Focal Lymphocytic Infiltration Research Articles

The prevalence of focal tubulo-interstitial lesions in various renal diseases.

The focal tubulo-interstitial lesions (FTIL) described in the present paper appear as short segments of tubules showing epithelial degeneration, necrosis and desquamation. The foci are surrounded by mononuclear cells, among which lymphocytes are most numerous. They infiltrate through the damaged tubular basement membranes and may thus be located between epithelial cells and in the tubular lumen. Older lesions show focal tubular atrophy with thickened basement membranes together with focal interstitial fibrosis and lymphocytic infiltrates. The overall prevalence of this type of lesion in a consecutive renal biopsy series was 36%. It was not detected in 24 biopsies from patients without renal disease. The frequency of FTIL was high in acute renal failure due to hemolysis, shock etc. or to the action of drugs, as well as in some types of glomerulonephritis (membranous, membrano-proliferative, SLE). Tubular immunoglobulins were not demonstrated in 38 biopsies with FTIL. The pathogenesis and possible consequence of the lesions are still unclear, but it is suggested that they may in some situations contribute to the nephron atrophy in chronic renal disease.

Lymphoid Hypophysitis With Selective Adrenocorticotropic Hormone Deficiency

This report describes a 31-year-old woman with evidences of selective adrenocorticotropic hormone deficiency associated with a remarkable pituitary lesion, lymphoid hypophysitis. Clinical manifestations of secondary hypocortisolism, which first appeared during the immediate postpartum period following normal pregnancy, included progressive weakness and mental aberrations, fasting hypoglycemia, transient hypercalcemia, and striking ECG changes. Sudden death resulted from cardiorespiratory collapse. Microscopic examination of the anterior pituitary disclosed focal fibrosis and extensive lymphocytic infiltrations with a marked reduction of basophils; immunostaining techniques demonstrated a selective loss of corticotropin-secreting cells. The histopathology of the pituitary and its association in this case with lymphoid thyroiditis suggest that selective damage to corticotrophs was due to an autoimmune process.

Observations on the Response of Dysgammaglobulinemic Chickens to Malarial Infection

Neonatal chickens were surgically bursectomized and irradiated to produce adults which were agammaglobulinemic or hypogammaglobulinemic. Those birds and intact birds were compared as to certain host responses to Plasmodium gallinaceum infection. In altered birds, the parasitemia appeared later and rose more slowly and all untreated bursectomized birds died at a low parasitemia. Dysgammaglobulinemic birds treated with an antimalarial drug recovered and were resistant to reinfection; serum-soluble antigens, but no measurable antibody, were recovered from their blood. The pathogenesis of the disease differed from that in unaltered birds. The following differences were observed: the lamina propria of the small intestine was thickened; the epithelial cells of the lungs were enlarged and increased in numbers and there was thickening of the peribronchial and alveolar walls; the kidney had widespread but patchy infiltration of leukocytes, with many glomerular tufts completely filled; there was widespread focal lymphocytic infiltration of the liver; the spleen suffered proliferation of the reticulum, with a highly disturbed architecture, but had little hemozoin deposited; the brain showed limited early neuronal degeneration.

Isolated lipodystrophy, a form of mesenteric tumor

A peculiar tumor-like alteration of the fat of the small bowel mesentery is described. This lesion was found in five adult patients, all with little or no relating symptomatology. In four an abdominal mass was palpable. Diagnosis was established at exploratory laparotomy in three patients, and at postmortem examination in the remaining two. Grossly, the entire small bowel mesentery was thickened and nodular, rubbery firm, opaque and mottled grey to yellowish orange. Microscopically, there was diffuse involvement of fat cells, most prominent about the periphery of the fat lobules. In the early stages individual fat cells appeared smaller than normal; their cytoplasm was opaque, granular and faintly basophilic, and the nucleus was centrally situated. Later, a mild focal lymphocytic infiltration and perilobular condensation of fibrous tissue were apparent. Only rarely and in small focal areas was there development of lipogranulomas. It is suggested that initial proliferation of mesenteric fat induces a perpetuating alteration in fat cell metabolism through either vascular or mechanical embarrassment. The fat cells, particularly those of the relatively more ischemic peripheral portions of the lobules, lose their ability to absorb fat and their lipolytic activity is compromised. These altered cells undergo the structural changes described heretofore; and as the process progresses, they may actually break down, liberating fatty acids and exciting focal inflammation and fibrosis. These mesenteric masses bear certain resemblances to Whipple's disease, Weber-Christian disease with systemic involvement, sclerosing lipogranuloma and traumatic or pancreatic fat necrosis. They must also be differentiated from true fat tumors, lymphosarcoma, tuberculosis and other less common conditions. The premortem diagnosis can be made only at operation. Biopsies should be taken not only of the mesentery but also of the bowel and mesenteric lymph nodes. Surgical resection usually is not feasible, as the process tends to surround the major mesenteric vessels. The prognosis apparently is favorable, for the lesion is slowly progressive and probably selflimited. Alteration in bowel function does not ensue, nor is there evidence that the process later involves other tissues.