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Journal articles on the topic 'Dyscrasite'

Author: Grafiati

Published: 6 September 2023

Last updated: 7 September 2023

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1

Osadchii, E., D. Boström, S. Lunin, and E. Rosén. "Thermodynamic properties of dyscrasite (Ag 3 Sb) at isostatic pressures 4000-8000 bar." Physics and Chemistry of Minerals 25, no. 4 (March 19, 1998): 288–91. http://dx.doi.org/10.1007/s002690050116.

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2

Kalinin, Arkadii A., Yevgeny E. Savchenko, and Ekaterina A. Selivanova. "Mustard Gold in the Oleninskoe Gold Deposit, Kolmozero–Voronya Greenstone Belt, Kola Peninsula, Russia." Minerals 9, no. 12 (December 13, 2019): 786. http://dx.doi.org/10.3390/min9120786.

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The Oleninskoe intrusion-related gold–silver deposit is the first deposit in the Precambrian of the Fennoscandian Shield, where mustard gold has been identified. The mustard gold replaces küstelite with impurities of Sb and, probably, gold-bearing dyscrasite and aurostibite. The mosaic structure of the mustard gold grains is due to different orientations and sizes of pores in the matrix of noble metals. Zonation in the mustard gold grains is connected with mobilization and partial removal of silver from küstelite, corresponding enrichment of the residual matter in gold, and also with the change in the composition of the substance filling the pores. Micropores in the mustard gold are filled with iron, antimony or thallium oxides, silver chlorides, bromides, and sulfides. The formation of mustard gold with chlorides and bromides shows that halogens played an important role in the remobilization of noble metals at the stage of hypergene transformation of the Oleninskoe deposit.

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3

Zachariáš, Jiří, and Matěj Němec. "Gold to aurostibite transformation and formation of Au-Ag-Sb phases: the Krásná Hora deposit, Czech Republic." Mineralogical Magazine 81, no. 4 (August 2017): 987–99. http://dx.doi.org/10.1180/minmag.2016.080.145.

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AbstractRare phases of the Au–Ag–Sb system were recognized in the Krásná Hora Sb-Au deposit (Sb 1.5–3 wt.%; Au 3–5 ppm), Czech Republic which correspond to auriferous dyscrasite (up to 7 at.% Au), auriferous allargentum (up to 34 at.% Au), and an unnamed phase with composition similar to the eutectics (E1, E2) of the experimental Au–Ag–Sb system. The dominant ore mineral is stibnite with rare native antimony, native gold and a Ag-Au alloy. Textural relationships are well established: stibnite (early) →gold → aurostibite → native antimony (late). Gold is present in four generations: Au-1 (0–15 at.% Ag) is the most abundant type; Au-2 (20–70 at.% Ag) forms thin rims along intra-grain boundaries of Au-1; Au-3 and Au-4 are rare and almost pure (∼0 at.% Ag). The formationof most of the Au-2 and of Au-Ag-Sb phases is associated with Ag-mobilization coupled with the Au-1 to aurostibite transformation via dissolution-precipitation and solid-state diffusion processes at temperatures <200°C.

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4

Hartshorn, Edward A., Gary M. Levin, and C. Lindsay DeVane. "A Review of Cyclic Antidepressant-Induced Blood Dyscrasias." Annals of Pharmacotherapy 26, no. 3 (March 1992): 378–83. http://dx.doi.org/10.1177/106002809202600313.

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OBJECTIVE: To review the literature for cases of blood dyscrasias associated with cyclic antidepressants. Several types of blood dyscrasias are discussed. DATA SOURCES: All references were selected through the use of MEDLINE. Indexing terms were blood, abnormalities, dyscrasias, antidepressants, agranulocytosis, and eosinophilia. The only constraints were English language and human subjects. STUDY SELECTION: All cases were included except for letters to the editor of various journals when pertinent data such as doses and additional medications were omitted. DATA SYNTHESIS: The review provides a table listing the different blood dyscrasias and the drug the patient was receiving. The table also includes time of onset, time to recovery, and several symptoms for each patient. CONCLUSIONS: Common symptoms of various blood dyscrasias are discussed. The chemical structures of the antidepressants are related to phenothiazines, which are also implicated in causing blood dyscrasias. Recommendations for treatment of both the dyscrasia and depression are discussed.

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5

Latif, Zahid, Faraz Jabbar, and Brendan D. Kelly. "Clozapine and blood dyscrasia." Psychiatrist 35, no. 1 (January 2011): 27–29. http://dx.doi.org/10.1192/pb.bp.109.026054.

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SummaryClozapine is an effective antipsychotic medication but is associated with agranulocytosis, neutropenia and leucopenia. The reintroduction of clozapine improved management of treatment-resistant schizophrenia, yet resulted in a paradoxical situation whereby the risk of blood dyscrasias is rigorously managed but other adverse effects (e.g. seizures, cardiovascular complications) are less well monitored. Monitoring of weight, lipids, plasma glucose and other metabolic parameters is recommended. There is also a need to reconsider routine haematological monitoring with other medications associated with blood dyscrasia (e.g. phenothiazines, carbamazepine). In particular, individuals who develop clozapine-induced blood dyscrasia may require haematological monitoring during treatment with other antipsychotics.

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6

Sutherland, Rory A., and Richard I. Crawford. "Scalp biopsy identifies systemic amyloidosis presenting as isolated telogen effluvium: A case report." SAGE Open Medical Case Reports 7 (January 2019): 2050313X1984778. http://dx.doi.org/10.1177/2050313x19847783.

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AL amyloidosis is a complication of B-cell dyscrasias and multiple myeloma, manifest as deposition of antibody fragments in many different organs, including the skin. We describe a rare case of this systemic disease which presented with isolated scalp alopecia. Further investigation led to the diagnosis of an occult plasma-cell dyscrasia, showing the benefit of including systemic amyloidosis in the differential diagnosis of alopecia. The biopsy finding of cutaneous amyloidosis should prompt further workup to exclude an underlying pathology.

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Dunk, Louisa R., Linda J. Annan, and Christopher D. Andrews. "Rechallenge with clozapine following leucopenia or neutropenia during previous therapy." British Journal of Psychiatry 188, no. 3 (March 2006): 255–63. http://dx.doi.org/10.1192/bjp.188.3.255.

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BackgroundFurther treatment with clozapine is contraindicated in any patient who has previously experienced leucopenia or neutropenia during clozapine therapy.AimsTo investigate the results of such a rechallenge in 53 patients.MethodAn analysis was made of the demographic, haematological and outcome data of patients in the UK and Ireland who were rechallenged with clozapine following leucopenia or neutropenia during previous clozapine therapy.ResultsOf 53 patients who were rechallenged, 20 (38%) experienced a further blood dyscrasia. In 17 of these 20 patients (85%) the second blood dyscrasia was more severe(P<0.001), in 12(60%) it lasted longer (P=0.0368) and in 17 (85%) it occurred more quickly on rechallenge (P<0.001). Of the original 53 patients, 55% (29 patients) are still receiving clozapine.ConclusionsNo clear risk factor for repeat blood dyscrasias was identified. Despite this, after risks and benefits have been considered, rechallenge may well be justified in some patients.

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8

Harris, Donald C., Andrew C. Roberts, J. H. Gilles Laflamme, and Chris J. Stanley. "Criddleite, TlAg2Au3Sb10S10, a New Gold-Bearing Mineral from Hemlo, Ontario, Canada." Mineralogical Magazine 52, no. 368 (December 1988): 691–97. http://dx.doi.org/10.1180/minmag.1988.052.368.13.

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AbstractCriddleite, ideally TlAg2Au3Sb10S10, is a rare constituent within the Hemlo gold deposit, Hemlo, Ontario, Canada. The mineral occurs as 20 to 50 µm-sized lath-like, tabular or anhedral grains usually surrounding or penetrating aurostibite, or associated with native antimony, native gold and stibnite. Criddleite is opaque with a metallic lustre and a black streak. It has been synthesized by reacting TlSbS2 and high purity Ag, Au, Sb and S in an evacuated silica glass tube at 400 °C. The measured density of the synthetic material is 6.86; the calculated density is 6.57 g/cm3. The difference is due to minor admixed aurostibite, native antimony and a dyscrasite-like phase within the charge. VHN25 is 94–129. Mohs hardness (calc.) = 3–3 ½. In reflected plane-polarized light in air, natural criddleite is weakly bireflectant with a discernible reflectance pleochroism from grey-blue to slightly greenish grey-blue. The mineral has a distinct to moderate anisotropy with rotation tints in shades of buff to slate grey. Reflectance spectra and colour values for both natural and synthetic criddleite are given. X-ray study showed that synthetic criddleite is monoclinic (pseudotetragonal) with refined unit-cell parameters a = 20.015(2), b = 8.075(2), c = 7.831(2) Å, β = 92.01(2)°, V = 1264.9 ± 1.0 Å3 and a:b:c = 2.4786: 1:0.9698. The space group choices are A2/m(12), A2(5) or Am(8), diffraction aspect A*/*. The seven strongest lines in the X-ray powder diffraction pattern [d in Å (I) (hkl)] are: 5.63(90) (011), 3.91(50) (002), 3.456(50) (320), 2.860(70) (700), 2.813(100) (022), 2.018(60) (040) and 1.959(70) (004). Electron microprobe analyses are reported of natural criddleite in five polished sections of drill core from four holes. The averaged empirical formulae, based on 26 atoms, are Tl0.92Ag1.99Au2.93Sb9.87S10.28 (natural) and Tl0.94Ag2.03Au2.89Sb9.76S10.38 (synthetic).

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9

Munshi, Tariq, Farooq Naeem, Mohammed Ayub, Saeed Farooq, Davit Khachatryan, Selim Asmer, Peter Wang, et al. "The haematological side effects of clozapine: literature review and meta-analysis." BJPsych Open 7, S1 (June 2021): S274. http://dx.doi.org/10.1192/bjo.2021.729.

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AimsThis review and meta-analysis aim to estimate the cumulative incidence of clozapine induced agranulocytosis and leukopenia the impact of the associated factors such as dose of clozapine, duration of follow-up, gender and race on the cumulative incidence.BackgroundClozapine is the only medication licensed for treatment-resistant schizophrenia. There has been a renewed interest in the role of Clozapine in the treatment of Schizophrenia based on strong evidence that favours its efficacy and safety. Despite the evidence that Clozapine has superior efficacy and has been recommended for treatment-resistant cases by the national guidelines, the drug is underutilised.MethodWe included all studies in which clozapine was used for a psychotic illness. We included studies which provided data on two primary indices; Leucopenia or agranulocytosis and neutropenia; defined according to the cut off used by CPMS for total WBC and neutrophil count. Additionally we included studies reporting another blood dyscrasia or death due to agranulocytosis. Studies were identified by searching AMED, BIOSIS, CINAHL, EMBASE, MEDLINE, PsycINFO, PubMed, and registries of Clinical Trials and their monthly updates, hand searches, gray literature, and conference proceedings from the first available date until 2nd February, 2015. The search was updated on 15th March, 2017. The Protocol was initiated and then registered with PROSPERO International prospective register of systematic reviews University of York, Centre for Reviews and Dissemination.ResultThe cumulative incidence of the agranulocytosis in all studies was 00.32 % (CI 00.1-0.63). The cumulative incidence in all studies for different types of blood dyscrasia were following: leucopenia 00.96 % (CI 0.39-1.70), neutropenia 2.93 % (CI 1.49-4.72), other blood dyscrasias 4.64% (CI 2.34-7.52) and any blood dyscrasia was 2.23 (CI 1.46-3.12).ConclusionThe limitations of this review are mainly due to the nature of evidence from the included studies. We adopted a broad inclusion criteria to include all the available evidence. Number of patients started on Clozapine may be withdrawn from the Clozapine on the earliest signs of blood dyscrasias since the introduction of Clozapine monitoring services. This means that the true incidence of agranulocytosis and neutropenia may be higher and this may be a major bias in finding the true incidence of Clozapine induced neutropenia.

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10

Michaeli, J., R. Niesvizky, D. Siegel, M. Ladanyi, PH Lieberman, and DA Filippa. "Proteinaceous (angiocentric sclerosing) lymphadenopathy: a polyclonal systemic, nonamyloid deposition disorder." Blood 86, no. 3 (August 1, 1995): 1159–62. http://dx.doi.org/10.1182/blood.v86.3.1159.1159.

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Abstract Proteinaceous lymphadenopathy with hypergammaglobulinemia (PLWH) is an exceedingly rare disease of unknown etiology. Described primarily as a pathologic entity, relatively little is known about its clinical manifestations or its response to therapy. The disease is often referred to and treated as an unusual form of plasma cell dyscrasia or light chain deposition disease. We have recently encountered a young patient with PLWH who presented with generalized lymphadenopathy, marked liver function abnormalities, hypocomplementemia, cryoglobulinemia, decreased T4/T8 ratio, and ophthalmopathy. Contrary to the notion that PLWH is a clonal disorder, we found no evidence of clonality in this patient. The most characteristic finding in this and in another patient, previously seen at our institution, was marked angiocentric hyaline sclerosis of the small and mid-sized blood vessels of involved lymph nodes and organs. Based on these findings, we propose the term angiocentric sclerosing lymphadenopathy, which more accurately defines this clinicopathologic entity that appears to be distinct from light chain deposition disease and other plasma cell dyscrasias.

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11

Michaeli, J., R. Niesvizky, D. Siegel, M. Ladanyi, PH Lieberman, and DA Filippa. "Proteinaceous (angiocentric sclerosing) lymphadenopathy: a polyclonal systemic, nonamyloid deposition disorder." Blood 86, no. 3 (August 1, 1995): 1159–62. http://dx.doi.org/10.1182/blood.v86.3.1159.bloodjournal8631159.

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Proteinaceous lymphadenopathy with hypergammaglobulinemia (PLWH) is an exceedingly rare disease of unknown etiology. Described primarily as a pathologic entity, relatively little is known about its clinical manifestations or its response to therapy. The disease is often referred to and treated as an unusual form of plasma cell dyscrasia or light chain deposition disease. We have recently encountered a young patient with PLWH who presented with generalized lymphadenopathy, marked liver function abnormalities, hypocomplementemia, cryoglobulinemia, decreased T4/T8 ratio, and ophthalmopathy. Contrary to the notion that PLWH is a clonal disorder, we found no evidence of clonality in this patient. The most characteristic finding in this and in another patient, previously seen at our institution, was marked angiocentric hyaline sclerosis of the small and mid-sized blood vessels of involved lymph nodes and organs. Based on these findings, we propose the term angiocentric sclerosing lymphadenopathy, which more accurately defines this clinicopathologic entity that appears to be distinct from light chain deposition disease and other plasma cell dyscrasias.

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12

Kapur, Umesh, Kevin Barton, Raoul Fresco, David J. Leehy, and Maria M. Picken. "Expanding the Pathologic Spectrum of Immunoglobulin Light Chain Proximal Tubulopathy." Archives of Pathology & Laboratory Medicine 131, no. 9 (September 1, 2007): 1368–72. http://dx.doi.org/10.5858/2007-131-1368-etpsoi.

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Abstract Context.—In plasma cell dyscrasias, involvement of the distal tubules is frequent and well characterized. In contrast, proximal tubules have only rarely been reported to show diagnostic pathology such as intracytoplasmic crystals. Objective.—To look for additional morphologic features that might be helpful in the diagnosis of proximal tubulopathy associated with an underlying plasma cell dyscrasia. Design.—We examined patients presenting with nonspecific renal symptoms who were found to have light chain restriction limited to proximal tubular epithelium by immunofluorescence. We correlated these results with light microscopy, electron microscopy, and the clinical findings. Results.—By immunofluorescence, 5 patients had light chain restriction in proximal tubular epithelium. By light microscopy, only 1 patient had focal rhomboid crystals in the proximal tubular epithelium; all other biopsies failed to show any discernible pathology within the proximal tubules or elsewhere in the kidney. By electron microscopy, proximal tubules from 2 patients showed crystals with a latticelike structure, whereas the remaining 3 patients had only prominent phagolysosomes. However, by immunoelectron microscopy, the lysosomal content showed light chain restriction (in 2 cases studied). Post–kidney biopsy, all patients were diagnosed with multiple myeloma or plasma cell dyscrasia. One patient developed renal failure and had recurrence of crystals in the allograft. Conclusions.—Light chain proximal tubulopathy may be associated with the presence of crystals or with the presence of phagolysosomes with light chain restriction as the sole abnormality. Both κ and λ light chains may be involved. The prognosis is variable and the pathology may recur in transplants.

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Woitge, Henning W., Eva Horn, Andrea V. Keck, Beatrice Auler, Markus J. Seibel, and Martin Pecherstorfer. "Biochemical Markers of Bone Formation in Patients with Plasma Cell Dyscrasias and Benign Osteoporosis." Clinical Chemistry 47, no. 4 (April 1, 2001): 686–93. http://dx.doi.org/10.1093/clinchem/47.4.686.

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Abstract Background: Myeloma-induced bone loss is related to an uncoupling of bone formation and bone resorption. The aim of the present study was to assess the potential clinical value of biochemical markers of bone formation in the work up of patients with plasma cell dyscrasias. Methods: Serum total alkaline phosphatase, bone-specific alkaline phosphatase (BAP), and osteocalcin (OC) were measured in 43 patients with newly diagnosed multiple myeloma (MM), in 40 patients with monoclonal gammopathy of undetermined significance (MGUS), in 40 patients with untreated benign vertebral osteoporosis (OPO), and in 48 healthy adults. Results: In MM and MGUS patients, serum BAP, but not serum OC, was lower than in healthy controls (P <0.05). Serum OC was higher in patients with OPO than in healthy controls (P <0.05). The strongest associations between markers were found in OPO patients and in healthy adults. MM patients with early-stage disease or without detectable osteolysis had decreased serum BAP values (P <0.05). Serum OC was higher in MM patients with stage III disease (P <0.05) than in healthy controls. MM patients with OPO-like bone involvement had lower BAP values than sex- and age-matched MGUS patients with OPO-like bone involvement and patients with benign OPO (P <0.05). Conclusions: In patients with plasma cell dyscrasias, serum BAP, rather than serum OC, appears to reflect a suppressed bone formation rate and may be helpful in the differentiation between benign and myeloma-induced OPO. However, the overall clinical use of biochemical markers of bone formation in patients with plasma cell dyscrasia appears limited.

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Bianchi, Giada, Maria Moscvin, and Raymond L. Comenzo. "Laboratory-Based Rationale for Targeting the Protein Homeostasis Network in AL Amyloidosis." Hemato 3, no. 2 (April 25, 2022): 298–317. http://dx.doi.org/10.3390/hemato3020022.

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AL amyloidosis is an incurable plasma cell dyscrasia with limited therapeutic options. The pathogenetic mechanism in AL amyloidosis is the deposition of insoluble fibrillary aggregates of misfolded immunoglobulin (Ig) free light chains (FLC) and chaperone proteins in target organs. Therefore, AL amyloidosis is the prototypic, protein-toxicity hematologic disorder. Based on laboratory evidence of increased, constitutive proteotoxic stress, PCs are intrinsically vulnerable to agents that target proteins whose function is to guarantee that nascent polypeptides either reach a functional conformation or are disposed of (proteostasis network). The clinical efficacy of proteasome inhibitors (PIs), such as bortezomib, in the treatment of plasma cell (PC) disorders has provided proof of concept that disrupting protein homeostasis is an effective and generally safe therapeutic approach. Therefore, the intrinsic biology of PC offers us the opportunity to rationally develop therapies that target this distinct proteostasis vulnerability of PC dyscrasias. In this manuscript, we will review the laboratory rationale for the effectiveness of FDA-approved and investigational agents targeting protein homeostasis in AL amyloidosis and related PC disorders.

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Bianchi, Giada, Maria Moscvin, and Raymond L. Comenzo. "Laboratory-Based Rationale for Targeting the Protein Homeostasis Network in AL Amyloidosis." Hemato 3, no. 2 (April 25, 2022): 298–317. http://dx.doi.org/10.3390/hemato3020022.

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AL amyloidosis is an incurable plasma cell dyscrasia with limited therapeutic options. The pathogenetic mechanism in AL amyloidosis is the deposition of insoluble fibrillary aggregates of misfolded immunoglobulin (Ig) free light chains (FLC) and chaperone proteins in target organs. Therefore, AL amyloidosis is the prototypic, protein-toxicity hematologic disorder. Based on laboratory evidence of increased, constitutive proteotoxic stress, PCs are intrinsically vulnerable to agents that target proteins whose function is to guarantee that nascent polypeptides either reach a functional conformation or are disposed of (proteostasis network). The clinical efficacy of proteasome inhibitors (PIs), such as bortezomib, in the treatment of plasma cell (PC) disorders has provided proof of concept that disrupting protein homeostasis is an effective and generally safe therapeutic approach. Therefore, the intrinsic biology of PC offers us the opportunity to rationally develop therapies that target this distinct proteostasis vulnerability of PC dyscrasias. In this manuscript, we will review the laboratory rationale for the effectiveness of FDA-approved and investigational agents targeting protein homeostasis in AL amyloidosis and related PC disorders.

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16

Patel, Jaymin M., Ankit V. Vahia, Puru Nanjappa, Ashun Bajwa, Sima Shah, Tai Yu-Tzu, Kenneth C. Anderson, Masood Shammas, and Nikhil C. Munshi. "Elevated Nuclease Activity Correlates With Clinical Spectrum Of Plasma Cell Dyscrasias." Blood 122, no. 21 (November 15, 2013): 4885. http://dx.doi.org/10.1182/blood.v122.21.4885.4885.

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Abstract Over the last decade, there has been increasing interest in mechanisms that underlie genomic instability which is implicated in tumor progression, development of drug resistance and possibly even oncogenesis. We have observed that dysregulated homologous recombination (HR) is an important contributor to genomic instability. In this study, we aim to broaden our understanding of HR by exploring alternate pathways that may affect genomic instability such as nuclease activity. Methods We have developed an assay to measure total cellular nuclease activity and compare activity levels across a spectrum of plasma cell dyscrasias. Total nuclease activity in cell lines and patient samples was assessed using a novel plasmid degradation assay. Briefly, multiple myeloma (MM) cell lines and primary MM patient cells were lysed at equal cell concentration. The lysates were mixed with plasmid DNA in triplicate/quadruplicate and incubated at 37°C for fixed time points ranging from 0 to 30 minutes. Following forced cessation of enzymatic activity, samples were fractionated on agarose gel and resultant image analyzed for band intensity by Kodak 1D Image analysis software. The ratio of degraded plasmid over time was analyzed via nonlinear regression to calculate a half-life and k-constant. Results Non-linear regression analysis of data derived from assays involving 6 MM cell lines (RPMI, OPM1, H292, U266, INA6 & MM1S) with three pellets each of equal size taken from non-confluent cell culture with > 85% viability showed statistically significant reproducibility of best fit curve with an average R-squared of 0.93. Similar regression analysis could not be performed on data derived from normal PBMC pellets because they showed minimal degradation with linear regression slope of (-0.62). Lastly, non-linear regression analysis on 22 patient samples with a plasma cell dyscrasia diagnosis, revealed a broader range of activity by half-life. Further differentiation of plasma cell dyscrasia patients into 2 groups revealed a significantly higher half-life in MGUS & smouldering (9499.8 minutes) versus newly diagnosed and refractory or relapsed multiple myeloma patients (9.4,19.3 minutes respectively). Conclusions In conclusion, we show that nuclease activity, implicated in elevated recombination and genomic instability, can be measured in a statistically reproducible fashion by our in vitro assay and may be used to differentiate plasma cell dyscrasias across a clinical spectrum. Further analysis of nuclease activity in clinically annotated samples for correlation with clinical features, genomic data and survival outcomes is ongoing. Disclosures: Anderson: celgene: Consultancy; onyx: Consultancy; gilead: Consultancy; sanofi aventis: Consultancy; oncopep: Equity Ownership; acetylon: Equity Ownership.

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Viny, Aaron D., Alan Lichtin, Brad Pohlman, Zachary Nearman, Thomas Loughran, and Jaroslaw P. Maciejewski. "Chronic B-Cell Dyscrasias Are an Important Clinical Feature of LGL Leukemia." Blood 110, no. 11 (November 16, 2007): 4675. http://dx.doi.org/10.1182/blood.v110.11.4675.4675.

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Abstract T-cell large granular lymphocyte leukemia (T-LGL) is a chronic clonal lymphoproliferation of CTL. The context of immune-mediated diseases led to the hypothesis that T-LGL represents an exaggerated clonal immune response to a persistent antigen such as an autoantigen or viral antigen or be associated with an immune surveillance reaction to occult malignancies. Based on the structural similarity of TCR CDR3 we have demonstrated that the transformation event in T-LGL may not be random and is driven by a related antigen. Similar to the clonal evolution in LGL, B cell expansion in low grade non-Hogkin lymphoma may also not be entirely stochastic. There have been coincidental case reports of T-LGL patients with concomitant B cell dyscrasia. It is therefore possible that similar pathogenic triggers may be operative in chronic proliferation of T and B cells, which subsequently predispose to clonal outgrowth. Consequently, we systematically examined a large series of T-LGL patients for evidence of B cell dyscrasias. When our patients (N=70) were studied we found a frequent association of low grade B cell lymphoproliferative disorders (28%). In general, all clinical comparisons with reported studies suggested that our LGL cohort had a composition equivalent to that of prior series and findings with regard to B cell dyscrasias are not due to selection bias. By comparison, a total of 51 patients with concomitant B and T cell dyscrasia were previously reported in small series or case reports. In our series, MGUS was the most common of the B cell disorders identified in T-LGL (21%), B-CLL also was present in 7%. Of note, 8 patients received rituximab and notably, evolution of clonal T cell expansion after therapy with rituximab has been identified in isolated case reports. In addition to clonal B cell expansion, polyclonal hyperglobulinemia was found in 26% of T-LGL, similar to previous report. Hypoglobulinemia was identified in 12% of patients. Evidence of involvement of both the T and B cell compartments in T-LGL fits into several models of disease pathogenesis. T-LGL may represent anti-tumor surveillance reflecting an exaggerated clonal expansion in the context of polyclonal anti-tumor response. An alternative theory is that both conditions may result from an initial polyclonal immune reaction directed against an unrelated common target; one could speculate that autoimmune/viral diseases associated with T-LGL or malignancies (e.g., MDS) provide antigenic triggers. It is also conceivable that impaired humoral immune response could result in an exuberant T cell reaction against an uncleared antigen. If B cell function is insufficient to fully clear the inciting pathogen, then chronic antigenic stimulation could polarize T cell-mediated response, resulting in LGL expansion. Finally, identification of decreased immunoglobulin levels in the context of LGL leukemia may also give merit to the theory that both B and T cell compartments are governed by regulatory/compensatory feedback mechanisms and T-LGL could evolve from unchecked T cell expansion in the context of B cell dysfunction. In sum, we describe here a high frequency of B cell dyscrasias in patients with T-LGL. The association is unlikely to be coincidental and provide important insight into dysregulated expression of T cell and B cell function.

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VATANSEVER, S., N. USTA SAGLAM, and E. BESTEPE. "LAMOTRIGINE INDUCED LEUCOPENIA IN A PATIENT WITH TYPE 2 BIPOLAR DISEASE." European Psychiatry 66, S1 (March 2023): S711. http://dx.doi.org/10.1192/j.eurpsy.2023.1488.

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IntroductionLamotrigine(LTG) is a widely used medication for bipolar disorder(BD) maintenance treatment, bipolar depression, epilepsy, trigeminal neuralgia.1The well-known common side effects of LTG are rash,fatigue, gastrointestinal symptoms,dizziness,headache,insomnia.2While one of the most refrained side effects of LTG is Steven Johnson’s syndrome, there have been reports of blood dyscrasia,such as agranulocytosis, neutropenia, pancytopenia.3,4Unfortunately, the exact mechanism of the blood dyscrasias isn’t fully explained.Here we report a case of LTG-induced leucopenia in a patient with BD type 2 patient.We obtained the patient’s consent.ObjectivesWe report a case of a 56-year-old female patient, brought to the emergency unit with complaints of feeling unhappy, hopeless,having trouble sleeping and suicidal thoughts for two months.She attempted suicide a few days ago,had multiple suicide attempts in the last two years.She had 3 psychiatric hospitalizations due to depressive episodes and 1 hypomanic episode.Her mood was depressed.She had psychomotor retardation,no psychotic feature.Due to active suicidal ideation,we admitted her to the inpatient unit with the diagnosis of BD type 2.Routine blood tests were within the normal range.We increased quetiapine XR 300 mg and venlafaxine 300 mg,which she had already taken;discontinued her aripiprazole treatment and added LTG 25 mg/d. 8 after initiation of LTG,there was a decrease in white blood coun(WBC) from a baseline level of 5.18x109/L to 3x109/L,while neutrophil count decreased from 3.8x109/L to 1.15x109/L in 12 days.Her medical records showed no sign of leucopenia.No pathology was detected in the peripheral smear or ultrasonography performed with the haematology consultation.Considering leucopenia might be an adverse drug reaction associated with LTG, we discontinued LTG treatment on the 9th day of administration. 9 days after discontinuation WBC was up to 4.22x109/L,neutrophil count was 2.78x109/L. We started valproate 500 mg/d and on the 27th day of her stay, she was discharged with a euthymic mood, having no depressive symptoms or suicidal thoughts.Her last treatment was venlafaxine 225 mg, quetiapine XR 300 mg, quetiapine IR 100 mg, valproate 500 mg, lorazepam 1 mg daily.MethodsIt is a retrospective review.ResultsIn this LTG naive patient,the WBC values were within the normal range at admission.There was a significant temporal relationship between the initiation of the LTG and the decrease in WBC values.The absence of other factors in the laboratory tests and examinations,the rapid increase of WBC levels after the LTG was discontinued suggests the observed effect may be a side effect of LTG.ConclusionsBlood dyscrasies aren’t a very common side effect of LTG, but it might be helpful to see CBC, especially in older populations, on patients with polypharmacy regimens and with severe mental illness that may interfere with patient’s ability to express any subtle side effect.Disclosure of InterestNone Declared

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19

Diljith, Hitha, Ambika Lokababu Pagadalu, Sreerekha Jinkala, Rakhee Kar, Sajini Elizabeth Jacob, and Debdatta Basu. "Acquired Coagulopathies Secondary to Plasma Cell Dyscrasias." Annals of Pathology and Laboratory Medicine 6, no. 6 (June 24, 2019): C67–71. http://dx.doi.org/10.21276/apalm.2398.

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Buss, David H., Robert W. Prichard, and M. Robert Cooper. "Plasma Cell Dyscrasias." Hematology/Oncology Clinics of North America 2, no. 4 (December 1988): 603–15. http://dx.doi.org/10.1016/s0889-8588(18)30587-2.

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21

Barlogie, Bart. "Plasma Cell Dyscrasias." JAMA: The Journal of the American Medical Association 268, no. 20 (November 25, 1992): 2946. http://dx.doi.org/10.1001/jama.1992.03490200198025.

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22

Barlogie, B. "Plasma cell dyscrasias." JAMA: The Journal of the American Medical Association 268, no. 20 (November 25, 1992): 2946–51. http://dx.doi.org/10.1001/jama.268.20.2946.

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23

Boselli, Bruce D. "Drug Induced Dyscrasias." Guthrie Journal 56, no. 3 (January 1987): 115–24. http://dx.doi.org/10.3138/guthrie.56.3.115.

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24

Yang, Daniel S., Edward E. Dickerson, Ling X. Zhang, Holly Richendrfer, Padmini N. Karamchedu, Gary J. Badger, Tannin A. Schmidt, Alger M. Fredericks, Khaled A. Elsaid, and Gregory D. Jay. "Quadruped Gait and Regulation of Apoptotic Factors in Tibiofemoral Joints following Intra-Articular rhPRG4 Injection in Prg4 Null Mice." International Journal of Molecular Sciences 23, no. 8 (April 12, 2022): 4245. http://dx.doi.org/10.3390/ijms23084245.

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Camptodactyly-arthropathy-coxa vara-pericarditis (CACP) syndrome leads to diarthrodial joint arthropathy and is caused by the absence of lubricin (proteoglycan 4—PRG4), a surface-active mucinous glycoprotein responsible for lubricating articular cartilage. In this study, mice lacking the orthologous gene Prg4 served as a model that recapitulates the destructive arthrosis that involves biofouling of cartilage by serum proteins in lieu of Prg4. This study hypothesized that Prg4-deficient mice would demonstrate a quadruped gait change and decreased markers of mitochondrial dyscrasia, following intra-articular injection of both hindlimbs with recombinant human PRG4 (rhPRG4). Prg4−/− (N = 44) mice of both sexes were injected with rhPRG4 and gait alterations were studied at post-injection day 3 and 6, before joints were harvested for immunohistochemistry for caspase-3 activation. Increased stance and propulsion was shown at 3 days post-injection in male mice. There were significantly fewer caspase-3-positive chondrocytes in tibiofemoral cartilage from rhPRG4-injected mice. The mitochondrial gene Mt-tn, and myosin heavy (Myh7) and light chains (Myl2 and Myl3), known to play a cytoskeletal stabilizing role, were significantly upregulated in both sexes (RNA-Seq) following IA rhPRG4. Chondrocyte mitochondrial dyscrasias attributable to the arthrosis in CACP may be mitigated by IA rhPRG4. In a supporting in vitro crystal microbalance experiment, molecular fouling by albumin did not block the surface activity of rhPRG4.

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25

Cates, Marshall, and Richard Powers. "Concomitant Rash and Blood Dyscrasias in Geriatric Psychiatry Patients Treated with Carbamazepine." Annals of Pharmacotherapy 32, no. 9 (September 1998): 884–87. http://dx.doi.org/10.1345/aph.17445.

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BACKGROUND: Rashes and blood dyscrasias are disconcerting adverse effects associated with carbamazepine therapy. Rashes are quite common, as are mild blood dyscrasias, such as mild leukopenias. Fortunately, severe rashes and blood dyscrasias are rare. There are few reports on the relationship between carbamazepine-induced rashes and blood dyscrasias, including a prospective study in which rash appeared concomitantly with leukopenia and/or thrombocytopenia in 10 patients, two case reports in which simultaneous rash and agranulocytosis occurred, and two case reports in which rashes served as harbingers of fatal aplastic anemia. CASE REPORTS: We report two cases of concomitant rashes and blood dyscrasias in geriatric psychiatry patients receiving carbamazepine therapy for bipolar disorder. One patient was found to have a severe leukopenia within several days after rash onset. The other patient was discovered to have a severe leukopenia and thrombocytopenia within about a month after rash onset. DISCUSSION: Current hematologic monitoring guidelines for carbamazepine rely heavily on the recognition of signs and symptoms of blood dyscrasias by clinicians and patients. We believe that our cases support the suggestion that patients who develop rashes receive more vigilant monitoring of the complete blood count, should carbamazepine therapy be continued. Given the currently available case reports and the fact that the incidence of drug-induced blood dyscrasias increases with advanced age, this recommendation may be particularly relevant for geriatric patients. CONCLUSIONS: Further study is required to establish whether carbamazepine-induced concomitant rashes and blood dyscrasias are valid associations insofar as monitoring is concerned.

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26

Comenzo, RL, E. Vosburgh, RW Simms, P. Bergethon, D. Sarnacki, K. Finn, S. Dubrey, et al. "Dose-intensive melphalan with blood stem cell support for the treatment of AL amyloidosis: one-year follow-up in five patients." Blood 88, no. 7 (October 1, 1996): 2801–6. http://dx.doi.org/10.1182/blood.v88.7.2801.bloodjournal8872801.

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The morbidity and lethality of AL amyloidosis is caused by the deposition of lg light chains as fibrillar amyloid protein in vital organs, disrupting their function, and not by the generally low burden of clonal plasma cells that produce the paraproteins. Survival of patients with AL amyloidosis is no more than 1 to 2 years from the time of diagnosis with current management approaches. Clearly, more effective therapies are needed for this rapidly lethal disease. Five patients were treated with dose-intensive melphalan and blood stem cell support and followed for a period of 1 year. Patients were diagnosed with AL amyloidosis by tissue biopsy and categorized by performance status and organ involvement. Their plasma cell dyscrasias were evaluated with immunofixation electrophoresis of serum and urine specimens, quantitative serum lgs, and immunohistochemical staining of bone marrow biopsy specimens. After treatment with dose-intensive intravenous melphalan followed by infusion of autologous growth-factor-mobilized blood stem cells, clinical evaluations and plasma cell studies were repeated at 3 and 12 months. Three men and 2 women aged 38 to 53 years were treated. Median performance status (SWOG) was 2 (1 to 3), and clinical presentations included nephrotic syndrome (n = 1), symptomatic cardiomyopathy (n = 1), gastrointestinal involvement with polyneuropathy (n = 2), and hepatomegaly (n = 1). With a median follow-up of 13 months (12 to 17 months), all five patients are well and have shown stable or improved performance status and clinical remission of organ-related dysfunction, including a 50% reduction in daily proteinuria with no change in creatinine, reversal of symptoms of cardiomyopathy and reductions of posterior wall and septal thickening, reversal of polyneuropathy and gastric atony, and resolution of hepatomegaly by computed tomographic scan. In 3 of the 5 patients (60%) at 12 months after treatment, plasma cell dyscrasias could not be detected. Dose-intensive chemotherapy with intravenous melphalan and growth-factor-mobilized blood stem cell support is feasible therapy for patients with AL amyloidosis, even when there is clinical evidence of cardiac involvement. At least some patients with AL amyloidosis achieve complete remission of their plasma cell dyscrasia, improvement in performance status, and clinical remission of organ-specific disease after this form of treatment.

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27

Neri, Antonino, Michela Mattioli, Luca Agnelli, Sonia Fabris, Luca Baldini, Fortunato Morabito, Silvio Bicciato, et al. "Gene Expression Profiling of Plasma Cell Dyscrasias: The Role of IGH Translocations in the Heterogeneity of Multiple Myeloma." Blood 104, no. 11 (November 16, 2004): 4845. http://dx.doi.org/10.1182/blood.v104.11.4845.4845.

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Abstract Multiple Myeloma (MM) is the most common form of plasma cell dyscrasia, characterized by a marked heterogeneity of genetic lesions and clinical course. It may develop from a premalignant condition (monoclonal gammopathy ofundetermined significance, MGUS) or progress from intra-medullary to extra-medullaryforms (plasma cell leukemia, PCL). To provide insights into the molecular characterization of plasma cell dyscrasias and to investigate the contribution of specific genetic lesions to the biological and clinical heterogeneity of MM, we analyzed the gene expression profiles of plasma cells isolated from 7 MGUS, 39 MM and 6 PCL patients by means of DNA microarrays. MMs resulted highly heterogeneous at transcriptional level, whereas the differential expression of genes mainly involved in DNA metabolism and proliferation distinguished MGUS from PCLs and the majority of MM cases. The clustering of MM patients was mainly driven by the presence of the most recurrent translocations involving the immunoglobulin heavy-chain locus. Distinct signatures have been found to be associated with different lesions: the overexpression of CCND2 and genes involved in cell adhesion pathways was observed in cases with deregulated MAF and MAFB, whereas genes upregulated in cases with the t(4;14) showed apoptosis related functions. In addition, we identified a set of cancer germ-line antigens specifically expressed in a sub-group of MM patients characterized by an aggressive clinical evolution, a finding that could have implications for patient classification and immunotherapy.

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Tong, AW, JC Lee, and MJ Stone. "Characterization of a monoclonal antibody having selective reactivity with normal and neoplastic plasma cells." Blood 69, no. 1 (January 1, 1987): 238–45. http://dx.doi.org/10.1182/blood.v69.1.238.238.

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Abstract A myeloma cell-reactive monoclonal antibody (MoAb), MM4, was generated from BALB/c mice immunized with alternate injections of cells from two human multiple myeloma (MM) cell lines. Screening by the enzyme-linked immunosorbent assay (ELISA) technique showed that MM4 reacted with human MM cell lines (7 of 7 positive), as well as bone marrow aspirates from MM patients (4 of 4 cases positive). MM4 did not react with marrow aspirates from control patients (3 cases), or with peripheral blood mononuclear (PBM) cells from normal subjects, lymphocytic (12 cases) and myelogenous (8 cases) leukemia patients. In addition, MM4 was negative with polymorphonuclear leukocytes and RBCs from normal donors. By means of the immunoperoxidase technique, the MM4-reactive antigen was detected in paraffin-embedded, Zenker formalin-fixed bone marrow biopsies of MM (12 of 12 cases positive), Waldenstrom's macroglobulinemia (2 of 2 cases positive), asymptomatic plasma cell dyscrasia (4 of 4 cases positive), and certain lymphomas (2 of 5 cases positive). Marrow biopsies from lymphocytic (5 cases) and myelogenous (5 cases) leukemias were uniformly negative. The MM4-reactive antigen also was expressed on plasma cells generated from pokeweed mitogen (PWM)-stimulated normal PBM cultures. The pattern of reactivity of MM4 with lymphocytes of B origin was similar to that of the plasma cell MoAb PCA-1. Competitive binding studies showed, however, that these two MoAbs recognized distinct antigenic determinants. These observations suggest that MM4 may be useful for the study of human plasma cell dyscrasias.

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29

Tong, AW, JC Lee, and MJ Stone. "Characterization of a monoclonal antibody having selective reactivity with normal and neoplastic plasma cells." Blood 69, no. 1 (January 1, 1987): 238–45. http://dx.doi.org/10.1182/blood.v69.1.238.bloodjournal691238.

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A myeloma cell-reactive monoclonal antibody (MoAb), MM4, was generated from BALB/c mice immunized with alternate injections of cells from two human multiple myeloma (MM) cell lines. Screening by the enzyme-linked immunosorbent assay (ELISA) technique showed that MM4 reacted with human MM cell lines (7 of 7 positive), as well as bone marrow aspirates from MM patients (4 of 4 cases positive). MM4 did not react with marrow aspirates from control patients (3 cases), or with peripheral blood mononuclear (PBM) cells from normal subjects, lymphocytic (12 cases) and myelogenous (8 cases) leukemia patients. In addition, MM4 was negative with polymorphonuclear leukocytes and RBCs from normal donors. By means of the immunoperoxidase technique, the MM4-reactive antigen was detected in paraffin-embedded, Zenker formalin-fixed bone marrow biopsies of MM (12 of 12 cases positive), Waldenstrom's macroglobulinemia (2 of 2 cases positive), asymptomatic plasma cell dyscrasia (4 of 4 cases positive), and certain lymphomas (2 of 5 cases positive). Marrow biopsies from lymphocytic (5 cases) and myelogenous (5 cases) leukemias were uniformly negative. The MM4-reactive antigen also was expressed on plasma cells generated from pokeweed mitogen (PWM)-stimulated normal PBM cultures. The pattern of reactivity of MM4 with lymphocytes of B origin was similar to that of the plasma cell MoAb PCA-1. Competitive binding studies showed, however, that these two MoAbs recognized distinct antigenic determinants. These observations suggest that MM4 may be useful for the study of human plasma cell dyscrasias.

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30

&NA;. "Ticlopidine-induced blood dyscrasias." Inpharma Weekly &NA;, no. 1057 (October 1996): 21. http://dx.doi.org/10.2165/00128413-199610570-00042.

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31

&NA;. "Blood dyscrasias with aminosalicylates." Reactions Weekly &NA;, no. 561 (July 1995): 2. http://dx.doi.org/10.2165/00128415-199505610-00001.

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32

&NA;. "Ticlopidine-induced blood dyscrasias." Reactions Weekly &NA;, no. 621 (October 1996): 2. http://dx.doi.org/10.2165/00128415-199606210-00003.

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33

&NA;. "Blood dyscrasias with aminosalicylates." Inpharma Weekly &NA;, no. 997 (July 1995): 21. http://dx.doi.org/10.2165/00128413-199509970-00047.

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34

Ancill, R. J. "Mianserin and Blood Dyscrasias." British Journal of Psychiatry 150, no. 4 (April 1987): 569–70. http://dx.doi.org/10.1192/s0007125000106920.

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35

Spielberg, Stephen P. "Pharmacogenetics and blood dyscrasias." European Journal of Haematology 57, S60 (April 24, 2009): 93–97. http://dx.doi.org/10.1111/j.1600-0609.1996.tb01653.x.

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36

Böttiger, L. E., A. K. Furhoff, and L. Holmberg. "Drug-Induced Blood Dyscrasias." Acta Medica Scandinavica 205, no. 1-6 (April 24, 2009): 457–61. http://dx.doi.org/10.1111/j.0954-6820.1979.tb06084.x.

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37

Medina, Patrick J., and James N. George. "Drug-associated blood dyscrasias." Adverse Drug Reaction Bulletin &NA;, no. 210 (October 2001): 803–6. http://dx.doi.org/10.1097/00012995-200110000-00001.

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38

Kaufman, David W., and Surapol Issaragrisil. "Aminopyrine and blood dyscrasias." Pharmacoepidemiology and Drug Safety 6, no. 4 (July 1997): 292. http://dx.doi.org/10.1002/(sici)1099-1557(199707)6:4<292::aid-pds302>3.0.co;2-f.

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39

Chan, Thomas Y. K., and Anthony W. K. Chan. "Aminopyrine-induced blood dyscrasias." Pharmacoepidemiology and Drug Safety 7, no. 2 (March 1998): 129. http://dx.doi.org/10.1002/(sici)1099-1557(199803/04)7:2<129::aid-pds326>3.0.co;2-#.

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40

Joseph, Geetha, Robert L. Barker, Bo Yuan, Alvin Martin, Jeffrey Medeiros, and Stephen C. Peiper. "Posttransplantation plasma cell dyscrasias." Cancer 74, no. 7 (October 1, 1994): 1959–64. http://dx.doi.org/10.1002/1097-0142(19941001)74:7<1959::aid-cncr2820740722>3.0.co;2-u.

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41

Danielly, Julie, Richard DeJong, Lyn C. Radke-Mitchell, and Andrew C. G. Uprichard. "Procainamide-associated blood dyscrasias." American Journal of Cardiology 74, no. 11 (December 1994): 1179–80. http://dx.doi.org/10.1016/0002-9149(94)90478-2.

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42

Bangolo, Ayrton, Trupti Waykole, Bilal Niazi, Chandini Sajja, Mahabuba Akhter, Bhavna Gupta, and Sameh Elias. "A Rare Cause of Acquired Factor X Deficiency in an 87-Year-Old Female." Case Reports in Hematology 2021 (November 17, 2021): 1–3. http://dx.doi.org/10.1155/2021/1138329.

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Factor X deficiency is a rare coagulopathy that can be inherited or acquired. Acquired factor X deficiency has been associated with plasma cell dyscrasias, amyloids, and use of vitamin K antagonists. Of plasma cell dyscrasias, most cases in the literature have been associated with multiple myeloma with or without concomitant AL amyloidosis. Here, we present a rare case of acquired isolated factor X deficiency in an elderly patient with immunoglobulin A (Ig A) monoclonal gammopathy of undetermined significance (MGUS). Herein, we highlight a rare cause of acquired factor X deficiency, and we hope to contribute to the growing literature of plasma cell dyscrasias associated with factor X deficiency.

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43

Yamakage, S. "Area Studies in Dyscrasia." Annuals of Japanese Political Science Association 37 (1986): 1–25. http://dx.doi.org/10.7218/nenpouseijigaku1953.37.0_1.

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44

Wisely, C. Ellis, Wenlan Zhang, and Dilraj S. Grewal. "Multiple Myeloma Presenting as Recalcitrant Macular Edema." Journal of VitreoRetinal Diseases 4, no. 3 (October 21, 2019): 248–52. http://dx.doi.org/10.1177/2474126419880491.

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Purpose: This article presents an unusual case of ocular involvement of multiple myeloma masquerading as macular edema associated with diabetic retinopathy. Methods: A report of a single case. Results: The presence of concomitant type 2 diabetes and scattered retinal hemorrhages presented a diagnostic challenge. Large globular vitreous opacities and significant weight loss were suggestive of a neoplastic process. We demonstrate multimodal imaging findings that can be associated with plasma cell dyscrasias and also describe the purported mechanism by which plasma cell dyscrasias cause macular edema and exudative retinal detachments. Conclusion: Although multiple myeloma and related plasma cell dyscrasias are rare causes of ocular disease, they should be considered in the differential diagnosis of recalcitrant macular edema, and there should be a low threshold for systemic evaluation.

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45

&NA;. "Mirtazapine linked to leucocyte dyscrasias?" Reactions Weekly &NA;, no. 1126 (November 2006): 5. http://dx.doi.org/10.2165/00128415-200611260-00013.

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46

Takeuchi, Yumiko. "Immuno-monitoring in blood dyscrasias." Japanese Journal of Clinical Immunology 9, no. 5 (1986): 391–96. http://dx.doi.org/10.2177/jsci.9.391.

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47

Kwaan, Hau C. "Hyperviscosity in plasma cell dyscrasias." Clinical Hemorheology and Microcirculation 55, no. 1 (2013): 75–83. http://dx.doi.org/10.3233/ch-131691.

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48

&NA;. "Ranitidine may cause blood dyscrasias." Reactions Weekly &NA;, no. 311 (July 1990): 2. http://dx.doi.org/10.2165/00128415-199003110-00003.

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49

Sidhu, Harleen, Almut Böer, and Albert Bernard Ackerman. "T-cell Dyscrasias in Dermatopathology." American Journal of Dermatopathology 28, no. 4 (August 2006): 353–56. http://dx.doi.org/10.1097/00000372-200608000-00013.

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50

Polak, B. C. P., H. Wesseling, Dien Schut, A. Herxheimer, and L. Meyler. "BLOOD DYSCRASIAS ATTRIBUTED TO CHLORAMPHENICOL." Acta Medica Scandinavica 192, no. 1-6 (April 24, 2009): 409–14. http://dx.doi.org/10.1111/j.0954-6820.1972.tb04838.x.

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