We investigated peripheral lymphocyte subsets in 34 consecutive acute pancreatitis patients (21 males, 13 females; mean age, 57 years; range, 16-85 years) studied within 48 h of pain onset and for 5 consecutive days to understand better the immunological response during the course of the disease. The diagnosis was based on characteristic abdominal pain associated with a twofold increase in serum lipase and confirmed by imaging techniques in all patients. Acute pancreatitis was of biliary origin in 25 patients, due to alcohol abuse in 5, due to pancreas divisum in 1 , and of unknown origin in 3. Fifteen patients had severe illness and 19 had mild disease. In all patients, total lymphocyte and lymphocyte subset counts were carried out on admission, as well as on the third and fifth day of hospitalization, using a flow cytometric analysis. Twenty-three patients (13 with severe illness and 10 with mild disease) also had a repeat count 1 month after recovery. Twenty-five healthy subjects and 27 patients with nonpancreatic acute abdomen comparable for sex and age were studied as controls. On the first day of the study, the leukocyte number was significantly higher in patients with acute pancreatitis and in those with nonpancreatic acute abdomen with respect to healthy subjects, whereas the number of total and CD4+, CD8+, CD3+DR-, and CD3-DRf lymphocytes was significantly lower in acute pancreatitis patients than in healthy subjects or in patients with nonpancreatic acute abdomen. These subset counts persisted on the third and fifth days of the study. Patients with nonpancreatic acute abdomen and healthy subjects had similar values of total and lymphocyte subsets. The patients with acute pancreatitis studied 1 month after complete recovery had numbers of leukocytes, total lymphocytes, and CD4', CD8+, CD3+DR-, and CD3-DR+ lymphocytes similar to those in healthy subjects. Regarding CD3 +DRf lymphocytes, the count in acute pancreatitis patients studied within the first 5 days of hospital admission was similar to that in healthy subjects, but 1 month after complete recovery it was significantly higher in the pancreatitis patients. CD4+ and CD3 +DR-lymphocyte counts were significantly lower in patients with severe acute pancreatitis than in patients with mild disease from the third day of illness onward. The CD4+-T cell difference was still present 1 month later. The number of total lymphocytes was significantly lower in patients with severe illness relative to those with mild pancreatitis on the fifth day of hospitalization. Results demonstrate that in early phases of acute pancreatitis there was a significant decrease in the number of total lymphocytes and lymphocyte subset counts relative to controls. These counts returned to normal with resolution of the illness.
When activated, lymphocytes secrete glycoproteins related to particular surface proteins, including soluble forms of the interleukin-2 receptor (sIL-2R) and of the surface proteins CD4 (sCD4) and CD8 (sCD8). We evaluated the release of these glycoproteins in order to assess the activation of the cellular immune system during the course of acute pancreatitis. Thirty-five patients with acute pancreatitis (22 M, 13 F, mean age 64 years, range 16-97) were studied. The diagnosis was based on typical abdominal pain associated with a twofold increase of serum lipase as well as morphological abnormalities compatible with acute pancreatitis seen at computed tomography and/or ultrasonography. The pancreatitis was of biliary origin in 22 patients, due to alcohol abuse in 8, due to pancreas divisum inl, due to type IV hyperlipoproteinemia in 1 and of unknown origin in 3. Based on clinical outcome, 22 patients had mild pancreatitis, whereas 13 had severe disease. In all patients serum sIL-2R, sCD4 and sCD8 were determined on admission and daily for the following 5 days using enzyme immunoassay (ElA) techniques. Serum concentrations of sIL-2R and sCD8 were significantly higher in acute pancreatitis patients relative to healthy controls during the entire observation period, whereas sCD4 levels were significantly lower in acute pancreatitis patients than in the control group from the 2nd to the 6th day of observation. Serum sIL·2R concentrations were significantly higher in patients with severe pancreatitis than in those with the mild form of the disease, whereas no differences in serum concentrations of sCD8 and sCD4 were found between patients with mild pancreatitis and those with severe disease. No differences in serum levels of sIL·2R, sCD8 and sCD4 were found between patients with biliary pancreatitis and those with other etiologic forms of the disease. The results indicate that in the early phases of acute pancreatitis there is an activation of the cellular suppres-sor-cytotoxic immune system and impaired activity of the CD4 T lymphocytes; furthermore, serum sIL-2R may be helpful in early assessment of the severity of this disease.
Patients with severe pancreatitis show impaired early activation of peripheral CD19+ cells.
Purpose: We evaluated the proliferative response of lymphocytes to phytohemagglutinin P (PHA P), concanavalin A (Con A), and pokeweed mitogen (PWM) during the course of acute pancreatitis. Patients and Methods: Sixty consecutive patients with acute pancreatitis were studied within 48 h of the onset of pain, and 16 of them were also studied 1 month after complete recovery. According to the Atlanta criteria, 21 patients had severe disease and 39 had mild disease. Fifteen healthy subjects and 11 patients with nonpancreatic acute abdomen were studied as controls. In 12 patients with acute pancreatitis the lymphocyte proliferation after stimulation with the three mitogens was also assessed in autologous and heterologous plasma. Results: The lymphocyte proliferative response to optimal doses of PHA P, Con A, and PWM was significantly lower (p < 0.001) in acute pancreatitis patients (mean ± SD; PHA P 74,310 ± 22,960 cpm; Con A 64,669 ± 20,188 cpm; PWM 26,714 ± 6,436 cpm) than in healthy subjects (PHAP Ill,316 ± 12,044 cpm; Con A 96,276 ± 12,327 cpm; PWM 33,957 ± 3,601 cpm). Patients with nonpancreatic acute abdomen had a significantly higher lymphocyte proliferative response to PHA P and Con A than acute pancreatitis patients (PHA P p < 0.002; Con A p < 0.01; PHAP 91,116 ± 22,995 cpm; Con A 77,879 ± 19,083 cpm). In patients with acute pancreatitis, lymphocyte proliferation stimulated with PHA P and Con A was significantly lower (PHA P p < 0.005; Con A p < 0.001) in those with severe disease (PHAP 63,190 ± 15,157 cpm; Con A 52,813 ± 13,324 cpm) than in those with mild disease (PHA P 80,298 ± 24,340 cpm; Con A 71,052 ± 20,490 cpm). In the group of 16 patients studied during the initial phase of acute pancreatitis and 1 month after recovery, lymphocyte proliferation significantly improved after remission of the disease but remained impaired compared with that of healthy subjects. No difference was found in the lymphocyte proliferation of the 12 patients with acute pancreatitis assayed in autologous and heterologous plasma. Conclusions: The peripheral lymphocyte proliferative response to mitogen stimulation in patients with acute pancreatitis was decreased during the early phases of the disease.
Objectives-To determine if the presence of low percentages of CD8 positive cells or high levels of soluble interleukin-2 receptors (sIL-2R) define a subgroup of patients with more severe polymyalgia rheumatica and giant cell arteritis (PMR/GCA). Methods-38 PMR/GCA patients were followed up prospectively. Serum levels of sIL-2R and peripheral blood CD8 lymphocytes were measured before the start of corticosteroid treatment, after six months of treatment and at the last visit. Phenotypical analysis of lymphocyte subpopulations was performed with a two colour technique, and assay of sIL-2R was performed using an enzyme-linked immunosorbent kit. Forty four healthy people matched for age and gender comprised a healthy control group. Results-The median duration of follow up was 28 months (range 7-65). Corticosteroid treatment lasted a median of 23-5 months
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