DOCSLIB.ORG

Multiple Myeloma

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Multiple Myeloma Multiple Myeloma Volume VII Thursday, January 30, 1936 Number 14 m~IV~1SI~Y OF MIN~~SOTA EOSPI'~LS=c...=...:==- _ Volume VII Ti:lUrsday, January 30, 1936 ----------_._--N\.1li1ber 14 I. ABS'l'RACT 1IDLTIPLE 1ITELOMA •••..••••.•. 142 - 148 II" CASE REPOR'r · · · · · · · ·· · ·· · · · 148 150 III. Lfi.ST WEEK ··· · · · · ·· ··· · · · 150 IV. EXEIBIT ···· · · · ··· · · · · · 150 V. MOVIE . · · · · · · · · · · · · ·· ···· 150 VI. GOSSIP ·· ·· ·· · · · ··· · ··· ·· 150 - 151 C 0 U R T E S Y 0 F CIT I ZEN S SOC lET Y 142 I. ABSTRACT---- from nearly every par t of the world. The greater incidence in certain places MULTIPLE MYELOMA appears to be due to the greater inter­ est shown in the dis ease in those places? C. M. Eklund VI. Among malignancies, Geschickter Multiple ffiJ-eloma is a primary and Copeland estimate that it myeloid tumor in which multiple tumor comprises about 0.03% of all foci arise in the red bone marrow. It mali gnanc i e s. is characterized by skeletal pain, spontaneous fractures, multiple tumors, Bence-Jones proteinuria, high plasma B. Presenting Symptoms and Signs pruteins and anemia. About 500 cases have been reported. Nothing is known as The clinical Gourse is vari ed. to etiology. Trauma is fre~uently cited May resemble chronic artbritis, kidney as an inciting agent but no good evi­ disease, severe anemia, pulmonary disease dence for this has been presented. or various neurological diseases. A. Incidence I. pain usually ushers in the disease and brings the patient to the 1. Age. physician. The onset may be definitely associated with some sudden movement or Wallgren, 90% over 40 years. follow lifting. The pain sometimes appears suddenly from no apparent cause. Geschickter and Copeland, 80% Wnen the pain has once appeared, it is between 40 and 70 with peak at 55. characteristically related to motion and is usually intermittent. In some, Up to 1933, Magnus-Levy consider­ the attack of pain is so sudden and of ed it doubtful if any proven case han such severity that the pat ient must been reported in childhood. grasp something for support. Wallgren cites a case where an attac~ occurred In 1934, Slavens collected 3 while tne patient was walking down cases from tne literature which he con­ stairs, and he fell the rest of the way. sidered as definitely proven histologic­ Occasionally, the pain is so severe as ally and presents a case of his own ­ to require general anesthesia. aE:ed 4. In tllis case, the history, ro entgenologic findings, biopsy and autop­ The pain is usually situated in sy all pointed to multiple myeloma. the back, especially the lumbar region. The chest and shoulders are involved II. Sex fre~uently: the arms and legs only occasionally; typically they are free. Various statistics agree on about 7CJ'~ males. The pain usually last s a few days to weeks, then the patient is more or less free until the next unguarded movemen t. The pain may recur spon­ Reported in white, yellow and taneously. As the disease progresses, the black races. pain tends to become more constant. In these patients, percussion of the thorax IV. Social Status or palpation of the abdomen or even the pressure of the stethoscope may be very In every class of society. painful. V. Countries The pain at first may originate in the bone itself but sooner or later Most cases reported from Germany it arises from pressure upon nerves. and the United States but others reported 143 II. A tumor ITk~y be the presenting VII. Some cases present themselves p~tient sign. The feels a lump wi th onlJl general sif:ns such as or a painful area. Occasionally, a weakness, weight loss and poor appetite. local tumor of the mediastin~, pelvis, nasophar;y-llX or orbit may be so large and grow so rapidly that it characterizes the C. Duration Qf the ;Qisease clinical picture. The tumors are de­ scrLled as feeling elastic and giving a The dis eteso is vcr:! insidious sensation of fluctuation. A parchment in its onset so tr~t no accurate know­ paper-like cre~itation may be present. ledge can be had as to its duration. Some tUJIlOrs pulsate. A tendency to Average duration is about 2 yeE1r s. spontaneous disappearance has been de­ Proven cases reported with a ciurati on sc:ribed.. of over 5 years. Magnus-Levy believes that tre clinical course is probably much J" ~. T:nc softening and compression of greater than is usually stated. the ',-cJ:tebrae may give a characteristic deformity. Tne sternum sinks in, the abdomen protrudes, the ribs rest upon D. Occurrence of Amyloid the ~elvis, the head sinks forward, the shc,ulCi.ers are braced back, the feet are Magnus-Levy reports 37 instances pbced far apart and the patient walks in less than 150 cases of multiule myelo­ with deliberation. A sllortening of the ma. It tends to have an unusual distri­ body up to 20 em. has occurred. bution. Large IIlc':\,sses may occur in bones or striated muscle. The intestines, IV. Fractures are reported in 62% heart and lungs may be infiltrated v~th of the c~ses (Geschickter and amyloid ani produce symptoms complicating Copeland). W:nile they are very common trB cl inical picture. and frequently multiple, they are usually not the presenting sign. Crushing of vertebrae, following lifting, has been E. BaboratoEY Findings noted in some of the cases here. The fractures usually involve the ribs. Fracture of the femur or humerus is fair­ ly common. a. Hemof~obin Rnd red _-blood cell£'. V. rrhe ma,;o,dty of the patients show The predominat e pictur e 801'18 nC"J.-:rological symntoms. is one of anEmia. In 70 cases~ the red Paraplegia is '::::J3 PJ8st important o Diplo­ blood cells were over four million in pia, paralysis of ;:,'1e hand, partial only 23% of the cases (Geschickter and laryng8al ,,,-nd r111.ryngeal paralysis !1-", ve Copeland). In the greater n~b8r the been reported. Iut8rcostal neuralgia and red blood count is between two [md three root pains are q~;tc common. million. Twenty-six of the above 70 had a high color index. VI. Thrombcsis of the intracrp~ial sinus due to pressure of tumors Wallgren also stat es thr\t the has b'"cn reported a few times. anemia is not the usual seconciary type. Thrombosis of the central artery Normoblasts are occasionally of the retina - once. seen and megaloblasts have been reyorted a few times. Thrombosis of the retinal vein onceo b. White -olood cells. (Geschickter and Copeland) One case presented signs of vascular disturbance resembling Raynaud's Seventy percent (100 disease. cpses) were within normal limits, 23% showed a leucocytosis and ?% a leukopenia. 144 In the cases with leucocytosis, Normal Levels: the white blood cells were usually 11,000 to 15,000. Total protein - 7.0 (6.0-7.0) Globulin - 2.0 (1.4-3.0) The highest count in definitely (Peter & Eise~~on) proven casas was 39,400. This is in Al Dumin - 5. a (4. 0-5. 5) contrast to metastatic malignancy in which counts as high dS 120,000 have been re­ Total plasma protein in multiple ported (Wallgren)~ mydoma may reach 16 grus. per 100 cc. A number of hematological and chemical peculiarities of the blood appear to be due to the increase of In Il about 60 cases,lI there euglobulin. were 15 with myelocytes (1 - 10%) (Geschickter and Copeland). Wallgren (a) Autohemagglutination: states that myelocytes do not usually Reimann was the first to exceed 2%. Geschickter and Copeland r·,?cognize the relation between autohe­ quote Vaughn as reporting myelocytes magglutination and high plasma ~orotein frequently present in a.dvanced carcinoma. in multiple myeloma. It rna;'{ be LIDOS­ Myeloma cells hwve ~een found in the siblG to do a red blood count because of blood smear in a small number of cases. the rapid. clumping of the cells. It is shown in blood smears by m:lrk0d rouleaux formation. Cross-matching of blood for d. Plasma Proteins blood transfusions may be vfery ciii'ficult bec0use tr£ patient's S8rum clumps red The great interest shown blood cells from any group. TIlis mal'ked in this comparatively rare disease at rouleaux formati on m0.y accoun t for the the present time is due to the unusual :rapid blood. sedimentati on in s erne cases disturbance in protein metabolism. This of multiple myeloma. Foard reports one disturbance is revealed in 3 ways. case of intravascular clum')jn,,:; visible uoon fundus examination after aoplying 1. Increased plasma protein. pressure to the eyeball to slow the 2. Bence-Jones protein in the urine. circulation. 3. Formation of amyloid deposits. (b) Presence of cloudines~, pre­ A marked increase in cipitation or coa~Jation plasma protein is an uncommon laboratow when the serum is inactiv[1.ted in carrying finding. It is s~lOwn more strikingly out the Wassermann react ion. in myltiple myeloma than in any other disease. Whe"t percentage of cases of (c) Increa~e in viscosity of multiple myeloma show an increased plasma the serum. protein is unk~o,n because plasma protein detarminations have been done in only a (d.) Spontaneous pr·3cbit'1.tion of few of the reported cases. protein from the blood. Wintrabe and Buell, while doing a In 1933, Magnus-Levy collected hematocrit determinat i on noti ceO. cl 18Ig8 36 cases; 21 of these h8.d plasma proteins runount of precipitate settle out above of more than 8 grams per 100 cc. The t.le red blood cell s and ~ the;y- s~.:.owed proteins were not fractionated in all thot it consisted of protein.
Load more

Recommended publications
  • Red Blood Cell Rheology in Sepsis K
    M. Piagnerelli Red blood cell rheology in sepsis K. Zouaoui Boudjeltia M. Vanhaeverbeek J.-L. Vincent Abstract Changes in red blood cell membrane components such as sialic (RBC) function can contribute to acid, and an increase in others such alterations in microcirculatory blood as 2,3 diphosphoglycerate. Other flow and cellular dysoxia in sepsis. factors include interactions with Decreases in RBC and neutrophil white blood cells and their products deformability impair the passage of (reactive oxygen species), or the these cells through the microcircula- effects of temperature variations. tion. While the role of leukocytes Understanding the mechanisms of has been the focus of many studies altered RBC rheology in sepsis, and in sepsis, the role of erythrocyte the effects on blood flow and oxygen rheological alterations in this syn- transport, may lead to improved drome has only recently been inves- patient management and reductions tigated. RBC rheology can be influ- in morbidity and mortality. enced by many factors, including alterations in intracellular calcium Keywords Erythrocyte · and adenosine triphosphate (ATP) Deformability · Nitric oxide · concentrations, the effects of nitric Sialic acid · Multiple organ failure · oxide, a decrease in some RBC Oxygen transport Introduction ogy of microcirculatory alterations and, perhaps, the treatment of sepsis. Severe sepsis and septic shock are the commonest causes This review evaluates alterations occurring in RBC of death in intensive care units (ICUs), with associated rheology during sepsis and possible underlying mecha- mortality rates of 30–50% [1]. Sepsis is a complex nisms. The potential implications of blood transfusion pathophysiological process that involves both alterations and erythropoietin administration in sepsis will not be in the microcirculation and changes in the biochemical discussed.
    [Show full text]
  • Canine Immune-Mediated Hemolytic Anemia – Brief Review
    TRADITION AND MODERNITY IN VETERINARY MEDICINE, 2018, vol. 3, No 1(4): 59–64 CANINE IMMUNE-MEDIATED HEMOLYTIC ANEMIA – BRIEF REVIEW Iliyan Manev1, Victoria Marincheva2 1University of Forestry, Faculty of Veterinary Medicine, Sofia, Bulgaria 2Animal Rescue, Sofia, Bulgaria E-mail: [email protected] ABSTRACT Immune-mediated hemolytic anemia (IMHA) is a common autoimmune disorder in dogs. It affects both sexes but occurs more often in female, middle-aged animals. IMHA can be idiopathic (primary) or secondary to infectious, neoplastic and autoimmune disorders. There is an acute regenerative anemia with accompanying hypoxia. Destruction of erythrocytes can be intravascular (as a result of complement system activation) or extravascular (removal of antibody-coated red blood cells by the macrophages in the liver and spleen). Diag- nosis is based on the presence of anemia, in vitro autoagglutination, positive direct antiglobulin test (Coomb`s test), detection of spherocytes. It is crucial to exclude possible secondary causes. The treatment protocol aims to cease cell destruction by high doses of corticosteroids, aggressive supportive care and long-term application of immunosuppressive drug combinations. Still lethality is high because of complications (pulmonary throm- boembolism, DIC), medication resistance, relapses. Key words: immune-mediated, anemia, canine, hemolysis, immunosuppressive drugs. Immune-mediated hemolytic anemia is one of the commonly diagnosed canine autoimmune diseases and a model of acute and clinically relevant anemia. Impaired
    [Show full text]
  • Cytology of Myeloma Cells
    J Clin Pathol: first published as 10.1136/jcp.29.10.916 on 1 October 1976. Downloaded from J. clin. Path., 1976, 29, 916-922 Cytology of myeloma cells F. G. J. HAYHOE AND ZOFIA NEUMAN1 From the Department of Haematological Medicine, Cambridge University SYNOPSIS A cytological, cytochemical, and cytometric study of plasma cells from 195 cases of multiple myeloma showed that, contrary to earlier reports, flaming cells, thesaurocytes, and intra- nuclear inclusions are not confined to IgA-secreting cases but are common also in IgG and Bence Jones varieties of myeloma. IgA-secreting cells are not larger, nor do they have a lower nuclear- cytoplasmic ratio than other myeloma cells. On average, for a given mass of tumour, Bence-Jones, IgG, and IgA varieties of myeloma produce amounts of paraprotein in the ratio 1 to 1 6 to 2-7. In 1961 Paraskevas et al reported a correlation the results of a larger scale survey carried out some between the morphological features of plasma cells years ago but previously unpublished. in myeloma and the type of immunoglobulin secreted. The cases studied included 12 with y1A Material and methods (f2A, IgA) myeloma, 30 with y (IgG) myeloma, and six myelomas without M protein (probably Bence The study was performed on bone marrow smearscopyright. Jones myelomas). Flaming cells, thesaurocytes, and from 200 consecutive patients newly entered into a intranuclear, PAS-positive inclusion bodies were comparative trial of treatments in myeloma, under found only in cases of IgA myeloma, and flaming the auspices of the Medical Research Council. Five cells especially were present in most cases and in patients were subsequently excluded as not confirmed high percentage in several.
    [Show full text]
  • Evidence-Based Practice Center Systematic Review Protocol
    Evidence-based Practice Center Systematic Review Protocol Project Title: Serum-Free Light Chain Analysis for the Diagnosis, Management, and Prognosis of Plasma Cell Dyscrasias I. Background and Objectives for the Systematic Review Plasma cell dyscrasias (PCDs) are a spectrum of disorders characterized by the expansion of a population of monoclonal bone-marrow plasma cells that produce monoclonal immunoglobulins.1 At the benign end of the spectrum is monoclonal gammopathy of undetermined significance (MGUS), where the plasma-cell clone usually does not expand. Multiple myeloma (MM) is a plasma cell disorder at the malignant end of the spectrum and is characterized by the neoplastic proliferation of a clone of plasma cells in the bone marrow with resulting end-organ damage, including skeletal destruction (lytic bone lesions), hypercalcemia, anemia, and renal insufficiency. Whereas monoclonal plasma cells generally secrete intact immunoglobulin, in about 20 percent of patients with MM these cells only produce light-chain monoclonal proteins (i.e., light-chain multiple myeloma [LCMM], formerly known as Bence Jones myeloma) and in 3 percent of patients they secrete neither light- nor heavy-chain monoclonal proteins that are detectable by immunofixation (i.e., nonsecretory multiple myeloma [NSMM]).1 In two-thirds of patients with NSMM, a monoclonal protein can be identified by the serum-free light chain (SFLC) assay. Patients with LCMM develop complications related to tissue deposition of light chains, including amyloidosis. Amyloid light-chain (AL) amyloidosis is the most common form of systemic amyloidosis seen in the United States and is characterized by a relatively stable, slow-growing plasma-cell clone that secretes light-chain proteins that form Table 1: Diagnostic criteria and clinical course of selected plasma cell dyscrasias (PCDs)2 Disorder Disease Definition Clinical Course Monoclonal gammopathy of .
    [Show full text]
  • Canine Multiple Myeloma
    Canine Multiple Myeloma Meredith Maczuzak, DVM; Kenneth S. Latimer, DVM, PhD; Paula M. Krimer, DVM, DVSc; and Perry J. Bain, DVM, PhD Class of 2003 (Maczuzak) and Department of Pathology (Latimer, Krimer, Bain), College of Veterinary Medicine, University of Georgia, Athens, GA 30602-7388 Introduction Multiple myeloma or plasma cell myeloma, is a neoplasm of well- differentiated B cell lymphocytes typically originating from the bone marrow. Neoplastic cells can metastasize widely, having a predilection for bone and resulting in osteolysis. The malignant transformation of a single B cell can secrete a homogenous immunoglobulin product known as paraprotein, which will mimic the structure of normal immunoglobulins. Overabundant production of paraprotein, consisting of any of the immunoglobulin classes, will appear as a sharp, well-defined peak or monoclonal gammopathy on serum electrophoresis. The most frequently encountered multiple myelomas secrete IgG or IgA paraproteins, however IgM myelomas (macroglobulinemia) have also been diagnosed in companion animals. Light chain disease is caused by plasma cell overproduction of the light chain segment of the immunoglobulin complex, consisting of either the lambda or kappa light chain. These proteins are referred to as Bence-Jones proteins and are the most commonly observed immunoglobulin fragments in the monoclonal gammopathies.2 There are rare instances where a malignant plasma cell neoplasm will be nonsecretory. These tumors occur in approximately 1% of all cases of multiple myeloma and are referred
    [Show full text]
  • Complete Blood Count in Primary Care
    Complete Blood Count in Primary Care bpac nz better medicine Editorial Team bpacnz Tony Fraser 10 George Street Professor Murray Tilyard PO Box 6032, Dunedin Clinical Advisory Group phone 03 477 5418 Dr Dave Colquhoun Michele Cray free fax 0800 bpac nz Dr Rosemary Ikram www.bpac.org.nz Dr Peter Jensen Dr Cam Kyle Dr Chris Leathart Dr Lynn McBain Associate Professor Jim Reid Dr David Reith Professor Murray Tilyard Programme Development Team Noni Allison Rachael Clarke Rebecca Didham Terry Ehau Peter Ellison Dr Malcolm Kendall-Smith Dr Anne Marie Tangney Dr Trevor Walker Dr Sharyn Willis Dave Woods Report Development Team Justine Broadley Todd Gillies Lana Johnson Web Gordon Smith Design Michael Crawford Management and Administration Kaye Baldwin Tony Fraser Kyla Letman Professor Murray Tilyard Distribution Zane Lindon Lyn Thomlinson Colleen Witchall All information is intended for use by competent health care professionals and should be utilised in conjunction with © May 2008 pertinent clinical data. Contents Key points/purpose 2 Introduction 2 Background ▪ Haematopoiesis - Cell development 3 ▪ Limitations of reference ranges for the CBC 4 ▪ Borderline abnormal results must be interpreted in clinical context 4 ▪ History and clinical examination 4 White Cells ▪ Neutrophils 5 ▪ Lymphocytes 9 ▪ Monocytes 11 ▪ Basophils 12 ▪ Eosinophils 12 ▪ Platelets 13 Haemoglobin and red cell indices ▪ Low haemoglobin 15 ▪ Microcytic anaemia 15 ▪ Normocytic anaemia 16 ▪ Macrocytic anaemia 17 ▪ High haemoglobin 17 ▪ Other red cell indices 18 Summary Table 19 Glossary 20 This resource is a consensus document, developed with haematology and general practice input. We would like to thank: Dr Liam Fernyhough, Haematologist, Canterbury Health Laboratories Dr Chris Leathart, GP, Christchurch Dr Edward Theakston, Haematologist, Diagnostic Medlab Ltd We would like to acknowledge their advice, expertise and valuable feedback on this document.
    [Show full text]
  • Chapter 7: Hematologic Disorders and Kidney Disease
    Chapter 7: Hematologic Disorders and Kidney Disease Ala Abudayyeh, MD,* and Kevin Finkel, MD, FACP, FASN, FCCM*† *Division of General Internal Medicine, Section of Nephrology, University of Texas MD Anderson Cancer Center, Houston, Texas; and †UTHealth Science Center at Houston Medical School, Department of Medicine, Division of Renal Diseases and Hypertension, Houston, Texas MULIPLE MYELOMA chains precipitate with Tamm-Horsfall protein (THP) secreted by the thick ascending limb of the Pathogenesis loop of Henle and produce casts in the distal tubule. Multiple myeloma (MM) is a hematologic malig- Decreased GFR may increase the concentration of nancy involving the pathologic proliferation of light chains in the distal tubule and enhance the terminally differentiated plasma cells. It is the formation of casts. Therefore, hypercalcemia, vol- second most common hematologic malignancy ume depletion, diuretics, and nonsteroidal anti- behind non-Hodgkin lymphoma, with an annual inflammatory drugs can exacerbate renal injury. incidence of 4–7 cases per 100,000 in the United In some cases of AKI associated with MM, cast States. Clinical symptoms are due to osteolysis of formation is rare on renal biopsy. Instead, renal the bone, suppression of normal hematopoiesis, injury is attributed to the direct toxic effects of and the overproduction of monoclonal immuno- urinary free light chains (FLCs) on proximal tubule globulins that deposit in organ tissues. Clinical cells (5,6). After reabsorption, lysosomal degrada- symptoms include bone pain and fractures, anemia, tion of FLCs can activate the NF-kB pathway lead- infections, hypercalcemia, edema, heart failure, and ing to oxidative stress with an inflammatory renal disease. response, apoptosis, and fibrosis.
    [Show full text]
  • 8 Erythrocyte Sedimentation Rate (Esr)
    MODULE Erythrocyte Sedimentation Rate (ESR) Hematology and Blood Bank Technique 8 Notes ERYTHROCYTE SEDIMENTATION RATE (ESR) 8.1 INTRODUCTION Erythryocyte Sedimentation Rate (ESR) is the measurement after 1hour of the sedimentation of red cells when blood is allowed to stand in an open ended glass tube mounted vertically on a stand. OBJECTIVES After reading this lesson, you will be able to: z describe the methods used for measuring ESR z enlist the factors influencing the sedimentation of red cells z discuss the significance of measuring ESR z describe the reticulocyte count and it’s significance 8.2 METHODS OF MEASURING ESR ESR can be measured in the laboratory by two methods z Westergren method z Automated ESR analyser The International Council for Standardization in Hematology recommends the use of Westergren method as the standard method for measuring ESR. Westergren method The Westergren pipette is a glass pipette 30 cm in length and 2.5mm in diameter. The bore is uniform to within 5% throughout. A graduated scale in mm extends over the lower 20 cm. 62 HEMATOLOGY AND BLOOD BANK TECHNIQUE Erythrocyte Sedimentation Rate (ESR) MODULE Sample: Venous blood collected in EDTA. Four volumes of blood is diluted in Hematology and Blood 1 volume of citrate. Alternatively, 2ml blood is directly collected in 0.5ml of Bank Technique 3.8% trisodium citrate. Equipment required 1. Westergren pipette 2. Stainless steel rack for holding pipette Notes 3. Timer Method 1. Mix the blood sample well and draw in the Westergren pipette to the 0mm mark with a rubber teat. 2. Place the tube exactly vertical in the rack which has a rubber cork at the bottom.
    [Show full text]
  • Intranuclear Inclusions in Myeloma Patient
    Published online: 2021-05-24 Letter to Editor Pathologist’s Feast: Intranuclear Inclusions in Myeloma Patient Sir, aspiration [Figure 2]. Plasma cells showed Dutcher body We present a case of a 36‑year‑old female admitted in bone marrow aspiration [Figure 3] as periodic acid– in hospital with complaints of pain in sacral region Schiff positive intranuclear inclusion [Figure 4]. The bone radiating toward right lower limb for 1 month. Laboratory marrow biopsy showed loss of normal architecture with examination revealed hemoglobin 8.1 g/dL, red blood packed marrow studded by plasma cells [Figure 5]. cell count – 2.61 × 109/mm3, white blood cell count Multiple myeloma account for 1% of all cancers and 16.16 × 103/mm3, and platelet count 299 × 109/mm3. The approximately 10% of all hematological malignancies.[1] The differential showed polymorphs – 74%, lymphocytes – 22%, eosinophils – 1%, and monocytes – 3%. Peripheral blood peak incidence is seventh decade, and it is quite rare, below smear showed rouleaux formation in red blood cells. The 40 years of age. The clinical and biological characteristics serum biochemistry showed blood urea – 54 mg/dl and of multiple myeloma in young patients are similar to those [2] creatinine – 3.8 mg/dl, angiotensin converting enzyme in elderly as in literature in studies by Usha et al. and [3] level – 64.25 U/L, and serum calcium – 13.3 mg/dl. Liver Bladé et al. The above case shows ditcher body inclusions function tests and serum electrolytes were normal and in plasma cells on bone marrow aspiration. HIV and HBsAg were nonreactive.
    [Show full text]
  • Successful Autologous Peripheral Blood Stem Cell Harvest and ­Transplantation After Splenectomy in a Patient with Multiple ­Myeloma with Hereditary Spherocytosis
    International Journal of Myeloma 8(3): 11–15, 2018 CASE REPORT ©Japanese Society of Myeloma Successful autologous peripheral blood stem cell harvest and transplantation after splenectomy in a patient with multiple myeloma with hereditary spherocytosis Daisuke FURUYA1,4, Rikio SUZUKI1,4, Jun AMAKI1, Daisuke OGIYA1, Hiromichi MURAYAMA1,2, Hidetsugu KAWAI1, Akifumi ICHIKI1,3, Sawako SHIRAIWA1, Shohei KAWAKAMI1, Kaito HARADA1, Yoshiaki OGAWA1, Hiroshi KAWADA1 and Kiyoshi ANDO1 Hereditary spherocytosis (HS) is the most common inherited red cell membrane disorder worldwide. We herein report a 58-year-old male HS patient with mild splenomegaly who developed symptomatic multiple myeloma (MM). Autologous stem cell transplantation (ASCT) was considered to be adopted against MM, although there was a possibility of splenic rupture following stem cell mobilization. Therefore, splenectomy was performed prior to stem cell harvest, and he was able to safely mobilize sufficient CD34+ cells with G-CSF and plerixafor and undergo ASCT. This case suggests that stem cell mobilization after splenectomy is safe and effective in HS patients complicated with malignancies. Key words: multiple myeloma, hereditary spherocytosis, splenectomy, autologous peripheral blood stem cell harvest Introduction Consolidation with melphalan-based HDT followed by ASCT is still the standard treatment option for transplant-eligible Multiple myeloma (MM) is characterized by clonal prolifera- patients with MM, leading to higher complete response rates tion of abnormal plasma cells in the bone marrow (BM) micro- and increased progression-free survival and overall survival environment, monoclonal protein in the blood and/or urine, compared with conventional chemotherapy regimens [2]. bone lesions, and immunodeficiency [1]. In recent years, the Importantly, the emergence of novel agent-based therapy introduction of high-dose chemotherapy (HDT) and autol- combined with ASCT has revolutionized MM therapy [2].
    [Show full text]
  • 10 11 Cyto Slides 81-85
    NEW YORK STATE CYTOHEMATOLOGY PROFICIENCY TESTING PROGRAM Glass Slide Critique ~ November 2010 Slide 081 Diagnosis: MDS to AML 9 WBC 51.0 x 10 /L 12 Available data: RBC 3.39 x 10 /L 72 year-old female Hemoglobin 9.6 g/dL Hematocrit 29.1 % MCV 86.0 fL Platelet count 16 x 109 /L The significant finding in this case of Acute Myelogenous Leukemia (AML) was the presence of many blast forms. The participant median for blasts, all types was 88. The blast cells in this case (Image 081) are large, irregular in shape and contain large prominent nucleoli. It is difficult to identify a blast cell as a myeloblast without the presence of an Auer rod in the cytoplasm. Auer rods were reported by three participants. Two systems are used to classify AML into subtypes, the French- American-British (FAB) and the World Health Organization (WHO). Most are familiar with the FAB classification. The WHO classification system takes into consideration prognostic factors in classifying AML. These factors include cytogenetic test results, patient’s age, white blood cell count, pre-existing blood disorders and a history of treatment with chemotherapy and/or radiation therapy for a prior cancer. The platelet count in this case was 16,000. Reduced number of platelets was correctly reported by 346 (94%) of participants. Approximately eight percent of participants commented that the red blood cells in this case were difficult to evaluate due to the presence of a bluish hue around the red blood cells. Comments received included, “On slide 081 the morphology was difficult to evaluate since there was a large amount of protein surrounding RBC’s”, “Slide 081 unable to distinguish red cell morphology due to protein” and “Unable to adequately assess morphology on slide 081 due to poor stain”.
    [Show full text]
  • Clinical Hematology 1
    CLINICAL HEMATOLOGY 1 CLINICAL HEMATOLOGY Editor Gamal Abdul Hamid, MD,PhD Associate Professor Faculty of Medicine and Health Sciences University of Aden CLINICAL HEMATOLOGY 2 PREFACE Clinical Hematology, first edition is written specifically for medical students, the clinician and resident doctors in training and general practioner. It is a practical guide to the diagnosis and treatment of the most common disorders of red blood cells, white blood cells, hemostasis and blood transfusion medicine. Each disease state is discussed in terms of the pathophysiology, clinical and paraclinical features which support the diagnosis and differential diagnosis. We bring together facts, concepts, and protocols important for the practice of hematology. In addition this book is also supported with review questions and quizzes. G.A-H 2012 CLINICAL HEMATOLOGY 3 CONTENTS Preface 1. Hematopoiesis 7 2. Anemia 26 3. Iron Deficiency Anemia 32 4. Hemolytic Anemia 41 5. Sickle Cell Hemoglobinopathies 49 6. Thalassemia 57 7. Hereditary Hemolytic Anemia 63 8. Acquired Hemolytic Anemia 68 9. Macrocytic Anemia 75 10. Bone Marrow Failure, Panctopenia 87 11. Spleen 95 12. Acute Leukemia 99 13. Chronic Myeloproliferative Disorders 125 14. Chronic Lymphoproliferative Disorders 137 15. Malignant Lymphoma 147 16. Multiple Myeloma and Related Paraproteinemia 171 17. Hemorrhagic Diseases 179 18. Transfusion Medicine 201 19. Bone Marrow Transplantations 214 CLINICAL HEMATOLOGY 4 Appendices: I. Hematological Tests and Normal Values 221 II. CD Nomenclature for Leukocytes Antigen 226 III. Cytotoxic Drugs 228 IV. Drugs Used in Hematology 230 Glossary 232 Answers 246 Bibliography 247 CLINICAL HEMATOLOGY 5 CLINICAL HEMATOLOGY 6 HEMATOPOIESIS 1 All of the cells in the peripheral blood have finite life spans and thus must be renewed continuously.
    [Show full text]