Ganoderma lucidum: a cause of pseudoparasitosis.

We report a pseudoparasitosis case due to Ganoderma lucidum, (lingzhi or reishi mushroom); we believe this to be a first reported case in Thailand. A 49-year-old male patient with non-Hodgkins lymphoma presented with chronic watery diarrhea. He had a history of consumption of powdered lingzhi extract as a dietary supplement and herbal medicine. Stool examination demonstrated many spores of G. lucidum, which must be differentiated from intestinal helminth ova and coccidia. After discontinuation of mushroom spores ingestion, the diarrheal symptoms improved and fecal examination subsequently showed no Ganoderma spores. Many artifacts in the stool may be confused with parasites. Differentiation of parasites from artifacts depends on characterization of the size, shape, structure, and reactivity with common stains.

A case with acute myelofibrosis and acute promyelocytic leukemia.

A 65-year-old man was admitted to a provincial hospital repeatedly over a period of years with a history of weakness, tiredness and progressive anemia. One occasion a bone marrow aspiration was found to contain normal marrow elements. On admission four months later, the patient was pale with pitting edema on both legs. His liver was barely palpable and the spleen was palpable 2 cm below the costal margin. He was anemic and peripheral blood showed anisopoikilocytosis, burr cells, ovalocytes and macrocytosis. The platelet level was very low, with some giant cells. The white blood cell count was normal, with some immature granulocytes. Bone marrow biopsy confirmed the diagnosis of acute myelofibrosis. The patient had very high levels of serum vitamin B12 and vitamin B12 binding proteins, especially transcobalamin I. After treatment with blood transfusion and prednisolone, his white cell count increased considerably. He died nine days after admission because of bronchopneumonia. This patient is an example of the simultaneous occurrence of acute myelofibrosis and acute promyelocytic leukemia that can terminate as acute myeloblastic or other stem – cell leukemia.

Differential diagnosis of myelofibrosis from polycythemia vera and chronic myelogenous leukemia by vitamin B12 determination.

Myelofibrosis (MF) has a close pathogenic relationship to polycythemia vera (PV), chronic myelongenous leukemia (CML) and primary thrombocythemia (PT). Sometimes, clinical, hematological and radioisotopic studies in these patients cannot give a definite diagnosis. As serum vitamin B12 and vitamin B12 binding proteins in patients with PV and CML show their own specific pattern. It would be of interest to see whether these determinations could separate MF from PV and CML. Serum vitamin B12 and vitamin B12 binding proteins were determined on 6 patients with MF. It was found that serum vitamin B12, UBBC and TBBC levels were elevated. Both TCI and TCIII were increased while TCII decreased. A shift to the left of the increased granulocytes in MFR resulted in an increased TCI synthesized by the myelocytes and metamyelocytes while in PV, the increased number of granulocytes, most of which are mature granulocytes is characterized by increased serum TCII resulting in a reverse ratio of TCI/TCIII. In CML, serum vitamin B12, UBBC, TCI and TCII are much more sharply elevated than those of MF. Therefore determination of serum vitamin B12 and vitamin B12 binding proteins with other hematological, bone marrow and clinical studies could be used for a differential diagnosis of MF from PV or CML.

Folates and vitamin B12 status in patients with multiple myeloma.

Serum and red cell folate, serum Vitamin B12 and Vitamin B12 binding proteins were multiple myeloma. Half of these patients were anaemic with a predominant macrocytic type. Altogether 17 and 33 percent had low serum and red cell folate levels, respectively. Low serum Vitamin B12 level was found in one third of these patients. Both TCI and TCIII increased while TCII decreased, while was different from the previous report of extremely elevated TCII in some patients with multiple myeloma. There was a direct relationship between serum Vitamin B12 and saturation of TCI. These finding indicated that folic acid and Vitamin B12 deficiency were relatively common in patients with multiple myeloma. The possible mechanisms of these vitamins deficiency were discussed in this paper.

Superoxide dismutase, catalase and acetylcholinesterase in the red cells of patients with multiple myeloma.

Serum cholinesterase (ChE), red cell acetylcholinesterase (AChE), superoxide dismutase (SOD) and catalase were determined in 12 patients with multiple myeloma. Serum ChE was significantly depressed and bore a derect relationship with serum albumin concentration or Hb level. Red cell AChE was significantly elevated and showed a tendency of a reverse relationship with Hb. There was increased serum uric acid and 25% of the patients had serum uric acid over 9 mg/dl. Both SOD and catalase activities were found to be within normal limits, and showed no relationship with serum uric acid. These finding indicated that hyperuricemia occurs quite commonly in multiple myeloma patients with increased extracellular oxidants released from the degradation of purines to uric acid. However, these toxic oxidants could not overcome the antioxidant capacity of the red cells as indicated by a finding of normal SOD and catalase activities.

Hyperuricaemia and antioxidant enzymes in red cells of patients with malignacy of haematological origin.

Serum uric acid, red cell SOD and catalase activities were determined in 117 patients acute lymphoblastic leukaemia, chronic myelocytic leukaemia, Hodgkin’s lymphoma, non-Hodgkin’s lymphoma, polycythemia vera and multiple myeloma in comparison to 40 healthy normal subjects. About 6-40 percent of these patients had serum uric acid level over 7 mg/dl. Altogether, 14 patients had hyperuricaemia, therefore they were grouped together. There was a reverse relationship between serum uric acid level and SOD activity in these patients. The hyperuricaemia is a result of increased proliferation and destruction of tumour cells which stimulates the generation of superoxide radicals. Therefore, red cell SOD will be decreased in patients with hyperuricaemia. In order to compensate for an elevated oxidant stress, SOD will therefore increase. These findings could explain the variable results of red cell SOD reported earlier in patients with malignancy of haematological origin. There was no relationship between serum uric acid and red cell catalase activity in these patients.

Serum and red cell folates in patients with leukaemia and lymphomas.

It has been suggested that leukaemia and lymphomas may cause folic acid depletion. The supporting evidence were obtained from urinary excretion of folic acid, rate of clearance of injected folic acid from the plasma and serum folic acid assays. However, no data red cell folate levels has been reported, the present study was there fore undertaken. Serum and red cell folate levels were determined in 144 patients with acute lymphocytic leukaemia, acute myeloblastic leukaemia, chronic myelocytic leukaemia, Hodgkin’s disease and non-Hodgkin’s lymphoma. The mean serum and red cell folate values in these patients were significantly lower than those of normal subjects. About 21.5% and 28.5% of these patients had serum folate levels lower than 3 ng/ml and red cell folate levels lower than 100 ng/ml, respectively. The elevated MCV and MCH values were also found in 42% and 30% of the patient’s groups. These findings indicated that some patients with leukaemia and lymphomas had macrocytiosis which was highly due to folic acid deficiency. The deficiency may be caused by various factors such as increased requirement due to an elevated production of leukaemic cells with higher folic acid content than normal leucocytes, poor dietary folic acid intake due to loss of appetite and intestinal malabsorption of lolic acid.

Erythrocyte superoxide dismutase and catalase activities and serum uric acid in patients with malignant lymphoma.

Many previous studies on superoxide dismutase (SOD) and catalase activities in red cells of patients with malignant lymphoma showed results. One possible factor may be the different oxidant stress in these patients. The objective of the present study was determine SOD and catalase activities in red cells of patients with untreated malignant lymphoma who had normal serum uric acid level. The studies were performed on 19 patients with Hodgkin's disease and 34 with non-Hodgkin's lymphoma (NHL) in comparison to 40 healthy normal subjects. The mean values of erythrocyte SOD activity in these patients were not significantly different from that of normal subjects. Serum uric acid levels were also within the normal ranges and only 4 out of 53 patients had serum uric acid over 7 mg/dl. There was no relationship between serum uric acid level would have red cell SOD within the normal limits. As hyperuricaemia may occur as a result of increased purine turnover from the increased destruction of tumor cells by therapy. The overproduction of uric acid would stimulate the generation of superoxide radicals. In such cases, red cell SOD would therefore be decreased during the hyperuicaemia. These findings may therefore explain why some previous authors found either increased or decreased SOD activity in red cell of patients with malignant lymphoma. No significant differentce of erythrocyte catalase activity between the groups of patients and the normal group was demonstrated in the present study.