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A leukemic child developed a pulmonary leukemic infiltration, confirmed by open lung biopsy. His radiograph showed a mixed interstitial and nodular pattern. Nodular lung lesions are rare in pediatric patients and may exceptionally represent leukemic invasion.
BACKGROUND: Patients with leukemia often manifest cutaneous findings, which include nonspecific lesions and specific leukemic infiltrates termed leukemia cutis. OBJECTIVE: A case of leukemia cutis involving distal finger pads is reported and literature describing hand involvement of specific leukemic infiltrates is reviewed. METHODS AND RESULTS: An 80-year-old woman with a 10-year history of chronic lymphocytic leukemia developed painful symmetric tumors of her distal finger pads. Histopathological examination of the biopsy specimen revealed infiltration by neoplastic lymphocytes. Only a few cases of leukemia cutis involving the hands have been reported in the literature, none with this particular presentation. The clinical and histopathologic features of leukemia cutis are reviewed. CONCLUSION: This case emphasizes the importance of obtaining a biopsy specimen for histopathological examination of any suspicious skin lesion in a patient with leukemia.
Acute lymphoblastic leukemia (ALL) was initially diagnosed in a 12-year-old girl. Maintenance chemotherapy was discontinued after 32 months of continuous remission. Relapse of ALL occurred ten months after cessation of chemotherapy. Twenty-one months after relapse, she presented with a large ovarian tumor due to leukemic infiltration while her bone marrow and central nervous system (CNS) were still in remission. She remained in bone marrow and CNS remission when disseminated leukemic infiltration of the peritoneum was found seven months later. She died of bone marrow relapse 11 months after ovarian relapse, six years and two months after the initial diagnosis. In contrast to testicular relapse, ovarian relapses in acute lymphoblastic leukemia are rarely reported.
OBJECTIVE: To present an unusual case of recurrent facial palsy resulting from acute leukemic infiltration of the parotid gland. STUDY DESIGN: Case report. METHODS: An 11-year-old boy who had been treated for acute lymphoblastic leukemia (ALL) from 3 to 6 years of age presented with intermittent left facial nerve palsy with concurrent ipsilateral parotid fullness. The initial findings at diagnosis and workup are presented, and the disease progression and resolution with therapy are documented. RESULTS: The patient had been off therapy when this finding developed. A workup for central and viral etiologies for the facial palsy was unrevealing. Biopsy of the parotid gland demonstrated a lymphoblastic leukemic infiltrate. The patient was placed on a chemotherapy protocol for relapsed leukemia, resulting in complete resolution of the facial palsy. CONCLUSION: Isolated facial nerve dysfunction, albeit rare, has been documented as a sign of central nervous system involvement in leukemia, but until now this presentation has not been described in the setting of leukemic relapse presenting with acute infiltration of the parotid gland.
Seven children with acute lymphocytic leukemia developed testicular swelling during bone marrow remission. Needle biopsies and one orchiectomy specimen revealed leukemic infiltration. Another patient encountered concurrent medullary and testicular relapses. The leukemic nature of the testicular infiltration can be readily confirmed on needle biopsies. Orchiectomy should be discouraged. The leukemic infiltration mainly took place in the interstitial spaces. The seminiferous tubules were atrophic and lined by Sertoli cells. Occasional spermatogenic cells could be found in some cases. The leukemic cells were also observed to invade and accumulate beneath the Sertoli cell layer. Destruction of the tubules by the infiltrate was seen in advanced cases. Postradiation biopsies were characterized by fibrosis. The sigeveloped subsequent marrow relapse despite the effective control of the testicular relapse by irradiation. Another important observation is the high incidence of testicular relapse (16.2% so far).
A previously healthy 4-year-old boy was admitted because of acute liver failure. He was icteric, lethargic, had elevated ammonia and abnormal liver function tests. Serology was negative for viral hepatitis. There was no history of hepatotoxic drugs. Family history was unremarkable. The child was taken to the operating room for a living-related hepatic transplant. Frozen section showed massive hepatic leukemic infiltration and hepatocellular necrosis. Bone marrow aspiration confirmed the diagnosis of acute lymphoblastic leukemia (ALL). Transplant was withheld and chemotherapy was attempted. He died the following day due to systemic leukemic infiltration, cerebral edema, and severe anoxic ischemic encephalopathy.
We report 3 children with leukemia cutis observed at the initial diagnosis of systemic leukemia. Leukemia subtypes in the three children were congenital monocytic, acute undifferentiated, and acute monocytic, respectively. The patients were girls age 10 days, 14 years, and 11 months, respectively, at diagnosis. We describe the clinical features of the cases and the results of immunohistochemical studies on paraffin-embedded skin biopsy specimens. The skin lesions were tumors and areas of reddish purple erythema in the first child, pigmented erythema in the second, and bright red erythema in the first child, pigmented erythema in the second, and bright red erythema in the third. In the first two patients skin lesion biopsy specimens had dense leukemic infiltrates in the dermis with reactive T lymphocytes scattered among them. In the third patient, the infiltrating cells were almost all reactive T lymphocytes, with a few leukemic cells. A relationship between the leukemic-reactive cell ratio and the prognosis was suggested; dense leukemic cell infiltrates may be associated with a poor prognosis.
The dimethyltriazenes p-(3,3-dimethyl-1-triazeno)benzoic acid potassium salt (DM-COOK) and 5-(3,3-dimethyl-1-triazeno)-imidazole-4-carboxamide (DTIC) increase, unlike cyclophosphamide (Cy), the survival time of mice bearing L1210 lymphoid leukemia, P388 lymphocytic leukemia and TLX5 lymphoma with a mechanism unrelated to cytotoxicity for tumor cells. The in vivo bioassays of brains, and the histologic examinations of the livers of leukemic mice show that DM-COOK and DTIC prevent leukemic infiltration in these organs at dosages devoid of cytotoxic effects for peritoneal tumor cells. At a dosage equitoxic with that of dimethyltriazenes, cyclophosphamide causes the absence of tumor cells in the peritoneal cavity and in the brains and livers of mice bearing P388 and L1210 leukemias. DM-COOK and DTIC thus possess a mild or insignificant cytotoxic action together with antimetastatic properties also on mouse transplantable leukemias. The use of DM-COOK appears advantageous over that of cyclophosphamide and DTIC because of a reduced host toxicity, which is particularly evident for cyclophosphamide and DTIC on liver parenchyma and bone marrow.
Endocardial fibroelastosis developed in the heart of a patient who had chronic lymphocytic leukemia. Leukemic infiltrates were found in the endocardial scar tissue, myocardium, coronary arteries, and other viscera. In view of the absence of any other known cause of endocardial fibroelastosis, it is postulated that endocardial fibroelastosis was caused by myocardial leukemic infiltration. This is the first reported case of endocardial fibroelastosis in a patient with chronic lymphocytic leukemia.
Ultrasonic computed tomography (UCT) can aid in characterizing tissue for the detection and diagnosis of leukemic infiltration of the testes. Preliminary studies in 6 healthy adults and 26 patients (3-20 years old) with leukemia or non-Hodgkin lymphoma suggest that elevated speed of sound in the testis may be an indicator of leukemic infiltration. UCT may become an important screening method for detecting testicular involvement. In long-term follow-up, UCT can be performed more frequently and easily than biopsy, which is the current screening method.
We report a case of acute lymphoblastic leukemia (ALL) with ocular involvement in which bilateral swelling of the optic disk head was noticed. Massive direct infiltration of the optic nerve head by leukemic cells can give rise to a clinical picture identical to that of a true papilledema. Ocular echography allowed a better and more complete interpretation of the optic disk involvement. No echographic description of a leukemic infiltration of the optic nerve head has been reported previously.
We describe a patient who developed unilateral papilledema after allogeneic BMT. This is a rare manifestation of pseudotumor cerebri, which results from elevated intracranial pressure caused by cyclosporin A. The papilledema usually involves the fundi bilaterally, but unilateral involvement has been described. Congenital anomalies, compression and adhesion of the optic nerve sheath are its causes. In this patient, the right optic fundus was spared although leukemic infiltration was present on this side and high-dose irradiation (72 Gy) was given. Although papilledema is a sensitive marker of elevated intracranial pressure, this sign may be masked by constriction of the optic sheath in patients who suffer from leukemic infiltration of the central nervous system and receive high doses of cranial irradiation.
An HTLV-I-transformed T cell line, obtained from the peripheral blood of a virus-infected (B/J X Chbb:HM) F1 rabbit, was able to kill syngeneic newborn rabbits within 7 days, when inoculated intraperitoneally at a dose of 1 X 10(8) cells. Inoculation of 1 X 10(7) cells killed or rendered moribund 50% of inoculated animals, while surviving animals exhibited cell-mediated cytotoxic activities against the transformed cells. The peripheral blood leukocyte counts increased in all surviving animals, in association with appearance of abnormal lymphocytes with convoluted or lobulated nuclei. Pathological examination of animals that died one week post-inoculation revealed no tumors in the abdominal cavity, but accumulation of ascites containing abnormal lymphocytes. Histological examination showed leukemic infiltration in the liver, lungs, spleen and mesenteric lymph nodes. The same cell line was also able to kill syngeneic adult rabbits in 8-10 days when inoculated intravenously, but not intraperitoneally, at a dose of 1 X 10(8) cells. Leukemic infiltration was observed in the major organs of these animals. Adult animals which were already virus carriers were resistant to this lethal inoculation. This rabbit ATL-like disease may prove to be useful as an experimental model for acute adult T cell leukemia.
PURPOSE: The purpose of this study was to report a case of bilateral blindness, bilateral necrotizing scleritis, and bilateral deafness in a patient with myelodysplastic syndrome (MDS). In such a patient, the possibility of relapsing polychondritis (RPC) associated with MDS must be considered. CASE REPORT/METHODS: A 66-year-old patient suffered from myelodysplastic syndrome (MDS). Shortly before his death, he became bilaterally blind and deaf. A biopsy was taken from the conjunctiva and the bone marrow, and both eyes were obtained after death for further investigation. Findings of the clinical and laboratory work-up for the patient's hematologic disorder as well as an examination of the eyes by light microscopy and immunohistochemistry are presented. RESULTS: Ocular sections showed a diffuse necrotizing scleritis with moderate uveitis and no identifiable infectious agent. Neither was there any evidence of a leukemic infiltration. The deafness had been due to inner ear failure, and the patient died of a cardiac failure. CONCLUSIONS: Non-infectious scleritis associated with inner ear deafness is a strong indication of relapsing polychondritis (RPC). Furthermore, RPC can be associated with MDS. Thus, in addition to leukemic infiltration and infection involving ocular structures, ophthalmologists and otolargyngologists should be aware of the association between MDS and RPC and the potential complications.
The medium-sized mononuclear cell with plasmacytoid features, formerly known as "T-associated plasma cell" or "plasmacytoid T cell," has recently been shown to express several myelomonocyte and monocyte-macrophage associated antigens, suggesting a monocytic origin, and it has been renamed "plasmacytoid monocyte." The present study describes the clinical and pathological features of two patients with generalized lymphadenopathy and leukemia (chronic myelomonocytic leukemia in Case 1, and acute non-B, non-T lymphoblastic leukemia in Case 2), and whose lymph node biopsies showed large numbers of plasmacytoid monocytes associated with the leukemic infiltrates. Case 1 was strikingly similar to three previously reported cases of so-called "plasmacytoid T cell" lymphoma, all associated with a myeloproliferative disorder. In our case, the destructive growth pattern of the plasmacytoid monocytes and the de novo expression of CD5 on these cells favored their neoplastic nature; the sharing of some markers of plasmacytoid monocytes with the myelomonocytic infiltrate suggested they were part of the tumoral proliferation. In Case 2, plasmacytoid monocytes displayed an immunophenotype guide similar to that reported in reactive conditions and were antigenically unrelated to the leukemic cells; plasmacytoid monocyte clusters occurred also in the lymphoid parenchyma spared by the leukemic infiltrate. These findings led us to interpret the large numbers of plasmacytoid monocytes in this second case as a tumor-associated host reaction.
Chronic lithium administration to 22 patients with oligoleukemia did not alleviate cytopenia or stimulate bone marrow proliferative activity. The authors identified, however, pretreatment characteristics discriminating two evolutionary endpoints of oligoleukemia (marrow failure, 10 patients; overt acute leukemia, 12 patients): higher marrow leukemic infiltrate, normal myeloid precursor proportion, platelet count, and female sex all favored eventual transition to overt leukemia which, in comparison with marrow failure, was associated with a significantly longer survival duration from symptoms. For patients developing overt leukemia, survival from diagnosis was inversely correlated with the degree of marrow leukemic infiltrate. The lack of lithium responsiveness in oligoleukemia is consistent with the concept of differentiated leukemia with abnormalities either at the level of a lithium-responsive adherent cell elaborating colony stimulating activity (CSA) or at the level of CSA-responsive CFUs.
A patient with oculomotor palsy with pupillary sparing was shown angiographically to have an aneurysm of the internal carotid artery, which proved at operation to arise distal to the origin of the ophthalmic artery. It did not impinge on the oculomotor nerve at any point. The oculomotor palsy persisted postoperatively, and complete intrinsic and extrinsic ophthalmoplegia developed. Cytological studies of cerebrospinal fluid were then made and were positive for malignant lymphocytic leukemic cells. Despite the fact that an aneurysm causing oculomotor palsy with pupillary sparing has been reported, we recommend that nonaneurysmal causes be considered first in patients presenting with that neurological sign.
Sweet's syndrome is characterized by the abrupt onset of fever, neutrophilic leukocytosis, and erythematous, tender pseudovesiculated plaques or nodules that respond readily to corticosteroid therapy. It is usually distinguished by the presence of mature neutrophils on histopathologic examination. We describe a 38-year-old man with acute myelogenous leukemia who had an erythematous vesicular eruption of the left eye develop that resembled cellulitis. A biopsy specimen revealed a dermal infiltrate of mature neutrophils and immature myeloblastic precursors. He later had hemorrhagic pseudovesiculated plaques develop bilaterally on his hands. A biopsy specimen again revealed abundant neutrophils with immature forms. A similar eruption developed at the site of a Hickman catheter placement 4 months later. His skin lesions responded rapidly to oral corticosteroids. This case is unique in that his initial presentation of Sweet's syndrome resembled orbital cellulitis that was characterized by immature myeloid precursors on histopathology.