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Fifty-nine lymph node biopsies from homosexual men with serum antibodies to HTLV-III/LAV were the subject of a detailed histopathological and immunohistochemical study. The histological findings were correlated to the patients clinical status, and the T4/T8 ratios in blood and lymph nodes. Four histological patterns predominated and were defined as follicular hyperplasia (FH), follicular fragmentation (FF), follicular atrophy (FA), and follicular depletion (FD). Immunocytochemical studies indicated that destruction of follicular dendritic cells is related to the initiation of follicular involution from FH to FF, but the possible role of follicular infiltrating T-cells cannot be excluded. Marked individual variations in lymph node angiogenesis increasing during involution were observed, which suggests that the degree of angiogenic host response may predispose for evolution of Kaposi's sarcoma. The majority of the patients with the clinical diagnosis of persistent generalized lymphadenopathy (PGL) were morphologically staged as FH or FF (89%), whereas most of the AIDS patients showed lymph node changes compatible with FA and FD (89%). Patients with AIDS-related complex (ARC) had a wider spectrum of morphological lymph node changes but a majority of cases (62%) were also classified as FA or FD. Clinical follow-up showed progression from PGL to ARC in seven of 21 cases with the FF pattern and only in three of 19 cases with FH, indicating a possible prognostic value in differentiating between FH and FF. Three cases with FD and one with FA progressed to AIDS during the time of observation. T4/T8 ratios in blood and lymph nodes were significantly lower in patients with FD histology compared to patients of the other histological groups. At autopsy, all AIDS cases showed the FD pattern of lymphadenopathy. Autopsy findings in seven patients emphasized the importance of post-mortem studies in clarifying the spectrum of opportunistic diseases, including tumors which afflict the AIDS patients.
P Biberfeld, and
A Ost, and
A Porwit, and
B Sandstedt, and
G Pallesen, and
B Böttiger, and
L Morfelt-Månsson, and
G Biberfeld
July 1986,
Quintessenz Journal,
P Biberfeld, and
A Ost, and
A Porwit, and
B Sandstedt, and
G Pallesen, and
B Böttiger, and
L Morfelt-Månsson, and
G Biberfeld
January 1986,
Pennsylvania medicine,
P Biberfeld, and
A Ost, and
A Porwit, and
B Sandstedt, and
G Pallesen, and
B Böttiger, and
L Morfelt-Månsson, and
G Biberfeld
January 1986,
International review of experimental pathology,
P Biberfeld, and
A Ost, and
A Porwit, and
B Sandstedt, and
G Pallesen, and
B Böttiger, and
L Morfelt-Månsson, and
G Biberfeld
November 1985,
The Journal of infectious diseases,
P Biberfeld, and
A Ost, and
A Porwit, and
B Sandstedt, and
G Pallesen, and
B Böttiger, and
L Morfelt-Månsson, and
G Biberfeld
September 1986,
Journal of immunological methods,
P Biberfeld, and
A Ost, and
A Porwit, and
B Sandstedt, and
G Pallesen, and
B Böttiger, and
L Morfelt-Månsson, and
G Biberfeld
April 1986,
The American journal of pathology,
P Biberfeld, and
A Ost, and
A Porwit, and
B Sandstedt, and
G Pallesen, and
B Böttiger, and
L Morfelt-Månsson, and
G Biberfeld
January 1987,
International archives of allergy and applied immunology,
P Biberfeld, and
A Ost, and
A Porwit, and
B Sandstedt, and
G Pallesen, and
B Böttiger, and
L Morfelt-Månsson, and
G Biberfeld
February 1986,
British medical journal (Clinical research ed.),
P Biberfeld, and
A Ost, and
A Porwit, and
B Sandstedt, and
G Pallesen, and
B Böttiger, and
L Morfelt-Månsson, and
G Biberfeld
June 1986,
Tumori,
P Biberfeld, and
A Ost, and
A Porwit, and
B Sandstedt, and
G Pallesen, and
B Böttiger, and
L Morfelt-Månsson, and
G Biberfeld
May 1986,
The Journal of infectious diseases,
