case presentation of ulcerative colitis

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The colon is a long tube-like organ in the abdomen. It's the largest part of the large intestine. The colon carries waste to be expelled from the body. The rectum makes up the last several inches of the colon.

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Ulcerative colitis (UL-sur-uh-tiv koe-LIE-tis) is an inflammatory bowel disease (IBD) that causes inflammation and ulcers (sores) in your digestive tract. Ulcerative colitis affects the innermost lining of your large intestine, also called the colon, and rectum. In most people, symptoms usually develop over time, rather than suddenly.

Ulcerative colitis can be draining and can sometimes lead to life-threatening complications. While it has no known cure, there are several new treatments that can greatly reduce signs and symptoms of the disease and bring about long-term remission.

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Ulcerative colitis symptoms can vary, depending on the severity of inflammation and where it occurs. Signs and symptoms may include:

Diarrhea, often with blood or pus
Rectal bleeding — passing small amount of blood with stool
Abdominal pain and cramping
Rectal pain
Urgency to defecate
Inability to defecate despite urgency
Weight loss
In children, failure to grow

Most people with ulcerative colitis have mild to moderate symptoms. The course of ulcerative colitis may vary, with some people having long periods when it goes away. This is called remission.

Health care providers often classify ulcerative colitis according to its location. Symptoms of each type often overlap. Types of ulcerative colitis include:

Ulcerative proctitis. Inflammation is confined to the area closest to the anus, also called the rectum. Rectal bleeding may be the only sign of the disease.
Proctosigmoiditis. Inflammation involves the rectum and sigmoid colon — the lower end of the colon. Symptoms include bloody diarrhea, abdominal cramps and pain, and an inability to move the bowels despite the urge to do so. This is called tenesmus.
Left-sided colitis. Inflammation extends from the rectum up through the sigmoid and descending portions of the colon. Symptoms include bloody diarrhea, abdominal cramping and pain on the left side, and urgency to defecate.
Pancolitis. This type often affects the entire colon and causes bouts of bloody diarrhea that may be severe, abdominal cramps and pain, fatigue, and significant weight loss.

When to see a doctor

See your health care provider if you experience a persistent change in your bowel habits or if you have signs and symptoms such as:

Abdominal pain
Blood in your stool
Ongoing diarrhea that doesn't respond to nonprescription medications
Diarrhea that awakens you from sleep
An unexplained fever lasting more than a day or two

Although ulcerative colitis usually isn't fatal, it's a serious disease. In some cases, ulcerative colitis may cause life-threatening complications.

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The exact cause of ulcerative colitis remains unknown. Previously, diet and stress were suspected. However, researchers now know that these factors may aggravate but don't cause ulcerative colitis.

One possible cause is an immune system malfunction. When your immune system tries to fight off an invading virus or bacterium, an irregular immune response causes the immune system to attack the cells in the digestive tract, too.

Heredity also seems to play a role in that ulcerative colitis is more common in people who have family members with the disease. However, most people with ulcerative colitis don't have this family history.

Risk factors

Ulcerative colitis affects about the same number of women and men. Risk factors may include:

Age. Ulcerative colitis usually begins before the age of 30, but it can occur at any age. Some people may not develop the disease until after age 60.
Race or ethnicity. Although white people have the highest risk of the disease, it can occur in any race. If you're of Ashkenazi Jewish descent, your risk is even higher.
Family history. You're at higher risk if you have a close relative, such as a parent, sibling or child, with the disease.

Complications

Possible complications of ulcerative colitis include:

Severe bleeding
Severe dehydration
A rapidly swelling colon, also called a toxic megacolon
A hole in the colon, also called a perforated colon
Increased risk of blood clots in veins and arteries
Inflammation of the skin, joints and eyes
An increased risk of colon cancer
Bone loss, also called osteoporosis

Ulcerative colitis care at Mayo Clinic

Feldman M, et al, eds. Epidemiology, pathogenesis, and diagnosis of inflammatory bowel diseases. In: Sleisenger and Fordtran's Gastrointestinal and Liver Disease: Pathophysiology, Diagnosis, Management. 11th ed. Elsevier; 2021. https://www.clinicalkey.com. Accessed July 22, 2020.
Goldman L, et al., eds. Inflammatory bowel disease. In: Goldman-Cecil Medicine. 26th ed. Elsevier; 2020. https://www.clinicalkey.com. Accessed July 22, 2020.
The facts about inflammatory bowel diseases. Crohn's and Colitis Foundation. https://www.crohnscolitisfoundation.org/. Accessed Sept. 6, 2022.
Ulcerative colitis. National Institute of Diabetes and Digestive and Kidney Diseases. https://www.niddk.nih.gov/health-information/digestive-diseases/ulcerative-colitis. Accessed Sept. 6, 2022.
What is ulcerative colitis? Crohn's and Colitis Foundation. https://www.crohnscolitisfoundation.org/what-is-ulcerative-colitis. Accessed Sept. 6, 2022.
Kliegman RM, et al. Inflammatory bowel diseases. In: Nelson Textbook of Pediatrics. 21st ed. Elsevier; 2020. https://www.clinicalkey.com. Accessed July 22, 2020.
AskMayoExpert. Chronic ulcerative colitis. Mayo Clinic; 2019.
Abraham B, et al. Antibiotics and probiotics in inflammatory bowel disease: When to use them? Frontline Gastroenterology. 2020; doi:10.1136/flgastro-2018-101057.
What should I eat? Crohn's and Colitis Foundation. https://www.crohnscolitisfoundation.org/diet-and-nutrition/what-should-i-eat. Accessed Sept. 6, 2022.
Mind-body therapies. Crohn's and Colitis Foundation. https://www.crohnscolitisfoundation.org/complementary-medicine/mind-body-therapies. Accessed Sept. 6, 2022.
Nguyen H. Allscripts EPSi. Mayo Clinic. April 1, 2022.
Special IBD diets. Crohn's and Colitis Foundation. https://www.crohnscolitisfoundation.org/diet-and-nutrition/special-ibd-diets. Accessed Sept. 6, 2022.
Shergill A, et al. Surveillance and management of dysplasia in patients with inflammatory bowel disease. https://www.uptodate.com/contents/search. Accessed Sept. 6, 2022.
Kashyap PC (expert opinion). Mayo Clinic. Aug. 13, 2020.
Kane SV (expert opinion). Mayo Clinic. Sept. 12, 2020.
Xeljanz, Xeljanz XR (tofacitinib): Drug safety communication — Initial safety trial results find increased risk of serious heart-related problems and cancer with arthritis and ulcerative colitis medicine. U.S. Food and Drug Administration. https://www.fda.gov/safety/medical-product-safety-information/xeljanz-xeljanz-xr-tofacitinib-drug-safety-communication-initial-safety-trial-results-find-increased?utm_medium=email&utm_source=govdelivery. Accessed Sept. 6, 2022.
Khanna S (expert opinion). Mayo Clinic. Aug. 20, 2022.
Cohen RD, et al. Management of moderate to severe ulcerative colitis in adults. https://www.uptodate.com/contents/search. Accessed Aug. 1, 2022.
Ulcerative colitis flare-ups: 5 tips to manage them

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Article Contents

Lay summary, introduction, case presentation, acknowledgment, author contributions, conflicts of interest, data availability.

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A Masking Effect: A Case of Initial Presentation of Ulcerative Colitis After Discontinuing Growth Hormone Therapy

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Onyinye Ugonabo, M'hamed Turki, Dane Stewart, Ahmed Sherif, Xavier Villa, A Masking Effect: A Case of Initial Presentation of Ulcerative Colitis After Discontinuing Growth Hormone Therapy, Crohn's & Colitis 360 , Volume 5, Issue 3, July 2023, otad041, https://doi.org/10.1093/crocol/otad041

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The inflammation and repair of the intestinal mucosa in inflammatory bowel disease (IBD) involve a complex interplay between innate, adaptive immune responses, and hormones. This may explain the relapsing clinical course of the disease.

We present the first reported case of a patient presenting their initial flare of ulcerative colitis immediately after discontinuing growth hormone (GH) therapy, suggesting treatment with GH or growth factors may prevent the development of IBD.

This is a case of a 13-year-old female with a history of GH deficiency, presenting with an 8-week history of abdominal pain, blood-stained diarrhea, and fecal calprotectin greater than 8000 mcg/g, 2 weeks after discontinuing GH therapy. The patient subsequently underwent an esophagoduodenoscopy and colonoscopy with biopsies showing histological features consistent with ulcerative colitis.

The finding of withdrawing GH or growth factors therapy potentially unmasking IBD in this patient raises a question of whether growth factors can inhibit the development of IBD and suggests beneficial effects of treatment with GH or growth factors as adjuvant therapy for IBD.

In a case of a 13-year-old patient with a history of growth hormone deficiency, she developed ulcerative colitis symptoms shortly after stopping treatment which supports the hypothesis that growth hormone may benefit inflammatory bowel disease patients as an adjuvant therapy.

Inflammatory bowel disease (IBD) is characterized by chronic recurrent inflammation of the gastrointestinal tract. The pathogenesis behind IBD is not well understood and is likely related to immune system disorders and imbalances between inflammatory mediators. Growth factors have antioxidant and anti-apoptotic properties aside from stimulating cellular differentiation. For example, epidermal growth factor (EGF) has been shown to ameliorate the effect of oxidative stress on the intestinal mucosa. Villa et al. demonstrated that pre-ischemic administration of intraluminal EGF significantly protects against intestinal ischemia-reperfusion injury in rats. 1 ; in a similar ischemia model, Arda-Pirincci et al. 2 demonstrated partially recovered intestinal mucosa architecture in rats treated with intraperitoneal EGF versus untreated rats.

Growth retardation has been recognized as a complication associated with IBD in pediatrics. It is reported to have an incidence at diagnosis ranging between 15% to 40% in Crohn’s disease (CD) and 3% to 10% in ulcerative colitis (UC). 3

The addition of growth hormone (GH) in treating children with established IBD has been previously studied. 4–6

A 13-year-old female presented from an outside facility with complaints of vague, intermittent, suprapubic abdominal pain, fatigue, and an abnormal fecal calprotectin of greater than 8000 ug/g. She also endorsed occasional blood-stained diarrhea but denied weight loss, fever, or skin rashes. Her past medical history included Kawasaki disease and GH deficiency. She was recently noted to have severe iron deficiency anemia believed to be secondary to menorrhagia (requiring blood and iron transfusions). Her home medications include ferrous sulfate and montelukast. She had a history of GH deficiency, treated with daily GH injections (1.8 mg) for 6 years, which was discontinued 2 weeks before the onset of symptoms, as the patient had achieved her expected height. The patient was pale on examination, with a height-for-age consistent with the 25th percentile. Significant laboratory findings included a white blood cell count 14.3 k/cm³, hemoglobin 10 gm/dL, platelet 506 k/µL, MCV 74.8 fL, C-reactive protein (CRP) 2.68 mg/dL, serum iron 9 ug/dL, percent iron saturation 3%, and ferritin 3 ng/mL. Other potential causes of acute colitis including infection were ruled out. esophagoduodenoscopy and colonoscopy showed erythematous gastric mucosa, congested mucosa at the appendiceal orifice, and contiguous nonbleeding ulcerated mucosa of the rectum, sigmoid colon, descending colon, and splenic flexure ( Figure 1 ). The biopsy reading showed mild-to-moderate acute inflammation, crypt architectural distortion, and increased chronic inflammatory cells in the lamina propria consistent with IBD ( Figure 2 ). The patient was treated with prednisone twice daily. The patient reported significant improvement in abdominal pain, and mesalamine was added to her medications on the 2-week follow-up clinic visit.

A, Ulcer in the terminal ileum (black arrow). B, Ulcerated rectal mucosa (black arrow).

Hematoxylin and Eosin (H&E) stains of colonoscopy biopsies from cecum (A), transverse colon (B), appendiceal orifice (C), splenic flexure (D), descending colon (E), sigmoid colon (F), rectum (G), splenic flexure higher power (H). Panels (A, B) demonstrate unremarkable colonic mucosa. While panels (C–H) display biopsies from the appendiceal orifice, splenic flexure, descending colon, sigmoid colon, and rectal biopsies show superficial fragments of colonic mucosa with mild-to-moderate acute inflammation ( black arrows ), crypt architectural distortion ( red arrows ), and increased chronic inflammatory cells in the lamina propria ( black boxes ). There is no granulomatous inflammation, dysplasia, or malignancy. Panels (A–G) were taken at 10X magnification. Panel (H) was taken at 40X magnification. These histologic findings are consistent with inflammatory bowel disease.

Ulcerative colitis is characterized by idiopathic chronic inflammation and ulcerations in the rectum in 95% of the cases and may present as continuous mucosal ulcers extending to involve other aspects of the colon. The inciting causes of the inflammatory cascade in IBD are not well understood. The treatment of IBD is directed at blocking factors involved in the inflammatory cascade with steroids, immune-modulating therapies, biologics, and small molecular agents. Growth factors have been shown to promote the renewal of epithelial and immune cells, enhance wound healing, mucosal integrity, and potentially modulate inflammation. 7 Growth factors help maintain mucosal barrier integrity by promoting colonic epithelial cell’s survival and inhibiting NF-kB activation by activating the Signal Transducer and Activator of Transcription Factor 5b (STAT5b). 8

Han et al., 8 using a 2,4,6-trinitro-benzene sulfonic acid-induced colitis (TNBS) model in STAT5B deficient mice, demonstrated that GH administration reduced colonic inflammation induced by TNBS in the control group of mice, causing a decrease in the severity score, while the effect of GH was blocked in STAT5b deficient mice. Kara et al., 9 using a similar TNBS-induced colitis model in mice, showed more serious intestinal damage in the TNBS-only-treated mice group compared to TNBS plus GH-treated group, with no damage found in saline-only-treated sham group.

Another study by Han et al. 10 in null mice with colitis discovered that GH increases the interaction of Src homolog 2 domain-containing protein tyrosine phosphatases (SHP2) with the glycoprotein 130 receptor, which negatively regulates the activation of Constitutive Signal Transducer and Activator of Transcription, STAT 3 (a protein that has been shown to promote chronic inflammation in IBD). Williams et al., 11 using a dextran sodium sulfate (DSS)-induced colitis model in transgenic mice overexpressing GH (MT1-bGH-TG) to determine whether increased plasma GH levels alter inflammation or crypt damage induced by the colitis, found that DSS induced similar colonic injury in the transgenic mice overexpressing GH and wild-type (WT) control groups; however, more transgenic MT1-bGH-TG mice survived than WT mice, and by recovery day 7, transgenic MT1-bGH-TG mice had less inflammation and crypt damage than WT mice, as well as improved survivability.

Our patient has a history of GH deficiency and has received GH supplements for 6 years. Her symptoms of UC presented after a short interval, 8 weeks, after discontinuing the GH therapy. Growth hormone has an average half-life of 20–30 minutes with a biological half-life of 9–17 hours. The possibility that our patient had IBD manifesting as growth failure cannot be ruled out. Short stature is a known complication of IBD in pediatrics. A retrospective study by Rinawi et al. 12 in 291 Crohn’s and 125 UC patients discovered a mean height Z -score lower than the control group, especially in males and those diagnosed before puberty. Growth retardation has been reported in less than 10% of patients with UC. The growth delay in IBD has been attributed to severe malnutrition due to malabsorption secondary to intestinal inflammation, anorexia, and metabolism related to systemic inflammation, particularly in CD. 3 Others have suggested GH resistance or deficiency as a possible cause of short stature seen in some patients with IBD. According to Tenore et al., 13 IBD patients may present with growth failure preceding abdominal symptoms by some years. This study further reported that 8 out of 10 patients with documented IBD and a history of decreased growth velocities had a mean basal GH higher than the control population, concluding that growth failure in IBD is not necessarily due to GH deficiency alone. A similar finding was also reported by Tietjen et al. 14 However, Wong et al. 15 reported a contrary finding in 28 patients with IBD, 4 of which showed biochemical evidence of GH deficiency, 5 had a normal serum response, and 11 had evidence suggesting GH resistance.

This patient presented with short stature years before developing intestinal symptoms of IBD and was successfully treated with GH for short stature for 6 years.

The onset of our patient’s first IBD flare following discontinuation of GH supports previous studies on the anti-inflammatory effects of growth factors in IBD. A double-blind and placebo-controlled study by Slonim et al. 5 in patients with moderate-to-severe CD showed that the use of a GH dose of 5 mg/day subcutaneously for 1 week, followed by 1.5 mg/day maintenance dose for 4 months was superior to placebo in reducing disease severity. In a randomized, double-blind control clinical trial by Sinha et al. 16 involving 24 patients with mild-to-moderate UC treated with 5 µg of EGF enema, 10 out of 12 treated with EGF enema and mesalamine were in remission after 2 weeks compared to 1/12 in the control group treated with only mesalamine. In a randomized control trial by Denson et al. 6 involving 20 patients with active CD receiving steroids 12 weeks after the initiation of 0.075 mg/kg of GH in half of the patients, 65% of those on GH achieved clinical remission compared to 20% of steroid only control group.

Improvement noted in subjects treated with growth factors is attributed to the anti-inflammatory effects. The effect of GH has also been noted with improved intestinal adaptation in short gut syndrome, occasionally seen in complicated IBD patients. In a study by Iannoli et al., 17 New Zealand rabbits with mid-duodenal ileal resection who were treated with GH (0.2 mg/kg/day) and EGF (1.5 pg/kg/h) for 7 days showed enhanced nutrient transport with an increase in microvillus height from 25% to 35%.

Growth factors cause the proliferation of both normal and malignant cells, and the possibility that treatment with growth factors may increase the risk of tumor occurrence in predisposed subjects may be an area of concern regarding the therapeutic use of growth factors in IBD. 18 However, none of the study trials reported cancer development in treated individuals during its use. GH therapy is the standard of care treatment for short stature secondary to GH deficiency. Further studies may need to be done in humans to support its efficacy as a therapy in IBD patients.

We would like to acknowledge our clinical laboratory scientist, Logan Lawrence, who provided us with pathology slides and captions, and the librarian, Hughes Anna, who provided us access to some articles.

X.V. and T.M. evaluated the patient and presented the case to O.U., who did a literature review and wrote the manuscript. D.S. did a literature review and contributed to the discussion. The manuscript was then submitted to T.N., A.S., and X.V., who edited and made changes before submission.

None to disclose.

Data not publicly available.

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Ishige T. Growth failure in pediatric onset inflammatory bowel disease: mechanisms, epidemiology, and management . Transl Pediatr . 2019 ; 8 ( 1 ): 16 – 22 . doi: 10.21037/tp.2018.12.04

Barahona-Garrido J , Hernández-Calleros J , García-Juárez I , Yamamoto-Furusho JK. Growth factors as treatment for inflammatory bowel disease: a concise review of the evidence toward their potential clinical utility . Saudi J Gastroenterol . 2009 ; 15 ( 3 ): 208 – 212 . doi: 10.4103/1319-3767.54742

Slonim AE , Bulone L , Damore MB , Goldberg T , Wingertzahn MA , McKinley MJ. A preliminary study of growth hormone therapy for Crohn’s disease . N Engl J Med. 2000 ; 342 ( 22 ): 1633 – 1637 . doi: 10.1056/NEJM200006013422203

Denson LA , Kim MO , Bezold R , et al. A randomized controlled trial of growth hormone in active pediatric Crohn disease . J Pediatr Gastroenterol Nutr. 2010 ; 51 ( 2 ): 130 – 139 . doi: 10.1097/MPG.0b013e3181c992d6

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Han X , Ren X , Jurickova I , et al. Regulation of intestinal barrier function by signal transducer and activator of transcription 5b . Gut. 2009 ; 58 ( 1 ): 49 – 58 . doi: 10.1136/gut.2007.145094

Kara E , Sungurtekin H , Sungurtekin U , Alkanat M , Ilkgul O. The effect of recombinant human growth hormone (rhGH) on trinitrobenzene sulfonic acid-induced colitis in rats: an experimental study . Inflamm Bowel Dis. 2004 ; 10 ( 2 ): 112 – 115 . doi: 10.1097/00054725-200403000-00008

Han X , Sosnowska D , Bonkowski EL , Denson LA. Growth hormone inhibits signal transducer and activator of transcription 3 activation and reduces disease activity in murine colitis . Gastroenterology. 2005 ; 129 ( 1 ): 185 – 203 . doi: 10.1053/j.gastro.2005.05.018

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Case Report
Open access
Published: 10 October 2012

Ulcerative colitis in a Nigerian girl: A case report

Idowu O Senbanjo 1 , 6 ,
Kazeem A Oshikoya 2 , 3 ,
Charles A Onyekwere 4 ,
Fatimah B Abdulkareem 5 &
Olisamedua F Njokanma 1

BMC Research Notes volume 5 , Article number: 564 ( 2012 ) Cite this article

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8 Citations

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Ulcerative colitis (UC) is uncommon in the tropics and sub-tropics. We report a case of UC in a 7 year old girl whose parents were both Nigerians. This report is to alert healthcare professionals in sub-Saharan Africa that UC is not a rare health problem, especially in children.

Case presentation

The patient presented with frequent passage of blood stained stool, abdominal pain and significant weight loss. The diagnosis was entertained after she was investigated for common causes of chronic diarrhea in our setting and the findings were negative. The patient symptoms abated after she was commenced on steroid therapy.

Under-diagnosis and misdiagnosis may account for a dearth of information on UC in African children.

Ulcerative colitis (UC) is a chronic inflammatory disease of unknown aetiology, localized to the colon and spares the upper gastrointestinal tract[ 1 ]. The inflammation is characteristically remitting and relapsing[ 2 ].

The prevalence of UC varies across geographical zones and from one country to another[ 3 ]. In North America, the prevalence varies from 37.5 to 238 per 100000 people[ 4 ]. The disease is less common in children than adults[ 2 ]. In patients with UC, 20% are younger than 20 years of age, 4% are children aged less than 5 years and 1% are infants[ 3 , 5 ]. Although, UC can occur at any age, the incidence peak in age group 15–25 years and in 55–65 years[ 6 ]. The first paediatric case was reported in 1923 by Helmholz[ 7 ], thereafter, several other cases have been reported in children[ 8 – 10 ]. UC usually exists in isolation and together with Crohn’s disease (CD) and indeterminate colitis (IC) constitutes a genetically, immunologically and histopathologically heterogeneous group of inflammatory bowel disorders called inflammatory bowel disease (IBD)[ 11 ]. Very rarely are these diseases diagnosed in the same patient[ 12 ]. However, a rare case of UC co-exiting with CD had been reported in an adult[ 13 ].

Many familial cases have been reported in the United States, yet no simple Mendelian genetic mechanism has been able to explain its transmission in those with associated family history of the disease[ 2 ]. The prevalence of UC is highest in Europe and America among Caucasians and Ashkenazic Jews and lowest in black Americans and in African countries and Japan[ 1 ]. Although, cases of UC in African-American children living in the United States of America have been reported[ 14 ], none has been reported in Africa. The rarity of the disease in Africa may limit the experience of clinicians in its diagnosis and management, especially in children. This case is therefore reported to create an awareness of UC among paediatric age group and to discuss the challenges facing the diagnosis and management of the disease in a resource poor country.

A 7 year old girl presented to the paediatric gastroenterology clinic at the Lagos State University Teaching Hospital (LASUTH), Ikeja with a history of prolonged diarrhoea of 10 weeks that progressed to frank haematochezia 2 weeks later. She also presented with abdominal pain weight loss of over 8 weeks duration. Stool was initially watery, not offensive or mucoid. Bowel motions were about 10 times per day. There was no vomiting, fever, jaundice, mouth ulcer or joint pains. The abdominal pain was crampy, diffusely localized to the umbilical and supra-pubic regions. It was neither aggravated nor relieved by any known factors. Pain did not radiate elsewhere nor, disturb the patient from sleep, associate with tenesmus or abdominal distension. The symptoms were however associated with a significant weight loss despite good appetite and adequate feeding. There were no associated respiratory and urinary symptoms. The past medical history was remarkable in the sense that she had initially presented to a general hospital where she was investigated and treated for dysentery with a course of metronidazole, co-trimoxazole and hyoscine bromide for 6 weeks without any appreciable improvement. There was no history or signs of past abdominal surgery. Patient is the first of three children to both monogamous parents. The parents are Nigerians and there was no history of similar illness in any member of the family.

On examination, she was afebrile, anicteric, mildly pale, weighed 19kg, not irritable or in respiratory distress, not dehydrated or had peripheral oedema. There was no peripheral lymphadenopathy, skin desquamation or skin discolorations. The mucous membranes and nails were normal. Mild tenderness was elicited in the peri-umbillical region but no palpable abdominal mass, hepatomegaly or splenomegaly. Rectal examination was painful, no palpable rectal mass. The rectum appeared to be narrowed and the examination finger was stained with frank blood.

The patient was admitted and investigated for causes of lower gastrointestinal bleeding. The investigations revealed Hb of 10g/dL, white blood cell count of 19,400/mm 3 with neutrophil differential of 61%, lymphocyte-32% and monocyte-7%. The ESR was elevated to 34mm/hr and serum protein significantly reduced with hypoalbuminaemia of 21g/dL. The liver function test and electrolyte with urea were essentially normal. The stool and urine cultures yielded no growth after 48 hours of incubation. No eggs, ova or intestinal parasites were seen on stool microscopy. Patient was commenced on a high protein diet and all antibiotics discontinued for 10 days. While the symptoms persisted, barium enema was requested which showed dilatation of the sigmoid and descending colon in association with persistent narrowing of the rectum and effacement of the mucosal pattern that was replaced by thumb printing appearances (Figure 1 ). These findings were suggestive of UC. Colonoscopy and rectal biopsy were performed later. The colonoscopy showed inflammatory changes extending from the anal opening up to the visible part of the descending colon. The bowel mucosa was erythemous and oedematous, with effaced vascular pattern. Tissue biopsy was granular and friable. The histology of the rectal tissue biopsy confirmed UC as shown in Figure 2 .

Barium enema showed dilatation of the sigmoid and descending colon, persistent narrowing of the rectum with effacement of the mucosal pattern that was replaced by thumb printing appearances.

Photomicrograph of UC (rectal mucosa) showing intense inflammation with disordered crypts and evidence of cryptitis and crypt abscess. H & E (magnification x 200).

Patient was commenced on sulfasalazine 50mg/kg/day in two divided doses and gradually increased to 60mg/kg/day after a week treatment as it was well tolerated. Patient was in remission until 6 months follow up. However, she defaulted from the clinic for about 6 months but continued taking her medications at home for another 5 months. She presented again with bleeding diarrhoea after stopping her medications for about a month. Sulfasalazine was re-commenced at the same dose plus prednisolone 1 mg/kg/day in two divided doses. Patient responded very well to the new regime and now in remission. She is being followed at the outpatient clinic every 4 weeks.

UC is known to affect children and adults globally. However, it is less common in Africa probably due to under-diagnosis, misdiagnosis or low racial distribution. Few cases of UC in adults have been reported in South Africa[ 15 ], Uganda[ 16 ] and Sudan[ 17 ]. Lack of reported cases in African children therefore underscores the importance of this current case report.

A major challenge in the management of UC in developing countries is making an accurate diagnosis. Our patient was presumptively treated for amoebic dysentery at a general hospital. In spite of persistent symptoms after 6 weeks of antibiotic therapy, UC was not suspected by her physician. Thus, a high index of suspicion may be required for early diagnosis of UC which should be considered as a differential diagnosis of blood stained chronic diarrhoeal diseases in children.

Presently, there is no permanent medical cure for UC[ 1 , 2 ]. The general goals of treatment in children are to control symptoms of the disease with minimal adverse effects of the medicines used and to achieve normal functioning of the patient[ 1 , 2 ]. A multidisciplinary approach has been suggested for effective management of UC in children[ 2 ]. Patient should be treated and followed up jointly by a team consisting of a paediatric gastroenterologist, paediatric surgeon, child psychiatrist, clinical psychologist and social worker. The intensity of treatment is dependent on the severity of the disease[ 1 ]. Less than 5% of children with UC may present predominantly with extraintestinal manifestations, such as growth failure; arthropathy; dermatological, genitourinary or pulmonary manifestations; coagulopathy; or liver disease[ 1 , 2 ]. However, none of these symptoms was manifested in the patient. Based on the symptoms and signs of bloody diarrhoea, abdominal cramps, urgency to defecate, abdominal tenderness, weight loss and mild anemia at presentation, and colonoscopy with histologic findings, the patient was diagnosed of moderate UC[ 2 ]. Mild to moderate UC is usually treated on an outpatient basis. Admission becomes inevitable upon failure of maximal outpatient therapy or progression to severe disease[ 1 , 2 ].

The patient was managed on outpatient basis after initial investigation and stabilization on admission. She was commenced on paediatric medical regimen for UC consisting of low residue diet, antimotility and sulfasalazine (a first line medicine)[ 1 , 2 ]. Sulfasalazine is known to treat UC effectively and prevents recurrence[ 1 , 2 ]. Its prolonged use, even during remission, has been recommended in children[ 1 ]. However, hypersensitivity adverse reaction to the sulfa component of sulfasalazine is a major limitation to its use as a first line medicine which may occur in 10-20% of patients[ 2 ]. Fortunately, the medicine was well tolerated by the patient. On rare occasions, sulfasalazine can exacerbate the symptoms and signs of UC which may prompt patient to self discontinue the medication. On the contrary, there was a tremendous improvement in the patient following the use of sulfasalazine. The medication was self discontinued as both the patient and the parents felt a permanent cure had been achieved after 11 months of remission. Lack of adequate counseling and psychosocial support might have contributed to the poor drug compliance exhibited by the patient at a later stage of treatment. The role of a clinical psychologist is to promote the psychological wellbeing of the patient and enable her to adjust to her daily normal life activities. The multidisciplinary approach to managing this type of patients is important and equally necessary when managing other chronic childhood illness. Unfortunately, the number of clinical psychologists and social workers in Nigeria is just a handful and are confined to academic institutions and tertiary health care facility.

Prednisolone is a second line medicine that was included in the treatment when the patient re-presented to our hospital. The use was justified by the slow response to sulfasalazine. However, both medicines were able to abate the symptoms and signs of the recurrent UC without any adverse effects. Corticosteroids are known to control acute flares of UC effectively but less effective at maintaining long term remission[ 2 , 18 ]. The numerous adverse effects of prolong use of corticosteroids also preclude their maintenance use during UC remission. We, therefore plan to taper off the dose of prednisolone over time and maintain the patient on sulfasalazine after achieving a prolonged remission.

Clinic default and poor medication compliance is a common problem of children with chronic diseases[ 19 ]. Poor follow-up has been reported in South African adults with UC[ 14 ]. Further default and poor medication compliance may put the patient at risks of progressing to fulminant colitis or becoming refractory to medical therapy[ 1 , 2 ]. Approximately 5-10% of such patients may require acute surgical intervention[ 2 , 20 ]. Surgery should, however, be seen as a complementary to medical therapy and as a means of preventing complications[ 20 ].

This is the first time UC is reported in an African child. Under-diagnosis and misdiagnosis may have accounted for lack of reports on this subject from Africa. Ingenuity may therefore be required for early diagnosis. UC should be suspected in childhood bloody chronic diarrhoeal diseases and patient should be investigated as such. Optimal management is required to achieve long term remission on medical therapy with minimal adverse effects.

A written informed consent was obtained from the patient’s legal guardian for publication of this case report and any accompanying images.

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Department of Paediatrics and Child Health, Lagos State University College of Medicine, PMB 21266, Ikeja, Lagos State, Nigeria

Idowu O Senbanjo & Olisamedua F Njokanma

Pharmacology Department, Lagos State University College of Medicine, PMB 21266, Ikeja, Lagos State, Nigeria

Kazeem A Oshikoya

Academic Division of Child Health, Medical School (University of Nottingham), Derbyshire Children’s Hospital, Uttoxeter Road, Derby, DE22 3DT, UK

Department of Medicine, Lagos State University College of Medicine, PMB 21266, Ikeja, Lagos State, Nigeria

Charles A Onyekwere

Gastrointesinal/Hepato-pathology Unit, Morbid Anatomy Department, College of Medicine, University of Lagos, P.M.B. 12003, Idi-Araba, Lagos, Nigeria

Fatimah B Abdulkareem

Paediatrics Gastroenterology, Hepatology and Nutrition Unit, Department of Paediatrics and Child Health, Lagos State University Teaching Hospital, Ikeja, Lagos, Nigeria

Idowu O Senbanjo

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IOS was the Pediatric gastroenterologist that managed the patient, conceived and designed the report. KAO participated in the management of the patient and the design of the report. CAO carried out the colonoscopy and biopsy assisted by IOS. FBA carried out the histopathologic evaluation of specimens and interpreted the patient samples. OFN guided and provided essential comments during production of the manuscipt. All the authors read and approved the final manuscript.

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Senbanjo, I.O., Oshikoya, K.A., Onyekwere, C.A. et al. Ulcerative colitis in a Nigerian girl: A case report. BMC Res Notes 5 , 564 (2012). https://doi.org/10.1186/1756-0500-5-564

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DOI : https://doi.org/10.1186/1756-0500-5-564

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Patient presentation

Differential diagnosis, examination, investigations, special investigations, final outcome.

Patient is a 22 year old female who presented to the surgery department of a tertiary level hospital having been referred from a private clinic, with a two month history of severe abdominal cramps, persistent bloody and mucoid diarrhoea, weight loss and tiredness.

Acknowledgement This case study was kindly provided by Dr Monica Mercer from Immunopaedia

2 months ago: Symptoms began with abdominal cramps and an intense urge to pass stool after every meal. Her symptoms rapidly worsened with passage of stool becoming more frequent. Within two days she was passing persistently watery diarrhoea mixed with fresh blood and mucous. She was seen by her general practitioner who treated her for gastritis.

One week later she collapsed at home and was admitted to hospital for investigations. She was discharged two days later without a diagnosis.

1 month ago: Symptoms persisted and she experienced diarrhoea and vomiting after eating or drinking, which lasted for 10 days. She was admitted to hospital for rehydration and further investigations. No conclusive diagnosis was made.

Currently: Patient is passing 10-20 liquid stools per day. Diarrhoea is mucoid and bloody. Occurs day and night. Patient complains of malaise, lethargy and anorexia. She has lost 8 kg in the past 2 months.

No past surgical history No significant medical history

Family history: Mother – type 2 Diabetes Mellitus No other family members with chronic disease

No known allergies

Cryptosporidium,
Shigella,
salmonella,
E.coli,
Campylobacter,
Clostridium difficile
If HIV positive consider- MAC, Isospera beli, cryptosporidium, TB
Functional bowel syndromes e.g. irritable bowel syndrome (IBS)
Malabsorbtion
Coeliac disease
Inflammatory bowel disease (IBD)

Thin ill looking young woman, conscious and alert, in obvious discomfort.

Vitals : Heart rate: 80bpm Respiratory rate: 18 bpm Blood pressure: 120/70 Temperature: 37˚C

Pale mucous membranes

Abdominal examination: Guarding and tenderness noted in the left iliac fossa and hypogastrium.

No results available from previous admissions. All results are from current admission.

Abdominal X-ray: No toxic megacolon

Gastroscopy Report: Oesophagus and gastro- oesopahageal junction were normal. Stomach mucosa was intact and normal. No gastritis, ulceration or blood was noted. Cardia was normal. Pylorus and duodenum normal.

Colonoscopy report: Very friable mucosa. Extensive ulceration with pseudopolyps, involving the rectum, entire sigmoid and left colon up to the transverse colon. Multiple biopsies of the colonic tissue were taken for histological analysis.

Histological Findings: Pathology is limited to the mucosa and submucosa. Intense infiltration of the mucosa and submucosa with neutrophils and crypt abscesses, lamina propria with lymphoid aggregates, plasma cells, mast cells and eosinophils, and shortening and branching of the crypts.

What is the Diagnosis?

Ulcerative Colitis, which is a chronic disease associated with diffuse mucosal inflammation of the colon, giving rise to significant morbidity and recurrent symptoms of intermittent bloody diarrhea, rectal urgency and tenesmus. Patients also present with fever, anemia, fatigue, weight loss, loss of appetite, loss of body fluids and nutrients, skin lesions, joint pain, and failure to grow. The latter is specifically seen in children. About half of the people diagnosed with ulcerative colitis have mild symptoms (Ulcerative colitis, no date). Onset of symptoms typically occurs between 15 and 40 years of age, with a second peak in incidence between 50 and 80 years of age.

Ulcerative colitis is closely related to another inflammatory intestinal condition called Crohn’s disease, which can lead to chronic inflammation in any part of the gastrointestinal tract. Together, these two conditions are collectively referred to as inflammatory bowel disease, or IBD. (Ulcerative colitis, no date).

Men and women are equally likely to develop ulcerative colitis. Extraintestinal manifestations may occur in up to 25% of patients. These include osteoporosis in 15%, oral ulcerations in 10%, arthritis in 5% to 10%, primary sclerosing cholangitis in 3%, uveitis in 0.5% to 3%, pyoderma gangrenosum in 0.5% to 2.0%, deep venous thrombosis in 0.3% and pulmonary embolism in 0.2%. Current cigarette smoking is associated with a reduction in the risk for ulcerative colitis, but former smokers have a higher risk of developing ulcerative colitis vs never smokers. Although the exact cause of ulcerative colitis is still unknown, there is strong evidence that primary dysregulation of the mucosal immune system causes an excessive immunologic response to normal microflora. Other contributing factors to ulcerative colitis are taken to be both genetic and environmental in nature (Richards, 2019).

What is the pathogenesis of ulcerative colitis?

What gene associations occur in ulcerative colitis?

The array of genetic polymorphisms associated with UC would point to the likelihood of abnormalities in the epithelial barrier contributing to the onset of this condition, one hypothesis supporting the presence of an epithelial cell defect that initiates the disease under pressure from the colonic microbiome (figure 4) (Fuss and Strober, 2015).

Figure 4:” Proposed mechanism of immune-mediated inflammation in UC. Inflammation in UC is initiated by release of glycolipid antigen(s) arising from genetically impaired epithelial cells under stress from exposure to components of the gut microbiome. These antigens are presented to and stimulate NK T cells in the context of CD1 on the surface of epithelial cells or on lamina propria dendritic cells. The NK T cells so stimulated cause epithelial cell damage by direct cytotoxic activity via interaction with CD1d loaded with glycolipid on the epithelial cell surface. Alternatively, the NK T cells cause epithelial apoptosis by release of IL-13 that then causes epithelial damage. Interleukin-13 also enhances inflammation by interacting with IL-13Rα2 on NK T cells, thereby inducing further NK T cell cytotoxic activity. Finally, epithelial ulceration resulting from these processes allows entry of bacterial components into the lamina propria that stimulates secondary inflammatory reactions.” Source: (Fuss and Strober, 2015)

What are Peyer’s patches?

Peyer’s patches are aggregations of lymphoid tissue, made up of lymphoid follicles located in the lamina propria of the mucosa. In adults, B lymphocytes are seen to predominate in the follicles’ germinal centers. T lymphocytes are found in the zones between follicles. With the lumen exposed to to the external environment, there are large numbers of potentially pathogenic microorganisms present. Peyer’s patches therefore carry out immune surveillance containing macrophages, dendritic cells, B-lymphocytes, and T-lymphocytes. The lymphoid tissue is covered by a special epithelium that contains specialized cells called M cells which sample antigen directly from the lumen and deliver it to antigen-presenting cells. These cells then pass to the mesenteric lymph nodes where the immune response is amplified.

How do you grade the severity of the disease?

Ulcerative Colits disease severity (based on Truelove and Witt classification):

Symptoms Mild Severe Fulminant
Stools per day 6 >10
Hematochaezia Intermittent Frequent Continuous
Temperature Normal >37.5 C
Pulse Normal >90
Haemoglobin Normal <75% of normal Transfusion
ESR 30mm/hr

Download images for case

Ulcerative colitis.

Treatment and management: On admission patient was rehydrated and given Solucortef 100 mg IMI tds. She continued to pass 10 stools the following day.

Day 3: Patient continued to experience diarrhoea and unable to tolerate food or water. Transfused with 2 units of packed cells Prescribed: Asacol 1.2g po, tds ( mesalazine ) Asacol suppository PR bds Morphine 15mg IMI PRN Flagyl 500mg tds

Day 6: Patient has continued to experience diarrhoea of watery, bloody stools. Abdominal pain has decreased and abdomen is soft and undistended. It was decided to continue medical management for a further 7 days, with the addition of: Cyclosporine 80mg IVI, infused over 2hrs Losec 20 mg po daily ( omeprazol ) Slow K rider IVI bds Slow Magnesium IVI daily Clexane 40 mg S/C daily ( enoxaparin )

Day 13: It was decided that medical management had failed as no relief of symptoms was achieved. Surgical management was therefore required.

A laparoscopic total colectomy and ileostomy was performed. Three months post surgery the patient is scheduled to return for ileal-anal pouch surgery, to eliminate the need to wear a bag.

Ulcerative colitis (no date) MedicineNet. Available at: https://www.medicinenet.com/ulcerative_colitis/article.htm (Accessed: November 14, 2022).
Richards, M. (2019) Immunopathogenesis of Ulcerative Colitis. USA: Maureen Richards Immunology & Microbiology: YouTube channel. Available at: https://www.youtube.com/watch?v=FnahtfSmP60 .
Fuss, I. J. and Strober, W. (2015) “Ulcerative Colitis,” in Mucosal Immunology. Elsevier, pp. 1573–1612.

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Published: 14 February 2024

An atypical presentation of ulcerative colitis: case report

Avanti Saoji 1 ,
Madhura Kavishwar 1 ,
Praveen Unki ORCID: orcid.org/0000-0002-0223-0622 1 &
Surbhi Rathi 1

Egyptian Pediatric Association Gazette volume 72 , Article number: 8 ( 2024 ) Cite this article

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Bloody diarrhea in children often indicates a severe gastrointestinal illness. Although infections are the most likely cause, inflammatory bowel disease (IBD) is a close mimic. IBD generally presents with chronic and persistent symptoms requiring long-term treatment. Hence, acute or atypical presentations may mislead the physician leading to delays in diagnosis. We report the case of an atypical presentation of ulcerative colitis.

Case presentation

We present the case of a 6-year-old girl with acute symptoms of bloody diarrhea, fever, abdominal pain, and tenesmus for 5 days. The child came to us after the non-resolution of symptoms after treatment from a local practitioner. The child was found to have signs of chronic malnutrition and clubbing on general examination. After ruling out infective causes, the child was evaluated further by colonoscopy, which revealed lesions suggestive of ulcerative colitis, and hence started on topical and oral treatment for the same.

Awareness about the disease and its atypical presentations like poor growth, anemia, or extraintestinal manifestations is necessary, especially in primary healthcare and resource-poor settings as it can lead to early diagnosis, referral, and treatment initiation.

Inflammatory bowel disease (IBD) comprises two chronic gastrointestinal (GI) inflammatory diseases—ulcerative colitis (UC) and Crohn’s disease (CD). They present with chronic and persistent GI symptoms and require long-term treatment and monitoring. Acute symptoms or atypical presentations may lead to delays in diagnosis. It may further lead to the affection of growth and development, bone health, and psychosocial functioning in children and adolescents and contribute to significant morbidity and mortality [ 1 ]. It also poses a significant load on the healthcare system [ 2 ]. Hence, awareness about the disease and its varied manifestations can aid in early detection and early initiation of treatment to improve outcomes. We report the case of one such atypical presentation of ulcerative colitis.

We present the case of a 6-year-old girl who came to our tertiary care center with acute bloody diarrhea for a duration of 5 days associated with fever, abdominal pain, and tenesmus. Her stools were non-foul-smelling, large in quantity, and had fresh blood (about 3–5 ml in each stool), associated with pain in the abdomen just prior to passage. The child had no similar complaints previously and no significant past medical or surgical history. For the above complaints, the child was started on antibiotics at a local hospital and was transfused with packed cells in view of severe anemia.

The child visited our hospital due to the non-resolution of symptoms despite treatment. Physical appearance revealed a pale, malnourished, and stunted girl. Anthropometry revealed weight and height for age less than the 3rd centile with a BMI of 11.5 kg/m 2 , thus suggesting a chronic cause for her malnutrition. On further evaluation, the child was noticed to have clubbing (as shown in Fig. 1 ) and cheilosis. No cyanosis, icterus, or lymphadenopathy was seen. The local perianal examination had no obvious abnormality. The abdomen was soft and non-tender, and the liver was palpable 3 cm below the right costal margin. Other systems were within normal limits.

Grade III clubbing seen in our case of ulcerative colitis

On investigations, a complete blood count revealed a hemoglobin of 8.4 g/dl, platelets of 77,000/mm 3 , and total counts of 15,000/mm 3 . Stool examination was positive for RBCs but, however, revealed no organisms or pus cells ruling out infective causes. Further testing was done to evaluate for etiology of chronic disease in the child. Liver functions, renal functions, and coagulation profile were within normal limits. C-reactive protein and erythrocyte sedimentation rates were normal. Tuberculosis and HIV were ruled out. Chest X-ray revealed no abnormal findings. 2D echo was within normal limits. Ultrasonography of the abdomen was suggestive of a thickened rectum, sigmoid colon, and part of the descending colon. Fetal calprotectin levels were inconclusive. Colonoscopy was planned, and it revealed diffuse inflammatory lesions from the rectum to the ascending colon sparing the terminal ileum and cecum as shown in Fig. 2 . Biopsy from the sites was suggestive of superficial ulcerations, lymphoplasmacytic infiltrates in lamina propria, cryptitis, and crypt abscess in the colon suggestive of ulcerative colitis. Hence, she was started on 5-aminosalicylic acid (Mesalamine) orally and topically in the form of an enema. Multivitamins and mineral supplements were also added, and parents were counseled about an appropriate diet. The child followed up after 2 weeks of discharge. There were no repeat episodes of bleeding. The child had resumed school and was active, and there was a weight gain of 1 kg.

Colonoscopy images of the patient showing A edematous and erythematous mucosa of the colon and B superficial ulcerations and bleeding

Inflammatory bowel disease constitutes chronic inflammatory disorders of the gastrointestinal tract [ 1 ]. These occur due to a complex interplay of various factors like genetic, environmental, microbial, and adaptive immunity of the host and result in a dysregulated mucosal immune response against the commensal intestinal microbiota [ 3 ]. Although most commonly seen during adolescence and young adulthood, an increasing number of children are now being diagnosed even at a younger age with early-onset (0–5 years) and very early-onset (VEO) diseases (0–2 years) [ 4 , 5 ].

The diagnosis of IBD is generally entertained in children with chronic or persistent symptoms like abdominal pain, diarrhea, rectal bleeding, and weight loss. Bloody diarrhea is the most common presenting complaint in UC whereas CD may present with vague abdominal pain, diarrhea, or chronic symptoms such as unexplained anemia, fever, weight loss, or growth retardation. The classic “triad” of abdominal pain, diarrhea, and weight loss occurs in only 25% of patients with CD [ 6 ]. Extraintestinal manifestations may involve nearly any organ system—but common ones include the musculoskeletal, dermatologic, hepato-pancreato-biliary, ocular, renal, and hematological systems [ 7 ]. These may present at diagnosis in 6 to 23% of children with a higher frequency in those > 6 years [ 8 , 9 ].

It is important to exclude enteric infections before making a diagnosis of IBD. The primary findings that differentiate infection from IBD are positive stool cultures and duration of diarrhea in these patients. Those who have no identified pathogen and/or symptoms with a duration of > 2 weeks are likely to have IBD [ 10 ]. Murphy [ 11 ] suggests that although GI infections may be the most likely cause of bloody diarrhea in children, the possibility of inflammatory bowel disease should always be kept in mind especially if associated with signs like impaired growth, clubbing, oral or perioral abnormalities. Impairment of growth in children may precede the intestinal mucosal lesion by months to years [ 12 , 13 ]. This is similar to what we observed in our case.

The classification of IBD is complex and characterized by some rare phenotypes that may be atypical or unusual. The recognition of the typical features of CD and UC, identification of atypical phenotypes that are still consistent with a diagnosis of CD or UC, and knowledge of those factors that preclude a diagnosis of one or the other are vital for diagnosis. Thus, a diagnosis of IBD should be supported on the basis of history, physical examination, laboratory investigations, histopathology, and imaging of the small bowel.

The revised Porto criteria accepted by the European Society for Paediatric Gastroenterology Hepatology and Nutrition (ESPGHAN) are a novel evidence-based approach to the definition of IBD [ 14 ]. It has a methodological approach and incorporates the Paris phenotypic classification of PIBD [ 15 ]. It also helps in the delineation of atypical phenotypes of IBD. Thus, it enables clinicians to properly diagnose each individual subtype. The criteria also consider advanced diagnostic imaging modalities like capsule endoscopy, along with serological and fecal biomarkers for diagnosis.

Reliable features to diagnose ulcerative colitis include continuous mucosal inflammation of the colon, starting from the rectum, without small bowel involvement and without granulomas on biopsy [ 8 , 10 , 16 ]. The typical macroscopic features seen are erythema, granularity, friability, purulent exudates, and ulcers that generally appear as superficial small ulcers. However, certain atypical phenotypes like macroscopic rectal sparing, isolated upper GI involvement in the form of non-serpiginous gastric ulcers, normal crypt architecture, absence of chronicity in biopsies, or a cecal patch may also be seen [ 14 ]. The results of the colonoscopy seen in our case match with the above findings.

Crohn’s disease typically manifests primarily in the ileum or colon, although any part of the GIT may be affected. CD may also present with extraintestinal manifestations initially. Key features of CD include the presence of skip lesions, non-contiguous serpentine and linear ulcerations, cobblestoning, stenosis/stricturing of the bowel, thickening of the bowel wall, or inflamed ileum with a normal cecum, with histological presence of well-formed non-caseating granulomas [ 14 ].

IBD type unclassified (IBD-U) is a term referring to patients with definite IBD, wherein the inflammation is limited to the colon and the differentiation between UC and CD remains uncertain even after a complete workup [ 14 ].

Fecal markers like calprotectin or lactoferrin are very sensitive in the detection of mucosal inflammation but are not very specific for IBD. Certain serological markers of IBD like anti- Saccharomyces cerevisiae antibody (ASCA) or perinuclear anti-neutrophil cytoplasmic antibodies (pANCA) may suggest an increased likelihood for IBD in atypical cases and may also help to differentiate CD from UC in cases of IBD-U [ 14 ].

An increasing number of cases of pediatric IBD are now being reported in India [ 17 ] which could be due to increasing awareness, improved diagnostic techniques, and enhanced access to specialized healthcare systems. However, atypical presentations and unique age-related issues of children make diagnoses of pediatric IBD challenging [ 18 , 19 , 20 ].

The treatment for IBD requires long-term care, follow-up, and support. The goals of treatment include the elimination of symptoms and restoring quality of life, restoring normal growth, and prevention of complications. Medical therapy includes drugs needed to induce remissions like aminosalicylates and corticosteroids; immunomodulators like azathioprine, methotrexate, and 6-mercaptompurine; and newer biologicals like monoclonal antibodies such as infliximab, adalimumab, and vedolizumab which are helpful in remission as well as maintenance and thus can heal the mucosa and augment growth [ 1 ].

Surgical intervention may be required in select cases like intractable disease and fulminant disease unresponsive to medical management. Psychosocial support for the child and family is also of utmost importance for adherence to treatment.

IBD is increasingly being reported in India. Knowledge about the disease and its atypical presentations in the form of poor growth, anemia, or extraintestinal manifestations is necessary, especially in primary healthcare and resource-poor settings to aid in early diagnosis, referral, and initiation of treatment.

Availability of data and materials

Not applicable.

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Department of Pediatrics, TNMC and BYL Nair Charitable Hospital, Mumbai, 400008, India

Avanti Saoji, Madhura Kavishwar, Praveen Unki & Surbhi Rathi

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AS: data curation, editing, writing—original draft preparation, and investigation. MK: data curation and investigation. PU: conceptualization, investigation, supervision, reviewing, and editing. SR: supervision and reviewing.

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Correspondence to Praveen Unki .

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Saoji, A., Kavishwar, M., Unki, P. et al. An atypical presentation of ulcerative colitis: case report. Egypt Pediatric Association Gaz 72 , 8 (2024). https://doi.org/10.1186/s43054-024-00252-8

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Published : 14 February 2024

DOI : https://doi.org/10.1186/s43054-024-00252-8

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Inflammatory bowel disease
Ulcerative colitis
Blood in stool
Chronic malnutrition
Case report

What is a stoma bag? Louise Thompson opens up about ulcerative colitis

F ormer Made in Chelsea reality TV star Louise Thompson opened up about her recent diagnosis of ulcerative colitis, sparking an outpouring of support on social media.

The 34-year-old has previously spoken candidly about battling both bowel condition ulcerative colitis and autoimmune disease lupus.

For those who don’t know, ulcerative colitis is a chronic bowel condition where the colon and rectum become inflamed. This causes small ulcers to develop on the colon's lining, which can bleed.

There is no cure for the condition but it can be effectively managed with time and treatment, such as a stoma bag.

This is the most recent update shared by Louise, posting a photo of her stoma bag on Instagram .

"HOW DO I DISCLOSE THIS SORT OF NEWS?” she wrote in the caption. "It’s not exactly exciting like a big pregnancy or gender reveal announcement!

"Hey look, I’m having a boy… Hey look, I’ve got a stoma! So I guess I’ll just stand here. Proud in stature. With my new friend. Le bum bag that represents life. And hopefully a better one.

"Isn’t it bizarre that this little grey pouch is the price I pay for good health! I say good riddance to that nasty menacing colon! Please be kind."

While Louise seems nervous yet proud about revealing her stoma bag, it’s a relatively common treatment. In fact, a reported 165,000 to 200,000 people are living with a stoma in the UK.

Here’s a closer look at what a stoma bag is and what it could be used to treat.

What is a stoma bag?

A stoma refers to one part of a larger process called a colostomy. A colostomy is an operation to divert one end of the colon, which is part of the bowel, through an opening in the tummy. This opening is known as a stoma.

A colostomy is usually needed for people who cannot pass stools through their anus, meaning it passes out of the stoma instead.

A stoma bag is therefore needed to collect the waste throughout the day.

Colostomies can be permanent or temporary, depending on the exact circumstances of the individual. It can be used to treat conditions such as bowel cancer , Crohn's disease, diverticulitis, forms of cancer, or – as in Louise’s case – ulcerative colitis.

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Pediatric Ulcerative Colitis in Siblings

Divya mamootil.

1 Internal Medicine, Ascension St. Agnes Hospital, Baltimore, USA

This case report discusses a nine-year-old female that presented with abdominal pain, diarrhea, and weight loss, suggestive of inflammatory bowel disease (IBD). She had an older brother previously diagnosed with ulcerative colitis (UC), which raised suspicion that she may have the same condition. CT scan of the abdomen/pelvis showed signs of bowel thickening. Stool studies revealed elevated inflammatory markers including lactoferrin and calprotectin, as well as occult blood. She underwent a colonoscopy and rectal biopsy which further confirmed the diagnosis of ulcerative colitis. This article aims to discuss the clinical presentation, role of genetic factors, diagnostic workup, and therapeutic management of ulcerative colitis in the pediatric population.

Introduction

Ulcerative colitis (UC) is a chronic and idiopathic inflammatory bowel disease (IBD) that causes ulcers and inflammation in the colon. The classic triad of IBD is abdominal pain, diarrhea, and weight loss, with the addition of rectal bleeding in UC patients. The pediatric population makes up 15-20% of all IBD cases in North America [ 1 ], and the incidence has continued to increase over the years. Pediatric IBD is classified based on the age they are diagnosed; very early onset (VEO) is < 10 years old and early onset (EO) is 10 to < 17 years old [ 2 ]. VEO cases tend to have increased severity of the disease or more extensive involvement in the colon, while EO cases present similarly to adult IBD [ 2 ]. Adult UC is mainly confined to the rectum or left side of the colon, while children generally present with pancolitis [ 3 ]. Pediatric IBD is suspected with persistent (≥4 weeks) or recurrent (≥2 episodes in 6 months) of these symptoms [ 3 ]. Children mainly complain of abdominal pain at the start of their diagnosis. 10-40% of pediatric patients can initially present with non-specific symptoms such as growth failure [ 3 ].

Case presentation

A nine-year-old previously healthy Caucasian female presented with a chief complaint of intermittent episodes of diarrhea and abdominal pain for three months. She also noticed bright red blood and mucus in her stools a few days prior to hospital admission. Associated symptoms included fatigue, generalized malaise, difficulty sleeping, and lack of appetite during that week. She denied any fever, chills, nausea, vomiting, recent travel, or consumption of poorly cooked food. Her past medical history only consisted of occasional upper respiratory symptoms and otitis media. She did not have allergies and was not taking any medications. Her family history was significant for a 13-year-old brother that had similar complaints of bloody stools a year ago and was diagnosed with ulcerative colitis at age 12.

Upon admission, she was afebrile with a blood pressure of 100/60 mmHg, a pulse of 90 beats/minute, a respiratory rate of 12 breaths/minute, and pulse oximetry of 100% on room air. Her BMI was 15.42. On the physical exam, there were no signs of scleral icterus, jaundice, pallor, rashes hepatomegaly, or splenomegaly. The cardiopulmonary exam was within normal limits. Her abdomen was non-distended, and soft, with mild generalized tenderness on palpation, without rigidity or guarding. Murphy's sign was negative.

Laboratory findings were significant for white blood cell (WBC) of 12.2 K/uL (reference range: 4-11 K/uL), hemoglobin 9.2 g/dL (reference range: 12-15 g/dL), lactic acid of 1.9 mmol/L (reference range: 0.5-1.6 mmol/L), Thyroid stimulating hormone (TSH) 3.11 mIU/L (reference range: 0.27-4.2 mIU/L), and free thyroxine (T4) of 1.2 ng/dL (reference range: 0.93-1.7 ng/dL). Aspartate aminotransferase (AST) was 38 U/L ( reference range: 0-34 U/L) and Alanine aminotransferase (ALT) was 24 U/L (reference range: 0-36 U/L). Inflammatory markers were elevated including Erythrocyte sedimentation rate (ESR) of 34 mm/hour (reference range: 0-20 mm/hour) and c-reactive protein (CRP) of 15.2 mg/L (reference range: 0-5 mg/L) (Table (Table1 1 ).

Stool samples were taken and revealed that the fecal lactoferrin assay was positive. Fecal calprotectin was 514 mcg/g (reference range: 0-50 mcg/g). Stool WBC showed 18-20 white blood cells/HPF. Occult blood was also positive. Ova and parasites were negative. Clostridium difficile toxin and antigen were both negative (Table (Table2 2 ).

CT scan of the abdomen/pelvis showed bowel wall thickening of the descending colon and rectum to 5.2 mm with irregularity of the wall contour and luminal narrowing. She underwent a colonoscopy, which revealed inflammation and friable mucosa with vascular effacement in the rectum and descending colon. Rectal biopsy was done and the pathology report showed crypt abscesses of varying sizes, crypt atrophy, and infiltration of polymorphonuclear leukocytes (<50% invasion), consistent with a diagnosis of ulcerative colitis (Figure (Figure1 1 ).

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Based on her clinical symptoms and pathology findings, her pediatric ulcerative colitis activity index (PUCAI) was classified as a score of 45 which is moderate disease severity. She was started on Prednisone 1 mg/kg daily concomitant with Mesalamine 50 mg/kg daily for one month with a gradual steroid taper. She was able to tolerate this well with improvement in her symptoms.

Gene studies

There is an estimated 7.9-12% prevalence of IBD among family members [ 4 ]. There are many studies that show strong gene linkage in patients with UC or Crohn’s, and a high monozygotic twin concordance rate of 15.4% compared to 3.9% dizygotic [ 4 ]. However, it is still a polygenic disease affected by environmental factors. One study showed siblings can influence the transmission and severity of clinical presentation of UC and Crohn’s disease [ 5 ]. They looked at the role of environmental exposures in relation to increased risk or protection from developing IBD within a specific window of susceptibility. Findings were remarkable for older siblings having a higher risk of developing UC [ 5 ]. One reason for this is that older siblings tend to develop asthma, allergies, and other atopic diseases more often due to the first exposure to certain antigens and environmental factors compared to their siblings. When younger siblings come along, they are in turn exposed to the same antigens and also have a high risk of developing the same disease, which may have more severe manifestations [ 5 ].

Genetics plays a strong role in the predisposition of some pediatric patients to developing UC. Genome-wide association studies (GWAS) in the past have shown a strong association of specific MHC class II alleles with UC, such as HLA DRB1*01:03 and HLA DQA1 [ 6 ]. These studies showed less heterozygosity in HLA genes, suggesting it would be protective for patients to have broader antigen recognition. This is particularly important for the pediatric population, as they are more prone to developing extensive colonic involvement, especially under the age of eight [ 7 ]. Another important factor to consider is the integrity of the intestinal epithelial barrier to prevent the development of colitis. Studies have shown patients with UC to have a deficiency in the MUC2 gene, which is responsible for producing mucins that help protect the lining of the colon [ 8 ]. UC patients have also had polymorphisms in ECM1, which is another gene that controls the strength of the epithelial basement membrane in the colon [ 9 ]. IBD patients tend to have increased inflammatory markers that cause colitis, such as interleukins that create an autoimmune response to attack the colon when they perceive a threat. IL-6, IL-12, and IL-23 exacerbate inflammation of the colon in IBD patients [ 10 ].

Diagnostic workup

A complete blood count (CBC) should be done in all patients to evaluate anemia, leukocytosis, or thrombocytosis. One study showed the combination of anemia and thrombocytosis in pediatric patients with IBD had a positive predictive value of 90% and a negative predictive value of 81%. [ 11 ]. ESR and CRP should also be tested as they are inflammatory markers, although they can also be elevated in infectious colitis as well. Stool samples are a common diagnostic tool used in the workup of IBD, as they can identify specific inflammatory markers. Lactoferrin is a glycoprotein that binds to and transports iron and is also a modulator of the immune system. There are elevated levels of lactoferrin when there is intestinal inflammation in IBD. One study indicated elevated lactoferrin had a sensitivity of 78% and specificity of 90% in IBD patients [ 12 ]. Osteoprotegerin is responsible for preventing osteoclast formation by blocking the (receptor activator of nuclear factor kappa beta) RANK ligand, as well as playing a role in the apoptosis pathway. Its pro-inflammatory effects identify colon inflammation in IBD patients. A study in children with IBD showed fecal osteoprotegerin had a sensitivity of 71% and specificity of 69% [ 13 ]. Calprotectin and S100A12 are other proinflammatory markers from a group called DAMP (damage-associated molecular pattern molecules) [ 14 ]. These markers are overexpressed when there is inflammation in the colon. A study revealed fecal calprotectin is significantly elevated in pediatric IBD patients with a sensitivity of 100% and specificity of 67% [ 15 ]. With all cases of bloody diarrhea, infectious causes must be ruled out first. Colonoscopy and upper endoscopy are essential to differentiate between Ulcerative Colitis and Crohn’s disease. Visualization of the ileum is also necessary to rule out pancolitis [ 3 ].

Therapeutic management

The PUCAI is a tool used to predict how children will respond to therapy based on disease severity. The mild disease has a score between 10 and 30. Moderate disease has a score between 35 and 60. Severe disease has a score greater than 65. Severe disease is characterized by ≥6 bloody stools/day and one of the following: anemia, fever, tachycardia, or elevated ESR [ 16 ]. There are several different treatment modalities used for UC usually based on their disease severity. Pediatric patients with mild disease usually begin treatment with an oral 5-Aminosalicylic acid (5-ASA) preparation such as mesalamine as first-line therapy to induce remission. Rectal mesalamine can also be used in conjunction with oral formulation to improve clinical outcomes [ 1 ]. One thing to be aware of is the possible transient exacerbation of diarrhea in the first few weeks following treatment, as this is a common side effect [ 1 ]. Oral glucocorticoids such as prednisone are often used as a second-line treatment for mild to moderate UC when unresponsive to mesalamine, or first-line therapy for moderate disease [ 17 ]. Intravenous (IV) glucocorticoids may also be used if unresponsive to oral therapy. Thiopurine therapy such as Azathioprine or 6-mercaptopurine may be added to maintain remission in patients that are dependent on steroids. [ 17 ].

Patients with severe UC with PUCAI score >65 are preferentially treated with IV steroids [ 16 ]. The scores are reassessed every two days to determine if additional therapy is warranted. For example on day five, if the patient is still unresponsive with a score >65, infliximab or IV cyclosporine may be given as second-line therapy [ 16 ]. If the score has improved to <35 on day five the patient may be switched to oral steroids [ 17 ]. Vedolizumab is a second-line biologic therapy that targets inflammation by blocking the recruitment of lymphocytes specific to the gut [ 18 ]. There is some evidence that a combination of broad-spectrum antibiotics (metronidazole, amoxicillin, doxycycline, and vancomycin [MADoV]) has been successful in children with UC that have failed other therapies [ 19 ]. There have also been a few studies in children with fecal microbial transplantation (FMT), as a proposed treatment of UC [ 20 ]. Pediatric patients with the refractory disease will have PUCAI scores that remain above 65 despite other therapies, so they may require surgical referral for a subtotal colectomy and ileostomy [ 16 ]. Other indications for colectomy include complications such as toxic megacolon, perforation, and hemorrhage.

Conclusions

As the incidence of ulcerative colitis increases in the pediatric population, further studies will need to be done to investigate the role of genetics and environmental factors in their susceptibility to the disease and response to management. It is also essential to spread awareness about the disease and educate children and their families about how Ulcerative Colitis will affect their lives. With advances in technology, there is great hope for the future of pediatric patients.

The authors have declared that no competing interests exist.

Human Ethics

Consent was obtained or waived by all participants in this study

On the Move

Palisade Bio stock slides 8% amid colitis drug presentation

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Shares of Palisade Bio ( NASDAQ: PALI ) were down 8% in late morning trading Wednesday after jumping in pre-market action around the time it announced a presentation on its ulcerative colitis drug candidate PALI-2108 at an industry event.

Palisade said early Wednesday that it made the presentation at the IBD Innovate: Product Development for Crohn’s & Colitis conference, currently underway in Cambridge, Mass. The presentation was also posted on the company’s website.

The company added that it remains on track to start a Phase 1 study for PALI-2108 in ulcerative colitis later this year.

On Monday, Palisade conducted a 1-for-15 reverse stock split .

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Case 25-2014: A 37-Year-Old Man with Ulcerative Colitis and Bloody
A 37-year-old man with ulcerative colitis was admitted to the hospital because of abdominal cramping, diarrhea, hematochezia, fever to a peak temperature of 38.8°C, and drenching night sweats.
Ulcerative Colitis Clinical Presentation
In some cases, ulcerative colitis has a fulminant course marked by severe diarrhea and cramps, fever, leukocytosis, and abdominal distention. Fulminant disease occurs more often in children than in adults. An estimated 15% of patients present with an attack severe enough to require hospitalization and steroid therapy.
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Clinical manifestations, diagnosis, and prognosis of ulcerative colitis
Colitis — Patients with ulcerative colitis usually present with diarrhea, which may be associated with blood. Bowel movements are frequent and small in volume as a result of rectal inflammation. Associated symptoms include colicky abdominal pain, urgency, tenesmus, and incontinence [ 1 ]. Patients with mainly distal disease may have ...
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Ulcerative colitis is an idiopathic inflammatory condition of the colon that results in diffuse friability and superficial erosions on the colonic wall associated with bleeding. It is the most common form of inflammatory bowel disease worldwide. It characteristically involves inflammation restricted to the mucosa and submucosa of the colon. Typically, the disease starts in the rectum and ...
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Case presentation. A 47-year-old man presented to Nambour General Hospital following a witnessed generalised tonic-clonic seizure. This was on the background of newly diagnosed and poorly controlled ulcerative colitis (UC), with symptoms of urgency, frequency (between 8 and 12 motions per day) and intermittent haematochezia stretching back 30 years.
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This case report describes the clinical course of a 64-year-old male with intermittent abdominal pain attributed to recurrent ulcers at the appendiceal orifice. Initial investigations in November 2019 revealed chronic gastritis and ulcers at the appendiceal orifice, prompting consideration of ulcerative colitis (UC).
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Source Reference: Cathomas M, et al "Herpes simplex virus colitis mimicking acute severe ulcerative colitis: A case report and review of the literature" J Surg Case Rep 2023; DOI: 10.1093/jscr ...
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Conclusion. Awareness about the disease and its atypical presentations like poor growth, anemia, or extraintestinal manifestations is necessary, especially in primary healthcare and resource-poor settings as it can lead to early diagno-sis, referral, and treatment initiation. Keywords Inflammatory bowel disease, Ulcerative colitis, Blood in ...
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In addition, 20% of patients with ulcerative colitis start with severe crises at diagnosis. In our study of 202 patients with inflammatory bowel disease at the Hospital Pablo Tobon Uribe, 23.1% of patients with ulcerative colitis showed severe activity (2). The mortality rate in these individuals in the UK is 2.8%.
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Case Report: An unusual presentation of ulcerative colitis
Ulcerative colitis (UC) may have diverse extraintestinal manifestations. Nutritional deficiencies, medications or immune-mediated epiphenomena are considered to be pathogenic mechanisms involved. We describe a case of a 56-year-old woman who presented with rapidly progressive tingling paraesthesias in both lower limbs followed by sensory ataxia ...
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In severe cases, ulcerative colitis can lead to complications. These could include: Significant bleeding if the bowel is very inflamed; A risk of the bowel perforating which is when a hole develops;
Bone marrow-derived mesenchymal stem cells mitigate chronic colitis and
Current treatments for inflammatory bowel disease (IBD) are often inadequate due to limited efficacy and toxicity, leading to surgical resection in refractory cases. IBD's broad and complex pathogenesis involving the immune system, enteric nervous system, microbiome, and oxidative stress requires more effective therapeutic strategies. In this study, we investigated the therapeutic potential of ...
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Ulcerative colitis (UC) is a chronic and idiopathic inflammatory bowel disease (IBD) that causes ulcers and inflammation in the colon. ... Case presentation. A nine-year-old previously healthy Caucasian female presented with a chief complaint of intermittent episodes of diarrhea and abdominal pain for three months.
Palisade Bio stock slides 8% amid colitis drug presentation
Shares of Palisade Bio (PALI) dropped 8% after announcing a presentation on its ulcerative colitis drug candidate PALI-2108 at an industry event. Read more here.
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To treat ulcerative colitis: 46. Loqtorzi: toripalimab-tpzi: 10/27/2023: To treat recurrent or metastatic nasopharyngeal carcinoma when used together with or following other therapies: 47 ...

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What is a stoma bag? Louise Thompson opens up about ulcerative colitis

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Pediatric Ulcerative Colitis in Siblings

Introduction

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Human Ethics

Palisade Bio stock slides 8% amid colitis drug presentation

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