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F Hentges

Publications and source records attributed to F Hentges.

30 records · Page 2Linked to original sources
PubMed1992

Prolonged clinically asymptomatic evolution after HIV-1 infection is marked by the absence of complement C4 null alleles at the MHC.

The length of time after which persons infected with HIV-1 progress to AIDS is variable. Certain alleles at the MHC have been shown to influence negatively the clinical outcome of HIV-1-infected persons and to be associated with special clinical manifestations. We investigated the MHC class I, class II and class III antigens in 54 Caucasian HIV-1-infected persons. The MHC profile of individuals with a prolonged period before AIDS is marked by a lower frequency of C4 null alleles.

Acquired Immunodeficiency Syndrome↗
PubMed1986

Acquired C1 esterase-inhibitor deficiency: case report with emphasis on complement and kallikrein activation during two patterns of clinical manifestations.

A case of severe angioedema with several episodes of life-threatening attacks during a follow-up of 7 years is presented. Although the biologic profile is that of an acquired C1 INH deficiency, no lymphoproliferative malignancy or immune-complex disease could be proven until now. However, the patient has had a small monoclonal IgG lambda-gammopathy for 4 years. During the last 4 years, edematous manifestations have stopped. The patient now suffers at regular intervals of about a week from short-lasting attacks with digestive and vasomotor symptoms. This clinical evolution is accompanied by a worsening in the complement abnormalities. The digestive and vasomotor attacks were found to be correlated with sudden prekallikrein and high-molecular-weight kininogen consumption. These findings demonstrate that prekallikrein is activated during acquired C1 INH deficiency and that the products of this pathway such as bradykinin are probably responsible for a part of the clinical manifestations associated with this disorder.

Aged↗
PubMed1982

[Salmonella dublin enteric fever in two compromised hosts].

Salmonella (S) dublin is a rare cause of human enteric fever. We studied 2 compromised hosts, one of them being treated for lymphocytic leukemia and the other for chronic lymphocytic leukemia. Both had recurrent enteric fever caused by S. dublin. Both strains were resistant to chloramphenicol and to ampicillin and the patients were treated by trimethoprim-sulfamethoxazole to which the organism was sensitive. Investigations failed to discover an extraintestinal localisation and stool cultures remained negative after antibiotic treatment. One patient had a relapse of enteric fever at every relapse of his leukemia; the second patient after his second episode of enteric fever was treated prophylactically during 3 months. When he stopped antibiotic prophylaxis a fatal S. dublin septicemia occurred. We suggest that compromised hosts with S. dublin infection be treated prophylactically to prevent relapse.

Adult↗