Bilateral quadriceps tendon rupture (BQTR) is an uncommon injury, with a recent review identifying approximately 105 cases reported in the English and German literature. Primary hyperparathyroidism (PHPT) is a rare cause, historically accounting for only about 5% of simultaneous BQTR cases described between 1949 and 2002 ^[1,2]. Quadriceps tendon rupture typically occurs in older adults or individuals with predisposing risk factors such as chronic renal failure, gout, rheumatoid arthritis, prolonged corticosteroid use, or metabolic bone disease ^[2]. PHPT, most often due to a solitary parathyroid adenoma, results in excessive secretion of parathyroid hormone (PTH), leading to hypercalcemia, increased osteoclastic bone resorption, and compromised osteotendinous integrity ^[3,4]. Chronic hypercalcemia and altered collagen metabolism may weaken tendon attachment sites, predisposing to rupture even after minimal trauma ^[3]. This report describes the case of a young adult with no prior comorbidities who sustained BQTR after minimal trauma, which led to the diagnosis of PHPT due to a parathyroid adenoma.

A 30-year-old male of African ancestry, born in France, working as a delivery man, presented to the emergency department with acute bilateral knee pain and inability to extend his legs. The injury occurred while descending stairs; he missed a step with his left foot and avoided falling by a rapid transfer of weight to his right leg. He denied direct trauma, falls, or previous knee problems. On examination, there was suprapatellar swelling bilaterally, palpable defects above both patellae, and inability to perform a straight leg raise. Knee flexion was limited due to pain. Distal neurovascular examination was intact.

Laboratory results

• Serum calcium: 3.96 mmol/L (ref: 2.15–2.55)
• PTH: 1908 pg/mL (ref: 15–65)
• Alkaline phosphatase (ALP): 1388 U/L (ref: 40–129)
• Vitamin D: 15.5 nmol/L (ref: 25–250).

Imaging

Magnet resonance imaging confirmed in sagittal T2-weighted sequences bilateral total distal quadriceps tendon rupture at the patella insertion site (Fig. 1 and 2). A parathyroid adenoma was diagnosed in axial T2-weighted sequence (Fig. 3).

Figure 1, 2: Magnet resonance imaging of both knees showing complete rupture of both distal quadriceps tendons with proximal retraction.

Figure 3: Magnet resonance imaging of the neck demonstrating a solitary hypoechoic nodule consistent with parathyroid adenoma.

Management

Bilateral quadriceps tendon repair was performed using transosseous sutures. During the same admission, a focused parathyroidectomy was performed, with histology confirming a parathyroid adenoma.

Outcome

Postoperatively, serum calcium and PTH levels normalized. At 6-month follow-up, the patient had regained full knee range of motion and strength, with no residual pain. Retrospective questioning revealed several months of generalized musculoskeletal aches prior to injury, which resolved completely after surgery.

BQTR is an uncommon event, with most reported cases occurring in older individuals or those with systemic comorbidities such as chronic renal insufficiency, gout, rheumatoid arthritis, or prolonged corticosteroid therapy ^[2]. The simultaneous rupture of both tendons in a young, otherwise healthy adult following minimal trauma is exceptionally rare. In the present case, the underlying cause was PHPT due to a solitary parathyroid adenoma. The pathophysiology of tendon rupture in PHPT is multifactorial. Chronically elevated PTH promotes osteoclastic bone resorption, particularly at the osteotendinous junction, where tendon integrity relies on strong mineralized anchorage ^[3,4]. Experimental and clinical data suggest that sustained PTH excess leads to structural weakening at the tendon–bone interface through several mechanisms. Chronic osteoclastic activity at the enthesis causes cortical bone resorption and subperiosteal thinning, reducing the mineralized anchor for tendon fibers ^[3]. At the same time, hypercalcemia and altered phosphate metabolism impair collagen synthesis and disrupt extracellular matrix organization, leading to reduced tensile strength of the tendon itself ^[5,6]. Secondary Vitamin D deficiency, often coexisting in PHPT, further compromises mineralization and muscle–tendon health ^[7]. The combination of osteotendinous junction fragility and intrinsic tendon degeneration explains why relatively trivial trauma may result in rupture in these patients ^[5,6]. A review of the literature reveals that fewer than 20 cases of tendon rupture as the first presentation of PHPT have been reported to date ^[1,2,8,9]. Soler and Giner also reported BQTR linked to PHPT ^[8], while Di Monaco et al. described a similar case in a relatively young patient ^[9]. Among reported cases, most occurred in middle-aged or older adults, often with additional comorbidities such as renal failure or parathyroid carcinoma. For example, Farrah et al. described simultaneous BQTR in association with parathyroid carcinoma, a much more aggressive endocrine disorder ^[1]. Shah, in an earlier series, noted PHPT as a rare but important risk factor for tendon rupture but primarily in patients with systemic disease ^[2]. Other authors have documented quadriceps tendon rupture in the setting of secondary hyperparathyroidism due to chronic renal failure ^[10]. In contrast, our patient was only 30 years old, had no other comorbidities, and presented with adenoma-driven PHPT as the sole precipitating factor. To the best of our knowledge, this makes him one of the youngest reported patients in the literature to present with BQTR as the initial manifestation of PHPT. From a clinical standpoint, this case highlights several important considerations. First, bilateral tendon rupture after low-energy trauma should immediately raise suspicion for systemic disease. A simple set of laboratory tests – including serum calcium, phosphate, ALP, and PTH – can rapidly uncover an endocrine or metabolic cause. Early recognition of PHPT is crucial, as delayed diagnosis not only predisposes patients to musculoskeletal complications but may also increase the risk of nephrolithiasis, neurocognitive impairment, and cardiovascular morbidity if untreated ^[3,4]. Second, management requires a dual approach: Surgical repair of the tendon injury to restore function and definitive treatment of the endocrine disorder to prevent recurrence. Our patient underwent successful bilateral tendon repair followed by parathyroidectomy in the same admission, with normalization of biochemical parameters and excellent functional recovery. Importantly, retrospective history revealed longstanding musculoskeletal aches that completely resolved after parathyroidectomy, reinforcing the systemic impact of PHPT on quality of life. Finally, this case underscores the value of preventive screening. Routine measurement of serum calcium is inexpensive and may allow diagnosis of PHPT at an earlier stage, before catastrophic musculoskeletal injuries occur. For orthopedic surgeons, awareness of this rare but important association is critical, as recognizing the systemic cause can change long-term outcomes ^[4].

While rare, PHPT should be considered in the differential diagnosis of tendon rupture in young patients, particularly when bilateral or associated with minimal trauma. Prompt diagnosis and surgical management of both the tendon injury and the underlying parathyroid pathology can result in excellent functional recovery and resolution of systemic symptoms.

Young patients presenting with tendon rupture after trivial trauma should prompt clinicians to search for systemic causes. Simple laboratory tests such as serum calcium and PTH can uncover PHPT. Timely diagnosis and combined surgical management of both the tendon injury and the endocrine disorder ensure excellent recovery and prevent recurrence.