Anti-lymphoma effect of naproxen and indomethacin in a patient with relapsed diffuse large B-cell lymphoma

A 77-year-old man with relapsed non-Hodgkin's lymphoma, diffuse large B-cell type, was treated with naproxen, a nonsteroidal anti-inflammatory drug (NSAID), for paraneoplastic fever. A dramatic disappearance of not only the fever but also generalized lymphadenopathy was observed. Naproxen was continued, and he maintained remission for 10 months. When relapse of lymphoma occurred in spite of continuous naproxen administration, indomethacin, another type of NSAID, was tried. Surprisingly, rapid regression of lymphoma occurred again and was maintained for almost 1 year. These results indicate that NSAIDs are effective in some patients with non-Hodgkin's lymphoma.     

Serum insulin-like growth factor II in chronic liver disease

Insulin-like growth factor II is secreted primarily by the liver and is reported to be transcribed in many primary hepatocellular carcinoma (PHC) cell lines. We have studied diagnostic significance of serum IGF-II in chronic liver diseases using specific enzyme immunoassay. Serum IGF-II levels (mean +/- SE) were decreased in chronic hepatitis (538 +/- 51 ng/ml; N = 29), liver cirrhosis (427 +/- 45; 50) and PHC (260 +/- 41; 17) compared to controls (830 +/- 49; 57). Serum IGF-II was not different from controls in any of nonhepatic diseases such as diabetes (1032 +/- 97; 19) pancreatic cancer (1413 +/- 282; 8), chronic pancreatitis (999 +/- 126; 17), peptic ulcer (1186 +/- 43; 11), irritable bowel syndrome (1002 +/- 109; 12), gastrointestinal tract cancer (1250 +/- 216; 21) and chronic renal failure (733 +/- 135; 14). In liver diseases serum IGF-II showed a significant correlation with liver function test (negative with retention of indocyanine green and total bile acids; positive with albumin, thrombo-test, and cholinesterase). These results suggest that serum IGF-II reflects a reduced production of IGF-II in the liver and that it can be an index for the residual capacity of liver function.     

Enzyme immunoassay and characterization of pancreatic stone proteins in human urine

An enzyme immunoassay of pancreatic stone protein (PSP) in human urine was developed. Mean analytical recovery of pure PSP-S_2-5 added to urine was 102.3% (SD 5.9%), and the precision of the assay was 2.0-2.7% within an assay and 2.5-2.9% between assays. In healthy volunteers (age 20-55 years), the mean value of the PSP concentration, expressed as ratios to urine creatinine, was 129 ± 88 (mean ± SD) μg/g without any differences for sex. Urine PSP correlated with urine N-acetylglucosaminidase (NAG) (r = 0.354). The molecular forms of immunoreactive PSP in urine were characterized by using cation exchange chromatography (Mono S), SDS-PAGE, N-terminal sequence, and enzyme immunoassay analysis. The urine PSP, eluted at the position corresponding to PSP-S_2-5 on cation exchange chromatography, was converted to PSP-S₁ by trypsin digestion. The difference in mobility on SDSPAGE between urine PSP and PSP-S_2-5 seems to be due to a glycosylated undecapeptide (N-terminal 1-11). The proposed method offers a sensitive, specific, and reproducible tool for laboratory analysis of human urine PSP levels. © 1993 Wiley-Liss, Inc.     

Neurological Manifestations Associated with Cold Hemagglutinin Syndrome Report of Two Cases

Two cases of cold hemagglutinin syndrome associated with neurological manifestations were reported. One was a 52-year-old woman with acute hemolytic anemia which developed following grippe. Cold hemagglutinin titer was elevated to 1:1,024. Neurological manifestations were apathy, confusion, auditory hallucination and EEG abnormality. Steroid administration cleared these neurological abnormalities and EEG was reverted to normal. The other was a 77-year-old man with chronic hemolytic anemia. Cold hemagglutinin titer was extraordinarily elevated (1:32,768, 1:524,-288). Neurological abnormalities were almost confined to the cerebellar system. Hormonal therapy was completely unrewarding and the patient was incapacitated from his daily activity. From the literature some of the reported cases of hemolytic anemia associated with neurological abnormalities, particularly in reference to cold hemagglutinin syndrome, were briefly described. The present authors consider 2 reported cases fall in the category of “Syndromes neuro-hémolytiques” by French school.     

Effect of recombinant GM-CSF and recombinant G-CSF on colony formation of blast progenitors in acute myeloblastic leukemia

The colony-promoting activities of recombinant granulocyte-macrophage colony-stimulating factor (rGM-CSF) and recombinant granulocyte colony-stimulating factor (rG-CSF) on primary and secondary colony formation by blast progenitors (leukemic colony-forming units [L-CFU]) from 21 patients with acute myeloblastic leukemia (AML) were examined using blast colony assay and compared to colony promotion stimulated by phytohemagglutinin-stimulated leukocyte-conditioned medium (PHA-LCM). Recombinant GM-CSF stimulated blast colonies in 13 out of 20 cases examined (1 case not done). The magnitude of stimulation by rGM-CSF varied significantly according to the type of AML, but in general was lower than that of PHA-LCM. Blast cells of type M1 did not form any colonies with rGM-CSF, although numerous colonies were produced with PHA-LCM. Type M4 blasts formed fairly large numbers of colonies, though slightly less than those stimulated by PHA-LCM. Blasts of type M2 and M5 formed colonies with the stimulation of rGM-CSF, but the numbers were considerably smaller than type M4 and those stimulated with PHA-LCM. Recombinant G-CSF stimulated blast colonies in only 5 out of 21 cases, 3 of them being type M2. The number of cases responding to rG-CSF was significantly smaller than that responding to rGM-CSF, and even in cases in which colonies were formed, the magnitude of stimulation was minimal. From these results it seems likely that blast cells of different types of AML require a different kind of CSF for their optimal growth; type M4 blasts responded to the stimulation of rGM-CSF well, but blasts of other types of AML responded poorly. Thus, except for type M4, CSF(s) other than rGM-CSF seems to be required for the sufficient growth of L-CFU. Recombinant G-CSF is not likely to play an essential role in the proliferation of leukemic blasts of most types. Previous exposure to rGM-CSF and rG-CSF did not alter the self-renewal capacity, cellular phenotype, and morphology of colony cells, indicating that the direction and degree of differentiation of L-CFU stimulated by rGM-CSF or rG-CSF were not different from those stimulated with PHA-LCM.     

Intraperitoneal Rupture of the Ureter as a Cause of Generalized Peritonitis: Report of a Case

We report a rare case of generalized peritonitis caused by nontraumatic, intraperitoneal rupture of the ureter. An 80-year-old woman with a history of bilateral vesicoureteral reflux and long-term urethral indwelling catheter drainage presented with a very distended abdomen. Computed tomography showed massive ascites and intraperitoneal free gas. We performed an emergency laparotomy, assuming a gastrointestinal perforation; but could not find a cause of generalized peritonitis. Postoperatively, she presented with anuria and massive peritoneal drainage. The findings of a cystogram confirmed intraperitoneal ureteral rupture. She was managed successfully with ureteral stenting. The diagnosis of this condition requires a high degree of clinical suspicion, along with radiographic evidence and peritoneal fluid analysis. Image-guided interventions play a crucial role in the management of ureteral urine leaks after a correct diagnosis has been made.