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Extensive splenic infarction, deep vein thrombosis and pulmonary emboli complicating induction therapy with all-trans-retinoic acid (ATRA) for acute promyelocytic leukemia.

Bleeding is a common complication during initial induction treatment for acute promyelocytic leukemia (APL). Administration of all-trans-retinoic acid (ATRA), which is in routine use for APL in the past decade improves the bleeding tendency dramatically. Nevertheless, thrombotic events have still been reported in a small proportion of APL patients treated with ATRA. Here we describe a case of splenic infarction and life threatening thrombosis in a young patient with APL treated with ATRA. We review the relevant literature and discuss the pathophysiology, risk factors and treatment of this complication occurring during therapy, for APL.

Adult↗

[Meningococcocemia complicated by disseminated intravascular coagulation, splenic infarction and pulmonary thromboembolism in a young adult: case report].

Mortality of meningococcal septicemia remains high in spite of the improvement of antibiotics treatment and critical care medicine. A 23-year-old male, who had been well until a day earlier, was admitted to the hospital because of a high-grade fever and headache. On the second hospital day, he was still febrile, and it was confirmed that he had disseminated intravascular coagulation. There was no purpuric skin lesion, and a lumbar puncture revealed no abnormality. The condition was complicated by a splenic infarction on the second hospital day, and he suffered a pulmonary infarction on the 8th hospital day. The blood culture was positive for Neisseria meningitidis, making the diagnosis meningococcal septicemia. He was successfully treated with antibiotics and intensive care. Although meningococcocemia in adults is relatively rare in Japan, the disease mortality is still high even in the modern era. Then, once the diagnosis is suspected, it is essential to keep in mind that meningococcal infection requires early recognition of the disease process, prompt initiation of adequate antiinfectious therapy and intensive treatment of multiorgan failure.

Adult↗

[Splenic infarct in heterozygote sickle cell trait (Hb AS)].

We present a carrier of the sickle cell trait who developed a serious splenic infarction. An antecedent hypoxaemic event and a blood coagulation disorder were ruled out. The observation shows that the sickle cell trait can represent a risk factor for a life-threatening thrombotic event, even in the absence of a predisposing condition.

Adult↗

[Acute abdominal pain due to splenic infarction in a patient with heterozygous sickle cell disease exposed to high altitude].

Hemoglobinopathy S, Depranocytosis or Sickle Cell Disease is the most common hemoglobinopathy in the world. In its heterozygous form (Sickle Cell Trait), it affects 8% of the black population in the U.S. and 25% of the black population in Africa, and is found less frequently in the Mediterranean area, India, Middle East and Latin America. The basic alteration is a substitution of glutamic acid by valin in the sixth position of the beta globin chain, which causes polymerization at low oxygen tension thereby distorting the structure of erythrocytes and increasing blood viscosity, which, in turn, generates obstructions of the capillary arterial blood flow to different areas of the body thus causing microinfarctions. Although Splenic Infarction is rare, it is recognized as a serious complication of Heterozygous Sickle Cell Disease (Sickle Cell Trait). We present the case of a 21 year-old mestizo male patient who came in with an acute case of abdominal pain after arriving to work in the Casapalca mining city (located in the Peruvian Andes at 4200 m.a.s.l.) and was referred to our Hospital in Lima for exams. We present the case because it is an unusual cause of acute abdominal pain, and because this condition is rare in Peru and there are few publications about it.

Abdominal Pain↗

Splenic infarction and spontaneous rupture of the spleen after therapeutic embolization.

Patients with major hematologic disorders who have hypersplenism and alterations in their immune mechanism are subject to a higher incidence of bacteremia after embolization procedures. In certain instances, these infectious complications can be fatal. Medical splenectomy for hematologic disorders is sometimes complicated by massive splenic infarction and spontaneous rupture; spontaneous rupture appears to be a function of both infarct size and underlying infectious complications. Prophylactic measures can be employed to avoid these complications after interventional splenic embolization.

Abscess↗

Fatal, complete splenic infarction and hepatic infection due to disseminated Trichosporon beigelii infection: CT findings.

We report on a 56-year-old woman with acute lymphocytic leukemia who presented with right upper quadrant pain, fever, nausea, and vomiting. Laboratory studies confirmed fungemia with Trichosporum beigelii, and contrast-enhanced computed tomography of the abdomen demonstrated numerous low-attenuation liver lesions and a hypodense spleen with capsular enhancement suggestive of complete splenic infarction. Subsequent splenectomy confirmed that the spleen was completely infarcted and infiltrated with Trichosporum. The patient had a difficult postoperative course and died despite aggressive antifungal therapy.

Antifungal Agents↗

Systemic mast cell disease with splenic infarction: a case report.

An autopsy case of systemic mast cell disease (SMCD) without primary skin lesions in a 57-year-old Japanese male is described. Initially the patient was suspected of having liver cirrhosis or malignant lymphoma because of hepatomegaly and lymph node enlargement on admission. However, a lymph node biopsy and bone marrow aspiration conducted on his third admission indicated a SMCD because of the existence of metachromatic cell aggregates stained with toluidine blue. At autopsy, the diagnosis was confirmed because the proliferating cells were histochemically proven to be mast cells by naphthol AS.D chloroacetate esterase, Giemsa and alcian blue, in addition to toluidine blue staining. The intra-abdominal and retroperitoneal lymph nodes were replaced by mast cell aggregates, which caused the splenic infarction and bilateral hydronephrosis, with infiltration of mast cells into the spleen and kidneys also being apparent. Mast cell infiltration was similarly found in the bone marrow, liver, ileum and ascending colon. Immunohistochemically, the mast cells were positive for antibodies of alpha 1-antichymotrypsin, CD45 (LCA), CD43 (MT-1), CD45R (MB-1) and the oncoprotein c-kit. Electron microscopic examination using formalin-fixed tissue gave supportive evidence of a mast cell origin for the lesions.

Fatal Outcome↗