Adenovirus-Associated Rhabdomyolysis Presenting With Gastrointestinal Symptoms and Preserved Renal Function in an Immunocompetent Young Adult: A Case Report

Abstract

Introduction

Rhabdomyolysis is characterized by skeletal muscle breakdown resulting in the release of intracellular contents into the circulation. Although trauma, medications, and metabolic disorders are common causes, viral infections are increasingly recognized as potential triggers.

Case Presentation

A 26-year-old previously healthy male presented with a 2-day history of abdominal pain, diarrhea, vomiting, bilateral thigh pain, and dark urine. Laboratory evaluation demonstrated severe rhabdomyolysis with a peak creatine phosphokinase (CK) level of 25,036 U/L, elevated aminotransferases, and preserved renal function. A stool gastrointestinal multiplex polymerase chain reaction (PCR) panel was positive for adenovirus and did not identify other enteric pathogens. Alternative etiologies, including significant recent exertion, medication-related muscle injury, toxin exposure, autoimmune myopathy, and inherited metabolic disorders, were considered but were not supported by the clinical history or disease course. The patient was treated with early intravenous isotonic fluid 1L every 6 hours and experienced progressive biochemical and clinical improvement without developing acute kidney injury.

Discussion

Adenovirus-associated rhabdomyolysis is an uncommon but increasingly recognized clinical entity in adults. The pathogenesis may involve direct viral muscle injury, immune-mediated inflammation, and contributory factors such as dehydration associated with gastrointestinal illness. Although adenovirus was considered the most likely precipitating factor in this case, a definitive causal relationship cannot be established.

Conclusion

This case highlights probable adenovirus-associated rhabdomyolysis in an immunocompetent young adult presenting predominantly with gastrointestinal symptoms and preserved renal function despite marked creatine kinase elevation. Early recognition, careful evaluation of alternative etiologies, and prompt supportive management are important for preventing complications and achieving favorable outcomes.

Introduction

Rhabdomyolysis is a clinical and biochemical syndrome resulting from skeletal muscle injury, leading to the release of intracellular components such as myoglobin, CK, and electrolytes into the bloodstream. The condition ranges in severity from asymptomatic elevations in muscle enzymes to life-threatening complications, including acute kidney injury (AKI), electrolyte imbalances, arrhythmias, and disseminated intravascular coagulation. ¹

The diagnosis is typically established when serum CK levels exceed five times the upper limit of normal. Common etiologies include trauma, prolonged immobilization, strenuous exercise, medications (e.g., statins), metabolic disturbances, and endocrine disorders. Infectious causes, particularly viral infections, are less commonly reported but increasingly recognized.

The underlying pathophysiology involves disruption of cellular energy production, leading to impaired ion homeostasis, cellular swelling, and eventual myocyte necrosis. Subsequent inflammatory responses further exacerbate muscle damage.

Adenovirus-associated rhabdomyolysis has been reported in the literature for several decades, with early adult cases described in the late 1970s and early 1980s and subsequent reports across diverse clinical settings. Although uncommon, the condition spans a spectrum of severity ranging from self-limited muscle injury to cases complicated by acute kidney injury and systemic complications.^1-9 We present a case of adenovirus-associated rhabdomyolysis in a young immunocompetent adult to further contribute to the growing body of literature and to highlight important diagnostic considerations in patients presenting with acute viral illness and marked creatine kinase elevation.

Case Presentation

A 26-year-old previously healthy male presented to the emergency department with a 2-day history of crampy abdominal pain, multiple episodes of diarrhea and vomiting, and bilateral thigh pain severe enough to limit ambulation. He also reported dark-colored urine.

He denied alcohol use, recent medication intake, or use of anabolic steroids or supplements. His past medical history was unremarkable except for rhinoplasty. Although physically active and a regular gym attendee, he denied recent excessive exertion, eccentric exercise, heat exposure, dehydration, prolonged fasting, pre-workout supplements, energy drinks, illicit stimulants, or immobilization.

On examination, he was hemodynamically stable. Abdominal examination revealed mild tenderness without guarding or rigidity. Cardiopulmonary examination was unremarkable.

Investigations

Initial laboratory findings included:

• • CK: 22,600 U/L

• • AST: 289 U/L, ALT: 141 U/L

• • Serum creatinine: 0.98 mg/dL

• • White blood cell count: 13.02 × 10⁹/L

• • CRP: 0.4 mg/dL

• • Electrolytes: within normal limits

• • INR: 0.98

Infectious workup, including stool studies and serologies for hepatitis A, was negative. A gastrointestinal multiplex PCR panel was positive for adenovirus. Chest radiography was unremarkable.

Beyond stool testing and hepatitis A serology, additional investigations for alternative infectious and noninfectious causes of rhabdomyolysis were not performed. Specifically, testing for hepatitis B virus, hepatitis C virus, Epstein–Barr virus, cytomegalovirus, influenza, SARS-CoV-2, human immunodeficiency virus (HIV), and leptospirosis was not obtained. Similarly, thyroid function testing, autoimmune myositis evaluation, and investigations for inherited metabolic myopathies were not performed during the hospitalization.

Although mild leukocytosis was present on admission, the patient remained hemodynamically stable, afebrile, and without features of systemic bacterial infection. CRP was minimally elevated, and no microbiological evidence of bacterial gastroenteritis was identified. In light of these findings and the detection of adenovirus on stool multiplex PCR testing, antibiotic therapy was not initiated.

Management and Outcome

The patient was admitted for monitoring and management of rhabdomyolysis. He received intravenous hydration with isotonic saline of 1 L every 6 hours and symptomatic treatment with paracetamol. Antibiotics were not administered.

Urine output was closely monitored and remained consistently above 0.5 mL/kg/hour throughout hospitalization, indicating preserved renal perfusion and adequate volume status. Sodium bicarbonate therapy was not administered, as there was no clinical or laboratory evidence suggestive of metabolic acidosis during hospitalization. Serum electrolytes and available biochemical parameters did not indicate the need for urinary alkalinization. Nephrology consultation was not required, as the patient maintained normal renal function throughout hospitalization, with stable serum creatinine, adequate urine output, and no electrolyte or acid–base abnormalities.

Serial laboratory monitoring demonstrated a progressive decline in CK and liver enzyme levels, with preserved renal function throughout hospitalization.

The patient was discharged after 4 days of hospitalization once clinical improvement was achieved, including resolution of gastrointestinal and muscle symptoms, down-trending creatine kinase levels, stable renal function, preserved oral intake, and continued hemodynamic stability.

At outpatient follow-up 2 weeks after discharge, the patient’s creatine phosphokinase level had decreased further to 3,048 U/L. The serum creatinine was 0.77 mg/dL, remaining within the normal range. The patient had no evidence of delayed renal dysfunction, and no complications were identified. He reported complete resolution of muscle pain, normalization of urine color, and no recurrence of gastrointestinal symptoms.

He was advised to maintain adequate hydration and to gradually resume physical activity only after continued clinical and biochemical improvement.

Relevant laboratory values’ trend is shown in the following table (Table 1):

Table 1.

Trend of Relevant Laboratory Values During Hospitalization

Laboratory test	Day 0	Day 1	Day 2	Day 4
CK	22600 U/L	25036 U/L	17827 U/L	6108 U/L
Gamma GT	18 U/L	16 U/L	15 U/L	15 U/L
ALT	141 U/L	134 U/L	118 U/L	119 U/L
AST	289 U/L	251 U/L	206 U/L	118 U/L
Creatinine	0.98 mg/dL	0.83 mg/dL	0.72 mg/dL	0.72 mg/dL
White blood cells	13.02 x 109/L	10.52 x 109/L	7.93 x 109/L	7.51 x 109/L

Of note, potassium, phosphate, calcium, bicarbonate, urinalysis, urine blood/myoglobin, bilirubin, alkaline phosphatase, and LDH are not in the table as these values were unavailable.

A structured timeline of the patient’s clinical course is provided in Table 2 in accordance with the CARE case report guidelines.

Table 2.

Timeline of Clinical Course

Time point	Clinical events and findings
Day -2	Onset of abdominal pain, diarrhea, vomiting, bilateral thigh pain, and dark urine
Day 0 (Emergency Department Presentation)	Hemodynamically stable. Laboratory evaluation showed CK 22,600 U/L, AST 289 U/L, ALT 141 U/L, creatinine 0.98 mg/dL, WBC 13.02 × 109/L. Stool gastrointestinal multiplex PCR positive for adenovirus
Day 0	Admission to hospital. Intravenous isotonic saline initiated (1 L every 6 hours). Serial monitoring of renal function, electrolytes, urine output, and CK levels
Day 1	Peak CK 25,036 U/L. Renal function remained normal
Day 2	Clinical improvement with decreasing muscle pain and improvement in gastrointestinal symptoms. CK decreased to 17,827 U/L
Day 4 (Discharge)	Resolution of gastrointestinal symptoms and significant improvement in myalgias. CK 6,108 U/L. Creatinine 0.72 mg/dL. Discharged with hydration advice and outpatient follow-up
2-Week Follow-Up	Complete symptom resolution. CK decreased further to 3,048 U/L. Creatinine 0.77 mg/dL. No evidence of delayed renal dysfunction or recurrence of symptoms

Discussion

Adenovirus is a well-known cause of respiratory and gastrointestinal infections, particularly in pediatric populations. However, its association with rhabdomyolysis in adults remains rare. ¹

Several case reports have described adenovirus-associated rhabdomyolysis, sometimes complicated by acute renal failure. Proposed mechanisms include direct viral invasion of myocytes and immune-mediated muscle injury, although definitive evidence is lacking. ²

In this case, adenovirus infection was identified in the context of gastrointestinal symptoms and significant muscle injury. However, alternative etiologies must be considered. Exercise-induced rhabdomyolysis remains a potential contributing factor, particularly in physically active individuals.^3,4 The absence of recent intense exertion and the presence of systemic symptoms support a viral etiology, although a multifactorial mechanism cannot be excluded. For instance, other potential causes of rhabdomyolysis were also considered. Autoimmune inflammatory myopathies were thought to be unlikely given the acute onset of symptoms, the absence of progressive muscle weakness or other systemic autoimmune manifestations, and the rapid improvement observed with supportive treatment alone. Similarly, toxin-induced rhabdomyolysis was considered less likely as the patient denied alcohol use, medications, supplements, anabolic steroids, or other relevant exposures. Although occult metabolic myopathies may predispose individuals to muscle injury, the absence of a history of recurrent rhabdomyolysis, exercise intolerance, or previous exertional symptoms made an underlying inherited metabolic disorder less probable. Taken together, these findings support adenoviral infection as the most plausible precipitating factor, while acknowledging that a multifactorial contribution cannot be entirely excluded.

The decision to withhold antibiotic therapy was based on the overall clinical and microbiological assessment. Although bacterial gastroenteritis and systemic infection were considered in the differential diagnosis, the patient’s stable clinical status, low inflammatory markers, absence of organ dysfunction suggestive of sepsis, and lack of evidence for bacterial enteric pathogens made a bacterial etiology less likely. This case highlights the importance of integrating clinical findings with microbiological testing to guide antimicrobial stewardship and avoid unnecessary antibiotic exposure.

The association between adenovirus infection and rhabdomyolysis in this case should be interpreted with appropriate caution. Although definitive proof of causality is lacking, several factors support a probable relationship. First, a clear temporal association existed between the onset of acute gastrointestinal symptoms and the development of rhabdomyolysis. Second, adenovirus was identified during the acute illness, and no alternative infectious pathogen was detected. Third, previous case reports and reviews have documented adenovirus-associated rhabdomyolysis in both pediatric and adult populations, providing biological plausibility and consistency with the existing literature. ³ Finally, other common causes of rhabdomyolysis, including medication exposure, toxin use, significant recent exertion, autoimmune myopathy, and metabolic muscle disease, were not supported by the clinical history or disease course. Nevertheless, the absence of serum adenovirus PCR, viral load measurements, repeat testing, or direct evidence of systemic adenoviral infection limits the strength of the causal inference. Accordingly, we consider adenovirus to be the most likely precipitating factor in this case while acknowledging that a multifactorial etiology cannot be completely excluded. In other words, the development of rhabdomyolysis in this patient likely resulted from a multifactorial process. The onset of gastrointestinal symptoms, including vomiting and diarrhea, preceded the development of significant muscle pain and marked elevation in creatine kinase, suggesting a temporal relationship between systemic illness and muscle injury. Volume depletion secondary to gastrointestinal fluid losses, combined with a possible systemic inflammatory response to adenoviral infection, may have contributed to reduced muscle perfusion and increased susceptibility to myocyte injury. Although the patient denied excessive exertion, his baseline physical activity may have further lowered the threshold for muscle injury in the context of acute viral illness. Taken together, these factors support a synergistic mechanism involving viral infection, systemic illness, and host susceptibility rather than a single isolated cause.

Exercise-induced rhabdomyolysis represents an important alternative consideration in this case given the patient’s regular participation in gym-based physical activity. Exertional rhabdomyolysis may occur following unaccustomed, excessive, or high-intensity exercise and can present with muscle pain, dark urine, and marked elevations in creatine kinase levels. ⁴ Although our patient denied recent excessive exertion and other recognized precipitating factors, including alcohol consumption, supplement use, and prolonged immobilization, exercise-related muscle injury cannot be entirely excluded. Therefore, it is possible that physical activity may have contributed to the severity of muscle injury, acting either independently or in conjunction with the concurrent adenoviral infection.

The elevated AST and ALT levels observed in this patient were likely attributable, at least in part, to skeletal muscle injury rather than primary hepatic disease. Aminotransferases, particularly AST, are present in skeletal muscle and may be released into the circulation during muscle breakdown. The parallel decline in transaminase and CK levels, together with normal GGT and preserved liver synthetic function, supports muscle injury as the principal source of these biochemical abnormalities. ⁴

Despite markedly elevated CK levels, the patient did not develop acute kidney injury. While the risk of renal complications generally increases with the severity of muscle breakdown, the occurrence of AKI is influenced by multiple factors, including baseline renal function, hydration status, and the promptness of treatment. In this case, serum creatinine was normal at presentation, and intravenous fluid resuscitation was initiated early, likely limiting myoglobin-induced renal tubular injury and preserving kidney function. This favorable outcome highlights the importance of early recognition and prompt supportive management in patients with rhabdomyolysis.^3,4

Management of rhabdomyolysis is primarily supportive, with fluid resuscitation with isotonic fluid of 1 L every 6 hours aimed at preventing AKI and focuses on early recognition, volume resuscitation, serial monitoring of renal function and electrolytes, and prevention of pigment-induced acute kidney injury. ⁵ The patient responded well to early hydration with isotonic fluid of 1 L every 6 hours, with no complications. Although intravenous fluid administration remains the cornerstone of treatment, the optimal rate and volume should be individualized according to the patient’s clinical status, renal function, comorbidities, and response to therapy. In the present case, preserved renal function at presentation and early initiation of intravenous fluids were likely important factors contributing to the favorable outcome and absence of renal complications. The patient received intravenous isotonic saline at approximately 1 L every 6 hours for the first days of hospitalization, with ongoing adjustment based on clinical status and laboratory trends. Renal function, electrolytes, and creatine kinase levels were monitored serially throughout admission. Urine output remained adequate during hospitalization, and no evidence of acute kidney injury developed. Clinical improvement was observed with progressive decline in creatine kinase levels and resolution of symptoms.

Although the detection of adenovirus on gastrointestinal multiplex PCR in the setting of acute gastrointestinal symptoms provides supportive evidence for adenovirus-associated rhabdomyolysis, a definitive causal relationship cannot be established from this case alone. The presence of adenovirus may indicate a concurrent infection rather than the sole cause of muscle injury. Furthermore, although the patient denied recent excessive exercise, his regular physical activity raises the possibility of subclinical exercise-related muscle injury contributing to the clinical presentation. Therefore, a multifactorial mechanism cannot be entirely excluded. Nevertheless, the temporal association between the viral illness and the onset of rhabdomyolysis, together with the absence of other identifiable causes, supports adenovirus infection as the most likely precipitating factor. ⁵

The potential for severe systemic complications in conditions characterized by substantial tissue injury and biochemical derangement highlights the importance of early recognition and prompt supportive management. Similar principles have been emphasized in other forms of acute systemic injury, including toxicological emergencies associated with multiorgan dysfunction and hemodynamic compromise. ⁵

The mechanisms underlying adenovirus-associated rhabdomyolysis remain incompletely understood. Several pathways have been proposed. Proposed pathways include direct viral invasion of skeletal muscle fibers, immune-mediated muscle injury triggered by systemic inflammation, and indirect effects related to dehydration and reduced tissue perfusion during acute illness. ⁶ In addition, the patient’s gastrointestinal illness may have contributed indirectly through volume depletion and reduced tissue perfusion resulting from vomiting and diarrhea. Although serum electrolyte concentrations were within normal limits at presentation, transient electrolyte disturbances prior to hospital admission cannot be excluded and may have increased susceptibility to muscle injury. Furthermore, while the patient denied recent excessive exertion, his regular participation in physical activity raises the possibility that exercise-related muscle stress may have acted synergistically with the viral illness. Therefore, the observed rhabdomyolysis may have resulted from a combination of viral and host-related factors rather than a single isolated mechanism. Although definitive evidence supporting one mechanism over another is lacking, the accumulation of published reports over several decades, beginning with the report by Meshkinpour and Vaziri, supports a genuine association between adenoviral infection and skeletal muscle injury. ⁷

Although adenovirus-associated rhabdomyolysis is often described as uncommon, the association has been recognized for several decades. Early reports published in the late 1970s and early 1980s documented severe rhabdomyolysis and myoglobinuria occurring in association with adenoviral infection, including cases complicated by acute renal failure. More recent reports have further expanded the clinical spectrum of disease, describing presentations in immunocompetent adults, collegiate athletes with concomitant hepatic injury, and pregnant patients with severe electrolyte disturbances. Collectively, these observations suggest that adenovirus-associated muscle injury may occur across a broad range of clinical settings and severity levels, ranging from self-limited disease to life-threatening complications requiring renal replacement therapy. The present case adds to this literature by demonstrating marked rhabdomyolysis associated with gastrointestinal adenoviral infection in an immunocompetent young adult who maintained preserved renal function throughout the course of illness. The association between viral infection and rhabdomyolysis has been recognized for several decades. Cases have been reported with influenza virus, Epstein–Barr virus, coxsackievirus, cytomegalovirus, and adenovirus, among others. Osamah and colleagues described rhabdomyolysis occurring during acute Epstein–Barr virus infection, further supporting the concept that viral pathogens may precipitate significant muscle injury through direct or immune-mediated mechanisms. The accumulating evidence from diverse viral infections provides biological plausibility for adenovirus as a potential trigger of rhabdomyolysis in susceptible individuals. ⁶

The available literature suggests that adenovirus-associated rhabdomyolysis can occur across a broad clinical spectrum. Meshkinpour and Vaziri reported one of the earliest adult cases in 1981, while subsequent reports have described severe disease complicated by acute kidney injury as well as less common presentations in specific populations. ⁷ Notably, Kishkovich et al reported adenovirus-associated rhabdomyolysis during pregnancy accompanied by significant hypokalemia and gastrointestinal symptoms. Together with previously published cases, these reports demonstrate the heterogeneous manifestations of adenovirus-associated muscle injury and underscore the importance of considering this diagnosis in patients presenting with acute viral illness and unexplained creatine kinase elevation (Table 3). ⁸

Table 3.

Published Adult Cases of Adenovirus-Associated Rhabdomyolysis Compared With the Present Case

Reference	Age/Sex	Immune status	Clinical presentation	Adenovirus diagnostic method	Peak CK (U/L)	Renal outcome	Treatment	Recovery
Tseytlin and Maynard, 2016 2	38/M	Immunocompetent	Flu-like illness, myalgias, dark urine, rhabdomyolysis	Respiratory viral panel positive for adenovirus	Markedly elevated (>100,000 reported)	Severe AKI requiring hemodialysis	Aggressive IV fluids, bicarbonate, temporary hemodialysis	Recovery of renal function after approximately 4 weeks
Hwang et al, 2021 9	Young adult male collegiate athlete	Immunocompetent	Nausea, vomiting, diarrhea, acute liver injury, rhabdomyolysis	Adenovirus testing positive during acute illness	Markedly elevated	No persistent renal dysfunction reported	Supportive care, IV hydration	Clinical and biochemical recovery with return-to-play protocol
Kishkovich et al, 2022 8	21/F (pregnant)	Immunocompetent (pregnancy)	Fever, abdominal pain, nausea, vomiting, diarrhea, hypokalemia, rhabdomyolysis	Respiratory pathogen panel positive for adenovirus	Elevated (exact peak CK not consistently reported)	No AKI reported	Supportive care, electrolyte replacement, monitoring	Recovery following prolonged hospital course
Present case	26/M	Immunocompetent	Abdominal pain, diarrhea, vomiting, bilateral thigh pain, dark urine	Stool gastrointestinal multiplex PCR positive for adenovirus	25,036	Preserved renal function; no AKI	​	​

A limitation of this case is that the association between adenovirus infection and rhabdomyolysis was based on a positive gastrointestinal multiplex PCR result rather than direct evidence of viral involvement in muscle tissue. Detection of adenovirus in stool may reflect active infection, prolonged viral shedding, or incidental carriage, depending on the clinical context and assay characteristics. Additional investigations such as serum adenovirus PCR, viral load assessment, or repeat testing were not available. Therefore, although the temporal relationship between the gastrointestinal illness and muscle injury supports adenovirus as the most likely trigger, a definitive causal relationship cannot be established. Another limitation of this manuscript is that only a qualitative positive adenovirus result was available and that Ct values, viral load measurements, and semi-quantitative data were not obtainable.

Although adenovirus was identified during the acute illness and represents the most plausible trigger for rhabdomyolysis in this case, the diagnostic evaluation was not exhaustive. Additional investigations for other infectious, autoimmune, endocrine, toxic, and inherited metabolic causes of rhabdomyolysis were not systematically performed. Furthermore, the absence of serum adenovirus PCR or other evidence of systemic viral dissemination limits the ability to establish a definitive causal relationship. Consequently, this case should be interpreted as probable adenovirus-associated rhabdomyolysis rather than conclusive proof of adenovirus-induced muscle injury.

This case report has several limitations that should be considered when interpreting its findings. First, as a single-patient report, it cannot establish a causal relationship between adenovirus infection and rhabdomyolysis, nor can it provide information regarding the incidence, risk factors, or prognosis of this uncommon clinical entity. Although the temporal association between the onset of gastrointestinal symptoms, the detection of adenovirus, and the development of rhabdomyolysis is suggestive, the findings remain observational and cannot be generalized to broader patient populations.

Another important limitation is that the diagnosis of adenovirus-associated rhabdomyolysis was based solely on a positive stool gastrointestinal multiplex polymerase chain reaction (PCR) result. Detection of adenoviral nucleic acid in stool does not necessarily indicate that adenovirus was the direct cause of skeletal muscle injury, as positive results may represent active enteric infection, prolonged viral shedding, or incidental viral carriage. Furthermore, serum adenovirus PCR, viral load measurements, repeat testing, and adenovirus serotyping were not available, limiting the ability to confirm systemic infection or strengthen the evidence supporting a causal relationship. Similarly, no muscle biopsy or histopathological evaluation was performed to demonstrate direct viral involvement or inflammatory muscle injury, although such investigations are not routinely indicated in clinically improving patients.

The diagnostic evaluation for alternative causes of rhabdomyolysis was also incomplete. While the patient’s history and clinical course made medication-related muscle injury, toxin exposure, autoimmune inflammatory myopathy, and inherited metabolic disorders less likely, these conditions were not systematically excluded through laboratory or genetic investigations. Likewise, additional infectious causes of rhabdomyolysis, including influenza, SARS-CoV-2, Epstein–Barr virus, cytomegalovirus, human immunodeficiency virus, hepatitis B and C viruses, leptospirosis, and other viral pathogens, were not investigated. Consequently, the possibility of an undetected coexisting infectious or noninfectious contributor cannot be entirely excluded.

Although the patient denied recent excessive physical exertion, exertional muscle injury remains a potential confounding factor. As a physically active individual who regularly attended the gym, subclinical exercise-induced muscle injury may have lowered the threshold for rhabdomyolysis, particularly in the setting of concurrent viral illness. In addition, gastrointestinal fluid losses resulting from vomiting and diarrhea may have contributed to muscle injury through dehydration and reduced tissue perfusion. Therefore, it is plausible that the patient’s presentation resulted from a multifactorial process involving viral infection, host susceptibility, and physiological stress rather than a single isolated cause.

Several laboratory parameters that are commonly evaluated in patients with rhabdomyolysis were unavailable, including serum and urine myoglobin, lactate dehydrogenase, serial calcium and phosphate concentrations, comprehensive urinalysis findings, and detailed acid-base measurements. The absence of these data limits the ability to fully characterize the severity of muscle injury and compare this case with previously published reports. Additionally, no skeletal muscle imaging, such as magnetic resonance imaging, was performed to assess for evidence of myositis or muscle edema.

Follow-up was limited to two weeks after hospital discharge. Although the patient demonstrated complete clinical recovery with continued improvement in creatine kinase levels and preserved renal function, longer-term follow-up would have been valuable to confirm complete biochemical normalization, assess for recurrent episodes, evaluate long-term renal outcomes, and document the patient’s tolerance of return to physical activity.

Finally, the available literature on adenovirus-associated rhabdomyolysis remains limited and consists predominantly of isolated case reports and small case series, making comparisons across studies inherently difficult and susceptible to publication bias. Consequently, the true incidence, clinical spectrum, and prognosis of adenovirus-associated rhabdomyolysis remain uncertain. Additional prospective studies and larger case series are needed to better define the epidemiology, underlying mechanisms, optimal diagnostic approach, and management of this uncommon condition.

Conclusion

This case underscores the importance of considering viral infections, including adenovirus, in the differential diagnosis of rhabdomyolysis, especially when accompanied by systemic or gastrointestinal symptoms. Further research is needed to better understand the mechanisms linking viral infections and muscle injury.

ORCID iDs

Philippe Attieh https://orcid.org/0009-0006-8491-0790

Karam Karam https://orcid.org/0009-0001-1914-320X

Elias Fiani https://orcid.org/0000-0003-3204-9098

Ethical Considerations

Case reports are exempted from ethical approval at our institution.

Consent to Participate

A signed written informed consent was obtained from the patient.