Journal
Granulocyte-colony stimulating factor producing cervical cancer with elevated levels of parathyroid hormone-related protein: a case report and literature review
Systemic effects associated with hormones and cytokines secreted by tumor cells can cause paraneoplastic syndrome. Leukemoid reactions and hypercalcemia are relatively common manifestations of paraneoplastic syndrome. Here, we describe the case of a 90-year-old woman who presented with leukocytosis and hypercalcemia and was diagnosed with granulocyte-colony stimulating factor (G-CSF)-producing cervical cancer with elevated levels of parathyroid hormone-related protein (PTHrP). The patient visited our hospital complaining of general fatigue and anorexia. On admission, she presented with marked leukocytosis, hypercalcemia, and an increase in C-reactive protein level. On the basis of abdominal magnetic resonance imaging and histopathological examination, the patient was diagnosed with cervical cancer. Additional tests confirmed elevated plasma levels of G-CSF, PTHrP, and serum interleukin-6. Immunostaining of pathological specimens of the uterine cervix showed expression of G-CSF in tumor cells. The patient was diagnosed with G-CSF-producing cervical cancer accompanied by elevation of PTHrP levels. As a treatment for hypercalcemia, discontinuation of oral vitamin D derivative and administration of saline and elcatonin were ineffective, and therapeutic intervention with zoledronic acid hydrate was required. Considering the patient's advanced age, surgical resection of cervical cancer was not performed. She died from congestive heart failure approximately 3 months after hospitalization. This case was indicated to be a paraneoplastic syndrome in which G-CSF and PTHrP-induced leukocytosis and hypercalcemia. To the best of our knowledge, there have been no reports of G-CSF-producing cervical cancer with elevated PTHrP levels, and our case is the first report.
Cervical cancer of the uterus complicated by renal AA amyloidosis
Cervical cancer of the uterus rarely develops systemic secondary amyloidosis. We present the case of a 66-year-old female patient who manifested systemic amyloid A (AA) amyloidosis in the kidney, digestive tract, and cervix of the uterus, secondary to cervical cancer. She exhibited nephrotic syndrome, intractable diarrhea, and mild fever 3 months after she underwent an extended hysterectomy with postoperative cisplatin-based chemotherapy and whole pelvic irradiation. Further examinations revealed AA amyloidosis of the kidney and colon and cytomegalovirus infection in the colon. AA amyloid deposition was positive in the resected tissues of uterine cancer. The patient was diagnosed with systemic AA amyloidosis consecutive to cervical cancer. Despite a decrease in urinary protein after antiviral therapy, it increased 14 months later with neither apparent symptoms nor an increase in tumor marker. A second renal biopsy revealed AA amyloidosis of the kidney. Subsequent investigations revealed the recurrence of cervical cancer in the lung, liver, and lymph nodes. This case report indicated that AA amyloidosis would complicate cervical cancer and recur even after resection of neoplasm owing to other stimulation. Moreover, urine protein could be a marker for cancer relapse in known cases of cancer-derived AA amyloidosis.
Localized solitary left renal vein thrombus complicating nutcracker syndrome: a case report and review of the literature
Nutcracker syndrome (NCS) refers to compression of the left renal vein (LRV) between the abdominal aorta and the superior mesenteric artery (SMA). The clinical presentation of NCS includes hematuria, abdominal and left flank pain, gonadal varices, and varicocele formation. Theoretically, thrombosis can occur in the LRV in patients with NCS. However, an isolated solitary left renal vein thrombus (LRVT) complicating NCS is rare. In addition, the clinical features of an LRVT complicating NCS remain unclear. We describe a 43-year-old woman presenting with an asymptomatic LRVT complicating NCS. She was referred to our hospital for investigation of dysfunctional uterine bleeding, and detailed examination revealed endometrial cancer. Computed tomography angiography (CTA) and Doppler ultrasonography revealed compression of the LRV between the aorta and the SMA, as well as an LRVT. CTA performed 4 months after the administration of an anticoagulant showed complete disappearance of the LRVT. We have also included a review of published reports describing LRVT complicating NCS and discussed the clinical features of such a presentation.
Vaginal bleeding as primary presentation of renal cell carcinoma
Vaginal metastases from renal cell carcinoma has been recorded as extremely rare. We present a patient with vaginal bleeding as primary manifestation of renal cell carcinoma. A 40-year-old woman presented to a local private clinic with intermittent vaginal bleeding for approximately one month. Gynecological examination revealed a mass on the vaginal wall at approximately 8 o'clock. She underwent dilation and curettage (D&C) and mass excision. Microscopic histopathology and immunohistochemical stains showed vaginal metastases of clear cell RCC. The patient was referred to our urology clinic. Magnetic Resonance Imaging (MRI) of abdomen and pelvic showed a well-defined solid mass lesion measuring 16 × 12 × 11 cm in left kidney. Patient underwent left side radical nephrectomy through a left subcostal intraperitoneal incision. Histopathological results and metastasis workup confirmed the diagnosis of RCC with solitary metastatic vaginal lesion. After radical nephrectomy, she was treated with Sunitinib. No local relapse or distant metastasis was recognized 5 months after radical nephrectomy. In conclusion, the incidence of RCC metastasis to the vagina is extremely rare; but, in cases of vaginal bleeding or lesions we have to keep in mind the possibility of metastatic RCC.
Bevacizumab-associated glomerular microangiopathy that occurred after postoperative chemotherapy for ovarian cancer
Bevacizumab is a monoclonal antibody against vascular endothelial growth factor (VEGF) that is used to treat patients with various cancers. However, it is known to be associated with adverse events, such as hypertension and proteinuria. The histology of bevacizumab-induced nephropathy is known as thrombotic microangiopathy or minimal change nephrotic syndrome. Recently, however, the terms "bevacizumab-associated glomerular microangiopathy" and "anti-VEGF therapy-induced glomerular microangiopathy" have been proposed. We present a case of a 68-year-old woman who was administered postoperative chemotherapy (carboplatin, paclitaxel, and bevacizumab) for stage IV ovarian cancer. Proteinuria and hypertension appeared after three courses; however, six courses were completed. Then, gemcitabine and carboplatin were administered for recurrence of her cancer. She was diagnosed with nephrotic syndrome after eight courses. Renal biopsy showed accumulation of periodic acid-Schiff (PAS)-positive substances in the capillary walls and para-mesangial areas. Double contouring of basement membranes was also observed. Immunofluorescence microscopy revealed positive staining for IgG, IgA, IgM, C3, C4, and C1q. Immunosuppressive therapy was administered, but was ineffective. Further examination by electron microscopy and immunostaining led to a diagnosis of bevacizumab-associated glomerular microangiopathy.
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