Vitamin B12 Deficiency in Infants With Axial Hypotonia and Psychomotor Regression: Insights From a Moroccan Case Study.

Vitamin B12 deficiency is a rare entity in the pediatric population. It is often of maternal origin in exclusively breast-fed infants. Its clinical manifestations are multiple and unspecific, encompassing hematological problems and neurodevelopmental consequences. Positive diagnosis and early treatment with vitamin B12 supplementation have a rapidly reversible effect on symptoms. Delayed diagnosis, however, may result in irreversible neurological sequelae. We report the case of a six-month-old infant, admitted with hypotonia and psychomotor regression since the age of four months. The laboratory work-up revealed macrocytic anemia with the presence of megakaryocytes and megaloblasts on the myelogram. Vitamin B12 levels were low, and homocysteine levels were high. A maternal workup showed vitamin B12 deficiency in the mother. A brain MRI showed bilateral frontoparietal cortical atrophy. The patient was put on vitamin B12 supplementation with good evolution. The aim of our work is to shed light on the misleading and varied clinical profile of vitamin B12 deficiency in an exclusively breastfed infant, the serious consequences of maternal vitamin B12 deficiency, and the importance of early diagnosis of this condition.

[Splenectomy as definitive surgical treatment for hemophagocytic lymphohistiocytosis]. / Esplenectomía como tratamiento quirúrgico definitivo para linfohistiocitosis hemofagocítica.

Background: Hemophagocytic syndrome or hemophagocytic lymphohistiocytosis (HL) is an immune hyperactivation of multifactorial etiology, characterized by excessive activation of lymphocytes and macrophages, as well as numerous pro-inflammatory cytokines. It has a non-specific and highly variable clinical presentation, with splenomegaly being one of the clinical manifestations. Due to its nature, it can manifest during childhood or adult life, which is why it is a disease of diagnostic and therapeutic complexity. Clinical case: 38-year-old male patient without comorbidities, who presented with abdominal pain, choluria, fever > 38 °C and diaphoresis of more than 10 days of evolution. A bone marrow aspirate was performed as part of the diagnostic approach with data compatible with hemophagocytosis and cytopenias. The immunosuppressive management did not show the expected response, which is why an open splenectomy was performed as the last therapeutic option with adequate hematological control. A documentary review of the disease was carried out, and of the therapeutic options, emphasizing surgical management in case of refractoriness to medical treatment. Conclusions: Splenectomy increases the overall survival rate and the time free of HL progression, even though there are still no studies to determine with certainty the ideal time to perform a splenectomy in patients with pancytopenia without splenomegaly who suffer from hemophagocytic syndrome.

Introducción: el síndrome hemofagocítico o linfohistiocitosis hemofagocítica (LH) es una hiperactivación inmune de etiología multifactorial, caracterizada por activación excesiva de linfocitos y macrófagos, así como por numerosas citocinas proinflamatorias. Tiene una presentación clínica poco específica y muy variable, y la esplenomegalia es una de las manifestaciones clínicas. Debido a su naturaleza puede manifestarse durante la infancia o la vida adulta, por lo que es una enfermedad de complejidad diagnóstica y terapéutica. Caso clínico: paciente del sexo masculino de 38 años sin comorbilidades, quien presentó dolor abdominal, coluria, fiebre > 38 °C y diaforesis de más de 10 días de evolución. Se le hizo aspirado de médula ósea como parte del abordaje diagnóstico con datos compatibles con hemofagocitosis y citopenias. El manejo inmunosupresor no mostró la respuesta esperada, por lo que se hizo esplenectomía abierta como última opción terapéutica con adecuado control hematológico. Se hizo una revisión documental de la enfermedad y de las opciones terapéuticas con énfasis en el manejo quirúrgico en caso de refractariedad al tratamiento médico. Conclusiones: la esplenectomía aumenta la tasa de supervivencia general y el tiempo libre de progresión de la LH, aunque no hay todavía estudios para determinar con certeza el tiempo ideal para hacer una esplenectomía en pacientes con pancitopenia sin esplenomegalia que padezcan síndrome hemofagocítico.

Bridging dermatology and hematology: a case of lepromatous leprosy with bone marrow involvement and pancytopenia.

Leprosy, caused by Mycobacterium leprae (M. leprae), primarily manifests with cutaneous and peripheral nerve involvement. Systemic involvement, particularly in the bone marrow, is exceedingly rare. This report presents a case of lepromatous leprosy with bone marrow involvement, emphasizing the systemic nature of the disease and the importance of comprehensive diagnostic and management approaches. We aim to present a case of lepromatous leprosy with bone marrow involvement, detailing the clinical presentation, diagnostic evaluation, and management approach. A 65-year-old male with lepromatous leprosy and severe erythema nodosum leprosum developed pancytopenia. After undergoing comprehensive clinical evaluation, including history taking, physical examination, and laboratory investigations, bone marrow examination and molecular diagnostics using polymerase chain reaction (PCR) were performed to confirm the presence of M. leprae as an etiology for his pancytopenia. The bone marrow aspirate revealed hypercellularity with erythropoiesis and thrombopoiesis within normal limits. Foamy histiocytes with erythrophagocytosis were observed, along with the presence of M. leprae on Modified Ziehl-Neelsen stain. Molecular analysis confirmed M. leprae DNA in the bone marrow aspirate. Treatment with multi-drug therapy (MDT) and thalidomide resulted in normalization of blood counts and healing of skin lesions. This case underscores the systemic nature of leprosy and the rarity of bone marrow involvement, highlighting the importance of thorough evaluation in cases of persistent symptoms. Comprehensive diagnostic approaches, including bone marrow examination and molecular diagnostics, are essential for accurate diagnosis and timely initiation of appropriate treatment, ultimately improving patient outcomes and minimizing disease complications.

Methimazole-Induced Pancytopenia in a Patient with Graves' Disease: A Case Report and Literature Review.

INTRODUCTION: Methimazole is an antithyroid drug known to cause hematological toxicity, including agranulocytosis and, very rarely, pancytopenia. We herein present a case of a patient with Graves' Disease (GD) who developed methimazole-induced pancytopenia. CASE REPORT: A 53-year-old Peruvian woman with GD, initially treated with methimazole 20 mg BID, experienced odynophagia, fever, and malaise after 37 days of treatment. The initial diagnosis was agranulocytosis, leading to the discontinuation of methimazole and initiation of antibiotics. Due to persistent neutropenia, a Granulocyte Colony-stimulating Factor (G-CSF) was administered. Eight days later, she developed pancytopenia and was managed with hematopoietic agents and platelet transfusions. The patient recovered with normalization of the blood count, eliminating the need for Bone Marrow (BM) examination. Radioiodine therapy was chosen as the definitive treatment, resulting in hypothyroidism. Currently, the patient is thyroidal and hematologically stable. CONCLUSION: Methimazole-induced pancytopenia is a rare and serious complication; however, with appropriate treatment, complete recovery can be achieved.

Infection-associated hemophagocytic lymphohistiocytosis: a case report.

Introduction: Hemophagocytic lymphohistiocytosis (HLH) is a rare hyperinflammatory disorder characterized by fever, cytopenia, splenomegaly, and hemophagocytosis. Without prompt treatment, HLH can rapidly progress to life-threatening multiorgan failure. The authors present a case of occult HLH with severe bicytopenia and organ dysfunction requiring intensive care. Case presentation: A 20-year-old male presented with fever, cough, and constitutional symptoms. He developed hypoxia, elevated transaminases, and bicytopenia. Despite transfusions, platelet counts remained critically low. With high suspicion for HLH, head computed tomography and bone marrow biopsy was although panned but couldn't be performed due to resource less settings. And with suspicion for HLH treatment with high-dose dexamethasone was initiated as counts improved. Clinical course: The patient required mechanical ventilation for pulmonary infiltrates. He exhibited seizure activity and epistaxis related to coagulopathy. On hospital day 9, he was successfully extubated as counts normalized. He was discharged from the intensive care unit once stable. Conclusion: This case illustrates a delayed diagnosis of HLH masquerading as a fever of unknown origin. HLH should be urgently considered in patients with unexplained cytopenia, organ dysfunction, and systemic inflammation. Early treatment with immunotherapy can be lifesaving, whereas delays may precipitate irreversible end-organ damage.

Asymptomatic Extrahepatic Portal Venous Obstruction: A Case Report.

This report describes a case of extrahepatic portal venous obstruction (EHPVO) with esophageal varices that would have led to significant bleeding if left untreated or inadequately managed. A 56-year-old diabetic and hypothyroid female visited our medical outpatient clinic to be assessed for pancytopenia and easy fatiguability. She experienced acute calculus cholecystitis 24 years ago, which was treated with a partial cholecystectomy. The laboratory tests showed indications of hypersplenism, characterized by anemia, leucopenia, and thrombocytopenia. The MRI results showed signs of long-term blockage of the portal vein outside the liver, with the liver tissue seeming normal. The upper gastrointestinal endoscopy showed grade IV esophageal varices, gastroesophageal varices 1, fundal varices, isolated gastric varices 2, and antral varices. The patient was diagnosed with EHPVO, and banding was performed as a preventive measure against upper gastrointestinal bleeding. Additionally, she was treated using conservative management techniques such as beta blockers. Endoscopic treatment is the standard of care for treating acute varices, while beta blockers are given as a secondary preventive measure. Despite cholelithiasis being a cause and/or sequelae to portal venous thrombosis, a clear explanation has not been offered to this patient while taking consent for cholecystectomy or thereafter. EHPVO is not frequently detected, and there is still a dearth of appropriate guidelines for managing this illness, even though it is a frequent cause of acute calculus cholecystitis and upper gastrointestinal bleeding.

Aplastic anemia triggered by the Bruton tyrosine kinase inhibitor acalabrutinib in two patients with mantle cell lymphoma - A case report.

The use of Bruton's tyrosine kinase inhibitors (BTKi) is rapidly increasing for patients with mantle cell lymphoma (MCL). Side effects reported so far are usually manageable. However, here we present two cases of life-threatening aplastic anemia (AA) upon treatment with the BTKi acalabrutinib for MCL. The first patient died of neutropenic infection secondary to AA. The second patient was successfully treated with immunosuppressive treatment but the MCL relapsed shortly thereafter. AA is a potentially fatal complication that should be considered when patients present with pancytopenia during treatment with BTKi.

Vitamin B12 Deficiency Manifesting As Pancytopenia, Lymphadenopathy, and Fever: A Clinical Mimic of Hematologic Malignancies.

Pancytopenia is a complex medical condition characterized by decreased levels of red blood cells (RBCs), white blood cells (WBCs), and platelets (PLTs). It can arise from impaired production, peripheral destruction, or a combination of both. The causes of pancytopenia range from reversible factors like infections and medication reactions to irreversible conditions. Vitamin B12 deficiency is a notable reversible cause that can take years to manifest in adults due to stored reserves. However, deficiencies caused by impaired absorption, especially due to the lack of intrinsic factors (IFs), can lead to rapid deterioration within two to five years. A healthy 39-year-old male with an athletic lifestyle presented with symptoms such as dizziness, nausea, vomiting, palpitations, and fainting over a few days. These symptoms were preceded by weeks of persistent body aches, headaches, weakness, daily fevers, chills, and night sweats. Vital signs were stable. The physical examination revealed conjunctival pallor and lymphadenopathy in the submandibular and superficial cervical regions. Initial blood tests showed normocytic anemia (Hgb 4.9, MCV 80), leukopenia (2.99), thrombocytopenia (142), and elevated liver enzymes (AST 199, ALT 96, and total bilirubin of 2.04). The peripheral smear showed tear-drop cells and hypochromic cells. The initial impression was hematologic malignancy, including but not limited to leukemia, lymphoma, or myelofibrosis given clinical findings such as B-symptoms like night sweats, neck lymphadenopathy, and subjective daily fever, along with pancytopenia. The patient received a bolus of normal saline and a transfusion of two units of packed RBCs. CT scans of the chest, abdomen, and pelvis showed no adenopathy or splenomegaly. Although initial clinical assessment pointed toward a potential hematologic malignancy, comprehensive testing, including SPEP, reticulocyte count/fraction, serum folate, and serum vitamin B12, revealed only severe vitamin B12 deficiency, with a level of less than 150, with the presence of IF antibodies. Treatment involved intensive in-patient vitamin B12 injections followed by a detailed outpatient regimen. The patient completed a daily dose of vitamin B12 injections for seven consecutive days, followed by weekly injections for the next four weeks. Subsequent laboratory results demonstrated an increase in WBC count to 8.39, Hgb level to 13.2, and PLT count of 249, indicating a continued positive response to the vitamin B12 replacement therapy. In summary, pancytopenia poses a diagnostic challenge that demands careful evaluation of patient data and comprehensive testing. Vitamin B12 deficiency, which encompasses pernicious anemia (PA), is among the reversible factors to consider. This aspect holds significance before opting for more invasive measures like a bone marrow biopsy. Nutritional deficiencies need to be considered first as differentials in pancytopenia, even in the absence of typical signs of vitamin B12 deficiency (like macrocytosis and hypersegmented neutrophils) and in the presence of compelling clinical indications pointing to a hematologic malignancy.

Pancytopenia Concurrent With Metabolic Encephalopathy.

Pancytopenia is a decrease in the number of cells in all peripheral blood cell lines and has been associated with anemias, cancers, chemotherapy, infections, and nutritional deficiencies. However, pancytopenia concurrent with encephalopathy is rare and not well-studied. We present a case of pancytopenia concurrent with metabolic encephalopathy. An 81-year-old female patient presented to the emergency department for two weeks of increased fatigue and hypersomnolence. The patient had trouble staying awake during the initial physical exam, and her laboratory results were significant for pancytopenia, hypercreatinemia, hypernatremia, hypermagnesemia, and alkalemia. She was admitted to the floor, diagnosed with metabolic encephalopathy and acute kidney injury, and treated with medication withholding, fluid resuscitation, and electrolyte repletion. She also received a comprehensive workup for pancytopenia, iron replacement, and red blood cell transfusion therapy. After her metabolic encephalopathy was resolved, she was discharged with plans to follow up with hematology/oncology for stable but unresolved pancytopenia. We hypothesize that the patient's metabolic encephalopathy was likely due to acute kidney injury-induced uremia or dehydration. We further hypothesize that parvovirus B19 and myelodysplastic syndrome are possible etiologies for pancytopenia. Our case highlights the importance of closely monitoring patients taking Sodium-glucose co-transporter-2 (SGLT-2) inhibitors and loop diuretics for dehydration and subsequent organ failure.

Approach to pancytopenia: From blood tests to the bedside.

Pancytopenia is an uncommon abnormality detected on a full blood count. Features of presentation tend to be non-specific, and are due to impaired functions of the cell lines involved. These can include fatigue, infection and bleeding. However, the aetiology of pancytopenia is extensive. This narrative review aims to provide a minimally invasive diagnostic algorithm for generalist clinicians to approach pancytopenia, including investigations into the underlying aetiology, and when a referral to the haematologist is warranted for further investigations such as bone marrow aspiration and trephine biopsy.

Contemplating dengue: the thinker's reflection on symptoms.

In this image, the autors reinterprate "The Thinker" from Auguste Rodin to transfer knowledge about dengue fever, which can range from flu-like illness to severe hemorrhagic fever. By fostering awareness and understanding of dengue fever, we strive to empower individuals and communities in the ongoing fight against dengue and other infectious threats.

Olaparib induced aplastic anemia in a patient with castrate resistant prostate cancer: A case report.

Olaparib is (ADP-ribose) polymerase inhibitor (PARPi), which stops the repair of single-stranded DNA breaks. This leads to the death of cancer cells with BRCA1/BRCA2 mutations or homologous recombination deficiency. Since being approved by the FDA in 2023 for treating castrate-resistant prostate cancer (CRPC), there have been some reports of myelodysplastic syndrome (MDS) and acute leukemia linked to PARP inhibitor use for ovarian, breast, pancreatic and breast cancers, there have been no reports of aplastic anemia after receiving PARPi therapy. This case report describes a 75-year-old man with BRCA2-positive metastatic castrate-resistant prostate cancer who developed aplastic anemia after taking olaparib.

Idiopathic aplastic anemia with concurrent complications of colonic perforation and mucormycosis: Case report.

We report a case of a 72-year-old female who presented with fever, abdominal pain, and diarrhea accompanied by leukopenia, anemia, and thrombocytopenia. The diagnosis of acute aplastic anemia was confirmed through bone marrow aspiration. Treatment included glucocorticoids, immunoglobulin therapy, and plasma exchange. Subsequently, the patient developed gastrointestinal bleeding and abdominal Computed Tomography (CT) revealed perforation of the transverse colon. Pathological examination of surgically removed diseased tissue confirmed mucor infection. Despite receiving antifungal therapy with amphotericin B, the patient's condition deteriorated due to the sepsis progression. Mucor infection in immunocompromised patients should be vigilant, and early diagnosis may help improve prognosis.

Single Low-Dose Methotrexate and Vitamin B12 Deficiency-Induced Pancytopenia Causing Fatality: A Case Report.

Methotrexate (MTX), a commonly used disease-modifying antirheumatic drug, is generally considered safe at low cumulative doses. However, severe pancytopenia can occur even with doses as low as 10 mg, as illustrated by a fatal case in an older adult with chronic kidney disease (CKI) and vitamin B12 deficiency. Despite the low dose and lack of folate supplementation, the patient developed severe mucositis and pancytopenia leading to fatal complications. This case underscores the challenges in diagnosing and managing MTX-induced pancytopenia, especially in patients with comorbidities such as CKI and vitamin B12 deficiency.

Ibuprofen-Induced Pancytopenia and Erythema Multiforme in an Elderly Female Patient.

Erythema multiforme (EM) is a delayed, cell-mediated cutaneous disease with varying clinical manifestations. It is most commonly associated with infections but can also be associated with medications, vaccines, and autoimmune diseases. Non-steroidal anti-inflammatory Drugs (NSAIDs) are commonly used analgesics that have rare associations with EM and pancytopenia. These adverse reactions to NSAIDs can obscure definitive diagnosis due to their rarity. We present a case where an elderly female patient taking 600mg of ibuprofen up to four times a day for shoulder bursitis developed EM and pancytopenia. In this case, a 75-year-old female with a medical history of atrial fibrillation, essential hypertension, non-insulin-dependent type 2 diabetes mellitus, and ischemic stroke with residual right-sided visual impairment presented to our Emergency Department in 2023 with neck swelling, skin rash, and ulceration of the oral cavity. She reported a generalized, targetoid body rash that occurred 15 days after she started taking ibuprofen regularly for left shoulder bursitis. No other medications were started before, after, or during this time period. CBC on admission was remarkable for a white blood cell count of 1.5x109/L, hemoglobin of 6.5 g/dL, and platelet count <10x109/L, consistent with pancytopenia. Ibuprofen was discontinued, and the patient was treated supportively with analgesia and packed red blood cell transfusions. Testing for HIV, antinuclear antibodies (ANA) panel, Hepatitis panel, and copper and zinc levels were negative. A biopsy of a targetoid lesion on the skin showed changes consistent with EM. Esophagogastroduodenoscopy revealed no actively bleeding lesions or ulcers in the stomach mucosa. The patient's blood counts eventually recovered with supportive treatment, and symptomatology improved. The patient was discharged six days after admission. Healthcare professionals should be aware of rare hematologic and immunologic side effects of NSAIDs, which may often be overlooked and misdiagnosed. More studies are needed to build on our wealth of knowledge regarding the etiology and management of EM, Steven Johnson syndrome (SJS), and toxic epidermal necrolysis (TEN).

Romiplostim for treatment of thrombocytopenia in dogs: A retrospective assessment and clinical outcomes.

BACKGROUND: Romiplostim, a thrombopoietin analog, is commonly used to treat immune-mediated thrombocytopenia (ITP) in humans, but its use in dogs remains limited. OBJECTIVES: Evaluate the effects and adverse events of romiplostim administration in dogs with thrombocytopenia caused by various underlying diseases. ANIMALS: Forty-two client-owned dogs with naturally occurring thrombocytopenia at 2 referral animal hospitals. METHODS: Retrospective, multi-institutional analysis to evaluate the outcomes of romiplostim treatment in dogs. RESULTS: Among the dogs treated with romiplostim, 27 experienced an increase in platelet count and 26 maintained a platelet count within the reference range. Platelet count improvement was observed in various conditions: primary ITP (90%, n = 18/20), pancytopenia of unknown etiology (42.9%, n = 3/7), chemotherapy-induced thrombocytopenia (50%, n = 3/6), babesiosis (100%, n = 1/1), radiotherapy-induced thrombocytopenia (0%, n = 0/1), and disseminated intravascular coagulopathy (33.3%, n = 2/6). The median time for platelet recovery (>50 000/µL) after romiplostim administration was 4 days, and the median time for platelet count normalization was 7 days. Median hospitalization time for the improvement group (I) was 5 days. The survival-to-discharge rates were 85%, 40%, and 28.6% for dogs with primary ITP, secondary thrombocytopenia, and thrombocytopenia of unknown etiology, respectively. CONCLUSIONS AND CLINICAL IMPORTANCE: Romiplostim is a well-tolerated and promising treatment for primary ITP in dogs, suggesting its potential as a valuable therapeutic option for dogs with thrombocytopenia caused by various underlying conditions. These findings emphasize the need for further research to optimize romiplostim dosing and understand its role in treating secondary thrombocytopenia and pancytopenia of unknown etiology.

Transcobalamin deficiency - a rare genetic defect in transportation of cobalamin; case report.

BACKGROUND: Vitamin B12 is primarily transported from plasma to cells by Transcobalamin. Deficiency of Transcobalamin is a rare autosomal recessive disorder that results in unavailability of cobalamin in cells and accumulation of homocysteine and methylmalonic acid. CASE REPORT: We report a case of a 2-year-old male child with persistent pancytopenia, recurrent infections, and megaloblastic anemia. Next-generation sequencing identified a novel variant in exon 8 of TCN2 gene. Substantial improvement has been observed following administration of high doses of parenteral methylcobalamin. CONCLUSION: In patients with unresolved pancytopenia and megaloblastic anemia, Transcobalamin deficiency should be investigated and treated promptly to prevent any irreversible and harmful outcome.

Stevens-Johnson syndrome associated with pancytopenia: a case report.

Introduction and importance: Stevens-Johnson syndrome (SJS) is a rare and unusual hypersensitivity reaction to certain drugs like allopurinol, commonly used for treating gout. SJS is recognized by extensive necrosis and detachment of skin and mucus membranes. Pancytopenia, characterized by decreased levels of red blood cells, white blood cells and platelets, is an exceedingly rare occurrence in the rare disorder SJS. Case presentation: The authors present a 61-year-old male who exhibited symptoms of fever and rash for 5 days accompanied by pancytopenia and liver injury. Clinical discussion: The abdomen and bilateral lower extremities exhibited several well-defined dusky-colored hyperpigmented macular lesions. Initially, these lesions were small, tender, erythematous, and raised, later transitioning to a dark red. Multiple distinct ulcerations were present on the lips and buccal cavity. Additionally, there was denudation of the skin with bleeding observed between the toes of both legs. The causality was assessed as a definite adverse drug reaction according to the Naranjo and ALDEN algorithm. The patient received treatment consisting of intravenous steroid along with prophylactics antibiotics. The individual's pancytopenia was resolved without requiring any blood cells or plasma or platelet concentrate transfusion. Conclusion: The exact pathophysiology of SJS associated with pancytopenia has not yet been fully elucidated. The authors' study hypothesized that the cause of pancytopenia in SJS could be either the direct cytotoxicity of drugs or immune-mediated damage to the bone marrow cells. Additional studies are necessary to establish the precise pathophysiology of the condition. Moreover, our study also indicates that pancytopenia can resolve in SJS without the need for blood cells or plasma or platelet concentrate transfusion. Once more, further studies are required to establish precise management strategies for managing SJS associated with pancytopenia.

Unveiling Neglected Concerns: Possible Severe Hepatic Complications after Nephrectomy in Autosomal Dominant Polycystic Kidney Disease - A Case Report.

Introduction: Autosomal dominant polycystic kidney disease (ADPKD) is the most common genetic kidney disease and the 4th leading cause of renal replacement therapy in the world. ADPKD is a systemic disorder as cysts may develop in several organs. Liver cysts are the most common extrarenal manifestations and are often incidentally detected. Even though cysts do not influence liver function, they can grow to a very great size and can significantly enlarge liver volume, causing structural distortion of the biliary tree and patient discomfort due to the mass effect. Nephrectomy is frequently considered in preparation for renal transplantation in patients with remarkable kidneys' enlargement. There are currently no globally recognized clinical guidelines for nephrectomy. Although cysts do not normally affect liver function in ADPKD, after nephrectomy cases of liver fibrosis and Budd-Chiari have been reported. These are uncommon disorders due to the obstruction of the blood flow in the hepatic venous causing spleen and liver volume enlargement, portal hypertension, and hepatic cirrhosis. Case Presentation: We present a case of hepatic fibrosis with splenomegaly and severe pancytopenia as a tardive complication after bilateral nephrectomy in 47-year-old ADPKD patient. Conclusion: This finding underscores the critical significance of meticulously examining the anatomical relationship between polycystic kidneys and the liver before performing nephrectomy. Additionally, it highlights the importance of assessing liver involvement and associated complications. By integrating liver assessment into the criteria, we can significantly enhance patient care and improve the overall management of ADPKD before kidney transplantation.

Reversible Pancytopenia Due to Severe Iron Deficiency Anemia in a 12-Year-Old Girl.

Iron deficiency anemia remains a global health challenge among young children starting from birth. Pancytopenia is a rare presentation of iron deficiency in children, being highly reversible with a simple treatment strategy including diet modification and iron supplementation. A 12-year-old Omani girl presented with a four-week history of fatigue, dizziness, and palpitations. Investigations revealed hemoglobin of 3.3 g/dL (11-14.5 g/dL), platelet of 47×109/L (150-450×109/L), white cell count of 3.9×109/L (2.4-9.5×109/L), and absolute neutrophil count of 0.5×109/L (1-4.8×109/L). Her red blood cell distribution width was high (34.1%; 11.5-16.5%), and her reticulocytes were normal (2.1%; 0.2-2%) with a mild elevation in the immature reticulocytes. Moreover, the ferritin level was profoundly low with a result of 1 ug/L only. Her peripheral blood smear showed pancytopenia in a background of microcytic and hypochromic red cells. After appropriate supplementation with oral ferrous sulfate in combination with an iron-rich diet, she showed complete recovery after six months from the initiation of management. This case report highlights that iron deficiency can be a cause of severe pancytopenia in children.