That the suggested criteria for diagnosis of polycythaemia vera (PV) are rather complicated, therefore accurate diagnosis of PV from other types of polycythaemia is needed. Serum Vitamin B 12 and Vitamin B 12 binding proteins were determined in a patients with PV and other 5 patients with secondary polycythaemia. Both serum Vitamin B 12 and unsaturated Vitamin B 12 binding capacity (UBBC) increased considerably. TCIII and TCI increased also markedly, i.e., 16 and 8 folds, respectively, resulting in a decreased ratio of TCI/TCIII from the normal value of 1.34 to 0.71. Patients with secondary polycythaemia had slightly increased serum Vitamin B 12 while serum UBBC, TCI and TCIII levels showed no significant alteration from those of normal subjects. These findings indicated that not only increased serum Vitamin B 12 and UBBC but also an increase of TCIII and the ratio of TCIII/TCI are the positive findings in patients with PV. Therefore determinations of serum Vitamin B 12 and its binding proteins can be used as a criteria for the differential diagnosis of PV from secondary polythaemia.

Introduction:​ The first epidemic of dengue hemorrhagic fever (DHF) occurred in Philippine and Thailand around 1952 and 1954. The clinical manifestations almost always presented with high fever, shock, severe bleeding with multiorgan failure and death. At that time, pathogenesis and pathophysiology including the knowledge of dengue virus was not known. Many studies were performed leading to the better understanding on the pathogenesis and pathophysiology including the knowledge of dengue virus (DV). This brought into the better management and decrease of mortality rate to 1-2%. During the last 50 years the natural history of DHF has changed a great deal with the tremendously progression of new knowledge. Endothelial cell derangement become to be an important factor. It played a big role in the occurrence of plasma leakage leading to shock, release of tissue factor resulting in DIC and increase platelet aggregation and then the formation of platelet fibrin thrombi. Furthermore, platelet dysfunction caused both bleeding and thrombosis. All of these event caused ischemia of the vital end organs. Recently, increased incidence of adult DHF along with high mortality rate became to be an important problem. Immunopathogenesis played an important role in the occurrence of the unusual manifestations in DHF such as hemophagocytic syndrome (HPCS) and related disorders. With better understanding, effective treatment by immunomodulator such as high dose corticosteroid and intravenous immunoglobulin G were given to save life of the patients. The key role for successful therapy was early diagnosis and effective treatment of hematophagocytic syndrome. The three topic discuss below included bone marrow suppression, DIC and hemophagocytic syndrome are important. These should lead to the better understanding on the natural history of Dengue infection, which has changed a great deal during the lest 50 years. This knowledge will bring into the early diagnosis and most effective treatment to decrease the high fatality of DHF at the present time.

During January 2008-February 2010, 157 adult patients who were admitted to Vichaiyut Hospital and Medical Center with acute phase of dengue hemorrhagic fever (DHF) were analyzed. Seven cases presented with very severe life-threatening complications. Among all, there were four cases presented with severe multiorgan failure during early first four days. The most significant organ failures were shock in 3 cases, acute respiratory distress syndrome (ARDS) in 3 cases, cardiac involvement in 4 cases, neurological involvement in 3 cases, severe hepatitis in 4 cases, acute renal failure in 2 cases, disseminated intravascular coagulopathy (DIC) in 3 cases and severe bleeding in 4 cases. Hemophagocytic syndrome (HPCS) was recognized in four cases in which 2 cases developed shock. Seven cases received high doses of corticosteroids and 5 cases received intravenous immunoglobulin G (IVIgG). Five cases survived with complete recovery. Two cases had delayed treatment and fatal outcome; one case with severe intracranial bleeding and the other case had co-infection with scrub typhus. (J Infect Dis Antimicrob Agents 2011;28:99-103.) *Department of Medicine, Vichaiyut Hospital and Medical Center, Bangkok 10400, Thailand. Received for publication: April 1, 2011. Reprint request: Ladda Sorakhunpipitkul, M.D., Department of Medicine, Vichaiyut Hospital and Medical Center, Bangkok 10400, Thailand. E-mail: annra33@gmail.com

Ferrokinetic and erythrokinetic studies were performed in 25 non-splenectomized patients with alpha or beta thalassaemia. Nine of these had HbH disease and six had HbE/beta thalassaemia or homozygous beta thalassaemia. In HbH disease, a mild anaemia was associated with severe peripheral haemolysis, increased splenic sequestration and only a moderate degree of ineffective erythropoiesis. By contrast, in the beta thalassaemia syndromes, a more marked anaemia was associated with prominent ineffective erythropoiesis and mild peripheral haemolysis. These findings indicate that the pathogenesis of anaemia in alpha and beta thalassaemia is different, haemolysis dominating in HbH disease and ineffective erythropoiesis in HbE/beta thalassaemia and homozygous beta thalassaemia.

Dengue fever (DF) and dengue haemorrhagic fever (DHF) are caused by the dengue virus. The major pathophysiological hallmark that distinguishes DHF from DF is plasma leakage as a result of increased vascular permeability. Following this leakage, hypovolaemic shock occurs as a consequence of a critical plasma volume loss. Constant haematological abnormalities occurring in DHF and frequently include bone marrow suppression, leucopenia and thrombocytopenia. An enhanced immune response of the host to a secondary DV infection is a feature of DHF and leads to many consequences. These are immune complex formation, complement activation, increased histamine release and a massive release of many cytokines into the circulation, leading to shock, vasculopathy, thrombopathy and disseminated intravascular coagulation (DIC). The mechanisms underlying the bleeding in DHF are multiple. These are vasculopathy, thrombopathy and DIC. Thrombopathy consists of thrombocytopenia and platelet dysfunction. DIC is prominent in patients with shock. The most severe DIC and massive bleeding are the result of prolonged shock and cause a fatal outcome. The mechanisms of thrombopathy and DIC and the proper management of DHF are reviewed and discussed.

We have performed an allogeneic stem cell transplant in an 18-year-old male patient who had Burkitt's lymphoma. The patient had disease which was refractory to conventional intensive chemotherapy and radiation therapy. High-dose chemotherapy with autologous stem cell rescue was given but the patient relapsed within 2 months after transplantation. He was then treated with allogeneic stem cell transplantation using a fludarabine, busulfan and anti-thymocyte globulin-based conditioning regimen. His GVHD prophylaxis included mycophenolate and tacrolimus. The patient had engraftment within 14 days. Investigation by FISH showed more than 95% of his peripheral blood nucleated cells to be of donor origin since day +14. He is now alive and well and remains disease-free 6-months after the transplant. A graft-versus-lymphoma effect is thought to be one of the factors contributing to his remission. Bone Marrow Transplantation (2000) 26, 1351–1354.

UNLABELLED:Concentrations of tumor necrosis factor alpha (TNF-alpha) in serum were measured in 17 Thai men infected with Plasmodium falciparum malarial infections to determine whether they were affected by severity of infections or exchange transfusions. Twelve patients were considered having complicated malarial infections, eight of whom had cerebral malaria. Five patients had uncomplicated malarial infections. The results showed that malarial infection markedly raised TNF-alpha level above normal values (mean +/- SEM 406 +/- 38 vs 15 +/- 5, p = 0.004). In complicated malaria, cerebral involvement appeared to significantly increase concentration of TNF-alpha when compared to values in uncomplicated malaria (mean +/- SEM 496 +/- 64 vs 339 +/- 12, p = 0.01). Degree of parasitemia, intravenous quinine (day 0 value vs day 7 value) and exchange transfusion did not significantly affect TNF-alpha levels.CONCLUSION:Serum level of TNF-alpha is increased in Plasmodium falciparum malarial infections and may be a useful index to predict severity of malarial infection, cerebral malaria in particular.

summary. The relationship of socioeconomic status to the risk of aplastic anaemia was evaluated in a case‐control study conducted in Bangkok and two rural regions of Thailand (Khonkaen and Songkla). Among 152 cases and 921 controls there were significant trends of increasing risk with decreasing years of education (P = O01) and total household income (P = 0–0001), after control for confounding. The relative risk estimate for those with monthly incomes of >1500 baht (about 60 U.S.) was 3–9 (95% confidence interval 2–1–7–3) compared to those with monthly incomes of at least 5000 baht (about 200). The pattern of increasing risk with decreasing income was observed in all three regions, with significant trends in Bangkok (P= 0–004) and Khonkaen (P = 0–003). This finding may partly explain the high incidence of aplastic anaemia in Thailand. Low socioeconomic status may be a surrogate for one or more environmental factors that could cause aplastic anaemia, such as infectious pathogens or toxic exposures.

Thirty-five patients diagnosed with "malignant histiocytosis" from 1984 to 1989 were studied for clinical, laboratory, histopathological features as well as survival and response to therapy, Immunocytochemistry and immunophenotypic studies were performed in 12 cases using the paraffin immunoperoxidase method. The staining included alpha-1 antichymotrypsin, muramidase, immunoglobulins and monoclonal antibodies specific for T, B lymphocytes and macrophage. From the clinical features, responsiveness to therapy and survival, the patients were divided into 2 groups: the non-responders (25 cases) and responders (10 cases) groups. Very short median survival of 1.25 months was found in the non-responders, whereas, longer median survival of 14.15 months was found in the responder group. Important different clinical and laboratory features were observed among these two groups. Unresponsiveness to treatment; rapidly progressive pancytopenia, increased hemophagocytosis, presentation of immature cells in blood with extensive infiltration of malignant cells in the bone marrow; severe jaundice and deterioration of hepatic function accompanied by early extranodal involvement were almost exclusively observed initially in the non-responder group. Satisfactory response to treatment was observed only in the responder group. Similarity of histopathology, cytology and immunophenotype was observed in these two groups. The immunophenotypic study in 12 cases showed 5 cases of B-cell lymphoma, 3 cases of T-cell (with 1 Ki-1 -positive) lymphoma; 1 case of Ki-1 positive non-T, non-B anaplastic large cell lymphoma; and 3 cases of undetermined cell lineage. From this study, so-called "malignant histiocytosis" appears to be a disorder of heterogeneity. The immunophenotypes of malignant cells indicated that their origin belonged mostly to lymphoid cell lineage. Based on their clinical feature of the early hematogenous spread along with the distinct histopathological and immunophenotypic findings, the term "pleomorphic large cell hematolymphoma" is proposed to be used instead of the old misnomer, "malignant histiocytosis" (MH).

The bone marrows of 21 Thai adults infected with Plasmodium falciparum malaria were cultured for CFU-E and BFU-E by using AB serum, autologous serum (parasitaemia) and autologous serum (post-parasitaemia). Six patients had no complication and 15 patients had pulmonary, renal or haematologic complications. In the non-complicated cases, sera during parasitaemia did not suppress the post-parasitaemia CFU-E and BFU-E. Post parasitaemia, there was suppression of CFU-E by parasitaemia sera. In the complicated cases, the autologous sera during parasitaemia suppressed the growth of both CFU-E and BFU-E both during and after parasitaemia (P < 0.05). The post-parasitaemia sera had neither a suppressive nor a stimulating effect. In the complicated cases, the progenitor cells cultured from the bone marrow post-parasitaemia were fewer in number than those cultured from the bone marrow during parasitaemia using the same sera. Two possible mechanisms of suppression are postulated, namely the reduction of erythropoietin or the increased tumour necrosis factor during malarial infection. Further studies to clarify this are being carried out.

Nine cases of severe complicated falciparum malaria treated by exchange transfusion were studied. Eight patients survived and one patient died. Multisystemic complications were found in all cases. The CNS complications, acute renal failure, pulmonary insufficiency, jaundice, bleeding, sepsis, and DIC were found in 9, 7, 5, 7, 2, 4 and 1 cases, respectively. The fatal case presented with severe multisystemic complications together with 40% parasitemia. In eight survivors, whose parasitemia ranged from 0.3%, to 90%, had milder degrees of systemic complications. With the use of blood exchange 10-15 units, the parasitemia was decreased to less than 5% within 24 hours in all expect one who had parasitemia 90%. In comparison with the other 10 matched non-exchanged patients, there was no significant difference in survival rate between these two group (89% vs 80%). However, in the patients with ARDS the survival rate in the group who received the exchange transfusion therapy was superior (75% vs 0%). The exchange transfusion therapy is therefore strongly recommended in the treatment of malarial patients who present with parasitemia > 30% and severe systemic complications, particularly those who have severe acute renal failure or have lung complications. The amount of blood used for exchange transfusion should at least 1.2 times the blood volume for rapid removal of parasites and toxic metabolites from the circulation.

Platelet aggregation, plasma betathromboglobulin (BTG) and platelet factor 4 (PF4) were studied in 35 children with dengue hemorrhagic fever. The suppression of platelet aggregation was demonstrated during acute phase of DHF in both shock and non-shock patients. Simultaneous with abnormal platelet aggregation, there was increased release of BTG and PF4 from platelets into plasma during the acute phase which lasted only 3-4 days after shock or subsidence of fever. Acute phase plasma during DHF infection was also shown to have a stimulatory effect on the aggregation of autologous platelets. In this study we showed that there was an increase in platelet secretory activity of BTG and PF4 along with an impairment of the platelet aggregation during acute phase of DHF.

This report of 8 cases (6 severe and 2 mild) heat stroke patients seen during the hot summer of 1987 at Pramongkutklao Hospital, Bangkok, represent the first report of this syndrome in Thailand. Severe cases presented with deep coma, shock, ARDS, DIC and other systemic complications. Two cases of mild heat stroke recovered completely with conventional treatment. Two of the 6 severe cases died with DIC, bleeding and acute renal failure. The other 4 surviving cases received early exchange transfusion and low dose heparin therapy. The clinical features of these 4 cases were as severe as those recorded for fatal heat stroke patients, including shock over 10 hours in 4, coma longer than 120 hours in 3, ARDS and DIC in 1. From these findings, early exchange transfusion plus low dose heparin should be considered as one effective treatment in severe fatal heat stroke patients.

Platelet function tests including platelet aggregation, PF3, bleeding time and clot retraction were studied in 48 malarial patients. The suppression of platelet aggregation was demonstrated in both P. vivax and P. falciparum infection. However, this abnormality was more prominent in malarial patients who had systemic complications and bleeding. The recovery of the impaired platelet aggregation was observed at period of 7 and 14 days after parasitemia in malarial patients without and with systemic complications. The correlation between the suppression of platelet aggregation and thrombocytopenia was observed. From this study, bleeding in malaria are operated by two mechanisms: thrombocytopenia and severely depressed platelet aggregation.

Twenty four cases of pure red cell aplasia were reported. No underlying diseases were found in two cases. Of the 22 cases with secondary form, 10 were from infections, mostly gram negative organisms. Three cases had systemic lupus erythematosus, two had autoimmune hemolytic anemia. The following conditions were found in one each: thymoma, thyroid carcinoma, protein calorie malnutrition, rheumatoid arthritis, non-Hodgkin lymphoma and Sheehan's syndrome. Three patients died, two from uncontrolled infection, the other from uncontrolled SLE and subsequently systemic fungal infection. Only one of the 2 primary cases responded to immunosuppressive drugs. The majority of patients with underlying infections, PRCA resolved after the infections were treated. This is the first reported series of PRCA in Thailand.