Some hematological problems in Indonesia

Indonesia consist of many island inhabited by many ethnic groups with different social economic condition. As in other parts of the world, anemia is still one of the major health problem in Indonesia. The reported anemia prevalence differs in each area and age groups, ranging from 5.4% in well nourished preschool children to 56.3% in primary school children; and 19% to 62.5% in pregnant women. The causes of anemia mostly reported were nutritional like iron deficiency, abnormal hemoglobin besides other conditions. In Cipto Mangunkusumo Hospital as the national referral hospital in Indonesia, in the adults groups, the cause of anemia reported were 14% with iron deficiency, 54% aplastic, 16% hemolytic and 16% other causes. Whereas in the child health department the cause were 29% nutritional deficiency, 31% thalassemia, 10% aplastic, 4% hemolytic and 26% other causes. Thalassemia is quite often reported in Indonesia. In 1955 Lie-Injo first reported the HbE as the most frequently found abnormality among many ethnic groups in Indonesia, ranging from 2.5% to 13.2%. In later studies the prevalence reported varies very much. It was reported as 9.5% in newborns, 22% in pregnant women, and 15.95% to 60% in athletes. The carrier frequency in some areas was between 6-10%, while the pattern of mutation varied widely within each region. Hemophilia cases in Indonesia is still not diagnosed adequately, only 530 cases were reported. The problems were lack of diagnostic laboratories and awareness. As many as 56.9% of the hemophilia patients who received cryoprecipitate were reported positive with HCV antibody. Hematological malignancy is now also became an increasing problem in Indonesia, in child health department the prevalence of leukemia was 57%, and lymphoma 13% among other malignancies. In National Cancer hospital, the prevalence leukemia as diagnosed using morphology and flowcytometry, were 51.4% AML, 19.7% B-ALL, 14.6% T-ALL, 4.5% preB-ALL, with 9.8% cases with co expression, and 30% other malignancies. Due to geographical situation, economic condition and lack of diagnostic laboratory facility many abnormalities were unable to be diagnosed properly.     

Diagnostic value of serum human Galactomannan aspergillus antigen and 1,3‐beta‐D‐glucan in immunocompromised patient suspected fungal infection

BackgroundThe prevalence of fungal infection (FI) in developing countries is high, but the diagnosis of FI is still challenging to determine, so it is needed evaluation of biomarkers other than microbiological culture, because the culture has low sensitivity, high cost, not available in every laboratory and needs a long time. The detection of human galactomannan Aspergillus antigen (GAL) and 1,3‐beta‐D‐glucan (BDG) on the fungal cell wall could be the promising biomarkers for fungal infection. Neutropenia, lymphopenia and CD4T cells in the immunocompromised patients are essential factors, but these cell associations with BDG and GAL levels have not been evaluated yet. The study aimed to evaluate GAL and BDG for detecting fungal infection and their association with total leucocyte count, neutrophil, monocyte, lymphocyte and CD4T cells.MethodA cross‐sectional study was conducted among 86 patient with suspected FI. Fungal infection established using EORTC/MSG criteria. Serology test performed using ELISA. Leucocyte cells were measured using a haematology autoanalyser, and CD4T cells were analysed using BD FACSPresto. Statistical analysis obtained using Spearman''s correlation coefficient, ROC curve analysis and 2 × 2 contingency table.ResultsSerum Galactomannan and BDG had a significant correlation with CD4T cells and total lymphocyte count (p < 0.05). The cut‐off OD GAL >0.3 had sensitivity 54.6%, specificity 87.5% and AUC 0.71; meanwhile, the BDG cut‐off >115.78 pg/ mL had sensitivity 71.2%, specificity 52.4% and AUC 0.63 for detecting fungal infection.ConclusionsThe immunocompromised patients can undergo GAL for determining the diagnose of FI. The lower the CD4T cells and total lymphocyte count, the higher the GAL and BDG serum levels.     

The mechanism of vagotomy-induced acute gastric mucosal injury in the rat

The present study investigated the integrity of the rat gastric mucosa after 6 hours of vagotomy without drainage. Transection vagotomy was employed to ensure complete gastric vagal denervation. Vagotomy without drainage produced gastric distension and mucosal injury confined to the glandular part. Anterior truncal vagotomy produced injury in 70% of rats, whereas truncal or transection vagotomy produced injury in all rats. The injury score with transection vagotomy was significantly higher than that with anterior truncal (21.2 mm2 +/- 1.6 vs. 8 mm2 +/- 2.7, mean +/- SEM, n = 10, p less than .01) or truncal vagotomy (21.2 mm2 +/- 1.6 vs. 15.6 mm2 +/- 1.4, mean +/- SEM, n = 10, p less than .05). Histologic examination of the mucosal injury revealed necrosis involving the epithelium and lamina propria. Cholestyramine, pyloroplasty, or gastric diversion protected the stomach against the vagotomy-induced mucosal injury. The results demonstrate in the rat that vagotomy without drainage produces within 6 hours injury of the gastric mucosa, which increases as vagal denervation is rendered more complete. Because cholestyramine protects the rat stomach against vagotomy-induced acute gastric mucosal injury, reflux of duodenal contents appears to be the principal factor behind this injury. Pyloroplasty prevents gastric distension but probably not duodenal contents refluxing, suggesting that this distention also may have a role in the mechanism of the said injury.     

Association of NT-ProBNP,Blood Pressure,and Cardiovascular Events: The ARIC Study

BackgroundAlthough intensive blood pressure reduction has cardiovascular benefits, the absolute benefit is greater in those at higher cardiovascular disease (CVD) risk.ObjectivesThis study examined whether N-terminal pro–B-type natriuretic peptide (NT-proBNP) helps identify subjects at higher risk for CVD events across systolic blood pressure (SBP), diastolic blood pressure (DBP), or pulse pressure (PP) categories.MethodsParticipants from the ARIC (Atherosclerosis Risk In Communities) study visit 4 (1996 to 98) were grouped according to SBP, DBP, or PP categories and further stratified by NT-proBNP categories. Cox regression models were used to estimate hazard ratios for incident CVD (coronary heart disease, ischemic stroke, or heart failure hospitalization) and mortality across combined NT-proBNP and/or BP categories, adjusting for CVD risk factors.ResultsThere were 9,309 participants (age: 62.6 ± 5.6 years; 58.3% women) with 2,416 CVD events over a median follow-up of 16.7 years. Within each SBP, DBP, or PP category, a higher category of NT-proBNP (100 to <300 or 300 pg/ml, compared with NT-proBNP <100 pg/ml) was associated with a graded increased risk for CVD events and mortality. Participants with SBP 130 to 139 mm Hg but NT-proBNP ≥300 pg/ml had a hazards ratio of 3.4 for CVD (95% confidence interval: 2.44 to 4.77) compared with a NT-proBNP of <100 pg/ml and SBP of 140 to 149 mm Hg.ConclusionsElevated NT-proBNP is independently associated with CVD and mortality across SBP, DBP, and PP categories and helps identify subjects at the highest risk. Participants with stage 1 hypertension but elevated NT-proBNP had greater cardiovascular risk compared with those with stage 2 SBP but lower NT-proBNP. Future studies are needed to evaluate use of biomarker-based strategies for CVD risk assessment to assist with initiation or intensification of BP treatment.     

Mixed gynecomastia

Gynecomastia is an enlargement of male breast resulting from a proliferation of its glandular component, and it is usually due to an altered estrogen-androgen balance. It should be differentiated from pseudogynecomastia, which is characterized by fat deposition without glandular proliferation and from breast carcinoma. Gynecomastia could be physiological in neonates and pubertal or pathological due to drug intake, chronic liver, or renal disease, hyperthyroidism, testicular or adrenal neoplasms, and hypogonadism whether primary, or secondary. Properly organized work-up is needed to reach the cause of gynecomastia. Here, we reported a case of a young Omani man with gynecomastia with the aim of creating awareness of the occurrence of Klinefelter’s syndrome (KS) in patients with gynecomastia, to observe any differences in clinical presentation of KS from those reported in the literature, and highlight the needed diagnostic work-up and treatment.Gynecomastia is an enlargement of male breast resulting from a proliferation of its glandular component. It is usually benign, bilateral, and characterized by the presence of a rubbery or firm mass around the nipples. It usually results from either increased estrogen level, increased breast sensitivity to estrogen,1 or low testosterone level. The highest incidence of gynecomastia is reported during neonatal period, puberty, and aging due to physiological disturbances. Pseudogynecomastia, which is often seen in obese men, refers to fat deposition without glandular proliferation and should be differentiated from gynecomastia. Therefore, male breast enlargement can be fatty (pseudogynecomastia or lipomastia), pure gynecomastia, or mixed. Our objective in presenting this particular case is to create awareness of the occurrence of Klinefelter’s syndrome (KS) in patients with gynecomastia, to observe any differences in clinical presentation of KS from those reported in the literature, and highlight the needed diagnostic work-up and treatment.     

A multicenter report of biologic agents for the treatment of secondary amyloidosis in Turkish rheumatoid arthritis and ankylosing spondylitis patients

In this multicenter, retrospective study, we evaluated the efficacy and safety of biologic therapies, including anti-TNFs, in secondary (AA) amyloidosis patients with ankylosing spondylitis (AS) and rheumatoid arthritis (RA). In addition, the frequency of secondary amyloidosis in RA and AS patients in a single center was estimated. Fifty-one AS (39M, 12F, mean age: 46.7) and 30 RA patients (11M, 19F, mean age: 51.7) with AA amyloidosis from 16 different centers in Turkey were included. Clinical and demographical features of patients were obtained from medical charts. A composite response index (CRI) to biologic therapy—based on creatinine level, proteinuria and disease activity—was used to evaluate the efficacy of treatment. The mean annual incidence of AA amyloidosis in RA and AS patients was 0.23 and 0.42/1000 patients/year, respectively. The point prevalence in RA and AS groups was 4.59 and 7.58/1000, respectively. In RA group with AA amyloidosis, effective response was obtained in 52.2 % of patients according to CRI. RA patients with RF positivity and more initial disease activity tended to have higher response rates to therapy (p values, 0.069 and 0.056). After biologic therapy (median 17 months), two RA patients died and two developed tuberculosis. In AS group, 45.7 % of patients fulfilled the criteria of good response according to CRI. AS patients with higher CRP levels at the time of AA diagnosis and at the beginning of anti-TNF therapy had higher response rates (p values, 0.011 and 0.017). During follow-up after anti-TNF therapy (median 38 months), one patient died and tuberculosis developed in two patients. Biologic therapy seems to be effective in at least half of RA and AS patients with AA amyloidosis. Tuberculosis was the most important safety concern.