Judith Staub
· Assistant Professor (Clinical)University of Utah · Gastroenterology & Hepatology
Active 2001–2026
Research topics
- Surgery
- Medicine
- Internal medicine
Selected publications
Gastroenterology · 2026-05-01
articleGastrointestinal Endoscopy · 2026-05-01
articleGastrointestinal Endoscopy · 2025-02-28
articleGastro Hep Advances · 2024-01-01 · 4 citations
articleOpen accessBackground and Aims: Lynch syndrome (LS) is caused by pathogenic mutations in mismatch repair (MMR) genes. There are limited data on differences in colorectal cancer (CRC) surveillance by MMR genes, and an international consensus on surveillance based on genes is not established. We aimed to evaluate colonoscopy and esophagogastroduodenoscopy (EGD) surveillance outcomes and compare CRC surveillance findings by the mutated gene. Methods: One hundred one patients with LS were included and colonoscopy results were compared by MMR mutation. Primary outcomes included the development and recurrence of adenoma, CRC, high-grade dysplasia, advanced adenoma, and sessile serrated lesions. Logistic regressions evaluated the relationship between genes and the development or recurrence of primary outcomes. Survival analysis evaluated primary outcomes in patients with ≥ 2 colonoscopies. EGD results were summarized. Results: (OR 11.89, 95% CI: 1.38-164.78). Of 170 EGDs, an actionable finding was identified in 16% of patients during their first 3 EGDs. Conclusion: Surveillance colonoscopy outcomes differed in patients with LS and suggest the need to guide surveillance based on MMR gene mutation.
The American Journal of Gastroenterology · 2024-10-01
articleSenior authorIntroduction: Multiple myeloma (MM) is a hematologic malignancy characterized by clonal proliferation of plasma cells originating in the bone marrow. It typically presents with myeloma-defining events such as hypercalcemia, renal failure, anemia and osteolytic bone lesions. Extramedullary MM (EMM) occurs when malignant plasma cells form tumors outside the bone marrow, and is associated with poor outcomes. We present a rare case of EMM with involvement of the Gastrointestinal (GI) tract manifesting as an acute upper gastrointestinal bleed (UGIB) and later a large bowel obstruction. Case Description/Methods: A 59-year-old male with IgG Kappa MM with history of a left shoulder plasmacytoma (on apixaban) presented with two weeks of melena, epigastric pain and worsening anemia with a hemoglobin of 6.6 while taking Nonsteroidal anti-inflammatory drug. Esophagogastroduodenoscopy showed four discrete atypical cratered gastric ulcers with heaped up edges and lacy vasculature in the gastric fundus and body, felt to be the source of UGIB (Figure 1a). Biopsies showed gastric mucosa with an atypical infiltrate of kappa restricted (Figure 1b), CD138 (Figure 1c), Leukocyte common antigen positive plasma cells, consistent with EMM. Congo red staining was negative for amyloid deposition. Bleeding resolved with continued chemotherapy and Omeprazole but he was readmitted 1 month later for a large bowel obstruction from a cecal mass requiring ileocolonic resection (Figure 1d). Pathology of the cecal mass again revealed kappa restricted, CD138 positive plasma cells with lymphovascular invasion. Positron emission tomography scan confirmed rapid progression of disease. Attempts at escalating chemotherapy were made, however he developed worsening obstructive bowel symptoms and abdominal pain and was found to have extensive bowel necrosis and perforation on repeat Computed tomography imaging. After further goals of care discussion, he was switched to comfort measures and quickly died. Discussion: EMM is seen in up to 15-30% of MM cases. However the GI tract is rarely involved, accounting for < 5% of cases. When present, it confers a poor prognosis and is a hallmark of aggressive disease. This case demonstrated two unique presentations of EMM of the GI tract - first as gastric ulcers resulting in an UGIB and subsequently as a cecal mass leading to bowel obstruction and perforation. Despite its rarity, physicians should be aware of these potential manifestations and its significance of advanced disease.Figure 1.: A) Non-bleeding gastric ulcer with heaped up edges and lacy vasculature, located in gastric body; B) Stomach biopsy with in-situ hybridization (ISH) for Kappa-restricted light chain plasma cell neoplasm; C) IHC stain of stomach biopsy for CD138 demonstrating a moderately well-circumscribed plasma cell neoplasm (blue arrow); D) CT A/P showing 6.9 x 3.5 cm soft tissue mass at the cecum resulting in early bowel obstruction (white arrow).
The American Journal of Gastroenterology · 2024-10-01
articleReplacement of PEG and PEJ Tubes
The American Journal of Gastroenterology · 2022-06-08 · 2 citations
article1Division of Gastroenterology, Hepatology and Nutrition, University of Utah, Salt Lake City, Utah, USA; 2Metabolic Nutrition Support Outpatient Clinic, Intermountain Medical Center, Murray, Utah, USA. Correspondence: John C. Fang, MD. E-mail: [email protected]. SUPPLEMENTARY MATERIAL accompanies this paper at https://links.lww.com/AJG/C544, https://links.lww.com/AJG/C545, https://links.lww.com/AJG/C546.
S246 Differences in Lynch Syndrome Colonoscopy Surveillance by Pathogenic Variant
The American Journal of Gastroenterology · 2022-10-01
articleIntroduction: Lynch syndrome is caused by pathogenic variants in 4 mismatch repair genes: MLH1, MSH2, MSH6, & PMS2. There is limited data on differences in endoscopic surveillance by pathogenic variant, and surveillance for colorectal cancer (CRC) with colonoscopy every 1-2 years is recommended for all patients. It is not known if occurrence of colonic lesions differs by mutation status. We aimed to evaluate colonoscopy surveillance outcomes in patients with Lynch syndrome overall and compare findings between patients by variant. Methods: We retrospectively reviewed colonoscopy results in patients with Lynch syndrome at our institution. Of 221 patients identified by participation in the Hereditary Gastrointestinal Cancer Registry (HGCR), 101 were included after excluding those without ≥1 colonoscopy available and 1 patient with a hereditary polyposis syndrome. Baseline variables and surveillance results from diagnosis to May 2020 were compared by variant (MLH1, MSH2, MSH6, PMS2). Primary outcomes included development and recurrence of adenoma, CRC, high grade dysplasia (HGD), advanced adenoma (AA), and sessile serrated lesions (SSL). Logistic regression analyses were completed to evaluate the relationship between pathogenic variant and development or recurrence of adenoma, SSL, and AA/HGD/CRC. A survival analysis evaluated the development of the primary outcomes in patients with ≥ 2 colonoscopies. Results: 327 colonoscopies were reviewed. Baseline characteristics did not differ by variant, and patients with MLH1 had more colonoscopies completed (Table). PMS2 was associated with decreased odds of AA/HGD/CRC development compared to MLH1 (OR .102, 95% CI .013-.507) and adenoma development compared to MSH2 (OR .240, 95% CI .057-.902). Among those with ≥2 colonoscopies (n=71), there was no significant difference in adenoma or AA/HGD/CRC development, but MSH2 had a lower risk of SSL compared to MLH1 (HR .053, 95% CI .004-.762) and MSH6 (HR .067, 95% CI .005-.861). For recurrence, PMS2 had a lower risk of adenoma recurrence compared to MLH1 (OR=.021, 95% CI .021-.001) and MSH2 (OR .084, 95% CI .006-.726). Similarly, MSH6 (OR .068, CI .004-.652) had a lower risk of adenoma recurrence compared to MLH1. Conclusion: Surveillance colonoscopy outcomes, including SSL risk, differed in patients with Lynch Syndrome based on the pathogenic variant present. These findings suggest the need to further evaluate appropriate surveillance intervals based on variant. Table 1. - Baseline Characteristics and Surveillance Colonoscopy Outcomes by Pathogenic Variant Key All n=101 MSH6 n=18 MSH2 n=32 PMS2 n-23 MLH1 n=28 p* Baseline Variables Age 45 (24) 50 (20) 46 (25) 44 (20.5) 40.5 (22.5) .509 BMI 27.3 (8.5) 29 (5.9) 26.2 (5.8) 25.9 (12.3) 26.8 (10.6) .584 Female 61 (60.4) 11 (61.1) 24 (75) 13 (56.5) 13 (46.4) .164 White 95 (97) 18 (100) 28 (93) 22 (96) 27 (100) .911 History of Malignancy 53 (52.5) 12 (66.7) 19 (59.4) 8 (34.8) 14 (50) .164 Colonoscopy Variables Total number 327 45 111 50 121 Per Patient 2 (4) 1.5 (2.8) 3 (2.2) 2 (2) 4 (4) .004 Surveillance (years) 3.6 (6) 0.3 (4.4) 3.9 (6.2) 1.1 (3.9) 4.5 (4.9) .023 Surveillance Outcomes Adenoma 54 (53.5) 9 (50) 18 (56.2) 10 (43.5) 17 (60.7) .650 SSL 17 (16.8) 5 (27.8) 5 (15.6) 3 (13) 4 (14.3) .621 AA/HGD/CRC 29 (28.7) 5 (27.8) 10 (31.2) 2 (8.7) 12 (42.9) .051 SSL: Sessile serrated lesion; AA: Advanced Adenoma; HGD: High grade dysplasia; CRC: Colorectal Cancer Values are n (%) or median (IQR); *Fisher’s exact for categorical variables & Kruskal-Wallis for continuous.
Endoscopic Management of Hamartomatous Polyposis Syndromes
Current Treatment Options in Gastroenterology · 2021-09-26 · 1 citations
articleDigestive Diseases and Sciences · 2020-08-20 · 18 citations
article
Frequent coauthors
- 6 shared
Priyanka Kanth
Georgetown University
- 4 shared
Linda J. Taylor
Western General Hospital
- 3 shared
Elena Gibson
University of Alabama at Birmingham
- 3 shared
Douglas G. Adler
- 3 shared
David E. Loren
Thomas Jefferson University Hospital
- 2 shared
Haojia Li
- 2 shared
John C. Fang
- 2 shared
David Jonason
Education
M.D.
Medical University of South Carolina
Other, Gastrointestinal and Hepatology
University of Utah School of Medicine
Other, Internal Medicine
University of Utah School of Medicine
Other, Internal Medicine
University of Utah School of Medicine
- Resume-aware match score
- Save to shortlist
- AI-drafted outreach
See your match with Judith Staub
PhdFit ranks faculty by your research interests, methods, and publications — grounded in their actual work, not templates.
- Free to start
- No credit card
- 30-second signup