Background
Acute pancreatitis is a recognized complication in people living with HIV (PLWH), with reported incidences historically higher than in the general population due to multiple concurrent risk factors, including alcohol use, biliary disease, opportunistic infections, and exposure to older antiretroviral agents [1–3]. Nucleoside reverse transcriptase inhibitors such as didanosine and stavudine, as well as protease inhibitors through induction of severe hypertriglyceridemia, are the best documented ART-related causes of pancreatitis [2].
Atraumatic splenic rupture (ASR) is rare but potentially fatal. Systematic reviews suggest that infection, neoplasia, and inflammatory conditions are predominant etiologies, with pancreatitis and pancreatic pseudocysts representing a small but important subset [4]. Several reports have described splenic subcapsular hematoma or rupture secondary to acute or chronic pancreatitis, often related to pancreatic tail pseudocysts eroding into perisplenic vessels or splenic parenchyma [5–8].
HIV-associated ASR has mainly been reported in the context of acute HIV seroconversion, opportunistic infections, or AIDS-related lymphoid hyperplasia [9, 10]. Atraumatic splenic rupture secondary to chronic HIV infection in the absence of overt alternative pathology has also been described, suggesting that HIV-related immune dysregulation and microangiopathy can, in rare cases, directly contribute to splenic fragility [10].
The coexistence of chronic HIV infection, pancreatitis with pancreatic tail pseudocyst, and atraumatic splenic rupture has only rarely been described. To our knowledge, very few reports have systematically discussed the interaction of these pathologies from both an infectious disease and surgical perspective. This case therefore adds to the literature by: (1) integrating detailed ART exposure history and immune status; (2) supporting a mechanistic link between pancreatic tail pseudocyst and splenic rupture; and (3) highlighting diagnostic and management considerations specific to PLWH.
The report is prepared according to the CARE case report guidelines [11].
Case presentation
Patient information and HIV history
A 35-year-old man presented to the emergency department with a 1-week history of epigastric pain that had acutely worsened over several hours, accompanied by dizziness and fatigue. He also reported intermittent upper abdominal pain over the preceding year, occasionally relieved by oral analgesics and fasting, for which no definitive diagnosis had been made.
He was diagnosed with HIV infection approximately nine years prior and had been followed at a local HIV clinic. Antiretroviral therapy (ART) history was as follows: from 28 December 2016 to 4 November 2019, nevirapine (NVP) plus zidovudine/lamivudine (AZT/3TC), discontinued due to adverse effects; from 24 December 2020 to 15 June 2022, the same NVP + AZT/3TC regimen was re-initiated; from 15 June 2022, lamivudine (3TC) plus efavirenz (EFV) plus tenofovir disoproxil fumarate (TDF); and from 31 July 2025, bictegravir/emtricitabine/tenofovir alafenamide (BIC/FTC/TAF).
He had never received didanosine or stavudine and had not been exposed to protease inhibitor–based regimens. There was no documented history of hypertriglyceridemia, pancreatotoxic medications such as pentamidine, high-dose steroids, or valproate, or opportunistic infections known to involve the pancreas. He denied alcohol abuse, smoking, or a family history of pancreatitis, and reported no history of trauma, recent endoscopic procedures, or anticoagulant therapy.
Longitudinal outpatient HIV records from 2016 to 2025 showed fluctuating immune and virologic control. CD4 cell counts were 131 cells/µL in 2016, 297 cells/µL in 2017, 246 cells/µL in 2018, 146 cells/µL in 2019, 79 cells/µL in 2022 (nadir), 189 cells/µL in 2023, 393 cells/µL in 2024, and 271 cells/µL in 2025. HIV RNA was below the lower limit of detection in 2017, 2018, and 2023, but became detectable again at 3,010 copies/mL in 2024 and 979 copies/mL in 2025.
Overall, these data indicate long-standing cumulative immunosuppression with partial, unstable immune reconstitution and intermittent low-level viremia before the index presentation.
Clinical findings on admission
On arrival, he was pale and appeared acutely ill. Vital signs showed low-grade fever, tachycardia, and borderline hypotension. Abdominal examination revealed generalized tenderness, maximal in the left upper quadrant and epigastrium, with guarding and rebound tenderness.
Bowel sounds were hypoactive. No external signs of trauma were evident.
Laboratory testing demonstrated anemia, leukocytosis with neutrophilia, thrombocytosis, and markedly elevated serum amylase and lipase compatible with acute pancreatitis [12]. C-reactive protein was elevated, while renal function and electrolytes were within normal limits. Serum triglycerides were not markedly elevated, and there was no clinical suspicion of hypertriglyceridemia-induced pancreatitis, as summarized in Table 1.
Table 1Laboratory results on admissionVariableValueReference rangeCD4 (cells/µL)393500—1600HIV RNA (copies/mL)3010<20WBC (10⁹/L)”15.804.0—10.0Absolute neutrophil count (10⁹/L)14.592.0—7.0Neutrophil percentage (%)92.40%50.0—70.0Absolute lymphocyte count (10⁹/L)0.30.8—4.0Lymphocyte percentage (%)1.9020.0—40.0Absolute monocyte count (10⁹/L)0.790.14—0.74Red blood cell count (10¹²/L)2.224.0—5.5Hemoglobin (g/L)68131—172Hematocrit (%)21.2038.0—50.8Platelet count (10⁹/L)565100—300AMY(U/L)895.0035.0—135.0CRP(mg/L)130.070—6.0TG(mmol/L)1.560—1.7
Imaging assessment
Contrast-enhanced CT of the abdomen revealed large-volume hyperdense free fluid consistent with hemoperitoneum in the perisplenic, perihepatic, peripancreatic spaces and pelvis (Fig. 1a). An irregular hypodense area with heterogeneous enhancement involving the upper pole of the spleen, extending towards the hilum, was seen, in keeping with splenic laceration and parenchymal disruption (Fig.
1b). Features of chronic pancreatitis were evident, including pancreatic atrophy, parenchymal calcifications, and a dilated main pancreatic duct (Fig. 1c).
A pseudocyst located in the pancreatic tail was closely adherent to the splenic hilum and upper pole, deforming the adjacent splenic contour (Fig. 1d). Preoperative CTA did not reveal any obvious pseudoaneurysm or “jet-like” high-density shadows.
Fig. 1A 35-year-old male patient with chronic HIV infection complicated by pancreatitis and atraumatic splenic rupture. a Pelvic fluid collection (brown arrow); b irregular, patchy hypodense lesion in the spleen (red arrow) with surrounding encapsulated fluid collection (blue arrow); c pancreatic atrophy with calcifications (yellow arrow) and dilatation of the main pancreatic duct (green arrow); d pancreatic tail pseudocyst (white arrow) and compressed splenic vein (gold arrow)
Based on clinical and radiological findings, a diagnosis of acute on chronic pancreatitis with pancreatic tail pseudocyst complicated by atraumatic splenic rupture and hemoperitoneum was made.
Therapeutic intervention
Given the patient’s evolving hemodynamic instability and generalized peritonitis, the multidisciplinary team (general surgery, interventional, infectious diseases, and anesthesiology) proceeded with emergency exploratory laparotomy.
Intraoperative findings included approximately 1500 mL of fresh and clotted intraperitoneal blood, most prominent around the spleen and left upper quadrant (Fig. 2a); a large laceration involving the upper pole of the spleen, extending toward the hilum with active bleeding (Fig. 2b); and a pseudocyst in the pancreatic tail, densely adherent to the splenic hilum, with surrounding inflammatory adhesions and evidence of chronic pancreatitis (Fig.
2c). No evidence of gastric or colonic perforation, portal hypertension, or intra-abdominal malignancy was noted.
Fig. 2Intraoperative findings and postoperative pathology. a Large blood clots adherent to the greater omentum, lesser sac, and liver surface (white arrow); b laceration of the upper pole of the spleen extending to the splenic hilum (yellow arrow); c pancreatic tail pseudocyst (white arrow); d Postoperative histological examination of the spleen showed local congestion and hemorrhage, with areas of degeneration and necrosis. No evidence of vasculitis, lymphoma, or granulomatous inflammation was found
According to the 2018 revision of the American Association for the Surgery of Trauma (AAST) spleen injury scale, the lesion was graded as at least Grade III, acknowledging that vascular lesions could not be fully characterized due to the lack of arterial-phase imaging.
The surgical team performed splenectomy and distal pancreatectomy (including resection of the pancreatic tail pseudocyst), followed by hemostasis, peritoneal lavage, and placement of drains in the pancreatic bed and pelvis. Total intraoperative blood loss was substantial and required transfusion of packed red blood cells and fresh frozen plasma. The patient was transferred to the intensive care unit postoperatively for close monitoring.
Postoperative course and follow-up
The patient was extubated on postoperative day (POD) 2 and transferred to the general ward once hemodynamically stable. Early postoperative complications included reactive thrombocytosis, with platelet counts approaching 900–1000 × 10⁹/L, which was managed with low-dose antiplatelet therapy. No clinically significant bleeding, pancreatic fistula, or intra-abdominal infection occurred.
Vaccination against Streptococcus pneumoniae, Haemophilus influenzae type b, and Neisseria meningitidis was administered prior to discharge in accordance with postsplenectomy guidelines. Postoperative histological examination of the spleen showed local congestion and hemorrhage, with areas of degeneration and necrosis. No evidence of vasculitis, lymphoma, or granulomatous inflammation was found.
Therefore, the possibility of spleen rupture caused by primary hematologic disorders or autoimmune diseases is unlikely. (Fig. 2d).
The patient resumed ART once oral intake was adequate and was co-managed by the infectious diseases team. At 15-month follow-up, he remained asymptomatic with no recurrence of abdominal pain, pancreatitis, or splenic/vascular complications. HIV viral load remained suppressed with stable CD4 counts on BIC/FTC/TAF.
Discussion
Relationship between HIV infection and pancreatitis
Pancreatic disease in PLWH is multifactorial. Pancreatitis can result from HIV itself, opportunistic infections (such as cytomegalovirus or mycobacteria), neoplasms, metabolic disturbances, and multiple drugs including some antiretrovirals [1–3]. Didanosine and stavudine carry the highest pancreatotoxic risk, particularly at cumulative high doses, while protease inhibitors are most often implicated through induction of severe hypertriglyceridemia [2].
In this patient, the ART history is notable for long-term NVP + AZT/3TC followed by EFV + TDF and, more recently, BIC/FTC/TAF—regimens with relatively low intrinsic risk of pancreatitis compared with didanosine/stavudine or some protease inhibitor–based combinations [2]. There was no exposure to didanosine, stavudine, or protease inhibitors, and no clinical evidence of hypertriglyceridemia. Therefore, while an ART contribution cannot be completely excluded, drug-induced pancreatitis appears unlikely and chronic pancreatitis probably has a multifactorial background, potentially including prior subclinical episodes of pancreatic injury [1–3].
Recent data suggest that acute pancreatitis in PLWH may present across the spectrum of immune status, and that the pattern and severity of pancreatitis do not strictly correlate with CD4 count [1]. In this case, HIV RNA was suppressed but CD4 counts remained only partially restored, suggesting incomplete immune reconstitution. Chronic low-grade immune activation in this setting might contribute to microvascular injury or impaired tissue repair in the pancreas and spleen, although this remains speculative.
Pancreatic tail pseudocyst and the “pancreas–spleen axis” of atraumatic Splenic rupture
In this report, we use the term “pancreas–spleen axis” to describe a proposed pathophysiological sequence—rather than a proven entity.Reported mechanisms include enzymatic digestion of splenic capsule and parenchyma by activated pancreatic enzymes, erosion of perisplenic arteries or veins by a pancreatic pseudocyst, and splenic vein thrombosis with left-sided portal hypertension and subsequent splenic congestion [4–8].
Several case reports have specifically described pancreatic tail pseudocysts causing splenic hematoma or rupture via direct contact and erosion into the splenic hilum or capsule, even in the absence of active acute pancreatitis [5–8]. In this patient, CT and intraoperative findings demonstrated chronic pancreatitis with a pancreatic tail pseudocyst; the pseudocyst adherent to and deforming the splenic hilum/upper pole; splenic rupture originating in the upper pole region in close proximity to the pseudocyst; and absence of malignancy or other focal splenic disease. These features strongly support a pancreas-driven mechanism of splenic injury.
Pancreatic enzymes and inflammatory mediators from the pseudocyst likely weakened the splenic capsule and perisplenic vessels, rendering the spleen vulnerable to rupture with minor increases in intra-abdominal pressure or spontaneous microtrauma. This “pancreas–spleen axis” is consistent with prior reports in non-HIV populations, in which pseudocyst-related splenic complications ranged from subcapsular hematoma to life-threatening rupture. Our case expands this concept to a PLWH with long-standing chronic pancreatitis, adding a layer of immunologic vulnerability.
HIV-related factors and atraumatic Splenic rupture
Atraumatic splenic rupture has been reported during acute HIV seroconversion, presumably due to acute lymphoid hyperplasia and capsular tension [9]. Cases of ASR secondary to chronic HIV infection without overt alternative pathology have also been described, emphasizing that HIV-related immune dysregulation and vasculopathy can occasionally predispose to splenic fragility [10].
Chronic HIV infection with incomplete immune reconstitution may have contributed to persistent immune activation and microvascular endothelial dysfunction [13, 14].In our patient, the CD4 nadir was 79 cells/µL in 2022, and CD4 counts remained below 200 cells/µL for several years before partially recovering to 393 cells/µL in 2024 and 271 cells/µL in 2025. HIV RNA was repeatedly undetectable in 2017, 2018, and 2023, but low-level viremia re-emerged with values of 3,010 and 979 copies/mL in 2024–2025. This trajectory is compatible with long-standing cumulative immunosuppression punctuated by episodes of renewed viral replication and immune activation.
This chronic, fluctuating pattern of immune dysfunction may contribute to microvascular fragility in the splenic and pancreatic circulation, thereby lowering the threshold for pancreas-driven vascular injury to progress to clinically overt atraumatic splenic rupture.However, our case does not provide direct histologic evidence of HIV-attributable vascular lesions in the spleen, and any contribution of HIV to splenic fragility in this patient remains inferential and hypothesis-generating rather than proven. we consider the temporal and anatomical relationship between the pancreatic tail psteudocyst and splenic rupture strongly suggests that pancreatitis-related mechanisms were dominant, with HIV acting as a potential background amplifier rather than the primary cause of splenic injury.
Diagnostic and management considerations
This case underscores several diagnostic lessons. First, clinicians should maintain a high suspicion for ASR in PLWH who present with sudden abdominal pain, hypotension, and signs of intra-abdominal bleeding, particularly when other causes such as trauma, ruptured ectopic pregnancy, or ruptured aortic aneurysm have been excluded [4–10]. Second, contrast-enhanced CT is the investigation of choice for suspected splenic injury, allowing assessment of lacerations, hematomas, hemoperitoneum, and vascular lesions [4, 8, 15].
The 2018 update of the AAST spleen injury scale, which incorporates vascular injuries, has improved correlation with management decisions and splenic salvage [15].
Contemporary trauma and splenic-injury guidelines support selective nonoperative management, with or without splenic artery embolization, in hemodynamically stable patients without generalized peritonitis, provided that close monitoring, interventional radiology, and rapid access to surgery are available. In such settings, observation with serial examinations and follow-up CT, combined with early angioembolization for vascular lesions, can achieve high splenic salvage rates and low failure rates even in higher-grade injuries. By contrast, emergent laparotomy and splenectomy remain the recommended strategy for patients who are hemodynamically unstable, require ongoing transfusion, or show diffuse peritonitis despite resuscitation [15, 16].
Our patient presented with evolving hypotension, generalized peritoneal signs, and a large volume hemoperitoneum, and was treated in a setting without immediate access to therapeutic angioembolization. In this context, nonoperative or purely endovascular management was not considered appropriate, and emergency splenectomy with distal pancreatectomy was chosen in line with current practice recommendations. Close collaboration between surgeons and infectious disease specialists ensured timely HIV-related management, optimal timing of ART resumption, and appropriate vaccination after splenectomy [17].
Our report also has several important limitations. First, as a single-patient case report, it can only generate hypotheses and cannot establish a causal relationship between chronic HIV infection and atraumatic splenic rupture; the mechanistic links we propose remain speculative. Second, although we were able to reconstruct selected historical CD4 and HIV RNA values, we did not systematically measure inflammatory or endothelial biomarkers (such as interleukin-6, high-sensitivity C-reactive protein, D-dimer, soluble CD14, angiopoietins, or asymmetric dimethylarginine), nor did we calculate formal metrics of cumulative viremia (e.g., viremia copy–years).
We therefore cannot precisely quantify this patient’s lifetime inflammatory and virologic burden or directly correlate it with the risk of splenic or pancreatic vascular injury. Third, no specialized vascular histopathology or immunostaining was undertaken to look for HIV-attributable microangiopathy in the spleen; as a result, any putative contribution of HIV to splenic fragility in this case remains circumstantial rather than proven. Finally, alternative spleen-preserving strategies such as observation with close monitoring and splenic artery embolization were not evaluated in this patient because of his evolving hemodynamic instability, generalized peritonitis, and limited local endovascular resources at the time of presentation, which may limit the generalizability of our management approach to other settings.
Why this case matters
This report adds to the literature in several ways. First, it describes the rare coexistence of chronic HIV infection, chronic pancreatitis with a pancreatic tail pseudocyst, and atraumatic splenic rupture, with a plausible mechanistic sequence linking these events. Second, detailed exposition of ART history shows the absence of high-risk agents such as didanosine/stavudine and protease inhibitors, helping to refine the differential diagnosis of pancreatitis in PLWH and avoid over-attribution to ART [1–3].
Third, the case supports the concept of a “pancreas–spleen axis,” whereby pancreatic tail pseudocysts can directly compromise splenic integrity, particularly in the setting of chronic inflammation and immune dysregulation [4–8, 10]. Finally, for clinicians caring for PLWH, the case reinforces the importance of early imaging, systematic evaluation of pancreatic tail lesions, and consideration of ASR in the differential diagnosis of acute abdomen.
Conclusions
In conclusion, we report a rare case of chronic HIV infection complicated by acute on chronic pancreatitis, pancreatic tail pseudocyst, and atraumatic splenic rupture. The clinical course supports a pancreas-driven mechanism of splenic injury, likely mediated by chronic pancreatic inflammation and pseudocyst-related erosion in a host with partial immune reconstitution.
For PLWH presenting with acute abdomen and imaging evidence of pancreatitis—especially involving the pancreatic tail—clinicians should maintain a high index of suspicion for splenic complications, including subcapsular hematoma and rupture. Early CT, timely surgical intervention when indicated, and coordinated postoperative HIV care are crucial for favorable outcomes.