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J Demonty

Publications and source records attributed to J Demonty.

At least 37 records · Page 2Linked to original sources
PubMed1998

[The clinical case of the month. Apropos of a case of unexplained fever].

An episode of fever of prolonged duration and undetermined origin always remains a difficult clinical problem. Several etiologies can indeed be responsible. If one wishes to obtain a diagnosis of the origin of the fever, one should adopt a well-structured strategy in which the various investigations are carried out in a strictly determined hierarchical order. This is badly needed if one wishes to reach a clue to the diagnosis and be able to implement an adequate therapy. In spite of all this, some cases will remain without precise diagnosis. The treatment of those cases will primary be empirical.

Aneurysm, Infected↗
PubMed1997

Extensive ulcerative colitis and extraintestinal manifestations in a patient with HIV infection and significant CD4 T-cell lymphopenia.

We report a heterosexual patient with HIV infection and a CD4 T-cell count of 0.45 x 10(9)/L who developed mild ulcerative proctitis, sacroileitis and oligoarthiritis. While he was treated with 5-aminosalicylic enemas, the patient rapidly developed severe pancolitis. An emergency colectomy without procetectomy was performed. A few months later, he suffered recurrence of ulcerative proctitis, aggravation of arthritic pain and developed anterior uveitis. All symptoms disappeared after proctectomy. There was no evidence for opportunistic infection or Kaposi's sarcoma. Antineutrophil cytoplasmic antibodies were positive and the HLA-B27 antigen was present. CD4 counts were lower during the phases of active disease than during remission. This case demonstrates that severe ulcerative colitis can occur in the presence of moderate T-cell defects. In view of a recent report of remission of Crohn's disease under comparable circumstances, it is possible that the extent of T-cell involvement in both diseases is radically different.

Acquired Immunodeficiency Syndrome↗
PubMed1994

Pathogenic tracks in fatigue syndromes.

This review analyses the recent literature devoted to two related fatigue syndromes: chronic fatigue syndrome (CFS) and acute onset postviral fatigue syndrome (PVFS). The articles are grouped into five pathogenic tracks: infectious agents, immune system, skeletic muscle, hypothalamo-pituitary-adrenal (HPA) axis and psychiatric factors. Although a particular infectious agent is unlikely to be responsible for all CFS cases, evidence is shown that host-parasite relationships are modified in a large proportion of patients with chronic fatigue. Antibody titres against infectious agents are often elevated and replication of several viruses could be increased. Chronic activation of the immune system is also observed and could be due to the reactivation of persistent or latent infectious agents such as herpes viruses (i.e. HHV-6) or enteroviruses. It could also be favorised by an impaired negative feedback of the HPA axis on the immune system. A model is proposed where the abnormalities of the HPA axis are primary events and are mainly responsible for a chronic activation of the immune system which in turn induces an increased replication of several viruses under the control of cellular transcription factors. These replicating viruses together with cytokines such as TNF-alpha would secondarily induce functional disorders of muscle and several aspects of asthenia itself.

Enterovirus↗
PubMed1992

Intrathoracic infections with bacteraemia due to Eikenella corrodens as a complication of peritonsillar abscesses: report of a case and review of the literature.

A 52-year-old man, without previous disease, presented with dysphagia, dyspnoea, high fever and sore throat after peritonsillar abscesses drainage. Physical and complementary examinations were consistent with pericarditis, mediastinitis, pneumonia and pleuritis. Blood cultures grew Eikenella corrodens resistant to clindamycin and amikacin. We emphasize the pathogenic potential of Eikenella corrodens. To the best of our knowledge, this is the first reported case of this organism as a pathogen in intrathoracic infections after peritonsillar abscesses drainage.

Bacteremia↗
PubMed1990

Protective effects of polyclonal sera and of monoclonal antibodies active to Salmonella minnesota Re595 lipopolysaccharide during experimental endotoxemia.

Mice were passively immunized with sera from blood donors active for rough lipopolysaccharides (LPS), the J5 (Rc chemotype) mutant of Escherichia coli O111:B4, and the Re595 (Re chemotype) mutant of Salmonella minnesota. All protected the mice against lethal challenge with smooth E. coli WF96 LPS, E. coli and Salmonella rough mutant LPS, or free lipid A. Epitopes recognized by monoclonal antibodies (MAbs) reacting with the LPS of S. minnesota Re595 or lipid A were localized in the 2-keto-3-deoxy-D-manno-octulosonic acid (KDO) region and on lipid A. Core-reactive MAbs reacted with their homologous Re LPS and with free lipid A. One, GL11, cross-reacted with the KDO alone. MAbs GL6, GL11, L.4, L.6, and L.8 protected the actinomycin D-sensitized mice against the lethal effects of LPS from E. coli WF96, Salmonella enteritidis, E. coli J5, S. minnesota Re595, and free lipid A. The GL11 antibody was also protective when injected after LPS challenge. These results indicate that antibodies directed against the core glycolipid of S. minnesota Re595 LPS may be useful as an additive form of therapy that may enable decreased mortality during gram-negative bacterial sepsis.

Animals↗
PubMed1989

Tumor necrosis factor and interleukin-1 serum levels during severe sepsis in humans.

In a study of serum levels of tumor necrosis factor (TNF alpha) and interleukin-1 beta (IL-1 beta) in patients developing sepsis in the ICU, high TNF alpha levels were found in patients with septic shock. Normal values are 75 +/- 15 pg/ml; in these patients, TNF alpha serum level ranged from 100 to 5000 pg/ml with a mean of 701 +/- 339 pg/ml and a median of 250 pg/ml. There was a correlation between TNF alpha level and sepsis severity score as well as with mortality. In contrast, IL-1 beta serum levels were only slightly increased and were not correlated with severity or mortality.

Adolescent↗
PubMed1988

Enzyme-linked immunosorbent assay for immunoglobulin G subclass antibodies specific for enterobacterial Re core glycolipid in healthy individuals and in patients infected by gram-negative bacteria.

An enzyme-linked immunosorbent assay was developed to study the subclass distribution of immunoglobulin G (IgG) specific to the core glycolipid (CGL) of the Re mutant of Salmonella minnesota R595 in serum samples from individuals with an IgG response toward these antigens. In a group of healthy blood donors, we detected predominantly the IgG2 and IgG1 subclasses. In a group of patients in an intensive care unit who developed infectious complications due to gram-negative bacteria, the anti-CGL IgG activity was due mainly to the IgG2 and IgG3 subclasses. In all serum samples found to be IgG positive, the assay for anti-CGL IgG2 was positive. This subclass was revealed to play a predominant role in patients displaying a seroconversion or a significant rise in their antibody response toward CGL. IgG4 was found or appeared only in patients with confirmed bacteremia. In addition, we observed a drop in anti-CGL IgG2 before the death of patients undergoing a septic shock or an irreversible organ failure, suggesting that the anti-CGL IgG2 activity could be used as a marker of the evolution of the illness in this group of patients.

Antibodies, Bacterial↗
PubMed1987

A direct enzyme-linked immunosorbent assay (ELISA) for antibodies to enterobacterial Re core glycolipid and lipid A. Results in healthy subjects and in patients infected by gram-negative bacteria.

We have developed an ELISA for IgM and IgG antibodies to the core glycolipid (CGL) of the Re mutant Salmonella minnesota R 595, and to lipid A. Anti-CGL antibodies have been detected in sera from 37% of healthy blood donors, whereas anti-lipid A activities were found in 13% of individuals only. The anti-CGL and anti-lipid A activities were examined in patients in a surgical intensive care unit, selected on the basis of a definite risk of infectious complications due to Gram-negative bacteria. Of the patients who developed such infections, the rate of favourable outcome was significantly higher in patients with either stable positive or increasing anti-CGL activities than in patients found to be negative. Our results provide clear evidence that anti-CGL antibodies contribute to host defence against various Gram-negative bacteria.

Animals↗