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PubMed1987

Antileukemic activity against L1210 leukemia, pharmacokinetics and hematological side effects of 5-hydroxymethyl-2'-deoxyuridine.

The chemotherapeutic potential of 5-hydroxymethyl-2'-deoxyuridine (5HmdUrd) was examined in vitro and in vivo. The compound was toxic in 2-day cultures; 7, 66 and 88% inhibition in the growth of L1210 cells was achieved with 1, 10 and 100 microM 5HmdUrd, respectively. The maximal plasma concentration of 5HmdUrd at 15 min after a single i.p. injection (100 mg/kg) in DBA/2 mice was 193-244 mumol./l and the compound had a logarithmic disappearance curve with a half-life of 20 min. Chemotherapy given as two daily i.p. injections of 5HmdUrd (100 mg/kg) for five successive days resulted in a 239% increase in median lifespan and 2/6 long-term survivals among DBA/2 mice bearing leukemia L1210. This treatment resulted in temporary neutropenia and thrombocytopenia, which were followed by rebound thrombocytosis and neutrophilia of short duration. Our data indicate that 5HmdUrd can successfully be used in experimental cancer chemotherapy in vivo.

Animals↗
PubMed1990

Analysis of bcr rearrangements in primary (essential) thrombocythaemia.

A clinical and molecular study was performed on 10 patients with the presumptive diagnosis of primary thrombocythaemia (PTH). In all cases conspicuous megakaryocytic proliferation in bone marrow smears was detected in the absence of the Philadelphia chromosome (Ph1), elevated red blood cell mass and evidence for a reactive cause of the thrombocytosis. We analyzed whether rearrangements of the bcr gene occurred in untreated patients. Bcr rearrangements were detected in the bone marrow cells but not in peripheral blood bells of one patient, indicating that this case might be related at the molecular level with Philadelphia chromosome negative CML, in which bcr rearrangements could be demonstrated.

Adult↗
PubMed1993

B-lymphoid/myeloid stem cell origin in Ph-positive acute leukemia with myeloid markers.

We report two cases of Philadelphia chromosome (Ph)-positive acute leukemia with definite myeloid markers. Ph was the sole chromosomal abnormality at presentation, and neither eosinophilia, basophilia, thrombocytosis nor hepatosplenomegaly was present. In both cases, Ph+ myeloblasts showed positive stain for myeloperoxidase and naphthol ASD chloroacetate esterase, which fulfilled the FAB criteria of acute myelogenous leukemia (AML). Ph+ myeloblasts co-expressed myeloid and B-lymphoid antigens (CD10, CD13, CD19 and CD33). In case 1, myeloblasts rearranged M-BCR, and the expression of M-BCR/ABL chimeric RNA was demonstrated by using the reverse transcription polymerase chain reaction (RT-PCR). They also clonally rearranged IGH. Ph clone disappeared on cytogenetic analysis in remission, and granulocytes in remission did not have rearranged M-BCR. In case 2, morphocytochemically distinct myeloid and lymphoid blast populations were seen. Myeloblasts and lymphoblasts were enriched > 96% as CD19-/CD33+ and CD19+/CD33- populations, respectively. Both of them possessed the identical rearrangement of IGH and M-BCR, indicating a common leukemic progenitor cell origin. Furthermore, m-BCR/ABL was detected in addition to M-BCR/ABL on RT-PCR. Accordingly, both cases were diagnosed as de novo Ph+ acute leukemia rather than as chronic myelogenous leukemia in blastic crisis. Their mixed B-lymphoid/myeloid characteristics strongly suggest that so-called 'Ph+ AML' is derived from Ph+ myeloid/B-lymphoid stem cells.

Adolescent↗
PubMed1995

Confirmation of spurious hypoxemia using continuous blood gas analysis in a patient with chronic myelogenous leukemia.

Patients with extreme leukocytosis or thrombocytosis who have hypoxemia on arterial blood gas analysis may demonstrate normal oxygen saturation using pulse oximetry. The most commonly invoked explanation for this phenomenon is oxygen consumption in the blood gas sample prior to analysis. However, others have challenged the premise that the hypoxemia is spurious. We describe a patient with extreme leukocytosis and hypoxemia in whom normoxia was confirmed by continuous blood gas analysis.

Adult↗
PubMed1996

Analysis of the erythropoietin receptor gene in patients with myeloproliferative and myelodysplastic syndromes.

The human erythropoietin receptor (EpoR) gene has been cloned and characterized. Very few EpoR genetic abnormalities have been reported so far. Polycythemia vera (PV) is characterized by low/normal serum erythropoietin (Epo) levels with proposed Epo hypersensitivity. Myelodysplastic syndromes (MDS) are characterized by refractory anemia with variable serum Epo levels. Several reports have suggested EpoR abnormalities in both types of stem cell disorders. We analyzed DNA obtained from peripheral blood mononuclear cells of seven healthy controls, 20 patients with myeloproliferative disorders (MPD, 11 patients with PV, five agnogenic myeloid metaplasia with myelofibrosis, four essential thrombocytosis) and eight patients with refractory anemia with ringed sideroblasts (RARS), an MDS variant. The DNA was digested with four restriction enzymes (BamHI, Bgl II, Sacl and HindIII), followed by Southern blot, using a 32P radiolabeled probe, containing 1.5 kb of the human EpoR cDNA. All 20 MPD patients and seven out of the eight MDS patients demonstrated a restriction pattern which was identical to the seven normal controls, as well as to the erythroid cell line K562, and also consistent with the expected restriction map, for all four enzymes tested. One RARS patient had a normal pattern with three enzymes but a different one with HindIII. The HindIII 12 kb large band was replaced by a faint 12 kb band and a new (about 9 kb) band appeared. The EpoR restriction map and the normal pattern obtained with the other three enzymes suggest that this patient has a 3 kb upstream deletion in one allelic EpoR gene. The same molecular pattern was detected in the patient's sister, who suffers from anemia with mild bone marrow (BM) dyserythropoiesis and plasmacytosis. Northern blot analysis showed that the patient's BM RNA carried normal EpoR message. This familial pattern may represent polymorphism. However, the patient's very high serum Epo level, her resistance to treatment with recombinant Epo, and the abnormally low growth rate of in vitro erythroid cultures, suggesting poor response to Epo in this MDS patient as well as the hematological abnormalities in her sister, support the speculation that the different EpoR gene might serve as a genetic predisposing marker and potentially could be involved (probably via post-transcriptional mechanisms and by an interaction with other factors or cytokines) in the pathogenesis. Our data suggest that the EpoR is intact in MPD and in most patients with RARS. One RARS patient had a familial different genetic structure, which could represent polymorphism. However, we can speculate also that it might be involved in the pathogenesis of the disease.

Aged↗
PubMed1983

The predictive value of initial cytogenetic studies in 148 adults with acute nonlymphocytic leukemia: a 12-year study (1970-1982).

When leukemic blood or marrow specimens from 148 adults with newly diagnosed acute nonlymphocytic leukemia (ANLL) were studied with chromosome banding techniques, 79 were found to have clonal abnormalities. Among 130 treated patients, the 53 with initially normal karyotypes had a significantly longer survival rate than the 16 in whom no normal metaphases were observed (p = 0.02). The 55 patients with both normal and abnormal metaphase cells had an intermediate survival. Once a complete remission had been attained, however, there was no significant difference in median survival between those patients with entirely normal karyotypes and those with abnormal karyotypes. Among the various FAB morphologic subsets of ANLL, the differences in complete remission rate and overall survival between the various cytogenetic subsets were greatest in acute myelogenous leukemia (AML, M1 + M2). The presence of an abnormal clone was a more important predictor of clinical outcome (p = 0.02) than the presence of normal stem cell clones. Aneuploidy alone (hyperdiploidy or hypodiploidy) was not of predictive value, indicating that the use of banding techniques to identify structural rearrangements in pseudodiploid cells was essential. Clonal chromosomal abnormalities were nonrandom and acquired, and specific abnormalities were closely associated with specific clinical-pathologic subsets of ANLL. All 13 patients with acute promyelocytic leukemia and adequate cytogenetic specimens had t(15;17); this translocation was not found in any other subset of ANLL. Six patients with AML (M2) had t(8;21) or a variant of this rearrangement. Seven patients had inv(16)(p13q22) associated with acute myelomonocytic leukemia (AMMoL, M4) and abnormal marrow eosinophils. Two patients had ins(3;3) and thrombocytosis. Four patients had a translocation involving 11q, but none of these had acute monocytic leukemia (AMoL, M5); no patient had del(11q).

Acute Disease↗
PubMed1987

Possible cytogenetic marker associated with myelofibrosis in chronic granulocytic leukemia and its prognostic significance.

An association between myelofibrosis (MF) and chronic granulocytic leukemia (CGL) has been recognized. MF is usually a sign of a poor prognosis but its relation to other important parameters of CGL is not known. We observed a 54-year-old, white male patient who was well until May 1983 when he began developing gradually increasing right hip and left shoulder pain. Clinical evaluation 3 months later revealed splenomegaly and a white blood count of 126,000 with 29 segmented neutrophils, 22 bands, 7 metamyelocytes, 11 myelocytes, 6 promyelocytes, 5 blasts, 2 eosinophils, 5 basophils, and 3 lymphocytes. Cytogenetic analysis by G-banding technique showed a male karyotype with all 20 bone marrow cells examined positive for the Philadelphia chromosome. The patient was placed on busulfan therapy with good symptomatic improvement, but later suffered severe thrombocytopenia. At the end of October 1983, he was admitted with blast crisis and thrombocytopenia and was initiated on vincristine and cytosine arabinoside therapy. His bone marrow was repeatedly inaspirable and the biopsy was characterized by diffuse fibrosis. Chromosome analysis of 16 spontaneously dividing cells in the blood at this time revealed that 86% of cells had a karyotype of 46,XY,t(9;22)(q34;q11),t(1;3)(p32;p21) with the rest of the cells having only the Ph chromosome. The patient died 4 months later of intracranial hemorrhage. Chromosome #3 involvement has been reported in acute MF and essential thrombocytosis, but no specific cytogenetic abnormalities have been found in MF associated with CGL. It is unclear whether t(1;3) in this case represents a cytogenetic marker of MF or blast transformation, but it is certainly associated with poor prognosis and short survival.

Blast Crisis↗
PubMed1989

Acute leukemia with abnormal thrombopoiesis and inversions of chromosome 3.

Abnormal thrombopoiesis has been described in acute leukemias associated with inv(3) (q21q26.2) or t(3;3)(q21;q26.2). We reviewed 13 patients seen at the Mayo Clinic since 1979 with inversions of chromosome 3 or related abnormalities; 12 acquired and one constitutional. The patient with the constitutional abnormality had an inv(3)(p21q29) and mild leukocytosis and thrombocytosis. Among the 12 patients with acquired abnormalities, five had inv(3) (q21q26.2), three had t(3;3)(q21;q26.2), one had del(3)(q12q21), one had ins(6;3) (p21;q21q26.2), one had inv(3)(p21q12), and one had r(3)(p?21q?21). Each of these patients developed acute leukemia; eight had antecedent myelodysplastic syndrome, eight presented with platelet counts greater than 100 x 10(3)/microliters, and six had atypical megakaryocytic hyperplasia. Five patients had ringed sideroblasts in their marrow, an antecedent refractory anemia with ringed sideroblasts, or erythroleukemia. Seven patients received chemotherapy but showed no response. From the time of chromosome study, the median duration of survival was 4 months. Our results suggest that 1) although abnormal megakaryocytopoiesis is observed in patients with inv(3)(q21q26.2), multiple hematopoietic lineages are also involved in the neoplastic process; 2) an antecedent myelodysplastic syndrome is common in acute leukemia with inv(3) or related abnormalities; 3) affected patients have a poor survival and are resistant to conventional chemotherapy; and 4) abnormal megakaryocytopoiesis in acute leukemia may also be associated with pericentric inversions of chromosome 3.

Acute Disease↗
PubMed1992

Deletion of the long arm of chromosome 5 in essential thrombocythemia.

A 51-year-old woman with no history of prior chemotherapy or radiation therapy was diagnosed with essential thrombocythemia (ET) according to the diagnostic criteria established by the Polycythemia Vera Study Group (PVSG). Cytogenetic analysis of bone marrow metaphases revealed both normal female karyotype and a single clonal abnormality, 46,XX,del(5)(q22q35). While chromosomal abnormalities have been reported in ET, their incidence is very low, and no specific abnormality has been found. Many of the reported cases of ET with chromosomal aberrations, including 5q-, do not meet the diagnostic criteria proposed by the PVSG, and may represent one of the other myeloproliferative disorders or a myelodysplastic syndrome. Furthermore, it is important to distinguish the 5q- syndrome, which may present with thrombocytosis and megakaryocytic hyperplasia, from ET. Our patient appears to be the first example of untreated ET clearly meeting the PVSG criteria in which 5q- was the only clonal abnormality seen at diagnosis.

Biopsy↗
PubMed1996

Translocation (3;3) in a patient with thrombocytopenia and erythroid dysplasia.

We describe a case with a translocation between the two chromosomes 3 with breakpoints q21 and q26, associated with a unique constellation of hematologic abnormalities. Megakaryocytic dysplasia and peripheral thrombocytosis are the most common abnormalities associated with this chromosome abnormality. Our patient had acute myeloid leukemia (AML), thrombocytopenia, dyserythropoiesis, and an increased myeloid/erythroid ration but no mekakaryocytic dysplasia. Although multilineage involvement has been reported, erythrocyte dysplasia associated with thrombocytopenia and without megakaryocyte dysplasia appears to be extremely rare. Our case supports the speculation that #3 abnormalities with breakpoints q21 and q26 affect a pluripotent stem cell and suggests that megakaryocytic involvement may not be pathognomonic in hematologic abnormalities with t(3;3)(q21;26).

Chromosomes, Human, Pair 3↗
PubMed1990

Prophylactic ribavirin treatment of dengue type 1 infection in rhesus monkeys.

The prophylactic efficacy of the broad-spectrum antiviral nucleoside analog ribavirin against flavivirus infection in non-human primates was investigated in a blinded, placebo-controlled study of rhesus monkeys infected with dengue virus. Both placebo- and ribavirin-treated monkeys developed viremia, as measured by direct plaque assay on Aedes albopictus C6/36 cells. Peak viremia occurred between days 3 and 9 after infection. No significant differences in time of onset, duration, or level of viremia were observed between placebo- and ribavirin-treated monkeys. Ribavirin induced predictable and reversible anemia and thrombocytosis. Serum ribavirin reached maximum levels of 30 microM by day 4, which approximates the in vitro minimum inhibitory concentration for dengue virus. Ribavirin appeared ineffective as a prophylactic drug for dengue type 1 viral infection, as evaluated by the magnitude of viremia in this monkey model.

Animals↗
PubMed1995

Effect of lithium in immunodeficiency: improved blood cell formation in mice with decreased hematopoiesis as the result of LP-BM5 MuLV infection.

Lithium salts have been demonstrated to induce the production of hematopoietic cells following administration in vivo and to minimize the reduction of these cells following treatment with either radiation, chemotherapeutic or antiviral drugs. We have previously demonstrated that lithium, when administered in vivo to immunodeficient mice infected with LP-BM5 MuLV (MAIDS) significantly reduced the development of lymphadenopathy, splenomegaly, and the lymphoma associated with late-stage immunodeficiency disease in this model, and increased the survival of these animals compared to virus-infected controls not receiving lithium. We report here the results of in vivo studies in the MAIDS model that determined the effect of lithium on peripheral blood indices and the number of myeloid (CFU-GM), erythroid (BFU-E) and megakaryocyte (CFU-Meg) hematopoietic progenitors from bone marrow and spleen harvested from immunodeficient mice receiving lithium carbonate (1 mM) placed in their drinking water compared to virus-infected controls not receiving lithium. Time-points evaluated were at weeks 1, 5, 9, 13, 17, and 21 postviral infection. Virus-control mice not receiving lithium demonstrated all the signs that are characteristic of MAIDS, i.e., splenomegaly, lymphadenopathy, hypergammaglobulinemia, reduced hematopoiesis, and death. Infected mice receiving lithium demonstrated diminished presence of splenomegaly, lymphadenopathy, hypergammaglobulinemia, no suppression of hematopoiesis nor mortality. Enhanced hematopoiesis was demonstrated by neutrophilia, lymphocytosis, thrombocytosis, and erythrocytosis that was evident by increased myeloid, erythroid, and megakaryocyte progenitor cells cultured from bone marrow and spleen. These studies further demonstrate that lithium influences the disease process in the MAIDS model and restricts the development of hematopoietic suppression that develops in this retroviral animal model of immunodeficiency.

Animals↗
PubMedDate not supplied

Anaemia and other haematological abnormalities in patients admitted to long-term care.

We investigated the occurence and causes of anaemia and other haematological abnormalities in 142 elderly patients (43 men, 99 women; median age 79 and 80 years), admitted to long-term care. Healthy 81-year-old subjects (n = 220) were used as reference group. Anaemia according to the WHO definition was much more common in the studied population (41%) than in a representative sample of 81-year-old subjects (10%). Somatically fit patients were less often anaemic (30%) than those with somatic illness (68%). The main causes for anaemia were: chronic disease (14.9%), recent haemorrhage (7.8%), iron deficiency (5.7%); and often multifactorial. Secondary leuko- or thrombocytosis occurred in 14 and 23%, drug-induced thrombocytopenia in 2.8% of the patients. Anaemia and other haematological abnormalities seen in elderly patients hospitalized for long-term care are often secondary to chronic or acute disorders. However, they also occur in patients without severe somatic impairment and many of them are reversible. Such findings should therefore not be neglected, but properly investigated, and if possible treated.

Journal Article↗
PubMed1991

alpha Interferon in the management of essential thrombocythaemia.

Thirteen patients (mean age 60.7 years; female:male ratio 10:3) with essential thrombocythaemia were treated with 3 million units (MU)/day interferon alfa-2b subcutaneously (s.c.) for 12 weeks, with all patients requiring a dose reduction after 4 weeks. The mean pretreatment platelet count was 1,400 x 10(9)/L and megakaryocytes were increased in all cases. Splenomegaly was present in six patients and haemorrhagic phenomena were observed in two. Nine patients (69.2%) had objective responses, including two (15.4%) complete responses (platelets less than 450 x 10(9)/L) which were then maintained with 5 MU interferon twice a week. Acute toxicity consisted of flu-like symptoms in 12 patients. Chronic toxicity (mainly leucopenia) was observed in nine patients. In conclusion, initial therapy and then requiring maintenance therapy at a reduced dose. However, the frequent side effects observed make it advisable to use a low dose of interferon alfa-2b, and to treat only those patients with significant symptoms and signs of thrombocytosis.

Adult↗
PubMed1990

Chronic toxicity and carcinogenicity of bis(tri-n-butyltin)oxide (TBTO) in the rat.

In a 106-wk toxicity and carcinogenicity study, groups of 60 male and 60 female weanling Wistar rats were fed 0, 0.5, or 50 mg bis(tri-n-butyltin)oxide (TBTO)/kg diet. In males, feed consumption was increased in all treated groups and increased water consumption occurred at 5 and 50 mg/kg. During the second year, body weight decreased in the 50-mg/kg males, while the females in that group showed no weight gain. Excess mortality was confined to the 50-mg/kg group towards the end of the study. Haematological changes, comprising anaemia, lymphocytopenia and thrombocytosis were noted mainly at the high-dose level. Also, signs of decreased kidney function and increased plasma enzyme activities (alanine aminotransferase, aspartate aminotransferase and alkaline phosphatase) were noted. No effects on serum hormone concentrations (thyrotropin, follicle stimulating hormone, luteinizing hormone or insulin) were observed, except for a decrease in the free thyroxin:thyroxin ratio in both sexes at the high-dose level. Higher serum IgM and IgA levels were present at 50 mg/kg, while, in females, IgG was decreased. At 50 mg/kg, the ovaries, adrenals, spleen (females), heart (males), pituitary, liver and kidneys were increased in weight, but the thyroid weight was decreased in females. The total tin concentrations in liver and kidneys showed a dose relationship and, in general, the concentrations were similar after 1 and 2 yr. Non-neoplastic histological alterations after 1 yr consisted of a decrease in the cell height of the thyroid follicles in all dose groups, with a reduced number of psammoma bodies at 50 mg/kg, a decrease in splenic iron content at 5 (females only) and 50 mg/kg, and a slight bile-duct activation. After 2 yr, only the thyroid changes were still present. In addition, at 2 yr, vacuolation and pigmentation of the proximal tubular epithelium and nephrosis were enhanced at 50 mg/kg. The incidence of benign tumours of the pituitary was significantly elevated and enhanced at 0.5 and 50 mg/kg. At 50 mg/kg increases in pheochromocytomas in the adrenal medulla and in parathyroid adenomas (males) were noted, while adrenal cortical tumours were decreased (males). There was a low, non-dose-related incidence of pancreatic carcinoma. Other tumour rates were in line with control data. It is concluded that lifetime feeding of 50 mg TBTO/kg diet induces toxicity in various organ systems. An increase in some common tumours was found at the high dose, probably due to hormonal or immunological changes.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenal Cortex Neoplasms↗
PubMed1991

Implication of thromboxane in the pathogenesis of Kawasaki disease and a suggestion for using novel thromboxane synthetase inhibitors in its treatment.

Kawasaki disease, a mucocutaneous lymph node syndrome predominantly prevalent in children, presents with coronary artery aneurysms and thrombocytosis, and investigators have suggested use of anticoagulants in addition to platelet inhibiting drugs. In Kawasaki disease, hypersensitivity reactions due to antigen/antibody complexes (Arthus type III) may damage the vessel wall and induce arteritis, and antigens may be of microbial or viral origin. Since thromboxane has been implicated in the pathogenesis of Kawasaki disease, I suggest use of ginger and carbon dioxide, novel thromboxane synthetase inhibitors. Thromboxane synthetase inhibitors may act as anticoagulants, platelet inhibitors, anti-inflammatory agents, and agents with both antimicrobial and antiviral activity.

Carbon Dioxide↗
PubMed1996

High-dose intravenous gamma globulin reduces macrophage colony-stimulating factor levels in idiopathic thrombocytopenic purpura.

We investigated the effect of high-dose intravenous gamma globulin therapy on the plasma level of macrophage-colony stimulating factor (M-CSF) level in 13 patients with chronic idiopathic thrombocytopenic purpura. M-CSF and interleukin-6 levels were determined by enzyme-linked immunosorbent assay. The mean +/- S.D. level of M-CSF in the patients was 1235 +/- 439 U/ml, and the level in 8 patients was higher than the mean + S.D. (903.6 U/ml) in normal controls. All 8 patients had steroid-refractory disease. M-CSF levels were significantly correlated with the serum levels of interleukin-6 (r = 0.66, P < 0.05). Interleukin-6 levels were also significantly raised in the high M-CSF group compared with the normal M-CSF group (P < 0.05). In the whole patient population, M-CSF levels decreased, but not significantly, after intravenous gamma globulin, while interleukin-6 decreased significantly. However, in the patients with high pretreatment M-CSF levels, both M-CSF and interleukin-6 decreased significantly after treatment (M-CSF, 4 weeks, P < 0.05; IL-6, 1 week, P < 0.05, 4 weeks, P < 0.01). These findings suggest that high-dose intravenous gamma globulin causes thrombocytosis by the decrease of M-CSF levels in idiopathic thrombocytopenic purpura.

Adult↗
PubMed2006

Prevalence of erythrocyte glucose-6-phosphate dehydrogenase (G6PD) deficiency in the population of western Turkey.

BACKGROUND: Newborn G6PD deficiency screening has been recognized as an essential component of public health care in most developed and some Mediterranean countries. However, such screening is yet to be widely embraced in Turkey. The aim of the present study was to determine the normal values of G6PD and deficiency prevalence of this enzyme in different age groups of people living in the western region of Turkey and accordingly inform and educate about favism to those asymptomatic carriers who usually are not aware of their G6PD deficient status. METHODS: A total of 1421 clinically healthy individuals without evidence of leukocytosis or thrombocytosis were included in the study. Activity of G6PD was quantitatively measured. RESULTS: Normal mean values of G6PD in healthy males were 8.94 +/- 8.65 IU/g Hb (or 231.73 +/- 43.16 IU/10(12) RBC), in females were 9.16 +/- 3.78 IU/g Hb (or 219.9 +/- 43.1 IU/10(12) RBC). The frequencies of severe and mild G6PD deficiencies were 0.44% and 6.07% in females, respectively, whereas in males it was 7.24%. Overall frequency of the G6PD-deficient phenotype was detected as 6.9%. CONCLUSIONS: There is no significant statistical difference of G6PD activity between males and females, although frequency of the G6PD-deficient phenotype is relatively high in western Turkey. The results emphasize a need for screening for G6PD deficiency before prescribing anti-malarial therapy with drugs like primaquine to patients in this region of Turkey known for its prevalence of malaria.

Erythrocytes↗