Pegfilgrastim is a granulocyte colony-stimulating factor used in non-myeloid cancer patients to prevent infections and neutropenic fevers. Although this medication is widely used to induce granulocytosis in pancytopenia patients, there are certain instances where such a situation can cause severe side effects. In this case, we present a patient with a history of metastatic colon cancer who is currently taking pegfilgrastim to counter the agranulocytosis caused by his chemotherapy treatment. However, the patient shortly developed localized left-sided jaw swelling, and upon further investigation, the granulocyte colony-stimulating factor revealed an underlying bacteremia. A discussion will also be held regarding the mechanism of action of how pegfilgrastim induced this patient\'s symptoms as well as the risks and benefits.

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An 81-year-old man with prostate cancer (cT3aN0M0), who had been undergoing hormonal therapy for 4 years and had maintained low prostate specific antigen levels, developed metastasized pelvic lymph nodes. A tissue biopsy revealed neuroendocrine differentiation of prostate cancer in the metastatic lymph nodes. Consequently, chemotherapy with carboplatin＋etoposide was initiated. During the first course, filgrastim was administered for 2 days due to a drop in his neutrophil count to 230/μl. During the second course, pegfilgrastim was administered as prophylaxis on day 4. However, on day 10 of the second course, he started to develop a fever and fatigue. Suspecting infection, antibiotics were administered, but failed to ameliorate his symptoms. On day 14, plain computed tomography revealed signs of aortic inflammation. Given the lack of improvement even after one week of antibiotic therapy, steroid treatment was initiated on the suspicion of granulocyte colony-stimulating factor (G-CSF) -induced aortitis, which rapidly improved his symptoms. Therefore, when encountering a case in which a fever remains unresponsive to antibiotics during chemotherapy with G-CSF agents, a differential diagnosis of aortic inflammation caused by G-CSF agents needs to be considered.

Pegylated recombinant human granulocyte colony-stimulating factor (PEG-rhG-CSF) has been introduced for the mobilization of peripheral blood stem cells (PBSCs). However, no cases of acute lung injury (ALI) in healthy donors have been reported, and the underlying mechanisms remain poorly understood. We first reported a case of ALI caused by PEG-rhG-CSF in a healthy Chinese donor, characterized by hemoptysis, hypoxemia, and patchy shadows. Ultimately, hormone administration, planned PBSC collection, leukocyte debridement, and planned PBSC collection resulted in active control of the donor\'s ALI. The donor\'s symptoms improved without any adverse effects, and the PBSC collection proceeded without incident. Over time, the lung lesion was gradually absorbed and eventually returned to normal. PEG-rhG-CSF may contribute to ALI in healthy donors via mechanisms involving neutrophil aggregation, adhesion, and the release of inflammatory mediators in the lung. This case report examines the clinical manifestations, treatment, and mechanism of lung injury induced by PEG-rhG-CSF-mobilized PBSCs.

卵巢癌是女性生殖系统常见的恶性肿瘤，早期多无明显临床症状，大多数患者就诊时已是中晚期，出现腹腔内扩散，伴发腹腔积液。对于中晚期卵巢癌，化疗是治疗的重要手段，而患者化疗后常产生骨髓抑制，导致中性粒细胞减少，严重者可影响患者的治疗及生存。聚乙二醇化重组人粒细胞集落刺激因子（PEG-rhG-CSF）是目前较常用的动员剂，可促进静息期造血干细胞进入细胞周期而大量增殖，增加外周血粒细胞，保证患者下一周期化疗顺利进行。本文报道1例卵巢癌患者化疗后白细胞低下，使用PEG-rhG-CSF后患者腹腔积液中出现大量幼稚粒细胞，在不了解病史的情况下容易误诊为髓系肿瘤，该情况罕见。.

Pegylated granulocyte colony-stimulating factor (G-CSF), commonly used in chemotherapy-induced neutropenia, has been associated with rare instances of aortitis. This study describes a 67-year-old female patient with estrogen receptor (ER)-positive, human epidermal growth factor receptor-2-positive breast cancer, undergoing chemotherapy with an epirubicin/cyclophosphamide (EC) regimen (epirubicin, cyclophosphamide) and pegylated G-CSF for neutropenia prophylaxis. Post-treatment, she developed symptoms including intermittent fever and severe arthralgia. Laboratory tests revealed an elevated white blood cell count, C-reactive protein levels, and erythrocyte sedimentation rate, while a computed tomography scan showed thickening in the aortic arch and descending aorta. Given the clinical presentation and exclusion of other potential causes, pegylated G-CSF-induced aortitis was suspected. The patient\'s symptoms improved significantly following the cessation of pegylated G-CSF, aiding in the differentiation from other types of aortitis. This study highlights the importance of considering pegylated G-CSF as a potential cause of aortitis in patients presenting with unexplained symptoms of fever and inflammation after chemotherapy. The rapid improvement upon discontinuation of the drug is a key feature distinguishing it from other aortitis causes. In conclusion, while rare, aortitis should be considered in the differential diagnosis of patients treated with pegylated G-CSF who exhibit relevant clinical symptoms. Early detection and management, including the discontinuation of the causative agent, are crucial for patient recovery and prognosis.

We describe a case of mandibular gingival carcinoma with hypercalcaemia and leukocytosis caused by tumour-derived parathyroid hormone-related protein (PTHrP) and granulocyte colony-stimulating factor (G-CSF). A 54-year-old man presented to our Department of Oral and Maxillofacial Surgery with a chief complaint of a left-sided mandibular gingival ulcer. A 42 mm × 20 mm sized ulcer was found on the left lower molar gingiva. Squamous cell carcinoma was pathologically diagnosed. The patient underwent a hemimandibulectomy, left-sided radical neck dissection, plate reconstruction, pectoralis major musculocutaneous flap reconstruction, and tracheostomy under general anaesthesia. Pathologically, two metastatic lymph nodes were identified. Residual tumour was suspected at the resection margins. Eight weeks after surgery, the patient started postoperative concurrent chemoradiotherapy (CCRT). Two weeks after CCRT, the patient developed hypercalcaemia. Serum levels of PTHrP and G-CSF increased in parallel with the progression of hypercalcaemia and leukocytosis. Immunohistochemical analysis of the surgical specimen showed positivity for G-CSF. Based on these clinical and pathological findings, the patient was diagnosed with hypercalcaemia and leukocytosis associated with malignancy and was treated with denosumab. Irradiation was terminated at 50 Gy because CT showed rapid disease progression. Chemotherapy was initiated, however, four weeks after the start of chemotherapy, a CT scan showed increased metastases and pleural dissemination. Therefore, chemotherapy was discontinued. One week after the chemotherapy was discontinued, the patient died of respiratory failure.

A 49-year-old woman was diagnosed with lung adenocarcinoma, stage IIIB, with increased leukocytes and neutrophils. Positron emission tomography showed dense uptake in right lung, but not in the bone marrow or bone. Biopsy revealed positive anaplastic lymphoma kinase (ALK) gene rearrangements. First-line ALK inhibitor, crizotinib, was used for 9 weeks and its effect was limited. Second-line ALK inhibitor did not show effect. Positive immunostaining and high serum granulocyte colony-stimulating factor (G-CSF) levels confirmed G-CSF-producing lung adenocarcinoma. The patient died after 4.5 months of diagnosis. This is the first reported case of G-CSF-producing lung cancer with ALK rearrangements.

Lung spindle cell carcinoma is an aggressive subtype of pleomorphic lung cancer resistant to cytotoxic chemotherapy. Programmed cell death-1 (PD-1) inhibitors have been reported to have clinical effects in patients with spindle cell carcinoma; however, the resistance mechanism to PD-1 inhibitors is yet to be fully elucidated. Herein, we report the case of an 88-year-old man with G-CSF-producing spindle cell carcinoma who acquired resistance to PD-1/PD-ligand 1 (L1) inhibitor in an early setting after a remarkable response. A histopathological review of the resistant specimen revealed a low count of CD8+ T cells and a predominant presence of M2 and TIM-3+ macrophages, indicating the presence of an immunosuppressive microenvironment. Our findings suggest a novel resistance mechanism to PD-1/PD-L1 inhibitors in G-CSF-producing spindle cell carcinoma.

Obsessive-compulsive disorder (OCD) is a mental condition that affects many people and is characterized by recurring obsessions and compulsions. It significantly impacts individuals\' ability to function ordinarily daily, affecting people of all ages. This study aimed to investigate whether or not the cytokines granulocyte macrophage colony-stimulating factor (GM-CSF) and interleukin-17 (IL-17) are involved in the pathophysiology of OCD. A case-control study with 50 OCD patients and 38 healthy volunteers served as the controls for this investigation. The levels of GM-CSF and IL-17 in the serum of both groups were measured with enzyme-linked immunosorbent assay (ELISA) kits. In addition, the sociodemographic characteristics of the population under study were studied. Based on the findings of this study, OCD patients had significantly elevated levels of IL-17 than the controls, it appears that there may be a function for IL-17 in the pathophysiology of OCD. It was also discovered that the severity of OCD and IL-17 levels had a significant positive correlation. On the other hand, when comparing the levels of GM-CSF, there was no significant difference between the patients and the controls. This study provides evidence supporting the involvement of cytokine IL-17 in the pathophysiology of OCD. This study suggests IL-17 as a diagnostic biomarker for OCD and adds to our knowledge of the function that the immune system plays in this condition.