Background . Fever of unknown origin (viral or bacterial) always presents diagnostic challenges for pediatricians, as it can accompany various conditions. Typically, when searching for the causes of fever, only infectious and somatic causes are considered, forgetting that it can be a manifestation of adverse drug reactions of drug products (DP). Our case report demonstrates an example of druginduced fever that occurred during teicoplanin therapy. Case report : A 13-year-old boy was examined in the pediatric diagnostics department due to the presence of fever and cytopenia. During the diagnostic process, common causes of fever—viral and bacterial infections—were ruled out. Considering the absence of “red flags” (severe weakness and lethargy, refusal to eat, breathing difficulties, focal and meningeal symptoms) in the patient’s condition, and the fact of prolonged hospital therapy, the hypothesis of a drug-induced fever associated with teicoplanin use was considered and subsequently confirmed. After discontinuation of the drug, all symptoms resolved spontaneously and did not recur. Conclusion . When conducting a differential diagnosis for the causes of fever, it is crucial to remember that fever can be caused by iatrogenic factors, such as the usage of certain DP. Polypharmacy and irrational prescription of DP are risk factors for the development of such reactions. Adherence to the principles of rational pharmacotherapy can help avoid such “human-made” complications in patient treatment.

Background. Idiopathic pulmonary hemosiderosis (IPH) is a rare interstitial lung disease associated with recurrent diffuse alveolar hemorrhage, anemia, and the risk of pulmonary fibrosis. Aim. To describe the clinical and laboratory, computed tomographic, diagnostic, therapeutic characteristics and outcomes of children with IPH. Materials and methods. This ambispective descriptive multicenter study included 11 patients with disease onset before 18 years of age and pulmonary hemorrhage/hemosiderosis documented by bronchoscopy with bronchoalveolar lavage, cytological and/or morphological examination, after exclusion of alternative causes. Clinical history, laboratory and instrumental findings, treatment, and outcomes were evaluated. Results. The cohort included 5 boys and 6 girls. The median age at IPH onset was 6.0 [3.7; 8.6] years, the median age at diagnosis was 8.0 [4.9; 9.7] years, the median diagnostic delay was 4.9 [1.8; 22.8] months, and the median minimum hemoglobin level was 52 [38.5; 98.5] g/L (data available for 10 patients). Anemia was documented in all patients, and hemoptysis in 6/11 (55%). Signs of diffuse lung involvement on chest CT were present in all patients; ground-glass opacities and consolidation were the most common findings. Six patients required ICU care, 3 required mechanical ventilation, and 8 received red blood cell transfusions. All patients received systemic glucocorticoids; azathioprine was used in 5, rituximab in 4, and cyclophosphamide in 1 patient. Three patients died. Conclusion. IPH debuts anemia in children. The absence of hemoptysis does not exclude diffuse alveolar hemorrhage. Early computed tomography of the chest organs, bronchoscopy with bronchoalveolar lavage, the search for siderophages and the exclusion of secondary causes are the key stages of diagnosis. In severe and recurrent cases, multidisciplinary management and steroid-sparing immunosuppressive therapy are required.

Background: Hemoglobin Rothschild (Hb Rothschild), NM_000518.5(HBB):c.112T>C, is an ultra-rare low-oxygen-affinity hemoglobin variant that persistently causes reduced peripheral oxygen saturation on pulse oximetry despite normal arterial oxygenation. Fewer than ten cases have been reported worldwide, and only one involved a child—an asymptomatic carrier identified incidentally. Methods: The patient underwent clinical examination, growth assessment, blood tests, hemoglobin electrophoresis, chest CT, abdominal ultrasound, echocardiography, and pulmonary perfusion scintigraphy. Whole genome sequencing (WGS) of the proband and parents was performed, followed by bioinformatic analysis and ACMG-based variant interpretation. A PRISMA-guided PubMed literature review was conducted. Results: We report on the first pediatric case exhibiting a symptomatic clinical course. A 4-year-old boy was referred for chronically low peripheral oxygen saturation (SpO₂), 78–86%, on pulse oximetry and recurrent lower respiratory tract infections. Early developmental history revealed episodes of apnea in infancy, perioral cyanosis, poor exercise tolerance, and low weight gain. Repeated cardiopulmonary assessments, chest computed tomography (CT), echocardiography, and pulmonary perfusion scintigraphy yielded unremarkable findings. Arterial blood gas analysis consistently showed normal arterial partial pressure of oxygen (PaO₂), excluding true hypoxemia. Hemoglobin electrophoresis revealed an abnormal HbD fraction; WGS identified a heterozygous variant NM_000518.5(HBB):c.112T>C inherited from the patient’s asymptomatic father. This variant increases the partial pressure of oxygen at which hemoglobin is 50% saturated (p50), thereby decreasing hemoglobin’s oxygen affinity and shifting the oxyhemoglobin dissociation curve to the right. These alterations explain the discordance between low peripheral oxygen saturation (SpO₂) and preserved oxygen delivery to tissues. Conclusions: This case expands the clinical spectrum of Hb Rothschild and demonstrates that symptomatic presentation may occur in early childhood. Awareness of low-affinity hemoglobin variants is essential to avoid misdiagnosis and unnecessary cardiopulmonary interventions. Early genetic testing facilitates accurate diagnosis and appropriate counseling.

Background. Hypokalemic periodic paralysis is a rare form of paralysis in children resulting from genetically determined electrolyte disorders. Its diagnosis is complicated due to transient nonspecific symptoms. Case description. The disease onset was at the age of 5 with episodes of muscle weakness and severe fatigue. Later, the number of these episodes has increased. After the surgery child was diagnosed with paralysis of lower limbs (mostly) accompanied by decreased level of potassium in blood serum. Next-generation sequencing, neuromuscular diseases gene panel, has revealed pathogenic variant in the CACNA1S gene (c.3716G>A, p.Arg1239His). The pathological allele was verified via Sanger sequencing in the proband, but not in his parents (de novo mutation). Diagnosis of “Hypokalemic periodic paralysis” was established. The child was transferred from parenteral administration of potassium solutions to oral therapy with KCl (4%) solution. Acetazolamide was added to the treatment regimen, and was subsequently discontinued due to an adverse reaction (persistent metabolic acidosis). Conclusion. Spontaneous paralysis in the patient, accompanied by decrease in serum potassium level, is a reason to suspect hypokalemic periodic paralysis. Administration of potassium medications allows us to prevent any symptoms of disease without reducing patient's quality of life.