Excessive Protein Loss Research Articles

Protein-losing disorders of the gastrointestinal tract: roentgen features.

The term “idiopathic” or “essential” hypoproteinemia is used to describe a chronic state characterized by a marked reduction in plasma proteins and by edema without evidence of kidney or liver disease, malnutrition, or other detectable underlying pathological condition. It has been referred to as nephrosis without albuminuria. It appears to be more common in children than in adults, and edema is the chief and often the only sign. All the protein fractions may be reduced or only the albumin may be affected. At autopsy, no lesion can be found to account adequately for the lowered serum albumin. Approximately 40 cases have been reported, which have been carefully studied, but only recently has there been a clue to the etiology. Hypoproteinemia can arise either through reduction in protein synthesis or through excessive loss of proteins. The inadequate synthesis can be due to lack of protein in the diet or to liver disease. Neither of these possibilities occurs in idiopathic hypoproteinemia. Nor is there excessive elimination of proteins via the kidneys, skin, or respiratory organs. Cope and Goadby in 1935 (3) first suggested the possibility of an internal loss of proteins. In recent years, isotope tracer technics have permitted a more detailed study of the protein metabolism of patients with this condition. In 1949, Albright and others (1) reported a greatly increased rate of disappearance of intravenously administered I131-labeled human serum albumin in a patient with “idiopathic hypoalbuminemia” and hypoglobulinemia. In 1957, Schwartz and Thomsen (13), using albumin labeled with I131, showed that this condition is marked by a two- or threefold increase in the turnover of albumin. The observation that the urinary excretion of I131 was correspondingly increased indicated that the protein was not only lost but broken down. This result was similar to that found in nephrosis, with the difference that, in idiopathic hypoproteinemia, the protein lost does not appear in the urine. Because of the increased protein breakdown, Schwartz and Thomsen designated this condition hypercatabolic hypoproteinemia. Although these studies showed that the hypoproteinemia must be due to excessive internal loss of protein with normal protein synthesis, they gave no clue as to the site of this loss. Recently, Citrin and co-workers (2) investigated a case of hypertrophic gastritis (Ménétriers disease) with associated hypoproteinemia and edema and detected a notable loss of I131-labeled albumin into the stomach. Gullberg and Olhagen (6) have shown that very small amounts of albumin can be demonstrated normally in human gastric juice only if achlorhydria is present or if the gastric contents are buffered to prevent peptic digestion.

Hypoproteinemia antedating intestinal lesions, and possibly due to excessive serum protein loss into the intestine

1. 1. Six patients are reported with “idiopathic” hypoproteinemia and rapid loss of albumin and γ-globulin from the plasma. The appearance of hypoproteinemia antedated the development of intestinal lesions in three of these patients. 2. 2. Albumin and γ-globulin have been demonstrated in the intestinal juice of these patients and of normal persons. The possibility exists that the hypoproteinemia is a consequence of excessive loss of serum protein into the intestine. 3. 3. Experiences with treatment are presented. Two patients improved greatly after resection of diseased intestine. 4. 4. Although all the intestinal lesions appeared to be inflammatory, no specific pathological classification was possible.

Excessive loss of protein and nitrogen in peritoneal fluid during peritoneal irrigation of nephrectomized dogs

Excessive loss of protein and nitrogen in peritoneal fluid during peritoneal irrigation of nephrectomized dogs

EXPERIMENTAL RENAL INSUFFICIENCY PRODUCED BY PARTIAL NEPHRECTOMY

Hypoproteinemia may follow excessive loss or deprivation of protein. Experimental hypoproteinemia has been produced by plasmapheresis and with diets low in protein. In man, hypoproteinemia is encountered after continued loss of protein in urine or during periods of dietary restriction of protein. Many investigators believe that the hypoproteinemia is entirely due to this loss of protein. However, in a recent discussion of the problem, Bloomfield 1 suggested: Part at least of the difficulty which leads to the lowering of the blood-proteins is an impairment of the blood-regenerating mechanism; lack and loss undoubtedly contribute an added burden which on occasion may be insuperable, but lack and loss clearly fail to explain the whole problem. In the present investigation, control and partially nephrectomized rats fed diets containing varying amounts of dried extracted beef muscle were used in studying the relation between the plasma protein content and the amount of protein ingested and excreted.

HYPOPROTEINEMIA PROBABLY DUE TO DEFICIENT FORMATION OF PLASMA PROTEINS

Attention has been repeatedly called to the association of hypoproteinemia with edema. Recently, Peters and Van Slyke1summarized the existing information. Hypoproteinemia has been observed repeatedly as a result of excessive loss of protein, decreased consumption of nitrogenous foodstuffs, and increased protein wastage. We are presenting a case with low plasma proteins and with edema which does not appear to be due to any one of these three causes. A man, aged 51, Irish born, was admitted to the hospital because of edema of the genitalia and lower extremities. He had been treated for six months at the age of 4 years for dropsy, which disappeared during that period of observation. For many years there was a slight but constant edema of the feet and ankles. The abdomen had been large since early childhood. Ten years before entry, a brownish discoloration, which was followed by some induration, appeared over