Superior Mesenteric Artery Syndrome: Disease-Characteristics Report

Scope and evidence note. Superior mesenteric artery syndrome (SMAS) is rare, and its literature is dominated by retrospective cohorts, small prospective series, and case reports rather than large randomized trials. The most recent 2023–2024 literature located was primarily surgical or case-based; therefore, foundational reviews and the prospective cohort indexed as PMID 30291587 remain important. Numerical epidemiologic and mortality estimates should be treated cautiously because they often derive from older, selected series rather than population registries.

Table: This table condenses the highest-yield disease-characteristics fields for Superior Mesenteric Artery Syndrome, including secure identifiers, anatomy, phenotypes, mechanism, diagnostic thresholds, treatment, epidemiology, and major evidence gaps. It is designed for direct use in a structured disease knowledge base.

1. Disease information

Definition

SMAS is an extrinsic mechanical obstruction of the third, horizontal portion of the duodenum (D3) where it passes between the superior mesenteric artery (SMA) anteriorly and the abdominal aorta/spine posteriorly. Reduction of the intervening mesenteric-retroperitoneal fat cushion narrows the aortomesenteric angle and distance, compressing D3. It is a structural gastrointestinal compression syndrome, not mesenteric ischemia or SMA dissection. (galimov2022thecomplicationof pages 2-3, galimov2022thecomplicationof pages 3-4, galimov2022thecomplicationof pages 1-2)

A useful exact abstract quotation from Galimov et al. (published July 2022) is: “the distal part of the duodenum is compressed between the abdominal aorta, spine, and SMA,” producing mechanical obstruction. The authors also emphasize that delayed diagnosis may lead to life-threatening complications. DOI: https://doi.org/10.24060/2076-3093-2022-12-2-123-127. (galimov2022thecomplicationof pages 1-2)

Identifiers and synonyms

• MeSH: D013478, Superior Mesenteric Artery Syndrome—securely present in the retrieved ClinicalTrials.gov records. (NCT03416647 chunk 1)
• MONDO, OMIM, Orphanet, ICD-10, ICD-11: an exact current identifier was not securely recovered from the accessed evidence and should be verified directly against the live ontology release before knowledge-base ingestion. SMAS is not established as an OMIM Mendelian disorder.
• Synonyms: Wilkie syndrome/Wilkie’s syndrome; chronic duodenal obstruction; arteriomesenteric duodenal compression syndrome; cast syndrome/CAST syndrome. “Chronic duodenal obstruction” and “Wilkie’s syndrome” occur in the prospective-study record. (galimov2022thecomplicationof pages 3-4, NCT03416647 chunk 1)
• Do not conflate with: SMA thrombosis, embolism, dissection, aneurysm, or acute/chronic mesenteric ischemia.

The report describes aggregated disease-level evidence. The cited prospective study included 39 consecutive patients; no individual EHR-derived patient record is used here. (NCT03416647 chunk 1)

2. Etiology

Causal and predisposing factors

The best-established causal sequence is rapid or substantial weight loss → depletion of the aortomesenteric fat pad → narrowing of the aortomesenteric angle/distance → D3 compression. Once obstruction impairs eating, further weight loss can create a self-amplifying cycle. (galimov2022thecomplicationof pages 2-3, NCT03937193 chunk 1)

Recognized clinical contexts include:

• severe or rapid weight loss, low BMI, malnutrition, cachexia, or feeding restriction;
• eating disorders and other illnesses causing reduced intake or catabolism;
• major burns, trauma, malignancy, malabsorption, prolonged immobilization, or severe systemic illness;
• corrective spinal surgery, marked scoliosis, body casting, or rapid linear growth, which can alter the relationship between the SMA, aorta, spine, and duodenum;
• abdominal or retroperitoneal operations that change intestinal fixation or tension.

The prospective surgical protocol regarded BMI below 18.5 kg/m² with difficulty eating as a major clinical feature. Imaging studies specifically examine BMI, visceral fat, and retroperitoneal fat because these influence angle and distance; severe scoliosis and spinal fixation are treated as important anatomical modifiers. (NCT03416647 chunk 1, NCT04515251 chunk 1, NCT03937193 chunk 1)

Genetics, environment, and protective factors

No validated causal gene, susceptibility locus, pathogenic variant, modifier gene, Mendelian inheritance pattern, or gene–environment interaction has been established. Congenital/anatomical configurations may predispose an individual, but that is not equivalent to a demonstrated genetic disorder.

No toxin, pollutant, occupational exposure, or infectious agent is established as a direct cause. Lifestyle and environmental effects are principally mediated through nutritional depletion or acquired anatomical change. Maintaining adequate nutrition and avoiding rapid, unmonitored weight loss in vulnerable patients are plausible protective measures, but no controlled study establishes a specific protective diet, allele, drug, or supplement.

3. Phenotypes

SMAS can occur in children or adults and may present acutely after a precipitating event or insidiously over months or years. Severity ranges from intermittent postprandial discomfort to complete high intestinal obstruction and severe malnutrition. The 39-patient protocol defined clinically important disease through severe symptoms occurring at least weekly, poor quality of life, refractory response to medical treatment, underweight, or serious complications. (NCT03416647 chunk 1)

Abdominal pain, nausea, vomiting, reflux, and bloating were explicitly captured in the prospective cohort’s symptom score; severe complications included gastric perforation, acute pancreatitis, and aspiration pneumonia. (NCT03416647 chunk 1)

Formal SMAS-specific EQ-5D, SF-36, or PROMIS norms were not identified. Nevertheless, inability to tolerate meals, recurrent vomiting, nutritional dependence, and chronic pain can markedly impair physical, psychological, educational, occupational, and social functioning. The prospective study explicitly required poor quality of life for one clinical inclusion pathway. (NCT03416647 chunk 1)

4. Genetic and molecular information

SMAS is not currently defined by a molecular lesion. No causal gene, HGNC identifier, pathogenic germline or somatic variant, variant class, allele frequency, penetrance, anticipation, founder effect, carrier frequency, modifier gene, epigenetic defect, or recurrent chromosomal abnormality was identified.

Accordingly:

• ClinVar-style variant classification: not applicable.
• WES/WGS, gene panels, CMA, karyotyping, FISH, mtDNA, and repeat-expansion testing: not indicated for diagnosing SMAS itself.
• Genetic evaluation may be appropriate only when a separate syndromic, connective-tissue, developmental, or neuromuscular disorder is clinically suspected.
• No validated pharmacogenomic recommendation exists for SMAS treatment.

5. Environmental and lifestyle information

The clinically meaningful “environmental” exposures are circumstances producing weight loss or anatomical distortion rather than toxicants. Restrictive eating, inadequate caloric intake, prolonged illness, catabolic states, spinal correction, and postoperative anatomical changes are the principal acquired contexts. Retroperitoneal fat is directly relevant: a 510-participant CT study was designed to relate aortomesenteric geometry to visceral and subcutaneous fat, with 500 non-SMAS and 10 SMAS participants. (NCT03937193 chunk 1)

Smoking and alcohol have no established disease-specific causal association. Exercise is not intrinsically causal, although extreme energy imbalance could contribute indirectly. No bacterial, viral, fungal, or parasitic trigger is established.

6. Mechanism and pathophysiology

Causal chain

1. Upstream trigger: rapid weight loss, low visceral fat, altered spinal/mesenteric anatomy, or postoperative tension.
2. Structural intermediate: reduced fat cushion and narrowing of the SMA–aorta angle and distance.
3. Primary lesion: extrinsic compression of D3.
4. Functional consequence: impaired chyme passage, proximal duodenal/gastric stasis and dilation, vomiting, reflux, and postprandial pain.
5. Downstream systemic effects: reduced intake, dehydration, electrolyte abnormalities, malnutrition, and additional fat loss.
6. Complications: mucosal injury/ulceration, aspiration, perforation, pancreatitis, and potentially severe metabolic deterioration. (galimov2022thecomplicationof pages 2-3, galimov2022thecomplicationof pages 3-4, NCT03416647 chunk 1, galimov2022thecomplicationof pages 4-5)

This is principally a biomechanical obstruction. No disease-defining Wnt, MAPK, mTOR, PI3K–AKT, immune, inflammatory, apoptotic, autophagic, protein-folding, receptor, ion-channel, or enzyme-deficiency pathway is established. Likewise, no reproducible transcriptomic, proteomic, metabolomic, lipidomic, single-cell, spatial-transcriptomic, multi-omic, or CRISPR-screen signature was identified.

Suggested GO biological-process labels: digestive-system process; gastrointestinal motility; regulation of body weight; response to nutrient; intestinal absorption. These are annotation suggestions, not demonstrated molecular mechanisms. Relevant cell populations are ordinary duodenal epithelium, smooth-muscle cells, enteric neurons, vascular endothelial/smooth-muscle cells, and adipocytes; none is a selectively diseased cell type. Suggested CL labels therefore include enterocyte, intestinal epithelial cell, smooth-muscle cell, enteric neuron, endothelial cell, and adipocyte.

7. Anatomical structures affected

• Primary organ/site: D3, the horizontal/transverse duodenum.
• Compression boundaries: SMA anteriorly; abdominal aorta and vertebral column posteriorly.
• Relevant tissue: the aortomesenteric/retroperitoneal adipose cushion.
• Secondary involvement: proximal duodenum and stomach through dilation and stasis; esophagus and lungs through reflux/aspiration; pancreas in rare obstructive pancreatitis.
• Body systems: primarily digestive; secondarily nutritional/metabolic and respiratory.
• Lateralization: not applicable.
• Subcellular compartment: none specifically implicated.

Suggested UBERON labels are duodenum, third part of duodenum, superior mesenteric artery, abdominal aorta, retroperitoneal region, adipose tissue, stomach, and vertebral column. Exact ontology IDs should be mapped against the selected UBERON release rather than inferred from names.

8. Temporal development

Onset can be acute following rapid weight loss, trauma, or spinal/abdominal surgery, or chronic and insidious. The highest reported occurrence is in adolescents and young adults, but disease is documented across childhood, adulthood, and older age. One reviewed source reports a peak at 10–30 years. (galimov2022thecomplicationof pages 2-3)

There is no universally accepted stage system. A practical clinical sequence is:

1. intermittent postprandial symptoms;
2. persistent obstruction with reduced intake and weight loss;
3. severe nutritional/metabolic compromise or complications;
4. recovery after restoration of the fat cushion or surgical bypass.

The course may remit with successful weight restoration, recur if weight is again lost, or remain chronic if obstruction and nutritional depletion perpetuate each other. The principal intervention window is before profound malnutrition, aspiration, perforation, or other complications develop.

9. Inheritance and population epidemiology

Reported prevalence estimates vary approximately from 0.1% to 0.78% in selected radiographic or clinical populations, with a reported female-to-male ratio near 2:1 and concentration in the 10–30-year age range. These are not robust population-incidence estimates and should not be interpreted as contemporary global prevalence. No reliable annual incidence per 100,000 was identified. (galimov2022thecomplicationof pages 2-3)

No established ethnic founder population, endemic geography, consanguinity association, carrier state, penetrance, or expressivity framework applies. Geographic differences are likely dominated by referral patterns, nutritional exposures, surgical practice, and ascertainment. The Chinese normative CT study illustrates active work to derive population-specific reference distributions rather than assuming one universal angle or distance threshold. (NCT03937193 chunk 1)

10. Diagnostics

Diagnostic approach

Diagnosis requires both a compatible obstructive phenotype and imaging evidence of D3 compression. A narrow angle or distance alone can occur without symptomatic SMAS and should not be treated as diagnostic in isolation.

Preferred imaging: contrast-enhanced abdominal CT with sagittal reconstruction measures the aortomesenteric angle; axial images measure distance and show D3 compression and proximal gastric/duodenal dilation. CT or MR angiography can define vascular geometry. Oral water-soluble contrast or an upper-GI/barium series may show proximal dilation, abrupt hold-up at D3, delayed transit, and sometimes positional improvement. Ultrasound can measure angle/distance without radiation but is operator- and body-habitus-dependent. (galimov2022thecomplicationof pages 2-3, galimov2022thecomplicationof pages 3-4, galimov2022thecomplicationof pages 1-2, NCT03416647 chunk 1)

Commonly used values are:

• normal angle approximately 35–65° or 38–80°;
• normal distance approximately 10–28 mm;
• strongly suggestive abnormal geometry: angle <22° and/or distance <8 mm;
• broader case-literature cutoffs: angle <35° and distance <10 mm.

A published case measured 14° and 6 mm. Variation in normal and abnormal cutoffs reinforces the need for clinical-radiological concordance. (galimov2022thecomplicationof pages 2-3, galimov2022thecomplicationof pages 3-4, NCT07115472 chunk 1)

A current pediatric observational study, NCT04515251, is prospectively establishing age-, BMI-, and fat-adjusted ultrasound ranges in 289 children aged 10–15 years, highlighting that pediatric reference standards remain under development. ClinicalTrials.gov: https://clinicaltrials.gov/study/NCT04515251. (NCT04515251 chunk 1)

Laboratory and other testing

There is no disease-specific blood, urine, tissue, genetic, or circulating biomarker. Laboratory studies assess consequences and alternative diagnoses: CBC, electrolytes, bicarbonate, renal and hepatic function, glucose, magnesium, phosphate, calcium, albumin/prealbumin with appropriate caution, inflammatory markers, lipase, and nutritional deficiencies. Endoscopy may exclude luminal lesions and evaluate retained contents or mucosal injury but cannot by itself establish extrinsic D3 compression. Biopsy, electrophysiology, PET, and omics testing have no routine role.

Differential diagnosis

Important alternatives include gastroparesis, functional dyspepsia, cyclic vomiting/cannabinoid hyperemesis, eating disorders, peptic ulcer disease, pancreatitis, annular pancreas, malrotation/Ladd bands, duodenal web or tumor, Crohn disease, retroperitoneal mass, adhesions, chronic intestinal pseudo-obstruction, and other vascular-compression syndromes. Malignancy, motility disorders, and severe psychiatric illness were specifically excluded from the prospective surgical protocol, illustrating the need to avoid attributing nonspecific symptoms to incidental vascular geometry. (NCT03416647 chunk 1)

There is no population, newborn, carrier, or cascade screening program. Targeted imaging is reasonable in a high-risk patient with rapid weight loss or recent spinal surgery who develops persistent postprandial pain and vomiting.

11. Outcome and prognosis

Timely diagnosis and reversal or bypass of obstruction generally permit nutritional recovery and symptom improvement. A prospective cohort enrolled 39 patients, all treated with duodenojejunostomy, and assessed symptoms, BMI, and medication requirements at a median 47 months (IQR 34–72). PMID 30291587; publication: Journal of Gastrointestinal Surgery, May 2019; https://pubmed.ncbi.nlm.nih.gov/30291587/. (NCT03416647 chunk 1)

A 2022 case had an uncomplicated postoperative course, pain relief, weight gain, and discharge nine days after surgery. This is illustrative but not a population response rate. (galimov2022thecomplicationof pages 3-4, galimov2022thecomplicationof pages 1-2)

Potential morbidity includes chronic pain, inability to eat, malnutrition, dehydration, electrolyte disorders, aspiration pneumonia, acute pancreatitis, gastric perforation, ulcer disease, and repeated hospitalization. Older case-based literature reports mortality as high as 33% in untreated or severely delayed disease, but this figure is likely affected by historical care and selection bias and should not be presented as a modern average mortality rate. (galimov2022thecomplicationof pages 2-3, galimov2022thecomplicationof pages 4-5)

No validated five- or ten-year survival estimate, life-expectancy decrement, prognostic molecular biomarker, or disease-specific quality-of-life instrument was identified. Favorable factors are early recognition, reversible weight-loss trigger, successful nutritional restoration, and absence of severe complications; persistent symptoms despite adequate nutrition and coexisting motility or functional disorders complicate prognosis.

12. Treatment

Initial conservative management

For a hemodynamically stable patient without perforation or another surgical emergency:

1. nasogastric decompression when vomiting or marked dilation is present;
2. intravenous fluid, electrolyte, and acid–base correction;
3. antiemetic and symptom-directed therapy;
4. small, frequent, energy-dense meals when tolerated;
5. enteral feeding distal to the obstruction, such as nasojejunal feeding, if oral intake is inadequate;
6. parenteral nutrition when enteral feeding is impossible or insufficient;
7. positional maneuvers—left lateral decubitus, prone, or knee-chest—may transiently reduce compression;
8. multidisciplinary treatment of the precipitating illness or eating disorder.

The objective is weight restoration and reconstitution of the fat pad, not merely suppression of nausea. The refractory-SMAS trial operationally defines failed conservative therapy as failure of decompression, enteral nutrition, and parenteral nutrition. (NCT07115472 chunk 1)

Suggested NCIT-style intervention labels include Gastrointestinal Decompression, Enteral Nutrition, Parenteral Nutrition, Nutritional Support, and Antiemetic Therapy. No SMAS-specific pharmacotherapy is approved, and no pharmacogenomic algorithm applies.

Surgery and intervention

Laparoscopic duodenojejunostomy bypasses the compressed segment and is the best-supported definitive operation for refractory disease. Indications include persistent obstruction despite an adequate nutritional trial, inability to restore weight, recurrent hospitalization, severe complications, or a fixed anatomical cause. The 39-patient prospective cohort used duodenojejunostomy, with or without duodenal resection. (NCT03416647 chunk 1)

Other operations include Strong’s procedure—division of the ligament of Treitz and duodenal mobilization—gastrojejunostomy, duodenal derotation, and selected alternative bypass procedures. Terminology must be used carefully: Strong’s procedure is anatomically distinct from duodenojejunostomy, although some case reports describe combined mobilization and anastomosis. A 2022 report achieved symptom resolution after laparoscopic operative treatment. (galimov2022thecomplicationof pages 3-4, galimov2022thecomplicationof pages 4-5)

Potential surgical adverse events include leak, bleeding, infection, delayed gastric emptying, persistent symptoms, adhesive obstruction, nutritional problems, and reoperation. Evidence comparing procedures remains limited.

Recent and ongoing clinical research

• NCT03416647: completed, single-group prospective cohort; 39 participants; duodenojejunostomy; outcomes included symptom score, BMI, and medical-treatment need over median 47 months. The linked publication is PMID 30291587. https://clinicaltrials.gov/study/NCT03416647. (NCT03416647 chunk 1)
• NCT06970093: small randomized, open-label comparison of one-anastomosis gastric bypass versus duodenojejunostomy; 20 participants, 12-month symptoms and BMI endpoints. Although enrollment began in March 2024, the registry was first posted in May 2025; no efficacy results were available in the retrieved record. https://clinicaltrials.gov/study/NCT06970093. (NCT06970093 chunk 1, NCT06970093 chunk 2)
• NCT07115472: 45-patient single-group study of fluoxetine, 20–60 mg/day, in refractory SMAS specifically with DSM-5 somatic symptom disorder. This tests treatment of a comorbidity, not reversal of anatomical compression, and should not be generalized to routine SMAS. No posted efficacy result was retrieved. https://clinicaltrials.gov/study/NCT07115472. (NCT07115472 chunk 1)
• NCT03937193: completed 510-participant CT study of angle, distance, and retroperitoneal fat in a young Chinese population. https://clinicaltrials.gov/study/NCT03937193. (NCT03937193 chunk 1)
• NCT04515251: recruiting pediatric normative ultrasound study with estimated enrollment of 289 and estimated completion in December 2026. (NCT04515251 chunk 1)

Gene, cell, RNA, targeted molecular, and immunotherapies have no established role.

13. Prevention

Primary prevention

There is no vaccine, prophylactic medication, genetic screening, or universal prevention program. In high-risk settings, practical measures are nutritional assessment before and after major surgery, prevention of excessive perioperative weight loss, early dietitian involvement, and close monitoring of patients with severe scoliosis, spinal correction, catabolic illness, or restrictive eating.

Secondary prevention

Persistent vomiting and postprandial pain after rapid weight loss or spinal/abdominal surgery should prompt early imaging. Angle and distance should be interpreted with demonstrated duodenal obstruction rather than used as asymptomatic screening tests.

Tertiary prevention

Prevent recurrence and complications through sustained nutritional rehabilitation, treatment of the precipitating disorder, monitoring of weight/electrolytes, aspiration precautions when vomiting is severe, and timely surgery when conservative treatment fails. Genetic counseling and reproductive testing are not indicated for isolated SMAS.

14. Other species and natural disease

No well-characterized naturally occurring veterinary counterpart, breed predisposition, orthologous causal gene, zoonotic potential, or cross-species transmission was identified. Because SMAS is a mechanical relationship among the duodenum, SMA, aorta, spine, and fat pad, conceptually similar compression could occur in another species, but this should not be entered as a validated comparative-disease association without veterinary primary evidence.

15. Model organisms

No standardized mouse, rat, zebrafish, invertebrate, cellular, organoid, iPSC, knockout, knock-in, or humanized model was identified. Experimental manipulation of body weight or surgical alteration of mesenteric anatomy might model selected biomechanical features, but such an induced model would not reproduce the full human symptom complex and could create major welfare and translational limitations. Human CT/MR/ultrasound measurements, computational geometry, and clinical cohorts are currently more directly relevant than molecular model organisms.

Expert synthesis and knowledge-base recommendations

1. Classify SMAS as an acquired structural duodenal-obstruction syndrome, not a genetic or primary vascular-occlusive disease.
2. Encode the primary causal chain as loss of aortomesenteric adipose cushion/anatomical distortion → reduced angle and distance → extrinsic D3 compression → proximal obstruction → reduced intake and further weight loss.
3. Require clinical-radiological concordance; <22° and <8 mm are supportive thresholds, not stand-alone diagnostic criteria. Population-, age-, BMI-, and technique-dependent reference variation remains an active research issue. (NCT07115472 chunk 1, NCT04515251 chunk 1, NCT03937193 chunk 1)
4. Treat nutritional restoration and decompression as first-line care, with laparoscopic duodenojejunostomy as the principal definitive operation for persistent, fixed, or complicated disease. (NCT03416647 chunk 1)
5. Mark gene, variant, inheritance, molecular pathway, omics, biomarker, animal-disease, and model-organism fields as “not established”, rather than filling them with speculative associations.
6. Evidence certainty is moderate for the core anatomy and diagnostic concept, but low-to-moderate for exact epidemiology, optimal duration of conservative therapy, comparative surgical effectiveness, and long-term quality-of-life outcomes.

References

1. (galimov2022thecomplicationof pages 2-3): O. V. Galimov, V. O. Khanov, H.M. H. Karkhani, Sh. Bhawna, and T. R. Ibragimov. The complication of decrease in aorto-mesenteric angle and distance its diagnosis and treatment: case report. Creative surgery and oncology, 12:123-127, Jul 2022. URL: https://doi.org/10.24060/2076-3093-2022-12-2-123-127, doi:10.24060/2076-3093-2022-12-2-123-127. This article has 0 citations.

2. (galimov2022thecomplicationof pages 1-2): O. V. Galimov, V. O. Khanov, H.M. H. Karkhani, Sh. Bhawna, and T. R. Ibragimov. The complication of decrease in aorto-mesenteric angle and distance its diagnosis and treatment: case report. Creative surgery and oncology, 12:123-127, Jul 2022. URL: https://doi.org/10.24060/2076-3093-2022-12-2-123-127, doi:10.24060/2076-3093-2022-12-2-123-127. This article has 0 citations.

3. (NCT03416647 chunk 1): Angelica Ganss. SMAS: a Prospective Study in a Single Institution. Azienda Ospedaliera di Padova. 2008. ClinicalTrials.gov Identifier: NCT03416647

4. (galimov2022thecomplicationof pages 3-4): O. V. Galimov, V. O. Khanov, H.M. H. Karkhani, Sh. Bhawna, and T. R. Ibragimov. The complication of decrease in aorto-mesenteric angle and distance its diagnosis and treatment: case report. Creative surgery and oncology, 12:123-127, Jul 2022. URL: https://doi.org/10.24060/2076-3093-2022-12-2-123-127, doi:10.24060/2076-3093-2022-12-2-123-127. This article has 0 citations.

5. (NCT07115472 chunk 1): Zhifeng Zhao, PhD. Fluoxetine in Refractory Superior Mesenteric Artery Syndrome by Targeting Comorbid Somatic Symptom Disorder. Xijing Hospital of Digestive Diseases. 2024. ClinicalTrials.gov Identifier: NCT07115472

6. (NCT04515251 chunk 1): Marirosa Cristallo Lacalamita. Ultrasound Evaluation of Superior Mesenteric Artery Measurements in a Healthy Pediatric Population. Ente Ospedaliero Cantonale, Bellinzona. 2020. ClinicalTrials.gov Identifier: NCT04515251

7. (NCT06970093 chunk 1): Comparison of One Anastomisis Gastric Bypass and Duodeno-Jejunostomy for Treating SMA Syndrome. Ain Shams University. 2024. ClinicalTrials.gov Identifier: NCT06970093

8. (NCT03937193 chunk 1): Professor Winnie W.C. Chu. Normal Range of Superior Mesenteric Artery in Young Chinese Population and Its Correlation With Retroperitoneal Adipose Tissue. Chinese University of Hong Kong. 2019. ClinicalTrials.gov Identifier: NCT03937193

9. (galimov2022thecomplicationof pages 4-5): O. V. Galimov, V. O. Khanov, H.M. H. Karkhani, Sh. Bhawna, and T. R. Ibragimov. The complication of decrease in aorto-mesenteric angle and distance its diagnosis and treatment: case report. Creative surgery and oncology, 12:123-127, Jul 2022. URL: https://doi.org/10.24060/2076-3093-2022-12-2-123-127, doi:10.24060/2076-3093-2022-12-2-123-127. This article has 0 citations.

10. (NCT06970093 chunk 2): Comparison of One Anastomisis Gastric Bypass and Duodeno-Jejunostomy for Treating SMA Syndrome. Ain Shams University. 2024. ClinicalTrials.gov Identifier: NCT06970093

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