However, there was a significantly lower expression of DDIT3 in the UC and FAP groups compared to the control (p≤0.05), which may suggest a deficiency in counterbalance the ER stress activation. On the other hand, concerning the UPR pathway markers, the levels of CALR and HSP90B1 were significantly higher in the IP of UC compared to the respective IP afferent loop (p≤0.05), supporting potential activation of the ER stress in the IP in the UC group. Additionally, the transcriptional level of ATF3 was significantly higher in the PAF group compared to the control (p≤0.05), which may indicate a counter-regulatory mechanism in response to tissue damage, which was not verified in the UC group.

Conclusion

Our findings demonstrated that markers of the unfolded protein response (UPR) signaling pathway, which is activated in response to ER stress, are modulated in the IP mucosa of UC patients, even in the absence of pouchitis. These results may explain the propensity to IP inflammation in UC patients. They may guide the identification of additional molecular pathways contributing to inflammation of the IP and the search for new therapeutic targets.

References

1. Negreiros LMV, Pascoal LB, Genaro LM, et al. Pouchitis: insight into the pathogenesis and clinical aspects. Am J Transl Res. 2022 Jul 15;14(7):4406-4425.
2. Rodrigues BL, Dotti I, Pascoal LB, et al. Endoplasmic Reticulum Stress in Colonic Mucosa of Ulcerative Colitis Patients Is Mediated by PERK and IRE1 Pathway Activation. Mediators Inflamm. 2022 Feb 9;2022:6049500.
3. Paiva NM, Pascoal LB, Negreiros LMV, et al. Ileal pouch of ulcerative colitis and familial adenomatous polyposis patients exhibit modulation of autophagy markers. Sci Rep. 2018 Feb 8;8(1):2619.
4. Qiao D, Zhang Z, Zhang Y, Chen Q, Chen Y, Tang Y, et al. Regulation of Endoplasmic Reticulum Stress-Autophagy: A Potential Therapeutic Target for Ulcerative Colitis. Front Pharmacol. 2021;Volume 12-2021.

Clinical Case Summary

Background: Chronic intestinal pseudo-obstruction (CIPO) is a rare syndrome in which the symptomatology of intestinal obstruction occurs without any mechanical cause. This syndrome may reveal or complicate celiac disease during follow-up.
Cases presentation: We report two cases of 40 and 24-year-old women. The first is followed since the age of 8 for celiac disease on a poorly followed gluten-free diet and consulted for repeated pseudo-occlusive syndromes. the second was admitted to the surgery department for a recurrent occlusive syndrome which resolves after gastric aspiration, then referred to our service for exploration of chronic diarrhea. For both, no mechanical obstruction was found. Ionic disorders and lymphoma were also ruled out. The diagnostic of CIPO was retained. The intestinal mucosal biopsy was characteristic of celiac disease. The evolution was favorable under a gluten-free diet. Symptoms of CIPO never recurred.
Conclusion: Our observations highlight that CIPO may be a rare and severe complication of celiac disease, which should always be suspected since the gluten-free diet can improve symptoms and prevent recurrences.

Clinical Case Summary

A 27-year-old woman is admitted to a tertiary hospital for a sudden painful wound on the inner side of her upper arm. The patient stated that she had been diagnosed with ulcerative colitis 6 years ago and had been treated with prednisone and mesalazine, but was currently in remission and discontinued treatment. She was treated twice in the surgical ward for similar ulcers 2-3 years ago. Physical examination revealed a redness of ~10x6 cm in the lower third of the left upper arm and a necrotic area of 3 cm in the middle of the upper arm which was very painful to palpate. The patient was hospitalized for suspected extraintestinal signs of ulcerative colitis, but colonoscopy revealed no changes. The wound was treated with incision, lavage, necrectomy and a/b therapy according to the culture results. During the course of treatment, the patient developed a new skin lesion on the right hip and an unexpected decrease in prothrombin from 70% to 6%, which normalized after vitamin K injections. A wound biopsy revealed necrotic-inflammatory lesions, differentiating between autoimmune vasculitis and possible chemical damage. Suspecting a factitious disorder (Munchausen syndrome) the patient's rucksack was searched and syringes together with a small vial of liquid (subsequently identified as formalin) were found. Furthermore, it was revealed that patient's son was treated for 10 months in the other hospital due to deep necrotic wounds that are difficult to heal, immunodeficiency of unknown origin, repeated disruptions in the coagulation system (prothrombin 3%) and dead at age 11 month from secondary sepsis 2 years ago.
The hospital appealed to the prosecutor's office, a forensic psychiatric expert found the patient guilty, and the court sentenced her to 16 years' imprisonment for killing her son.