Epidermoid inclusion cyst of the perineum--a rare case report in a 50 years old male.

A 50 year old male presented with a history of mid line painless swelling in the perineum for last 4 years. The patient's only concern was a perineal swelling which was gradually increasing in size. Clinical examination mimics subcutaneous lipoma with soft lobulated surface with positive slip sign. The base line investigations were within normal limits. Complete surgical excision of the cyst performed. Histopathology confirmed epidermal inclusion cyst with no evidence of malignancy. Patient discharged on next day. The follow-up visits were un-remarkable. Perineal epidermal inclusion cyst is a rare entity and only few cases have been reported.

Pattern of pathogens and their sensitivity isolated from superficial surgical site infections in a tertiary care hospital.

BACKGROUND: Infection is an important cause of morbidity and mortality in surgical patients. Rapidly emerging nosocomial pathogens and the problem of multi-drug resistance necessitates periodic review of isolation patterns and sensitivity in surgical practice. Surgical site infections (SSI) are defined as an infections that occurs at the incision site within thirty days after surgery. Objectives of the study were to determine the pattern of pathogens involved and their antibiotic sensitivity isolated from superficial surgical site infections in a teaching hospital. METHODS: This observational study was conducted for 1 year from January 2008 to December 2008 in all 4 surgical units of Liaquat University Hospital Hyderabad which caters to patients from low socioeconomic status. Pus culture and sensitivity reports were collected prospectively from hospitalised patients who developed postoperative wound infection. The patients who developed fecal/biliary/urinary fistula or operated for malignancies, and with negative cultures were excluded from the study. Analysis was carried out using SPSS 10. RESULTS: During the study period 112 pus culture and sensitivity reports were analyzed. E. coli 68 (60.7%) was the most common organism isolated followed by Klebsiella 23 (20.5%). The least frequent organism was staph. Epidermidis 1 (0.9%). All isolates were sensitive to penicillin derivatives and carbapenem. Quinolones, Aminoglycosides and Monobactum were also showing some promise in our study. However, Cephalosporins were ineffective against most of the important isolates in our study. CONCLUSION: E. coli and klebsiella were the most important isolates form SSI in our study, and penicillin derivatives and carbapenem were showing 100% antibiotic sensitivity to all of the isolates.

Role of serum leptin level as a marker of severity of pre eclampsia.

BACKGROUND: To explore the possibility of serum leptin being a marker of severity of pre-eclampsia, so that risk of imminent eclampsia and eclampsia can be reduced. METHODS: This observational study was conducted at a private hospital of Hyderabad from 31st July to 1st December 2007. Forty primipara with same age, body mass indices and gestational age were included in this study. Twenty women had raised blood pressure in third trimester of pregnancy and 20 women with a normal blood pressure in third trimester of pregnancy. The exclusion criteria included history of diabetes, twin pregnancy, chronic hypertension, liver or renal disease. After counselling and affordability of laboratory testing their blood sample was taken for serum leptin, uric acid, serum creatinine and urine for albumin. The serum leptin level was measured by radio-immunoassay (RIA) kits. All data was filled in a pre-designed proforma after taking detailed history and examination. Statistical analysis was performed on SPSS. Student's t-test was applied where applicable. RESULTS: Mean systolic and diastolic blood pressure between pre-eclamptic and control group showed a marked difference (p < 0.001) ranging from 149.50 +/- 3.44 and 104.40 +/- 3.03 as compared to control 107 +/- 1.56 and 74.50 +/- 1.49 respectively, similarly proteinuria was present in 20 (100%) cases of pre-eclampsia and 07 (35%) of normotensive women. Mean serum leptin level was significantly high in pre-eclampstic (79.380 +/- 3.287), when compared with a control group (27.825 +/- 1.050). Mean serum uric acid in pre-eclamptic (5.040 +/- 0.147) showed significant changes than control (3.600 +/- 0.141), while serum creatinine level was insignificant in both groups. It has been observed that Mean +/- SEM value of serum leptin level was much higher in severe pre-eclamptics (76.418 +/- 5.056) than in women with mild pre-eclampsia (40.856 +/- 2.807). All the parameters correlated positively and significantly with increased blood pressure. CONCLUSION: Elevated plasma leptin concentration appears to be a marker of pre-eclampsia independently or along with other parameters of pre-eclampsia could be used to reduce the severity of pre-eclampsia thus avoiding risk effects of pre-eclampsia to mother and foetus. This study still needs more research work to prove our results.

Serum creatine phosphokinase as prognostic indicator in the management of electrical burn.

OBJECTIVE: To determine the mean difference of serum creatine phosphokinase according to the extent of tissue damage and prognosis of the patients suffering from electrical burn injuries. STUDY DESIGN: A case series study. PLACE AND DURATION OF STUDY: Department of Burns, Liaquat University Hospital, Hyderabad, from September 2005 to August 2006. PATIENTS AND METHODS: During the study period, 38 patients with electrical burn injuries were enrolled. Victims of electrical burns with evidence of myocardial injury were excluded. Following admission, serum creatine phosphokinase was measured serially on 10 consecutive occasions. The data was later analyzed statistically using SPSS-10.0. RESULTS: Of the 38 patients, the mean age of the victims was 28 years, with males dominating the study population (82%). A statistically significant association was found between the level of serum creatine phosphokinase and likelihood of death (p=0.000). It was also found that serial monitoring of this enzyme can be used as prognostic indicator in the management of electrical burns injury. CONCLUSION: The level of creatine phosphokinase increased with the degree of tissue injuries in patients with electrical burns. This prognostic value is of great importance in the local setup, where sophisticated investigations to detect extent of injuries are not available.

A major fraction of human bone marrow lymphocytes are Th2-like CD1d-reactive T cells that can suppress mixed lymphocyte responses.

Murine bone marrow (BM) NK T cells can suppress graft-vs-host disease, transplant rejection, and MLRs. Human BM contains T cells with similar potential. Human BM was enriched for NK T cells, approximately 50% of which recognized the nonpolymorphic CD1d molecule. In contrast to the well-characterized blood-derived CD1d-reactive invariant NK T cells, the majority of human BM CD1d-reactive T cells used diverse TCR. Healthy donor invariant NK T cells rapidly produce large amounts of IL-4 and IFN-gamma and can influence Th1/Th2 decision-making. Healthy donor BM CD1d-reactive T cells were Th2-biased and suppressed MLR and, unlike the former, responded preferentially to CD1d(+) lymphoid cells. These results identify a novel population of human T cells which may contribute to B cell development and/or maintain Th2 bias against autoimmune T cell responses against new B cell Ag receptors. Distinct CD1d-reactive T cell populations have the potential to suppress graft-vs-host disease and stimulate antitumor responses.

Loss of IFN-gamma production by invariant NK T cells in advanced cancer.

Invariant NK T cells express certain NK cell receptors and an invariant TCRalpha chain specific for the MHC class I-like CD1d protein. These invariant NK T cells can regulate diverse immune responses in mice, including antitumor responses, through mechanisms including rapid production of IL-4 and IFN-gamma, but their physiological functions remain uncertain. Invariant NK T cells were markedly decreased in peripheral blood from advanced prostate cancer patients, and their ex vivo expansion with a CD1d-presented lipid Ag (alpha-galactosylceramide) was diminished compared with healthy donors. Invariant NK T cells from healthy donors produced high levels of both IFN-gamma and IL-4. In contrast, whereas invariant NK T cells from prostate cancer patients also produced IL-4, they had diminished IFN-gamma production and a striking decrease in their IFN-gamma:IL-4 ratio. The IFN-gamma deficit was specific to the invariant NK T cells, as bulk T cells from prostate cancer patients produced normal levels of IFN-gamma and IL-4. These findings support an immunoregulatory function for invariant NK T cells in humans mediated by differential production of Th1 vs Th2 cytokines. They further indicate that antitumor responses may be suppressed by the marked Th2 bias of invariant NK T cells in advanced cancer patients.

CD1d-reactive T-cell activation leads to amelioration of disease caused by diabetogenic encephalomyocarditis virus.

A subset of CD161 (NK1) T cells express an invariant Valpha14Jalpha281 TCR-alpha chain (Valpha(invt) T cells) and produce Th2 and Th1 cytokines rapidly in response to CD1d, but their physiological function(s) remain unclear. We have found that CD1d-reactive T cells mediate to resistance against the acute, cytopathic virus diabetogenic encephalomyocarditis virus (EMCV-D) in relatively Th1-biased, C57BL/6-based backgrounds. We show now that these results generalize to Th2-biased, hypersensitive BALB/c mice. CD1d-KO BALB/c mice were more susceptible to EMCV-D. Furthermore, alpha-galactosylceramide (alpha-GalCer), a CD1d-presented lipid antigen that specifically activates Valpha(invt) T cells, protected wild-type (WT) mice against EMCV-D-induced encephalitis, myocarditis, and diabetes. In contrast, neither CD1d-KO nor Jalpha281-KO mice were protected by alpha-GALCER: Finally, disease in Jalpha281-KO mice was comparable to WT, indicating for the first time equivalent roles for CD1d-reactive Valpha(invt) and noninvariant T cells in resistance to acute viral infection. A model for how CD1d-reactive T cells can initiate immune responses, which synthesizes current results, is presented.

Involvement of CD1 in peripheral deletion of T lymphocytes is independent of NK T cells.

During peripheral T cell deletion, lymphocytes accumulate in nonlymphoid organs including the liver, a tissue that expresses the nonclassical, MHC-like molecule, CD1. Injection of anti-CD3 Ab results in T cell activation, which in normal mice is followed by peripheral T cell deletion. However, in CD1-deficient mice, the deletion of the activated T cells from the lymph nodes was impaired. This defect in peripheral T cell deletion was accompanied by attenuated accumulation of CD8(+) T cells in the liver. In tetra-parental bone marrow chimeras, expression of CD1 on the T cells themselves was not required for T cell deletion, suggesting a role for CD1 on other cells with which the T cells interact. We tested whether this role was dependent on the Ag receptor-invariant, CD1-reactive subset of NK T cells using two other mutant mouse lines that lack most NK T cells, due to deletion of the genes encoding either beta(2)-microglobulin or the TCR element J alpha 281. However, these mice had no abnormality of peripheral T cell deletion. These findings indicate a novel role for CD1 in T cell deletion, and show that CD1 functions in this process through mechanisms that does not involve the major, TCR-invariant set of NK T cells.

CD1d structure and regulation on human thymocytes, peripheral blood T cells, B cells and monocytes.

Human T cells expressing CD161 and an invariant T-cell receptor (TCR) alpha-chain (Valpha24invt T cells) specifically recognize CD1d and appear to have immunoregulatory functions. However, the physiological target cells for this T-cell population, and whether alterations in CD1d expression contribute to the regulation of Valpha24invt T-cell responses, remain to be determined. A series of antibodies were generated to assess CD1d expression, structure and regulation on human lymphoid and myeloid cells. CD1d was expressed at high levels by human cortical thymocytes and immunoprecipitation analyses showed it to be a 48 000-MW glycosylated protein. However, after solubilization, the majority of the thymocyte CD1d protein, but not CD1d expressed by transfected cells, lost reactivity with monoclonal antibodies (mAbs) against native CD1d, indicating that it was alternatively processed. Moreover, thymocytes were not recognized by CD1d-reactive Valpha24invt T-cell clones. Medullary thymocytes and resting peripheral blood T cells were CD1d-, but low-level CD1d expression was induced on activated T cells. CD1d was expressed by B cells in peripheral blood and lymph node mantle zones, but germinal centres were CD1d-. Resting monocytes were CD1d+ but, in contrast to CD1a, b and c, their surface expression of CD1d was not up-regulated by granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-4 (IL-4) activation. These results demonstrate constitutive CD1d expression by human professional antigen-presenting cells and that post-translational processing of CD1d may contribute to regulation of the activity of CD1d-specific T cells.