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Case Reports
. 2023 Sep 8;102(36):e34965.
doi: 10.1097/MD.0000000000034965.

Severe complications in the induction phase of therapy in a pediatric patient with T-cell acute lymphoblastic leukemia: A case report

Affiliations
Case Reports

Severe complications in the induction phase of therapy in a pediatric patient with T-cell acute lymphoblastic leukemia: A case report

Agata Rocka et al. Medicine (Baltimore). .

Abstract

Rationale: Acute lymphoblastic leukemia (ALL) represents approximately 1-quarter of all new cases of childhood cancer. Although overall survival following diagnosis has improved in recent years, the toxicity of chemotherapy remains a concern.

Patient concerns: We describe an 11-year-old male patient diagnosed with T-cell precursor ALL who developed compounded complications during the induction phase of chemotherapy. Patient was hospitalized in the Department of Pediatric Hematology, Oncology, and Transplantology of the Medical University of Lublin, Poland. The patient's induction therapy was started according to the AIEOP-BFM ALL 2017 protocol IAp (International Collaborative Treatment Protocol for Children and Adolescents with Acute Lymphoblastic Leukemia).

Diagnoses: Patient developed compounded complications such as cholecystitis, hepatotoxicity, pancreatitis and myelosuppression.

Interventions: The patient was treated with leukapheresis, received a broad-spectrum antibiotic, potassium supplementation and hepatoprotective treatment and laparotomy cholecystectomy.

Outcomes: In the available literature, there is a limited amount of similar clinical cases with multiple complications in pediatric patients with ALL. Toxicities cause delays in the treatment of the underlying disease.

Lessons: In children with acute lymphoblastic leukemia, there are side effects during the treatment such as cholecystitis and pancreatitis. Complications during treatment require a quick response and modification of disease management. Abdominal ultrasound performed before treatment makes it possible to observe the dynamics of lesions. Genetic mutation analysis could allow us to more precisely respond to the possible susceptibility to and appearance of complications after the use of a given chemotherapeutic agent.

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Conflict of interest statement

The authors have no funding and conflicts of interest to disclose.

Figures

Figure 1.
Figure 1.
Fluorescence in situ hybridization (FISH) probe of the described patient’s case. (A) Mo-lecular Abbott. Vysis LSI BCR/ABL dual color, dual fusion translocation probe hybridized to a nucleus containing a simple balanced t (9;22). 9q34.1 region, (B) CytoCell MLL (KMT2A) Breakapart. The KMT2A (lysine methyltransferase 2A) gene at 11q23.3.
Figure 2.
Figure 2.
(A). Karyotype 48, XY, + mar1, + mar2 [16]/46, XY [4]. (B) The genetic microarray SNP analysis. (C) PRSS1 del biallelic. PRSS1 = serine protease 1.
Figure 3.
Figure 3.
Abdominal ultrasound. (A) US of the abdominal cavity which had been done before treatment. Gallbladder without stones. The common bile duct and bile ducts were not dilated. (B) A gallbladder was measured approximately 121 × 47 mm (red tags) with a slightly echogenic bile. (C–D) The presence of several stones, up to 7 mm long (red tag). Common bile duct and bile ducts did not dilate. The gallbladder was reaching the level of the navel, of considerable size 146 × 52 mm (red tags), hydrocele lesion with the level of echogenic contents. Compression soreness in the projection of the gallbladder. (E) The gallbladder wall was marked, with slightly increased vascularization in Kolor Doppler. Compression soreness in the projection of the gallbladder. (F) A liver with a markedly elevated heterogeneous echogenicity, significantly enlarged, dim. in the front armpit line approx. 237 mm (red tag) (progression of dimensions). US = Ultrasound.
Figure 4.
Figure 4.
(A–B) Abdominal CT. Siemens Definition AS + spiral protocol before and after iv. admin-istration of a contrast agent. The liver was enlarged (dimension CC approx. 292 mm-red arrow), homogeneous, with clearly reduced density, without visible focal lesions. The gallbladder was partially constricted with signs of wall edema. In the lumen of the gallbladder there were 3 small gallstones 2–3.5 mm long. Pancreatic (green arrow) head was enlarged by dim. AP 29 mm with slightly blurred contours. The pancreatic parenchyma presented normal contrast enhancement (no areas of necrosis). Body and tail of pancreas were not enlarged, dim. AP 13 mm and 20 mm. Edema of adipose tissue and banded fluid areas were visible in the region of the head of the pancreas. In the area of the pancreas and along the mesentery of the intestine, there were moderately numerous lymph nodes with a diameter of in the short axis up to 10 mm. AP = acute pancreatitis, CT = computed tomography.
Figure 5.
Figure 5.
Abdominal ultrasound. Routine checkup. Status after cholecystectomy, surrounding area, liver parenchyma with lower echogenicity (red arrows). In addition, the liver was visible fragmentarily, enlarged, with increased echogenicity of the parenchyma. Intrahepatic bile ducts did not dilated. The pancreas in the area of the head was not enlarged, discreetly heterogeneous, otherwise obscured.

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