Extranodal posttransplant plasmacytic hyperplasia with subsequent posttransplant plasmacytic malignancy: six-year interval case report and review of the literature

Posttransplant lymphoproliferative disorders (PTLDs) represent a morphologic, immunophenotypic, and genotypic spectrum of disease. Most recently, Knowles et al divided PTLDs into 3 distinct categories: (1) plasmacytic hyperplasia, (2) polymorphic B-cell hyperplasia and polymorphic B-cell lymphoma, and (3) immunoblastic lymphoma and multiple myeloma. Although one form of PTLD may progress to another form, only 1 previous case has been reported in which multiple myeloma developed 14 months after an original diagnosis of plasmacytic hyperplasia. The type of solid organ transplant was not specified in that case. We report a post--cardiac transplant plasmacytic hyperplasia developing 7 years posttransplant. Six years subsequent to the plasmacytic hyperplasia, the patient developed a posttransplant plasmacytic malignancy, supported by morphology, flow cytometric immunophenotyping, and genotypic studies. Since we have no data to support disseminated bony disease or an abnormal serum protein, we have not used the term "multiple myeloma" for this case.     

Lectins in the unicellular Tetrahymena. II. Impact of nutrition and sugar treatment on anti-lectin binding

Tetrahymena pyriformis GL cells showed partly intracytoplasmic, partly intramembraneous accumulation of lectin-like proteins in conditions of starvation, as demonstrated cytochemically by reaction with antibodies to pea, lens, bean, Datura, and snail lectin. The lectins binding to simple sugars tended to accumulate in the membrane, whereas those capable of interacting with hexosamines in the cytoplasm. While the fluorescence pattern of lectin localization was generally homogeneous in normally nourished cells, it assumed a variegated appearance in starved cells, owing to patching of the membrane, and spot-like accumulation of lectins in the cytoplasm, presumably within membranes of endocytosed vesicles. Snail lectin was an exception, since its distribution remained homogeneous also in conditions of starvation.     

Analysis of the genetic variability of the 1st (CCC/ACC,P52T) and the 10th exons (bp 1012–1704) of the TSH receptor gene in Graves’ disease

We determined the genetic variability of the 1st (CCC/ACC, P52T polymorphic variant) and 10th exons (bp 1012–1704) of the TSH receptor (TSHR) gene in Graves’ disease. A total of 101 Graves’ patients and 163 control subjects were screened. The A253 mutant allele was carried by nine patients with Graves’ disease (8.91%) and 13 control subjects (7.98%) in heterozygous genotype. No significant difference in the frequency of the mutant allele was found between Graves’ patients and control subjects. These results provide evidence that the A253 polymorphism has no genetic relevance in Graves’ disease. Moreover, the DNA nucleotide sequence of 693 bp of the 10th exon (bp 1012–1704) of the TSHR gene was determined in 15 Graves’ patients. Six patients were homozygous for the wild‐type allele and nine were heterozygous for the mutant allele at the 253rd nucleotide of the first exon. No polymorphism was found in the DNA sequences obtained from leukocytes of Graves’ patients, similarly to the sequences obtained from the nine control subjects. None of the nine patients carrying the A253 polymorphism in the 1st exon of the TSHR had polymorphism in the examined part of the 10th exon, including two additional patients whose thyroid tissue was directly analysed. In all likelihood, the polymorphisms of the examined regions of either the 1st or the 10th exon of the THSR gene do not contribute to the genetic susceptibility to Graves’ disease.     

Differentiation of Rhizomucor Species by Carbon Source Utilization and Isoenzyme Analysis

Nineteen Rhizomucor miehei and Rhizomucor pusillus isolates were assayed for their ability to utilize 87 various substrates as a single carbon source. Besides a difference in sucrose utilization, distinctive differences were found in the utilization of glycine, phenylalanine, and β-alanine. Five isoenzyme systems also proved useful for the determination of markers of distinctive value at a species level. Data were used to obtain information about the genetic polymorphism of these species: a high degree of variability was found among the R. pusillus isolates, whereas the group of R. miehei isolates was more homogeneous genetically.     

Prostanoid response in the kidney of hypertensive subjects as part of renal counteraction to gallopamil-induced blood pressure decrease

The purpose of the study was to characterize the renal TxA2, PGI2 and PGF2 alpha release in response to arterial blood pressure (BP) fall induced by systemic and intrarenal vasorelaxation in subjects with essential hypertension. Significantly enhanced TxB2- and PGF2 alpha excretion and no change in ratio TxB2/6-keto-PGF1 alpha were found in urine in hypertensive patients after administration of the Ca++ entry blocker gallopamil, used to induce BP fall. This response was associated with significant PRA elevation in peripheral venous samples. In in vitro experiments, direct and indirect effects of gallopamil on renal tissue could be distinguished. Gallopamil resulted in significant diminution of TxA2 production and a decrease in TxB2/6-keto PGF1 alpha ratio in incubated rat kidney slices. This model was also used to test biochemically the effect of reflex sympathetic activation on prostanoid generation in kidney. It was concluded that this mechanism was only one among the indirect mechanisms by which gallopamil could induce that renal prostanoid response in hypertensive subjects. The response in urinary TxB2- and PGF2 alpha excretion was found to be significantly related to the changes in sodium reabsorption. These results suggested, that the increase in renal TxA2 and PGF2 alpha production in response to systemic and intrarenal "vasodilation" induced by gallopamil in hypertensive subjects can be interpreted as part of counteraction of the kidneys to BP fall.     

High co-prevalence of genogroup 1 TT virus and human papillomavirus is associated with poor clinical outcome of laryngeal carcinoma

BACKGROUND: The aetiology and factors leading to the progression of laryngeal cancer are still unclear. Although human papillomavirus (HPV) has been suggested to play a role, reports concerning the effect of HPV infection on tumour development are controversial. Recently, transfusion transmitted virus (TTV) was suggested to play a role in certain infections as a causative or coinfecting agent. AIMS: To investigate whether the development and progression of laryngeal squamous cell carcinoma is associated with coinfection with TTV and HPV. METHODS: The prevalence of TTV and HPV was investigated using the polymerase chain reaction in tissue samples from 40 healthy individuals, 10 patients with recurrent papillomatosis, five patients with papillomatosis with malignant transformation, and 25 patients with laryngeal carcinoma. The obtained prevalence data were compared and analysed statistically. RESULTS: In the 11 patients with carcinoma who had metastasis or relapse there was a high rate of coinfection with genogroup 1 TTV and HPV (eight of 11), whereas in the 14 without tumour progression no coinfection was found. Coinfection was associated with significantly lower tumour free survival in patients with carcinoma (p < 0.001). Furthermore, four of five patients who had papillomatosis with malignant transformation were coinfected with genogroup 1 TTV and HPV. CONCLUSIONS: Although the nature of cooperation between HPV and TTV needs to be investigated further, coinfection with genogroup 1 TTV and HPV appears to be associated with poor clinical outcome in laryngeal cancer.     

Dexamethasone suppression and multiple hormonal responses (TSH,prolactin and growth hormone) to TRH in some psychiatric disorders

Summary Baseline and TRH-induced changes of thyroid stimulating hormone (TSH), prolactin (PRL), and growth hormone (GH) were measured in 15 healthy control subjects and 63 psychiatric inpatients with DSM-III diagnoses of major depression (n = 19), schizophrenic disorder (n = 20), alcohol dependence (n = 10), and adjustment disorder (n = 14); baseline and postdexamethasone cortisol (CS) were also determined 3–6 days after the TRH-challenge. All patients and controls were women of similar mean age, weight, height, and they were free from interfering illness or drugs.Baseline TSH and PRL were lower in depression, TRH-induced TSH and PRL responses were lower in the whole patient group, but most markedly in depression and alcohol dependence. Postdexamethasone CS was significantly higher in depression, schizophrenia and alcohol dependence. Basal GH did not differentiate the subgroups; TRH-induced pathological GH responses were sometimes found in the patient groups. The differences were most marked quantitatively in major depression: a multivariate analysis of variance showed that TSH, postdexamethasone CS and PRL were the most important variables in separating patients from controls. A discriminant function derived from these variables classified all controls and 18 of 19 depressed patients correctly; however, 25 of the 44 other patients were also classified with depression.It was confirmed that psychiatric patients show significantly more endocrine disturbances than controls, and this was seen not only in major depression but also in at least three other conditions. Further work is needed to identify other neuroendocrine patterns more specific to depressive disorder.     

H1-receptor blocker antihistamine, terfenadine durably influences the glucocorticoid receptor, and lymphocyte histamine content of weanling rats.

Hormonal imprinting takes place perinatally when a hormone and its maturing target receptor meet. As a consequence of imprinting the receptor accomplishes its maturation reaching the binding capacity characteristic to the adult age. In this critical period the presence of foreign molecules which are able to bind to the receptor can cause faulty imprinting with life-long consequences. In the recent years it was cleared that not only receptors are influenced by faulty imprinting, however, also the hormone production of the given cell. In addition imprinting was provoked at non-perinatal periods (adolescence and adult age) in cytogenic organs. In the present experiment the prolonged effect of a non-perinatal imprinting by an antihistamine to the histamine content of white blood cells and glucocorticoid receptors of liver and thymus was studied. Two weeks after 3-day terfenadine treatment at weaning, flow cytometry of peritoneal cells and blood lymphocytes for histamine, and receptor kinetic analysis of dexamethasone binding were done. Histamine content of blood lymphocytes and glucocorticoid receptor density of liver cells were significantly decreased. This means that a short treatment with a H(1)-receptor blocker antihistamine durably influences physiological indexes which were not known till now. This means that not only the acute effects, but the prolonged side-effects must be considered.