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A 64-year-old male presented for a baseline ophthalmic exam before beginning erdafitinib, a fibroblast growth factor receptor (FGFR) inhibitor, for stage 4 papillary urothelial cancer. Baseline optical coherence tomography (OCT) and ophthalmic examination were unremarkable. After one month of treatment, his OCT demonstrated a significant thickening of the ellipsoid zone and prominence of the interdigitation zones along with a small amount of subretinal fluid. Two months after discontinuation of the medication, the OCT returned to baseline. Erdafitinib is a Food and Drug Administration (FDA)-approved treatment for unresectable or metastatic urothelial cancer with FGFR2 or FGFR3 mutations. However, retinal toxicity can ensue with the initiation of the drug and cause subjective vision changes and OCT abnormalities. The drug may exert toxic effects on retinal pigment epithelium, which may be seen through interval OCTs and visualization of the interdigitation zone. Therefore, pronunciation of the ellipsoid and interdigitation zone on OCT may allow for surveillance of early manifestations of erdafitinib-induced retinal toxicity.

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Combination immune checkpoint inhibitor (ICI) therapy is an emerging chemotherapy strategy for patients with solid tumor malignancies. Cardiotoxicity is a rare adverse effect of ICI therapy, most commonly presenting as acute myocarditis and, less frequently, as significant conduction abnormalities. We present a unique case of a 68-year-old female with urothelial cancer who developed shortness of breath and chest pain one week after receiving combination ICI therapy with ipilimumab and nivolumab. Biomarkers were elevated, including high-sensitivity troponin to 14,000 ng/L and creatine phosphokinase to 20,000 U/L. Due to suspicion of acute ICI-related myocarditis, a transthoracic echocardiogram (TTE) was obtained and demonstrated preserved ejection fraction (EF). Pulse-dose methylprednisolone therapy was initiated. However, the patient's clinical status continued to decline, and she developed bradycardia due to a complete heart block (CHB). This was initially treated with a dopamine infusion, but due to hypotension and hemodynamic instability, a transvenous pacemaker was placed. She continued to decline from a heart failure standpoint and developed acute hypoxic respiratory failure, requiring intubation due to pulmonary edema. A repeat TTE acquired three days following the initial echocardiogram demonstrated a newly reduced EF of 30%-35%. Additional anti-inflammatory agents were administered, including mycophenolate, infliximab, and anti-thymocyte globulin, with little improvement in clinical status. Unfortunately, she rapidly deteriorated, resulting in pulseless electrical activity (PEA) arrest and circulatory death. The autopsy revealed severe biventricular myocarditis with partial involvement of the atrioventricular node, consistent with her clinical syndrome of acute heart failure and CHB. A literature review demonstrated very few cases of ICI-related CHB. This case highlights a rare instance of atrioventricular dissociation in a patient with cardiotoxicity due to combination ICI therapy.

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Gray zone lymphoma (GZL) is an extremely uncommon hematological cancer with characteristics in common with both classical Hodgkin's lymphoma (HL) and diffuse large B-cell lymphoma. In this case report, we present a rare case of a 22-year-old male who developed HL initially and then transitioned to relapsed or refractory GZL. The disease relapsed twice throughout, even after the peripheral blood stem cell transplant. The initial biopsy suggested it was classical HL, and the biopsy was done late in the progression of the disease; the features suggested it was GZL. The treatment consisted of curative and preventive chemotherapy, radiation therapy, and immunotherapy.

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This case highlights the occurrence of hand-foot syndrome due to the use of an antimetabolite group of drugs, capecitabine, which was used in the chemotherapy of a 56-year-old male patient who was diagnosed with rectosigmoid carcinoma. The patient was diagnosed with rectosigmoid carcinoma two months ago and underwent laparoscopic lower anterior resection and colorectal anastomosis. Subsequently, the patient commenced chemotherapy treatment with a combination of oxaliplatin and capecitabine. The patient presented to us with complaints of loose stools for the past three days, and discoloration of the palms, soles, and tongue was noted and subjected to a biopsy, which revealed features compatible with chronic, nonspecific dermatitis. The occurrence of such palmar-plantar erythrodysesthesia with capecitabine is yet to be extensively studied.

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Pegylated (PEG)-asparaginase is used during the induction and intensification phases of treatment for B-cell acute lymphoblastic leukemia (B-ALL). It works by depleting the external sources of asparagine, causing the death of lymphoblasts. It has several adverse effects, including pancreatitis and hypertriglyceridemia; however, the simultaneous occurrence of both is uncommon. We present the case of an 18-year-old man with B-ALL who developed acute epigastric pain radiating to the back and non-bloody, non-bilious emesis following treatment with PEG-asparaginase. He was diagnosed with acute interstitial pancreatitis and severe hypertriglyceridemia. Conservative management was used for the pancreatitis, while hypertriglyceridemia was treated with an insulin infusion. Pancreatic toxicity and hypertriglyceridemia can necessitate the discontinuation of PEG-asparaginase, limiting treatment options and potentially increasing the risk of relapse. Therefore, further studies are needed to identify the factors contributing to hypertriglyceridemia and pancreatitis, aiding clinicians in monitoring and prevention.

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Gemcitabine-induced thrombotic microangiopathy (GITMA) is a rare but severe complication seen in cancer patients on gemcitabine therapy. This case report describes a 45-year-old female with metastatic cholangiocarcinoma on gemcitabine-capecitabine who developed acute kidney injury and hypertension without typical hematologic signs of thrombotic microangiopathy (TMA). Despite initial management targeting hypertensive urgency and acute kidney injury, renal function continued to decline and progressed to end-stage renal disease requiring hemodialysis. Laboratory tests revealed TMA features such as elevated lactate dehydrogenase (LDH), decreased haptoglobin, and schistocytes. Renal biopsy confirmed TMA with chronic features. This case highlights the challenge of diagnosing drug-induced TMA without typical hematologic findings.

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Aim: To describe treatment-induced toxicities (TITs) and associated factors in Zimbabwean cancer patients receiving cisplatin. Methods: In total, 252 Zimbabwean women with cervical cancer, receiving cisplatin were followed up over 12 months for TITs and disease status. Results: Peripheral neuropathy (70%) and ototoxicity (53%) were most prevalent. Advanced disease (OR = 1.3; 95% CI = 1.1-1.5; p = 0.02), pain comedications (OR = 1.3; 95% CI = 1.1-1.5; p = 0.03), alcohol (OR = 2.8; 95% CI = 1.1-7.5; p = 0.04) and comorbidities (OR = 1.2; 95% CI = 1.1-1.4; p = 0.04) increased peripheral neuropathy and ototoxicity risk. Older age increased risk of disease progression (OR = 1.9; 95% CI = 1.4-3.0; p = 0.033). Conclusion: High peripheral neuropathy and ototoxicity prevalence were observed, which are not routinely monitored in Zimbabwe. There is a need for capacity building to incorporate comprehensive TIT testing and optimize cancer care in Zimbabwe.

Cancer treatment has side effects, also known as treatment-induced toxicities (TITs), that can lead to death if not management properly. African populations are more likely to develop TITs, however, not many studies research on TITs in Africans and why they are more prone to TITs. This study followed up 252 Zimbabwean women with cervical cancer, over 12 months for TITs and found that loss of sensation and ear complications most commonly occurred after treatment. Advanced disease, prescribed pain medication, alcohol consumption history and underlying diseases such as diabetes increased likelihood of TITs, while older age increased risk of unresponsive cancer. This study highlights a need to incorporate comprehensive monitoring for TITs for at-risk individuals toward improving cancer care.

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Platinum-based chemotherapeutic agents such as cisplatin, carboplatin, and oxaliplatin are used as adjuvant or neoadjuvant agents in malignancies of the ovary, cervix, lymphoma, head and neck, and breast. Cisplatin is most commonly used until the carboplatin is approved by the Food and Drug Administration (FDA). Cisplatin is not tolerated in many patients due to severe nausea and renal tubular injury. Carboplatin is used in patients where side effects limit the uses of cisplatin. Although carboplatin is least commonly associated with hematuria, we report a case of carboplatin-induced hematuria with obstructive acute kidney injury (AKI). Our patient, a 63-year-old female diagnosed with triple-negative breast carcinoma and post-mastectomy, was started on adjuvant chemotherapy, with carboplatin 700 mg and paclitaxel 250 mg. She developed hematuria with ureter obstruction due to clots, resulting in obstructive AKI. The patient continued to have oliguria and worsening symptoms, and thus, the ureter was stented. The patient's renal function returned to the baseline. In this case, we highlight the fact that carboplatin can cause hematuria with ureter obstruction. Adequate hydration before infusing carboplatin as in cisplatin can reduce the complications.

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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.

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Pembrolizumab is a programmed death 1 receptor (PD-1) inhibitor. It is used as immunotherapy in various cancers, including metastatic melanoma, non-small cell lung cancer, and, notably, high-risk triple-negative breast cancer. We discuss a case of a 44-year-old female with a past medical history of triple-negative breast cancer who presented with a chief complaint of poor oral intake and fatigue after her fourth cycle of pembrolizumab therapy. The patient was diagnosed with pembrolizumab-induced isolated secondary adrenal insufficiency (AI) and was treated with corticosteroids with improvement in her symptoms. Secondary AI due to pembrolizumab use is a rare yet potentially life-threatening complication. If initial serum cortisol is borderline low, as observed in our patient, repeated testing within shorter intervals should be considered to optimize patient outcomes.

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5-Fluorouracil (5-FU) and its prodrug, capecitabine, are commonly used chemotherapeutic agents for solid tumor management. While these agents can present with adverse side effects such as nausea, vomiting, diarrhea, and myelosuppression, they can also, less commonly, cause cardiovascular toxicity. This toxicity may manifest as cardiac arrhythmias, myocarditis, heart failure, myocardial infarction, and even death. The management of 5-FU-related cardiotoxicity includes early recognition of symptom manifestation so that medication can be discontinued promptly and symptoms can be addressed appropriately. Here, we describe the case of a 72-year-old male who developed coronary vasospasm and ST-segment elevation myocardial infarction shortly after the initiation of chemotherapy with 5-FU.

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Sarcomatoid carcinoma of the esophagus, a mixed tumor comprising both carcinomatous and sarcomatoid components and known as carcinosarcoma, is a rare malignancy. Clinically and radiologically, it presents like other esophageal cancers. Here we discuss the case of a 69-year-old male patient with sarcomatoid carcinoma of the esophagus who developed Stevens-Johnson syndrome (SJS) after chemotherapy with carboplatin and paclitaxel. The patient was evaluated for dysphagia and odynophagia. He was initially misdiagnosed to have an esophageal polyp and underwent excision for the same. He presented with recurrent growth at the local site, with histopathological examination showing sarcomatoid carcinoma of the esophagus. After the development of paclitaxel-carboplatin-induced SJS, the patient was subsequently treated with palliative radiotherapy at the primary site for symptomatic relief. He underwent feeding gastrostomy as a supportive nutritional measure and was on best supportive care after a multidisciplinary tumor board discussion. Paclitaxel-carboplatin-induced SJS poses numerous diagnostic conundrums, on account of there being only one reported incident prior to this in literature, to the best of our knowledge. In this report, we explore the diagnostic and therapeutic predicaments associated with a rare disease that is under-reported and understudied in literature and delve into the various treatment modalities that can benefit the patients. The case also demonstrates the delicate balance between cancer chemotherapeutics and their Pandora's box of adverse effects.

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The causes of variation in toxicity to the same treatment regimen among seemingly similar patients remain largely unknown. There was tremendous optimism that the patient's germline genome would be strongly predictive of treatment-related toxicity and could be used to personalize treatment and improve therapeutic outcomes. However, there has been limited success in discovering robust pharmacogenetic predictors of treatment-related toxicity and even less progress in translating the few validated predictors into clinical practice. It is apparent that identification of toxicity predictors that can be used to predict and prevent treatment-related toxicity will require thinking beyond germline genomics. To that end, we propose an integrated biomarker discovery approach that recognizes that a patient's toxicity risk is determined by the cumulative effects of a broad range of "omic" and non-omic factors. This commentary describes the limited success in discovering and translating clinical and pharmacogenetic toxicity predictors into clinical practice. We illustrate the evolution of cancer toxicity biomarker discovery and translation through studies of taxane-induced peripheral neuropathy, which is one of the most common and debilitating side effects of cancer treatment. We then discuss the opportunities for discovering non-genomic (e.g., metabolomic, lipidomic, transcriptomic, proteomic, microbiomic, medical, behavioral, environmental) and integrated biomarkers that may be more strongly predictive of toxicity risk and the potential challenges with translating integrated biomarkers into clinical practice. This integrated biomarker discovery approach may circumvent some of the major limitations in toxicity biomarker science and move precision oncology treatment forward so that patients receive maximum treatment benefit with minimal toxicity.

Asunto(s)

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Tracheoesophageal puncture (TEP) is a voice restorative option adopted by many head and neck cancer patients following laryngectomy. Though generally safe, TEP may develop leakage. Lenvatinib is a tyrosine kinase inhibitor (TKI) with anti-tumoral activity against head and neck malignancies.TKIs, including lenvatinib, have been associated with organ perforation or fistula formation. There remains a paucity of literature on the association between lenvatinib and TEP leakage. In this report, we described a patient with adenoid cystic carcinoma of the larynx who had a TEP. After approximately two weeks of treatment with lenvatinib, the patient developed a leakage of TEP. Despite several interventions, the patient died three months afterward due to a retropharyngeal abscess secondary to Fusobacterium nucleatum. To our knowledge, this is the first report of fatal lenvatinib-associated TEP leakage. Clinicians should be cognizant of a potentially rapid development of this complication when prescribing TKI for patients with TEP.

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Introduction Sexual dysfunction is rarely studied in Indonesian patients with breast cancer. We aimed to assess the prevalence of sexual dysfunction symptoms following chemotherapy, as well as the pattern and the associated factors. Methods This cross-sectional study included 135 female breast cancer patients receiving primary chemotherapy. The present study measured the prevalence of sexual dysfunction symptoms using an e-questionnaire containing Common Toxicity Criteria for Adverse Events (CTCAE) version 4 at different time points. Other data included sociodemography, clinicopathology, treatment, and other concurrent symptom characteristics. Bivariate and multivariate logistic regression tests were used to analyze any association among variables. Results In the whole panel, 86 (63.7%) of 135 cases experienced sexual dysfunction. The most common symptom was vaginal dryness (45.9%), followed by decreased libido (45.2%), dyspareunia (13.3%), delayed orgasm (11.1%), and anorgasmia (8.9%). When observed at five different time points, the frequency of symptoms increased during chemotherapy and persisted until six months after completing treatment. Chemotherapy duration of >120 days was associated with a higher probability of vaginal dryness (p=0.012) and decreased libido (p=0.033). Spouse age ≥55 years old and body mass index (BMI) ≥23 kg/m2 were associated with a reduced probability of decreased libido (p=0.033 and 0.025, respectively). The presence of comorbidity was associated with a reduced probability of delayed orgasm (p=0.034). Conclusions A significant proportion of patients with breast cancer had sexual dysfunction following chemotherapy. Vaginal dryness, decreased libido, and dyspareunia were the commonest symptoms observed. Duration of chemotherapy, spouse age, BMI, and comorbidity were associated with the risk of sexual dysfunction occurrence.

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Despite ongoing breakthroughs in novel anticancer therapies, chemotherapy remains a mainstream therapeutic modality in different types of cancer. Unfortunately, chemotherapy-related toxicity (CRT) often leads to dose limitation, and even results in treatment termination. Over the past few years, accumulating evidence has indicated that the gut microbiota is extensively engaged in various toxicities initiated by chemotherapeutic drugs, either directly or indirectly. The gut microbiota can now be targeted to reduce the toxicity of chemotherapy. In the current review, we summarized the clinical relationship between the gut microbiota and CRT, as well as the critical role of the gut microbiota in the occurrence and development of CRT. We then summarized the key mechanisms by which the gut microbiota modulates CRT. Furthermore, currently available strategies to mitigate CRT by targeting the gut microbiota were summarized and discussed. This review offers a novel perspective for the mitigation of diverse chemotherapy-associated toxic reactions in cancer patients and the future development of innovative drugs or functional supplements to alleviate CRT via targeting the gut microbiota.

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Cancer is one of the leading causes of morbidity and mortality in the pediatric population with the most common cancer being acute lymphoblastic leukemia. One of the most common drugs used in the treatment is the anthracycline group of chemotherapeutic agents, and a major side effect is cardiotoxicity. Dexrazoxane, a member of the cardioprotective agents' group of medications, is the only current FDA-approved medication to tackle cardiotoxicity. The mechanism of action in which dexrazoxane is cardioprotective is by halting necroptosis in cardiomyocytes after anthracycline therapy and concurrently binds with iron and reduces the formation of anthracycline-iron complexes and reactive oxygen species. The efficacy of dexrazoxane has been demonstrated in clinical trials within the pediatric population with roughly 60%-80% reduction in risk of developing cardiotoxicity with a very tolerable and limited side effect profile. Further research is required to not only establish the efficacy of dexrazoxane within the pediatric population but also to explore other medications that may serve alongside the function of dexrazoxane.

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Acute lymphoblastic leukemia (ALL) is a hematological cancer that can cause ocular tissue involvement. Asparaginase is a chemotherapy regimen that is commonly used in leukemia which could lead to similar ocular manifestations. We report a patient with a history of ALL for seven months on asparaginase therapy and persistent cerebral sinus venous thrombosis (CSVT) with acute venous infarction in the left frontal lobe presented with worsening vision. On examination, he had a visual acuity (VA) of (6/21) in the right eye and (6/60) in the left eye, with a mild left eye abduction limitation. Fundal examination showed bilateral prominent multilayered retinal hemorrhages and papilledema with absence of leukemic infiltration. His chemotherapy regimen was held and a one month follow up was scheduled. Follow up after one month of chemotherapy cessation showed resolution of both VA and fundal exam findings. It is crucial to differentiate between asparaginase toxicity and infiltration of the disease in ALL patients. As this would determine whether the treatment should be continued or suspended.

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Dermatologic toxicities, such as urticaria and mucositis, with docetaxel, have been commonly reported; however, fixed-plaque erythrodysesthesia is a rare adverse phenomenon with a reported incidence of less than 5% of patients. Docetaxel-induced psoriasis is extremely rare, and to date, very few cases have been reported in the literature. We present a literature review of psoriasis cases secondary to docetaxel and report our own case of severe docetaxel-induced psoriasis in the setting of treatment of metastatic prostate cancer. Our patient received topical steroids and narrow-band ultraviolet B (NBUVB) light therapy with resolution of their psoriasis and was able to complete their chemotherapy without discontinuation or interruption of their docetaxel.

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The purpose of this case report is to present the first case of neratinib maculopathy. We describe the initial presentation, baseline characteristics, imaging findings, and outcomes. The case report is accompanied by a thorough literature review including possible mechanisms of tyrosine kinase inhibitor (TKI) maculopathy. Neratinib is a novel TKI that is commonly used in the treatment of breast-associated malignancies. Neratinib toxicity presents similarly to macular telangiectasia type II but differs with the fine granular hypofluorescent areas spanning the limit of the posterior pole and vascular arcades as well as the nasal aspect of the optic nerve.  We report a case of suspected macular toxicity secondary to neratinib. Concomitant use of neratinib in conjunction with docetaxel and other chemotherapeutics with known retinal side effects should alert clinicians of an increase in the risk of macular toxicity. Albeit commonly reported ocular side effects of TKIs, maculopathy is a rare and potentially overlooked side effect. Patients that have planned chemotherapy should undergo a baseline retinal examination.