Lamotrigine hypersensitivity in childhood epilepsy

PURPOSE: To evaluate the effect of lamotrigine (LTG) on several humoral and cellular immune functions in children with epilepsy and the change in immunological status in patients with LTG-induced rash. METHODS: Sixteen children with epilepsy of unknown origin or secondary to various etiologies undergoing treatment with LTG participated in the humoral and cellular immunological study. Of these, 2 patients developed a rash during LTG treatment and are described in detail. RESULTS: No modifications of humoral or cellular immunity (measured at 1 and 3 months) were noted in 14 of the 16 patients during this treatment. In the 2 children who manifested rash, basal immune function was normal. In both, immediately after the skin rash appeared, there was a high increase in the percentage of activated T-helper lymphocytes (CD4-DR) and activated T-suppressor lymphocytes (CD8-DR), a slight increase in percentage of B lymphocytes (CD19), and a greater increase in serum concentration of IgE. In 1 of the 2 patients, reevaluation of immunity 20 days after the rash appeared and after LTG suspension showed normal percentages of CD4-DR, CD8-DR, and CD19, whereas the serum concentration of IgE had decreased. CONCLUSIONS: The observed immunological results indicate that LTG-induced rash may be considered an immune-mediated hypersensitivity reaction.     

Common expression of the multidrug resistance marker P-glycoprotein in B-cell chronic lymphocytic leukaemia and correlation with in vitro drug resistance

The expression of P-glycoprotein (Pgp), which is associated with multidrug resistance (MDR), was investigated in 20 B-cell chronic lymphocytic leukaemia (B-CLL) patients by flow cytometry using two Pgp-specific monoclonal antibodies (mAb), MRK-16 which recognizes an extracellular epitope, and JSB-1 which recognizes an intracellular epitope. Sixteen (80%) patients were positive with MRK-16 whereas all patients were positive with JSB-1. The proportion of Pgp-positive lymphocytes from each patient sample varied from 2-94% for MRK-16 and 20-93% for JSB-1. There was no correlation between the level of positivity and disease stage or treatment history. In vitro drug resistance to vincristine (VCR) and doxorubicin (DOX) was determined by the colorimetric MTT assay. All patients were resistant to one or both drugs being consistent with the expression of Pgp. There was no correlation between the level of resistance and disease stage or drug treatment. We investigated the expression of Pgp in the normal counterpart of the B-CLL cells, CD5+CD19+ B-lymphocytes. A minor subpopulation (3%) of CD5+CD19+ lymphocytes isolated from normal controls expressed Pgp suggesting that these cells may be the potential precursors to the B-CLL cell. We conclude that Pgp expression and drug resistance are inherent characteristics of the B-CLL lymphocyte.     

Clinical features of primary and secondary atypical mycobacteriosis

A clinical investigation was carried out in 39 patients with atypical mycobacteriosis (AM). The patients at our hospital diagnosed as having AM during an 11-year period from 1981 to 1991 were reviewed in this study. The incidence of AM among all of mycobacterial infections has been increasing since 1988. The atypical mycobacteria detected included M. avium complex (MAC) in 79%, M. kansasii in 26%, and other organisms in 5%. Patients who had primary infection without underlying respiratory disease were compared with those who had secondary infection. In secondary infection, MAC was detected in the sputum of a high percentage of patients and was positive for more than 6 months despite therapy. Gamma globulin levels were also increased in patients with secondary infection. Cell mediated immunity was examined by the DNCB reaction and the detection of CD4- and CD8- positive T lymphocytes. The DNCB skin reaction was positive in 6 out of 26 patients with secondary infection. The percentage of CD8- positive T lymphocytes was higher in patients with secondary disease. Fischer's ratio (indicating the balance of plasma amino acids) was also examined as an index of the nutritional status. It was significantly lower in secondary infection compared with primary infection. Moreover, secondary infection was associated with a lower positive rate for the DNCB skin reaction and a lower Fischer's ratio when compared with pulmonary tuberculosis. Thus impairment of cell-mediated immunity, malnutrition, and a poor prognosis were significantly more common in secondary infection compared with primary infection.     

Differential diagnosis between classic Hodgkin's lymphoma, T-cell-rich B-cell lymphoma, and paragranuloma by paraffin immunohistochemistry

There are significant difficulties in the differential diagnosis of lymphomas at the interface between classic Hodgkin's lymphoma and both paragranuloma and T-cell-rich B-cell lymphoma as well as at the interface between T-cell-rich B-cell lymphoma and paragranuloma. We therefore investigated 197 cases (155 classic Hodgkin's lymphomas, 32 T-cell-rich B-cell lymphomas, and 10 paragranulomas) by paraffin immunohistochemistry. Special interest was given to cases with a B-cell phenotype of tumor cells. The reactive inflammatory infiltrate in both classic Hodgkin's lymphoma and T-cell-rich B-cell lymphoma was rich in TIA-1-positive cytolytic lymphocytes, and CD57-positive cells were rarely encountered. In contrast, in paragranuloma CD57-positive cells and small B-lymphocytes predominated the background infiltrate. The tumor cells in cases of classic Hodgkin's lymphoma were positive for CD30 in 95%, for CD15 in 75%, and for CD20 in 22%. Apart from this, vimentin was expressed in >95% of the cases. All cases of T-cell-rich B-cell lymphoma were negative for vimentin, CD30, and CD15. The reactivity of the tumor cells for CD30, CD15, CD20, and vimentin together with the background reactivity for CD57 and TIA-1 seem to reliably discriminate between the entities and should therefore help to increase the interobserver reproducibility of diagnoses in the gray zone around Hodgkin's lymphoma.     

Myelomonocytic antigens in B-cell chronic lymphocytic leukemia

The clinical significance of myelomonocytic (MyMo) antigens in B-cell chronic lymphocytic leukemia (B-CLL) is unclear. We have analyzed the expression of MyMo antigens (CD13, CD14 (LeuM3, My4, Mo2), CD15, CD11b, CD11c, CD33 and CD68) on B-lymphocytes (CD19+) in 105 B-CLL patients and in 35 controls. A double direct staining technique and flow cytometric analysis was performed. The expression of MyMo antigens on the control group did not exceed 4% B-lymphocytes. A MyMo antigen was considered as positive when present in > or = 10% of B-lymphocytes. Among the B-CLL patients, 28 (26.7%) were positive for CD11c, 21 (20.0%) for CD11b, nine (8.6%) for CD15, five (4.8%) for CD13, two (1.9%) for Mo2, and one (1.0%) for My4. No patient was positive for LeuM3, CD33 or CD68. CD11c was more frequently expressed in patients with a short lymphocyte doubling time (< 12 months) (P = 0.05) and CD11b in the group with a higher number of lymphoid areas involved (P = 0.02). No correlation was found between lymphoid morphology and MyMo antigen expression. Fourteen of the 80 patients at risk subsequently progressed to a more advanced stage. Multivariate analysis identified hemoglobin (P = 0.004) and CD11b positivity (P = 0.009) as independent variables for disease progression. Fifteen patients died during evolution. Seven out of the 21 CD11b positive patients and eight of the 84 CD11b negative patients died (LR: P = 0.02, BG: P = 0.05). In the multivariate analysis, only CD11b positivity (> or = 10%) added prognostic value to clinical stages.     

Complexities of primary generalized epilepsy

Abnormal arousal responses paired with paroxysmal discharges and photosensitivity are the principal mechanisms in the precipitation of seizures in primary generalized epilepsy. The abnormal arousal responses show a consistent maximum over the frontal midline region. An exception from this rule was found in two children with primary generalized epilepsy (petit mal absences, one also with grand mal) with a strongly positive family history. In these patients, the generalized-synchronous bursts showed a maximum over the vertex (Cz electrode). Both of these children also had single spikes over the Rolandic region. A relationship between primary generalized and benign Rolandic epilepsy is demonstrated. Both forms of seizure disorder are based on dysfunction (hyperexcitability) rather than on a structural epileptogenic lesion. A dichotomy of dysfunctional and structural epilepsies is presented but gray zones of overlap indubitably exist. The limitations of the dichotomy concept are pointed out.     

The autonomic nervous system and the immune system in juvenile rheumatoid arthritis

CD16, the low affinity receptor for monomeric IgG (Fc gamma RIIIA), is a well characterized activation molecule on NK cells. In this study we investigated the role of CD16 in NK cell-mediated regulation of immunoglobulin production. Cocultures of the CD16+ human NK clone CNK6 and highly purified SAC/IL-2-activated B lymphocytes with various CD16 antibodies showed significantly diminished NK-enhanced immunoglobulin production in a dose-dependent manner, indicating that CD16 is relevant in NK-B cell interaction. Similarly, recombinant soluble CD16 incubated with B cells before cultures, suppressed the NK cell-stimulated B cell antibody response. Enhanced immunoglobulin production was also inhibited by Fc-specific F(ab')2 anti-body fragments. Coculture of NK cells with B lymphocytes resulted in induction of mRNA for IFN-gamma and TNF-alpha. The accumulation of mRNA for these cytokines was prevented by addition of CD16 and Fc-specific antibodies. It is proposed that interaction of CD16 on NK cells with B cell bound immunoglobulin leads to induction of cytokines in NK cells which stimulate immunoglobulin production by B cells.     

4-Hydroxynonenal and cell signalling

Donor leukocyte transfusions (DLT) have an anti-leukemic effect in most patients with a relapse of chronic myeloid leukemia (CML) after allogeneic stem cell transplantation. However, DLT are often complicated by graft-versus-host disease. Selection of donor lymphocytes with a relative specificity for leukemic cells is desirable. The generation of leukemia-reactive cytotoxic T lymphocyte (CTL) responses between HLA-identical donors and patients in bulk cultures showed major variations, and false negative results were observed. In a modification of a limiting dilution analysis (LDA) two-fold serial dilutions of HLA-identical donor mononuclear cells (MNC) were cultured in the presence of CML cells. The anti-leukemic CTL precursor frequencies in these donors varied between <1 and 9 per 106 MNC. HLA-restricted CD4+ or CD8+ lymphocytes as well as MHC non-restricted gammadelta T cells were responsible for the anti-leukemic responses. A positive correlation between cytotoxicity in the various wells after 3, 4 and 5 weeks of culture could be found. The LDA may be superior to bulk cultures in selecting stable immune responses and in separating multiple different anti-leukemic T cell responses in each donor-patient combination.     

Interleukin 1 beta synergises with interleukin 2 in the outgrowth of autologous tumour-reactive CD8+ effectors

Using peritoneal fluid or pleural effusion obtained from 20 patients with lung, ovarian or metastatic breast cancer, we separated tumour cells from malignant effusion-associated mononuclear cells (MEMNCs) using discontinuous Ficoll-Hypaque density gradients. CD3+ T lymphocytes represented the main population of MEMNCs. The mean +/- s.d. CD4/CD8 ratio of MEMNC suspensions was 1.18 +/- 0.40. MEMNCs proliferated and expanded in vitro with human interleukin 2 (IL-2) either as CD3+ CD8+ cells or as CD3+ CD4+ cells or as mixed populations of CD8+ and CD4+ cells. Preferential cytolytic activity against autologous tumour cells was demonstrated in IL-2-activated MEMNC cultures with excess CD3+ CD8+ cells. In contrast, effectors derived from IL-2-activated cultures with excess CD3+ CD4+ cells lysed both autologous and allogeneic tumour target cells. The addition on day 0 of interleukin 1 beta (IL-1 beta) to MEMNCs cultured in the presence of IL-2 was effective in promoting the growth of CD3+ CD8+ cells and augmenting the cytotoxicity against autologous tumour. Simultaneously, the production of gamma-interferon (IFN-gamma) was increased in these cultures. This is the first report suggesting that IL-1 beta synergises with IL-2 to induce autologous tumour-specific CD8+ cytotoxic T lymphocytes (CTLs) within the MEMNC population. Selective enrichment in T-cell subsets by IL-1 beta may be useful in cellular adoptive immunotherapy using cells isolated from malignant effusions.     

Follicular dendritic cells in non-Hodgkin's lymphomas

Follicular dendritic cells (FDC) are restricted to the B-cell regions of secondary lymphoid tissue and to non-Hodgkin's lymphomas derived from the follicular center or the mantle zone. With their cytoplasmic ramifications they form a dense network which contains the B-lymphocytes. In situ, FDC are only detectable at the ultrastructural level or when stained with anti FDC-reagents. On the surface of their dendritic extensions they express transferrin receptors (CD71), the B-cell epitope CD20, class II antigens, the myelomonocytic molecule CD14, the glycoprotein gp50 (CD40), and several receptors for components of the complement system (CD11b, CD21, CD35). Subsequent to an antigen challenge, FDC trap and retain immune-complexes for a long period of time. In vitro FDC and neoplastic lymphocytes spontaneously form small cellular aggregates. This adhesion is mediated by the LFA-1-alpha/beta = ICAM-1, the VLA-4 = VCAM-1, and the ICAM-1 = C3bi- receptor ligand pathways on B-cells and on FDC, respectively. The loss of LFA-1- alpha/beta and ICAM-1 molecules may enable neoplastic lymphocytes to detach from FDC. The monoclonal B-cells now invade new compartments. In vitro, FDC have the capacity to activate resting B-cells and to save them from dying by apoptosis. Signals involved in this activation include cell-surface immunoglobulin and CD40. Immunocytochemistry and autoradiography with single cell suspensions of neoplastic B cells suggest that FDC also provide signals leading to the continued stimulation of lymphoma lymphocytes. During the early stage of HIV infection lymph nodes show an immense follicular hyperplasia, with a massive increase of the dendritic network of FDC. In the later stage of the disease, the continuous involution of the germinal centers is associated with a progressive destruction of FDC.     

Epidermodysplasia verruciformis accompanied by familial large granular lymphocytosis and a decrease in T lymphocytes

A 40-year-old man with epidermodysplasia verruciformis showed a decrease in peripheral blood T cells and abnormal expansion of large granular lymphocytes, accompanied by increased natural killer cell activity. Surface marker analysis of his large granular lymphocytes demonstrated that the subset, CD 57+ and CD 16+, had increased. His father, who had no skin lesions of epidermodysplasia verruciformis, displayed similar blood changes and his brother showed a decrease in T cells and a slight increase in CD 16+ natural killer cells, whereas his mother revealed only a slight decrease in T cells. Our present study indicates that epidermodysplasia verruciformis might be associated with hereditary abnormal expansion of large granular lymphocytes and a decrease in T cells.     

Nickel subsulfide is genotoxic in vitro but shows no mutagenic potential in respiratory tract tissues of BigBlue rats and Muta Mouse mice in vivo after inhalation

The immunostimulatory capacity of Acanthospermum hispidum, a tropical plant which is used in the traditional medicine of Benin for the treatment of infectious diseases, was studied in the porcine immune system. These in vitro studies revealed the capacity of A. hispidum to enhance the proliferation of T lymphocytes after stimulation with ConA or allogeneic stimulator cells in the mixed leucocyte culture (MLC). The virus-specific MHC class II-restricted in vitro immune response against pseudorabies virus (PRV) was also enhanced in a co-stimulating manner. Phenotyping of T lymphocytes that had been activated in vitro in the presence of A. hispidum revealed an increase of activated gamma delta T lymphocytes with the phenotype CD2-CD5low+CD8-. In vitro analysis of the influence on the lymphocyte function demonstrated neither an increase of the immunoglobulin synthesis, nor of the interleukin-2 production, nor of the cytolytic activities. Experiments using separated T-lymphocyte subpopulations showed that the co-stimulatory activity was based on a synergism between T helper and gamma delta T lymphocytes, and that gamma delta T lymphocytes were the targets of the plant-derived extract. The gamma delta T cells which could not activated in mixed leukocyte cultures or with pseudorabies virus antigen in a secondary immune response, were reactive to the interleukin-2 released from antigen-stimulated T helper lymphocytes.     

Temperament profiles and their role in neurodevelopmental assessed preterm children at two years of age

CD26 antigen, a 110 kDa membrane glycoprotein with exopeptidase activity (DAP IV), is an activation marker of T lymphocytes preferentially expressed on CD4+ memory cells and involved in T cell proliferation and IL-2 production after antigenic stimulation. We employed cytochemical and immunocytochemical techniques to study DAP IV/CD26 expression in circulating lymphocytes from 40 hemophilic patients, chronically treated with coagulation factors, in order to verify the possible involvement of this molecule in the immunological alterations of hemophilia. In all the hemophiliacs DAP IV activity was significantly lower than in the controls, independently of the quantity of blood transfused and previous exposure to viruses. This reduction may be responsible for the impaired proliferative response of lymphocytes to antigens and mitogens, notoriously observed in hemophilia. Whereas in the group of HIV- patients CD26 expression was similar to that of normal controls, in the 8 HIV+ hemophilic patients both percentages of positive lymphocytes and intensity of staining were significantly lower. In only 4 of the 8 cases was this deficit associated with CD4+ cell depletion. The significant selective loss of CD26 expression observed in HIV+ patients is probably an early event after HIV infection and seems to occur even before CD4 cell depletion. In conclusion, evaluation of DAP IV/CD26 might be a useful option for monitoring the immunological alterations of all hemophilic patients, HIV positive or not, chronically treated with coagulation factors.     

Concurrent hypercortisolism and hypermineralocorticoidism

The clinical and pathologic findings in 16 cases of carcinoid tumor of the testis are presented: 10 tumors were primary in the testis, 2 were teratomas, 2 were in the spermatic cord and 2 were metastatic. Most of these tumors occurred in middle-aged patients and the symptoms were those of testicular tumor in general, that is swelling, pain and tenderness. In none of the primary case was there evidence of carcinoid syndrome and no determination of serotonin was made before orchiectomy. Followup in 12 cases was from 4 months to 16 years postoperatively. Three patients died 2 to 4 years after orchiectomy: 1 with generalized metastasis and 2 with intercurrent diseases. Two patients were lost to followup and the remaining patients are well. Although ovarian carcinoids usually occur in teratoma and do not metastasize 1 of the primary cases produced generalized metastasis.     

The interrelation of the expression of HLA class I and II proteins and of the costimulatory proteins CD11a/CD18 and CD16 with the lytic activity of resting and activated natural killer lymphocytes

It has been presumed that: 1) rheumatoid arthritis (RA) is a genuine model of activation of the peripheral natural killers (NK); 2) methods of NK separation can cause their activation, and therefore only peripheral mononuclear cells were used. The aim of this research was to study the role of cytolysis of HLA-I, HLA-DR, and costimulatory proteins CD11a and CD16 expressed on resting and activated peripheral NK cells. A total of 74 healthy volunteers (HV) and 74 RA patients were compared before corticosteroid or gold treatment. Two-colour immunofluorescence and cytofluorimetric analysis, cytotoxic test against the target K 562 cells (class I negative) before and after incubation of PMC with monoclonal antibodies (MoAB) to HLA-I (E3D8), HLA-DR (ICO-1), CD11 (ICO-11), PXx63 Ag8.653 as control, and also incubation with recombinant alpha 2-IFN were used. VEP-13 MoAB was used for CD16 determination. Compared with HV PMC, the RA PMC showed a statistically significant increase of activated NK lymphocytes (CD11a+DR+ and CD16+DR+ by 2.03 and 1.96 times, resp.), and increased level of expression of HLA-I, HLA-DR, and CD16 on CD11a+ lymphocytes, resulting in significantly diminished cytolytic activity (CA) by 1.9 times. A short-term incubation with alpha 2-IFN (100 U/ml, 1 h) increased the level of expression of HLA- and costimulatory proteins and the CA of the HV PMC, while the RA PMC did not react. HV peripheral NK are concluded to be mainly resting cells, and the RA peripheral NK are mainly the activated ones. Only using the level of expression of HLA-DR on CD11a lymphocytes, as a ranking criterion, allowed to reveal two types of correlation between the CA and immunocytological parameters of PMC. The first type: in HV, the CA correlated positively (P < 0.025) with the percentage of CD11a+CD16+, and with levels of expression of HLA-I (P < 0.025) and CD16 (P < 0.025) expressed on CD11a lymphocytes (5-9.5 MFI DR--the mean fluorescence intensity of HLA-DR). The second type: the CA positively correlated (P < 0.05) with the percentage of CD11a+CD16-, and with levels of expression of HLA-DR (P < 0.05) and CD11a (P < 0.05) expressed on CD11a lymphocytes (12.4-16 MFI DR). In RA patients with a "normal" density expression of HLA-DR on CD11a lymphocytes (up to 14 MFI) there exists a mixed type: the CA correlated positively (P < 0.05) with the percentage of CD11a+CD16+, and with levels of expression of HLA-DR (P < 0.05) and CD11a (P < 0.05) expressed on CD11a lymphocytes. In RA patients with a very high density expression of HLA-DR on CD11a lymphocytes (VH-DR group, 18-26 MFI) the CA correlated negatively with the percentage of CD11a+CD1 6+ (P < 0.05), and with levels of expression of HLA-DR (P < 0.025) and CD11a (P < 0.025) expressed on CD11a lymphocytes. The anti-HLA-I,-DR, -CD11a MoABs strongly inhibit the Ca in HV- and RA-PMC. However, in the VH-DR group the anti-DR MoAB stimulates the CA from 27.06 +/- 10.25 up to 41.69 +/- 14.23%. Thus, activated peripheral CD11a+CD16+ lymphocytes suppress the CA of other NK.     

Inflammatory pseudotumor of nerve

Two cases of inflammatory pseudotumor are described. The first patient, a 35-year-old white man, developed a progressive sensorimotor deficit in the right leg associated with a fusiform sciatic nerve mass in the posterior thigh. The lesion, compressive in nature and situated entirely within the epineurium, was totally resected. Histology revealed lymphocytic and plasmacellular inflammation as well as extensive fibrosis and collagen deposition. The patchy infiltrate consisted equally of CD2, CD3, CD5, and CD7 positive T-lymphocytes as well as CD20-and CD22-positive B-lymphocytes expressing both kappa and lambda immunoglobulin light chains. A selective biopsy of the encompassed and compressed nerve fascicles demonstrated both myelin loss and axonal injury. The second case was that of an 18-year-old woman with focal enlargement of a radial nerve by an epineurial infiltrate of multinucleate histiocytes and T as well as occasional B lymphocytes. No etiology was apparent in either case. The differential diagnosis includes non-neoplastic processes (amyloidoma and tuberculoid leprosy) as well as tumors (benign and malignant peripheral nerve sheath tumors, lymphoma). Although rare, inflammatory pseudotumors must be included in the differential diagnosis of tumor-like lesions of peripheral nerve.     

Mechanism of human immunodeficiency virus type 1 localization in CD4-negative thymocytes: differentiation from a CD4-positive precursor allows productive infection

Human immunodeficiency virus (HIV) infection of the thymus could have profound effects on development of the immune response, particularly in children. We and others have established that in addition to infecting and depleting CD4-bearing thymocytes, functional HIV proviruses are found in thymocytes lacking surface CD4 expression. Using in vitro thymocyte cultures, we show that neither HIV-mediated down regulation of CD4 nor CD4-independent infection contributes to the localization of HIV in cells lacking the primary virus receptor. Rather, infection of a CD4-positive precursor cell (CD4 positive/CD8 positive) with subsequent differentiation into a mature CD4-negative phenotype results in productively infected CD4-negative cells. This novel mechanism may contribute to pathogenesis by distributing viral sequences into functional subsets of T cells typically refractory to HIV infection and could account for the presence of viral DNA in CD8-positive lymphocytes recently observed in patients.     

Migration resistant, blood-compatible plasticized polyvinyl chloride for medical and related applications

AIMS: To determine the morphology, immunophenotype and bcl-2 protein status of intraepithelial lymphocytes in HIV-positive lymphoepithelial lesions. METHODS AND RESULTS: Seventeen cases (from adults and children) of HIV-associated parotid and lung lymphoid lesions were examined. In addition, three lymphoepithelial cysts from HIV-negative patients were studied in parallel. Immunohistochemistry was performed on paraffin embedded tissue with the following antibodies: CD20, CD79a, CD3, CD4, CD8, bcl-2, CAM5.2, AE1/3, MIB1, kappa/lambda light chains and EBV-LMP-1. Heavy chain rearrangement was sought by polymerase chain reaction (PCR) in four of the cases. The lymphocytes participating in lymphoepithelial lesions of HIV-positive patients had the morphology of centrocyte-like cells with occasional cells resembling centroblasts. The majority of these cells were of B-cell lineage, but occasional intraepithelial T-cells (CD8 positive, CD4 negative) were also present. T-cells also formed a significant component of the infiltrative lymphoid cells outside the lymphoepithelial lesions. These were mainly CD8 positive, but very occasional CD4-positive T-cells were also noted. None of the cases showed light chain restriction and the four cases did not demonstrate heavy chain rearrangement by molecular biology. The interesting finding was the absence of bcl-2 expression by the intraepithelial lymphocytes. In contrast, the intraepithelial lymphocytes seen in the non-HIV setting were strongly bcl-2 positive. The majority of these were B-cells, and very occasional CD8 and CD4 positive T-cells formed the intraepithelial population. CONCLUSION: It is postulated that this finding is due to the HIV causing down-regulation of bcl-2 protein.     

Pain in the hip area accompanied by a fever]

In 3 patients, 2 women aged 16 and 64 years and 1 man aged 64 years, with pain in the left hip region and fever, the diagnosis psoas abscess was made. After antibiotic treatment and drainage they recovered well. The primary from of psoas abscess is presumably caused by haematogenous spread of bacteria, mostly Staphylococcus aureus. The secondary form is caused by spread of infection from surrounding tissue, mostly gastrointestinal micro-organisms with Crohn's disease and diverticulitis. Painful passive extension and endorotation as well as a painful flexion stress-test of the hip joint can indicate a psoas abscess. Echography and blood cultures should be performed if a psoas abscess is suspected. If echography is inconclusive, CT-scan can establish the diagnosis. The psoas abscess should be treated by percutaneous or surgical drainage combined with antibiotic therapy. The underlying cause of a secondary psoas abscess should be treated separately.