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A 2-year-old boy with acute lymphoblastic leukemia initially experienced pericardial effusion during the maintenance treatment due to leukemic infiltration of the pericardium and cardiac muscle. He subsequently died suddenly owing to leukemic occlusion of the left coronary artery.
SJL/J mice which developed a high incidence of spontaneous reticulum cell neoplasms, developed a low rate incidence (20-25%) of myeloid leukemia (ML) after X-irradiation. The possible effect of adrenal steroid imbalance to radiation-induced ML in SJL/J mice was tested. Intact and thymectomized animals were exposed to a single dose of 300 r whole body irradiation and treated with either hydrocortisone acetate, prednisone, metyrapone and adrenocorticotropin as coleukemogenic agents. Hydrocortisone and prednisone exerted a marked coleukemogenic effect, increasing the ML incidence to a similar rate of about 50-70%, at a mean latent period of 300 days. Prominent leukemic infiltration were observed in the bone marrow, spleen, lymph nodes and liver of the leukemic animals. Results of cytological and histological studies, including cytochemistry and ultrastructure, were all consistent with the diagnosis of acute myeloid leukemia (AML). Since AML is the type of human secondary leukemia which appears increasingly in patients treated with alkylating drugs and/or irradiation and corticosteroids for Hodgkin's disease or other neoplastic diseases, the experimental model of AML induced in SJL/J mice could be used for elucidation of mechanisms of leukemogenesis in secondary leukemia.
Twenty-nine of 60 boys with acute lymphoblastic leukemia survived for more than 30 months and were potential candidates for discontinuation of therapy. Six patients developed overt clinical testicular leukemia: one at 34 months from diagnosis while receiving therapy and five at three to 17 months after therapy was stopped. Elective wedge biopsy of the testes has become part of the evaluation prior to discontinuation of therapy since 1977. Six of 18 boys had microscopic evidence of leukemic infiltration of the testes: four with diffuse involvement and two with focal clusters of leukemic cells. Testicular biopsy is recommended at the time of discontinuation of therapy and perhaps early in the course of the disease, although a negative biopsy does not exclude some focal lesions. The eventual outcome of those with occult testicular leukemia remains to be determined.
The antileukemic activity of karminomycin and rubomycin was studied comparatively in parallel experiments with respect to 4 strains of transplantable leukemia, i.e. acute non-differentiated leukemia La, acute lymphoblast leukemia, L-1210 and P-388 and subacute lymphoblast leukemia No. 8 CRIHBT. The doses used were adequate by their toxicity. The tests of the therapeutic effectiveness were: an increase in the life time of the animals treated as compared to the control ones, a decrease in the leukocyte count and the number of the blast cells in the peripheral blood, a decrease in the leukemic infiltration of the organs and tissues of the animals treated. It was shown that karminomycin was more effective in the studied leukemia strains when it was used in the doses with equivalent toxicity. The more pronounced antileukemic activity of karminomycin was especially evident from histological examinations, which showed lower infiltration of the organs and tissues of the mice treated with karminomycin by the leukemic cells as compared to the animals treated with rubomycin.
Results on morphologic and hematologic characterization of a hamster leukemia capable of both cellular and cellfree transmission are described. Solid tumors removed in the course of several passages of leukemia animals, after producing blood smears, and spleen, liver, lymph nodes, bone marrow, thymus, kidney and lung were investigated histologically and histochemically. The morphological picture of the hamster leukemia has not changed during several transplantation generations. In addition to solid tumours, typical leukemic infiltration were detected histologically in spleen, liver, lymph nodes, bone marrow, kidneys and lung. No leukemic proliferation was noticed in the thymus. The final stage of the disease is characterized by an abrupt occurrence of high leukemic cell counts. The demonstration of alkaline phosphatase, but especially of naphtol-AS-D-chloroacetate esterase, in the leukemic cells is interpreted as indicating malignization of cells of the granulocytic line.
We describe a patient with myelomonocytic leukemia who demonstrated striking leukemic infiltration in the scar of a recent Hickman catheter placement. This cutaneous involvement occurred initially without signs of systemic relapse. A comparative review of leukemic cell physiology provides several possible reasons for this extramedullary infiltration, including the greater functional maturity, deformability, adhesiveness, and ability to cluster of myelomonocytic and monocytic leukemia cells relative to other leukemias. A careful cutaneous examination, with particular attention to recent scars, may provide the only evidence of relapse in adult leukemia.
Hairy cell leukemia (in french: leucémie à tricholeucocytes) is a distinctive form of chronic leukemia with splenomegaly, pancytopenia, presence of a particular circulating mononuclear cell, myelofibrosis and leukemic infiltration of the bone marrow. Generally, a tartrate resistant acid phosphatase activity is found in the leukemic cells. Hairy cell leukemia is the main leukemia in which the treatment is first surgical. Splenectomy has a good result for survival median and infectious risk. The disease is still mysterious for the origin of the leukemic cell; monocyte, B lymphocyte or in few cases T lymphocyte, even though a spectrum of immunological patterns pleads for the B lymphocyte origin of the leukemic cells.
A patient with leukemic optic nerve infiltration is presented. It occurred as an isolated manifestation of leukemia 17 months after therapy for acute lymphocytic leukemia was discontinued. Therapy with prednisone and vincristine was effective in reducing optic nerve infiltration in a short period of time. This observation leads to the conclusion that the optic nerve does not belong to the pharmacological sanctuary.
Out of 70 cases of leukemia studied, 19 had neurological manifestations. All cases were autopsied. Leukemic infiltrates and intracranial hemorrhages produced various neurological manifestations. In autopsied cases 37.2% showed infiltrative changes. Intracranial hemorrhages contributed to 20%, the cause of which were due to thrombocytopenia and leukostasis. Leukemic nodules, demyelination and astrocytosis, gliosis were also seen on histopathology.
Electrolyte disturbances in leukemia can be the result of the disease process or drug therapy. One group of electrolyte abnormalities is related to the stage of the leukemic process. Included in this group are newly diagnosed patients who may show elevated serum potassium, phosphorus, and magnesium--a result of their release from malignant cells after cytotoxic therapy or their accumulation due to urate nephropathy. Patients in remission usually have normal serum electrolyte concentrations, but acute leukemia patients during relapse may have hypokalemia, hypophosphatemia, and hypomagnesemia. This imbalance may be related to cellular uptake of these electrolytes in the presence of inadequate dietary intake. Other factors contributing to electrolyte derangements, and related to the leukemic process, include hyponatremia and hypochloremia secondary to the SIADH, hypokalemia in acute monocytic or acute myelomonocytic leukemia due to lysozyme-induced tubular damage, hypercalcemia possibly secondary to leukemic infiltration of bone or parathyroid glands (with PTH release), or production of a PTH-like substance by leukemic cells. Nonspecific factors related to the disease process which may aggravate the electrolyte imbalance include gastrointestinal loss through nausea, vomiting, and malnutrition. The drug-related electrolyte abnormalities include cyclophosphamide- and vincristine-induced SIADH; decreased serum sodium, chloride, potassium, and calcium concentrations as a result of polymyxin B nephrotoxicity; hypokalemia and hypomagnesemia secondary to amphotericin B; hypocalcemia, hypophosphatemia, and hyperphosphaturia due to L-asparaginase-induced hypoparathyroidism; hypokalemia due to a nonreabsorbable anion effect of antibiotics in the distal tubule or changes in membrane ionic transport of all cells by large doses of antibiotics. Electrolyte disturbance in leukemia thus have a multifactorial pathogenesis which can best be delineated according to the stage of the leukemic process and the drugs being used. Recognition of the cause or causes in a particular patient is essential for an effective approach to management. This review emphasizes the need for routine measurement of serum electrolytes during all phases of the leukemic process.
A 6-year-old boy with a diagnosis of acute myeoblastic leukemia in remission developed iris infiltration accompanied by uveitis, hypopyon, and vitreous hemorrhage, which was initially unilateral, later becoming bilateral. Pathologically, the eyes showed leukemic infiltrates in the conjunctiva, episclera, sclera, ciliary body, trabecular meshwork, canal of Schlemm, choroid, vitreous, and the iris. Leder stain studies showed positive esterase activity, indicating granulocytic sarcoma. Granulocytic sarcoma may appear intraocularly as iris nodules. These iris nodules may be the initial manifestation of granulocytic leukemia.
A 28-year-old woman in the third trimester of her pregnancy was found to have acute myelocytic leukemia. The baby was delivered by Cesarean section and her leukemia underwent spontaneous remission. However, 3 months later, she presented with massive painful leukemic infiltration of the breasts as initial manifestation of relapse, followed by systemic symptoms of leukemia. In vitro culture of the leukemic cells demonstrated characteristics of macrophage cell line. This case illustrates a unique sequence of events: spontaneous remission after the termination of pregnancy, which has profound hormonal alterations, and relapse in a very hormone-sensitive organ, the breast, a few months later when the hormonal milieu was resumed. This suggests hormonal dependence of her leukemic cells and potential for hormonal manipulation in a certain subset of human leukemia.
PURPOSE: To retrospectively review the pathologic diagnoses and clinical characteristics of patients undergoing dacryocystorhinostomy (DCR). METHODS: Specimens accessioned between 1991 and 2001 in a single ophthalmic pathology laboratory were reviewed. All of the specimens included a lacrimal sac biopsy specimen. The pathologic diagnoses were recorded. The clinical features of the patients with significant pathologic abnormalities were reviewed to determine if the pathology was suspected before or at the time of the DCR. RESULTS: There were 377 DCR specimens from 316 patients representing 1.8% of 21,018 ophthalmic pathology specimens accessioned between 1991 and 2001. Diagnoses, in decreasing order of frequency, were nongranulomatous inflammation (321, 85.1%), granulomatous inflammation consistent with sarcoidosis (8, 2.1%), lymphoma (7, 1.9%), papilloma (4, 1.11%), lymphoplasmacytic infiltrate (4, 1.1%), transitional cell carcinoma (2, 0.5%), and single cases of adenocarcinoma, undifferentiated carcinoma, granular cell tumor, plasmacytoma, and leukemic infiltrate. A total of 31 (8.2%) specimens from 25 (7.9%) of patients demonstrated significant pathology. Among 17 specimens (4.5%) from 14 patients with neoplasms whose clinical histories were available, 8 (2.1%) were not suspected before surgery. CONCLUSIONS: Nongranulomatous inflammation consistent with chronic dacryocystitis is the most common diagnosis in lacrimal sac specimens obtained at DCR. Neoplasms resulting in chronic nasolacrimal duct obstruction occurred in 4.6% of cases and were unsuspected before surgery in 2.1% of patients. We recommend pathologic examination of DCR specimens.
Hairy cell leukemia can be responsible for polyarthritis due either to leukemic infiltration or to immunity-drive inflammation. The second variant can antedate or post-date the clinical onset of leukemic symptoms and usually presents as rheumatoid arthritis, more rarely as lupus or scleroderma. The presence of hairy cells in the joint fluid does not rule out autoimmune polyarthritis. The main differential diagnoses are Felty's syndrome and large granular lymphocyte leukemia. We report a case of hairy cell leukemia with seropositive rheumatoid arthritis.
The sensitivity of different wild-type and 5-azacytidine-resistant lines of AKR leukemic mice to 5-azacytidine varies in relation to the activity of uridine kinase isolated from corresponding leukemic livers. The enhancement of liver uridine kinase activity observed in leukemic mice following the administration of a single dose of 5-azacytidine is accounted for by the presence of hepatocytes in infiltrated leukemic livers. The optimal schedule for the treatment of AKR leukemic mice with 5-azacytidine requires equally divided doses administered daily and not an initial high dose followed by low doses.
The eyes of 60 children dying of acute leukemia between 1968 and 1976 at the Children's Hospital Medical Center have been examined pathologically. An attempt has been made to relate eye findings to the state of the systemic disease at the time of death. Eight of the 60 patients had leukemia retinal infiltrates and all eight had fulminant disease with terminal leukocyte counts over 100,000 per cubic millimeter and a high percentage of "blast" cells. Twenty-six patients (43%) had leukemic infiltration of the choroid which was not apparent clinically, but which would require therapy in any effort to eradicate leukemic cells from the body. Five of six patients with optic nervic involvement had coexistant meningeal leukemia. Isolated retinal hemorrhages could not be correlated with other parameters of the leukemic process.
The sonographic findings present in three surgically-proven cases of testicular leukemic infiltration are discussed. The diagnosis is strongly suggested when an enlarged testis with focal or diffuse internal sonolucency is encountered in the leukemic patient in bone marrow remission.
The selectivity of action of 1-beta-D-arabinofuranosylcytosine (ara-C) against leukemic cells was studied in vivo. Dynamic state tissue levels of ara-C and of its mono-, di-, and triphosphate (ara-CTP) were measured in L1210 leukemic cells and in C57BL x DBA/2 F1 host tissues at different times after various doses of the agent. The levels were correlated with inhibition of thymidine incorporation into DNA and with cytocidal effects as measured by loss of isotopically prelabeled DNA. ara-CTP levels, but not those of the mono- and diphosphates of ara-C, were higher in leukemic cells and in host cell renewal systems than in other host tissues. DNA synthesis was equally inhibited by similar levels of ara-CTP in ascitic L1210 cells, in leukemic infiltrates in liver, and in small intestine. However, L1210 cells accumulated higher levels of ara-CTP for longer periods than did small intestine, and correspondingly the inhibition of DNA synthesis was greater and more prolonged in leukemic cells. ara-C caused greater losses of prelabeled DNA in ascites cells and in infiltrated liver than in host small intestine. It appears that the differential net tissue level of ara-CTP and its duration are the determinants of chemotherapeutic efficacy of ara-C against L1210 leukemia. ara-C was the predominant nucleoside present in hydrolysates of ara-CTP fractions. By contrast, 1-beta-D-arabinofuranosyluracil predominated in hydrolysates of monophosphate nucleotide fractions from ascites cells, liver, small intestine, and blood. Monophosphate nucleotide was also present in ascites fluid and plasma.