“
“In Escherichia coli, cytosine DNA methylation is catalyzed by the DNA cytosine methyltransferase (Dcm) protein and occurs at the second cytosine in the sequence 5′CCWGG3′. Although the presence of cytosine DNA methylation was reported over 35 years ago, the biological role of 5-methylcytosine in E. coli remains unclear. To gain insight into the role of cytosine DNA methylation in E. coli, we (1) screened the 72 strains of the ECOR collection and 90 recently isolated environmental samples for the presence

of the full-length dcm gene using the polymerase chain reaction; (2) examined the same Cabozantinib ic50 strains for the presence of 5-methylcytosine at 5′CCWGG3′ sites using a restriction enzyme isoschizomer digestion assay; and (3) quantified the levels of 5-methyl-2′-deoxycytidine in selected strains using liquid chromatography tandem mass spectrometry. Dcm-mediated cytosine DNA methylation is conserved in all 162 strains examined, and the level of 5-methylcytosine ranges from 0.86% to 1.30% of the cytosines. We also demonstrate that Dcm reduces the expression of ribosomal protein genes during stationary phase, and this may explain the highly

conserved nature of this DNA modification pathway. DNA bases are modified by postreplicative methylation by enzymes MEK inhibitor termed DNA methyltransferases. In prokaryotes, the most common modified DNA bases are 6-methyladenine and 5-methylcytosine (5mC). The most recognized role of modified DNA bases is in restriction-modification (R-M) systems (Ishikawa et al., 2010). In each R-M system, there Alanine-glyoxylate transaminase is a restriction endonuclease that cleaves foreign DNA and a site-specific DNA methyltransferase that prevents cleavage of host DNA, and in some cases controls expression of the R-M system (O’Driscoll et al., 2005). However, some DNA methyltransferases are not found in conjunction with a cognate restriction enzyme and are termed solitary DNA methyltransferases. In addition to DNA adenine methyltransferase

(Dam), Escherichia coli possesses another solitary DNA methyltransferase termed Dcm for DNA cytosine methyltransferase (Marinus & Lobner-Olesen, 2009). The presence of Dcm was discovered in 1973 by Marinus & Morris. The dcm gene of E. coli K-12 contains 1419 base pairs, and the predicted protein is 472 amino acids (Bhagwat et al., 1986; Hanck et al., 1989). The protein contains ten conserved motifs and a catalytic cysteine residue that is found in all cytosine-5 DNA methyltransferases (Posfai et al., 1989). The Dcm protein methylates the internal C in the sequence 5′CCWGG3′ where W = A/T (Palmer & Marinus, 1994). 5mC is occasionally spontaneously deaminated in an existing C:G base pair, and a T:G mismatch is formed. The dcm gene is in an operon with the very short patch repair (vsr) gene and is controlled by the same promoter.

Fig.

S2. Nucleotide sequences of tclipG (GenBank accession no. AB237774). Please note: Wiley-Blackwell is not responsible for the content or functionality of any supporting materials supplied by the authors. Any queries (other than missing material) should be directed to the corresponding author for the article. “
“Bacteria often have multiple copies of ribosomal RNA (rrn) genes in their genomes. The presence of multiple rrn operons suggests an advantage to the organism, perhaps HDAC inhibitor through adjustable control of protein expression in response to altered environmental conditions. In the work described here, the strengths of the seven rRNA promoters of Pseudomonas sp. UW4 were individually assessed by separately cloning each promoter region into an expression vector and monitoring the activity of the reporter protein, the Escherichia coli lacZ gene product. The lacZ expression was the highest for the rrnE promoter under all growth conditions, with the various promoters demonstrating a range of strengths. These findings indicate that these promoters are not functionally identical. This observation suggests that the differential expression of rrn operons under various physiological conditions and growth stages allows better regulation

of rRNA, conferring an advantage to P. sp. UW4 through a more fine-tuned control of protein expression in a wide range of environmental situations. “
“Nitrogenase produces hydrogen as a normal byproduct of the reduction of dinitrogen to ammonia. The Nif2 nitrogenase in Anabaena variabilis is an alternative Mo-nitrogenase and is expressed in vegetative cells grown with fructose Sorafenib solubility dmso under strictly anaerobic conditions. We report here that the V75I substitution in the α-subunit of Nif2 showed greatly impaired acetylene reduction and reduced levels of 15N2 fixation but had similar hydrogen production rates as the wild-type enzyme under argon. Another mutant containing a substitution in the α-subunit, V76I, would result in a decrease in the size of the putative gas channel of nitrogenase and, thus, was hypothesized to affect substrate selectivity of nitrogenase.

However, this substitution Pyruvate dehydrogenase lipoamide kinase isozyme 1 had no effect on the enzyme selectivity, suggesting that access by gases to the active site through this putative gas channel is not limited by the increased size of the amino acid side chain in the α-subunit, V76I substitution. Hydrogen produced from photosynthetic microorganisms such as cyanobacteria is an attractive biofuel because it is made from water using sunlight as the energy source. In filamentous cyanobacteria, the primary enzyme used to produce H2 is nitrogenase, which reduces H+ to H2 as part of the mechanism of reduction of N2 to ammonia (Tamagnini et al., 2007). Hydrogen production by nitrogenase is not dependent upon the reduction of N2; in an argon atmosphere, nitrogenase produces only H2 (Benemann & Weare, 1974; Barney et al., 2004).

In addition, three cases of fatal hepatotoxicity occurred in women who had baseline CD4 counts <100 cells/μL and were receiving anti-tuberculosis Pictilisib solubility dmso therapy. We did not detect the association between rash-associated hepatotoxicity

and initiation of nevirapine-based ART at CD4 counts ≥250 cells/μL that was reported in the retrospective analysis of Boehringer-Ingelheim trials [11–15]. These discordant results can probably be explained by differences in the study populations and elevated rates of rash-associated hepatotoxicity among participants with a CD4 count <50 cells/μL. Regarding differences in the study populations, the Boehringer-Ingelheim trials enrolled participants who were mainly white (57%), from high-income settings, and older I-BET-762 in vivo (mean age 37 years) [13]. Genetics [28], nutrition [29], cigarette smoking [30], tuberculosis [31] and age [32] can affect CD4 cell count and several studies have reported lower CD4 cell counts among HIV-negative Southeast Asians [33] and Zambians [34,35] compared with white adults from high-income settings. In the context of these differences in genetics, nutrition and population-level CD4 cell counts, an absolute CD4 cell count cut-off

demonstrated to predict an increased risk of rash-associated hepatotoxicity in one setting may not be valid in other settings. In addition, previous studies have not reported the incidence of rash-associated hepatotoxicity among women with CD4 counts <50 cells/μL. In our study, among participants with CD4 counts <50 cells/μL, rates of both severe hepatotoxicity

and rash-associated hepatotoxicity were substantially elevated. Differences in comorbidities (e.g. tuberculosis and hepatitis B virus coinfection), concomitant medications and environmental exposures (e.g. to aflatoxins [36]) might explain the high rates of both severe hepatotoxicity and rash-associated hepatotoxicity that we observed at CD4 counts <50 cells/μL. Our results demonstrate that severe hepatotoxicity and rash-associated hepatotoxicity occur among Lonafarnib molecular weight Zambian, Thai and Kenyan women but are not accurately predicted by a CD4 count ≥250 cells/μL. Although our study demonstrated a decreased risk of rash-associated hepatotoxicity among women with a CD4 count of 50–199 cells/μL compared with women with CD4 counts <50 and ≥200 cells/μL, this finding should not be interpreted as evidence that a CD4 count of 50–199 cells/μL is a safe zone for initiating nevirapine use. One of the three fatal hepatotoxicity events occurred within this range (CD4 count 68 cells/μL). Clinicians in resource-limited settings must be vigilant for nevirapine-associated hepatotoxicity in all women initiating ART regardless of the baseline CD4 cell count.

Infection of the culture at OD600 nm 0.5 only rarely resulted in cell lysis and the turbidity test showed no sensitivity to ΦBP. However, Torin 1 the result of plaque assay indicated the sensitivity of P. polymyxa CCM 1465 to ΦBP. We observed the plaques on the plates where the culture of this strain with ΦBP had been plated. Phage particles examined by TEM (Fig. 1) were recovered from the cell-free supernatant of spontaneously lysed culture of P. polymyxa CCM 7400 and CsCl gradient purified. The phages had polyhedral heads with a diameter of 56±4 nm (mean±SD) (n=24) and tails with

a length of 144±8 nm (n=6) (n=number of measurements). The structural proteins of ΦBP were analyzed by SDS-PAGE (Fig. 2). At least 11 bands were revealed with molecular masses of putative proteins estimated at 13, 16, 22, 25, 26, 28, 35, 38, 51, 79 and 160 kDa. The most abundant protein bands were 28, 35, 38 and 51 kDa in size. We extracted nucleic acid from purified phage particles. The purified nucleic acid was sensitive to DNAse and resistant to RNAse treatment. To determine the genome size, ΦBP DNA was cut with restriction endonucleases HindIII,

EcoRV and XbaI. The length of the genome of about 43 kb was calculated as the sum of the Volasertib molecular weight lengths of the restriction fragments (Fig. 3a). Restriction enzymes XhoI, PstI, BamHI and SalI did not cut ΦBP DNA. Analysis with four restriction enzymes (EcoRI, HindIII, XbaI, SpeI) showed an identical restriction pattern for DNA extracted from phage particles, which were recovered from both spontaneously lysed culture of P. polymyxa CCM 7400 and culture after external ΦBP infection (data not shown). Sequence homology analysis of eight DNA fragments from EcoRI-digested ΦBP DNA (Fig. 3b, Sclareol Table 1) revealed regions

with significant similarity to typical phage genes for two of them. Two regions within the 2.5-kbp fragment with predicted ORFs of 507 and 996 bp shared significant homology to phage holin and lysin genes, respectively. They represent a putative cassette of lytic genes, where the gene coding for predicted holin is closely followed by the lysin gene. We detected an overlap of both genes over a 23-bp region. The third gene of this cluster seems to be the second holin gene (555 bp). Two predicted ORFs with the length of 552 and 744 bp were identified within the 1.2-kbp fragment as putative small and large terminase subunit genes. These ORFs are incomplete due to the interruption caused by EcoRI digestion with the genes overlapping by 83 bp. Restriction and ORF maps of the 1.2- and 2.5-kbp fragments were constructed from the primary sequencing data (Fig. 4). The basic data of eight analyzed sequenced fragments, the sizes of the known sequences and results of the homology search are summarized in Table 1. Two pairs of specific oligonucleotide primers were derived from the proposed small terminase and holin gene sequences to detect the presence of ΦBP DNA sequences on P. polymyxa chromosome.

The pol gene sequences and recommended subtype reference

sequences (http://www.hiv.lanl.gov) were also used to construct neighbour-joining phylogenetic trees using the mega 4 software [15]. Phylogenetic tree analysis was used to determine the subtype of the pol gene sequence and to facilitate detection of Selleck PD 332991 possible PCR contamination and sample mix-up. The prevalence of drug resistance mutations was calculated with a 95% confidence interval (CI) based on the binomial distribution. Univariable and multivariable logistic regression analyses were used to estimate odds ratios (ORs) with 95% CIs for the association between resistance status and various factors. Statistical analyses were carried out using statistica version 8.0 (StatSoft Inc., Tulsa, OK, Screening Library ic50 USA) and stata version 8.2 (StataCorp LP, College Station, TX, USA). A total of 138 HIV-1-infected individuals with treatment failure were included in the study (Table 2); 97 were adults and 41 were children under 18 years of age. A little more than half of the study subjects were male (57%). The median age was 38 years for the adults

and 10 years for the children. All individuals were native Hondurans; the most frequent route of transmission was heterosexual transmission (66%), followed by mother-to-child transmission (28%), blood products (3%) and homosexual transmission (3%). The severity of disease according to the MycoClean Mycoplasma Removal Kit Centers for Disease Control and Prevention (CDC) Classification System [16] was stage A for 12 patients, stage B for 60 patients and stage C for 66 patients. Adherence was scored as good in 99 patients (72%), intermediate in 26 patients (19%) and poor in 13 patients (9%). The median time on antiretroviral therapy was 3.2 years (range 1–12 years). The median CD4 count was 185 cells/μL

and the median VL was 4.5 log10 copies/mL (Table 2). The median time span between sampling for the resistance test and the last available CD4 cell count was 5 months (range 0–36 months); one patient had never undergone CD4 cell count measurements. The median time span between the last VL measurement and sampling for resistance was 5 months (range 0–25 months); seven patients had never undergone VL testing. Only 37 patients (28%) had CD4 cell counts and VL determined simultaneously with the resistance test. The patients were recruited using three different criteria for treatment failure (virological, immunological and clinical) because access to plasma HIV-1 RNA and CD4 quantification was irregular during the study period. Table 2 shows that 51% of the treatment failures were identified virologically, 21% immunologically and 28% clinically.

This is consistent with findings from another study of this cohort, in which a substantial proportion of individuals delayed starting HAART even when national guidelines recommended initiation of treatment [17], and a recent UK analysis showing that a high proportion of patients who experience a CD4 decline to <200 cells/μL do so while under regular follow-up [18]. Among those initiating HAART at a low CD4 cell count, the median Selleck LDK378 follow-up

after diagnosis was 5 years, suggesting that rapid decline in CD4 cell count is not the main explanation for this. Late presenters are known to have a high risk of clinical progression in the first 3 months after HIV diagnosis, regardless of HAART initiation. As we wished to capture

the inherent efficacy of HAART rather than any consequence of poor adherence or loss to follow-up, our main analyses were restricted to individuals who remained under follow-up and on treatment at each time-point – our question, therefore, was whether patients who managed to remain alive and under care throughout this high-risk period Selleck Veliparib could ultimately achieve as good an outcome on treatment as other patients. We did, however, perform sensitivity analyses to assess the robustness of our findings to patients who were lost to follow-up after the first 3 months. On the whole, our conclusions remained unchanged in these analyses. However, as loss to follow-up rates were (somewhat Cyclic nucleotide phosphodiesterase unexpectedly) highest in ideal starters, clinical progression rates were significantly higher in ideal starters in these sensitivity analyses. However,

we do not believe that this higher loss to follow-up rate really reflects a higher clinical progression rate in this group – it is more likely that patients with a higher CD4 cell count felt more able to discontinue treatment, attend less frequently (with reduced viral load monitoring) or transfer their care to other centres. There are some important limitations of this study to note. Firstly, we have considered two arbitrary time-points (48 and 96 weeks) in order to be consistent with those used in many randomized trials. Alternative analyses that we could have used may have considered the time to an initial virological response, time to virological rebound or time to clinical progression after starting HAART. However, these approaches can be heavily affected by the frequency of monitoring; if monitoring is less (or more) frequent in late presenters, then the degree of bias that is introduced may be greater. Secondly, as already noted, our analyses excluded patients who presented late but who did not start HAART, either because they died very soon after diagnosis or because they chose to remain untreated. Thus, our outcomes cannot be applied to all patients who present late, but only to the group who survive long enough to initiate HAART.

With treatment increasing patient survival, comparisons of therapeutic regimens should consider treatment-associated AEs. Findings from this study could be informative for clinicians and payers in managing HIV infection with NNRTIs. “
“These 96-week, ECHO/THRIVE pooled analyses evaluated data for antiretroviral treatment-naïve, HIV-1-infected adults with viral load (VL) ≤ 100 000 HIV-1 RNA copies/mL receiving rilpivirine or efavirenz. ECHO and THRIVE were phase 3, randomized, double-blind trials. Patients received rilpivirine 25 mg once daily (qd) or efavirenz 600 mg qd,

with a fixed (ECHO) or investigator-chosen (THRIVE) nucleoside/tide reverse transcriptase inhibitor (N[t]RTI) background regimen. Response rate (the percentage of patients with VL < 50 copies/mL, click here using an intent-to-treat-population, time-to-loss-of-virological-response selleck chemical algorithm), virological failure (VF), resistance development, safety and tolerability were evaluated. Baseline characteristics were comparable between the rilpivirine (n = 368) and efavirenz (n = 329) groups. At week 96, response rates [84% for rilpivirine vs. 80% for efavirenz; difference 4.0%; 95% confidence interval (CI) –1.7% to 9.7%] and incidences of VF for the resistance analysis (VFres) (8% for

rilpivirine vs. 6% for efavirenz; P = 0.46) were similar in the two groups. Among patients with VFres, a comparable proportion in each group developed nonnucleoside reverse transcriptase inhibitor (NNRTI) resistance-associated mutations (RAMs). Among those with VFres, more patients in the rilpivirine group than in the efavirenz group developed N[t]RTI RAMs, second mostly M184I/V. The mean (95% CI) CD4 cell count increased from baseline to week 96 by 224 (208–240)

cells/μL in the rilpivirine group and by 206 (188–225) cells/μL in the efavirenz group. Treatment-related grade 2–4 overall adverse events, any rash and dizziness were less frequent for rilpivirine than for efavirenz (P < 0.0001). Rilpivirine demonstrated antiviral efficacy similar to that of efavirenz in antiretroviral treatment-naïve adults with baseline VL ≤ 100 000 copies/mL over 96 weeks. Frequencies of VFres and emergent NNRTI RAMs in each group were similar. More patients with VFres in the rilpivirine group than in the efavirenz group developed N[t]RTI RAMs (mostly M184I/V). Rilpivirine had a more favourable safety/tolerability profile than efavirenz. "
“Objectives. Female sex workers (FSW) have been considered reservoirs and vectors of sexually transmitted infections (STI) in the community. This study estimated the prevalence of STI/human immunodeficiency virus (HIV) among FSW of various migration and residential status in Hong Kong and identified possible risk factors. Methods. An outreach “Well-women” clinic was set up at Ziteng, a non-governmental organization working with FSW.

All had fasting low-density lipoprotein (LDL) cholesterol ≤ 130mg/dL. Seventy-eight per cent of patients were men and 65% were African-American. Median (interquartile range) age and CD4 count were 47 (43, 52) years and 648 (511, 857) cells/μL, respectively. All had HIV-1 RNA < 400 HIV-1 RNA copies/mL. Mean CCA-IMT BIBW2992 was correlated with log-transformed CD8+CD38+HLA-DR+ percentage (r = 0.326; P = 0.043), and concentrations of interleukin-6 (r = 0.283; P = 0.028), soluble vascular cell

adhesion molecule (sVCAM; r = 0.434; P = 0.004), tumour necrosis factor-α receptor-I (TNFR-I; r = 0.591; P < 0.0001) and fibrinogen (r = 0.257; P = 0.047). After adjustment for traditional cardiovascular disease (CVD) risk factors, the association with TNFR-I (P = 0.007) and fibrinogen (P = 0.033) remained significant. Subjects with plaque (n = 22; 37%) were older [mean (standard deviation) 51 (7.7) vs. 43 (9.4) years, respectively; P = 0.002], and had

a higher CD8+CD38+HLA-DR+ percentage [median (interquartile range) 31% (24, 41%) vs. 23% (20, 29%), respectively; P = 0.046] and a higher sVCAM concentration [mean (standard deviation) 737 (159) vs. 592 (160) ng/mL, respectively; P = 0.008] compared with those without plaque. Pro-inflammatory monocyte find more subsets and serum markers of monocyte activation (soluble CD163 and soluble CD14) were not associated with CCA-IMT or plaque. Participants in SATURN-HIV have a high level of inflammation and immune activation that is associated with subclinical vascular disease despite low serum LDL cholesterol. “
“The incidence of sexually transmitted hepatitis C virus (HCV) reinfection is on the rise in HIV-infected men who have sex with men (MSM). Data on natural history of acute

hepatitis C and possible factors associated with spontaneous clearance are limited. The Baf-A1 cell line aim of this study was to analyse the outcome of HCV reinfections in HIV-positive MSM. A retrospective analysis was carried out on patients with more than one sexually acquired HCV infection who were diagnosed at four major German HIV and hepatitis care centres. Reinfection was defined by genotype or phylogenetic clade switch, detectable HCV RNA after a sustained virological response (SVR) or after spontaneous clearance (SC). In total, 48 HIV-positive MSM were identified with HCV reinfection, among them 11 with a third episode and one patient with four episodes. At the first episode, 43 and five patients had an SVR and SC, respectively. The second episode was accompanied by a genotype switch in 29 patients (60%). Whereas 30 and nine patients showed an SVR and SC, respectively, eight patients developed chronic hepatitis. Neither HCV genotype switch nor interleukin-28B genotype was associated with SC. However, SC rates at the second episode were higher for patients with SC at the first episode compared with patients without SC (60 vs. 14%, respectively; P = 0.03).

[23] Religious influences,[21, 22, 32, 34] high expectations and negative perceptions and attitudes towards healthcare services and healthcare providers have also been identified across Selleckchem MDV3100 the studies as a potential cause of MRPs.[15, 20, 23] Lack of knowledge of the healthcare services and how to use them is also a further possible contributing factor for MRPs that has been identified; for example, some ethnic minority patients have no knowledge of the pharmaceutical care role of pharmacists which may lead to lack of regular monitoring and review of their medicines.[15, 20] According

to the literature, underestimating patients’ desire Ion Channel Ligand Library cost for information, which may be a consequence of a lack of awareness of the extent of patients’ decision-making regarding the use of their medicines and/or poor appreciation of their experience of MRPs,[36] may well cause MRPs. Some recommendations were made across the studies to support patients in the use of medicines. The recommendations involved providing patient counselling and education programmes about their disease, its management and medicines and the service available,[23, 35] providing an interpreter for ethnic minorities who cannot speak

English, using pictorial flashcards to provide information for illiterate people,[34] providing bilingual link-workers

who explain reasons for regular appointments and provide encouragement and a cultural bridge between healthcare professionals and patients,[34, 35] increasing involvement of ethnic minorities in decisions about healthcare provision and utilisation,[20] involving patients in evidence-informed decision making for safer and more effective disease and medicine managements.[32] Further recommendations included not only improving provider–patients communication by understanding of cultural factors that inform their beliefs and practices but also ensuring PJ34 HCl that mechanisms are in place for the effective transfer of information,[35] encouraging pharmacists and patients to work together and share their experiences regarding the use of medicines as well as exchanging information that will support patients achieving optimal outcomes from their medicines,[36] encouraging effective reliable communication between secondary and primary care, surgeries, pharmacies and patients for the continuity of safe and effective therapy,[36] providing enhanced pharmaceutical services in areas of health inequalities and to such minority groups.[15] This review brings together the information in the current literature regarding medicine use and MRPs experienced by ethnic minority groups in the UK.

AOSD is a rare, inflammatory disease of unknown etiology, affecting primarily young adults, and

characterized by high spiking fevers, arthritis and an evanescent, macular, non-pruritic, salmon-colored rash, distributed on the trunk and the extremities. Organomegaly and lymphadenopathy are common associations. Laboratory tests reveal neutrophilic leukocytosis, negative rheumatoid factor (RF) and antinuclear antibodies (ANA), as well as high serum ferritin levels and low serum glycosylated ferritin levels.[1] A small number of AOSD cases complicated by secondary hemophagocytic lymphohistiocytosis (HLH) have been described.[2-4] Our patient, a 36-year-old INNO-406 solubility dmso man, presented with asymmetric, recurrent, multiple large joint arthritis associated with spikes of high grade fever (> 39°C) for the last 8 months and hyper-pigmentation for 4 months. There CP-868596 clinical trial was no history of long-term drug intake, photosensitivity, diarrhea or weight loss. Examination revealed pigmented non-pruritic patches and plaques on his chest wall (Fig. 1), dermal and mucosal hyper-pigmentation, anemia, fixed flexion deformity with arthritis in both knees and mild splenomegaly. Examination was notable for absence of lymphadenopathy and hepatomegaly. Initially, investigations included microcytic

hypochromic anemia (hemoglobin: 6.9 g/dL), neutrophilic leukocytosis (total leukocyte count: 16 800; neutrophil 78%) and high erythrocyte sedimentation rate (ESR) of 58 mm in the 1st hour, and hypoalbuminemia (2.4 g/dL). He had normal plasma glucose,

urea, creatinine, electrolytes and liver enzymes. He had elevated C-reactive protein, and raised serum ferritin (4821 ng/mL; normal: 30–400). Anti nuclear antibody (ANA) and rheumatoid factor (RF) Interleukin-2 receptor were negative, as was HFE mutation assay. Serum cortisol at 6 a.m. was normal. The patient was not immuno-compromised, and hepatitis B surface antigen and anti-hepatitis C virus were negative. Ultrasonography of abdomen showed splenomegaly. Skin biopsy showed multiple necrotic keratinocytes in aggregates, located in the upper epidermis and a para-keratotic horny layer, associated with infiltration of lymphocytes and neutrophils in the papillary and mid-dermis. The patient was diagnosed as AOSD according to Yamaguchi criteria (Table 1).[5] During the course of his hospital stay (2 weeks from the day of presentation), he developed pancytopenia (Hb 5.6 g/dL, TC 2100, platelet 50 000), increment of spleen size to 5 cm below the costal margin and hepatomegaly in face of a decreasing ESR (16 mm). A course of antibiotics and analgesics failed to relieve the symptoms. He had raised fasting serum triglyceride (286 g/dL) and persistently raised serum ferritin at that time (5132 ng/mL). Bone marrow biopsy showed severe hemophagocytosis with decrease in all hematopoietic precursors (Fig. 2). Thus, a diagnosis of HLH according to HLH 2004 criteria was established (Table 1).