Category Archives: Heamatology

Blood, Bone Marrow and Lymphatic system.


Hemophagocytic Lymphohistiocytosis (HLH) is a type of Cytokine Storm Syndrome caused due to uncontrolled proliferation of morphologically benign Macropages and Lymphocytes secreting copious amount of Inflamatory Cytokines resulting into Hyperinflamation.



Mutations or Single Neuclotide Polymorphism in certain genes gives rise to HLH it can be germ-line defect or may be acquired. There are other factors as well which may cause secondary HLH(sHLH).

  • PRIMARY HLH -Primary that is without any other underlying disease in background it is termed as HLH
  • SECONDARY HLH (sHLH) – HLH secondary to some other primary underlying disease condition or Iatrogenic factors in the backgroung is termed as Secondary HLH or (sHLH)


  • T-cell lymphoma
  • B-cell lymphoma
  • ALL – Acute Lymphocytic Leukemia, 
  • AML – Acute Myeloid Leukemia,
  • Myelodysplastic Syndrome
  • Juvenile Idiopathic Arthritis
  • Juvenile Kawasaki Disease
  • SLE – Systemic Lupus Erythematosus
  • Juvenile/Adult onset Still’s Disease,
  • RA- Rheumatoid Arthritis
  •  Severe Combined Immunodeficiency 
  • DiGeorge Syndrome
  • Wiskott – Aldrich Syndrome
  • Ataxia – Telangiectasia
  • Dyskeratosis congenita
  • EBV -Epstein Barr Virus
  • CMV -Cytomegalovirus
  • HIV – Human Immunodeficiency Virus
  • nCoV2019/SARS-CoV-2 probable
  • Certain Bacterias, Fungus and Protozoas


  • Bone Marrow Transplant
  • Organ transplantations
  • Chemotherapy
  • immunosuppressive treatment


HLH is caused due to genetic mutations that may be germ-line defect or acquired

Mutation in gene responsible for decoding a proyien protein in Cytotoxic T-cells and Natural Killer cells which killes virus infected is one of the known factor causing HLH

Genes that have been identified as contributor to HLH are UNC13D, STX11, RAB27A, STXBP2, LYST, PRF1, SH2D1A, BIRC4, ITK, CD27, MAGT1 any SNP or mutation in above mentioned gene that causes decfect in ability to kill virus infected cells or damaged cells.

As the Cytotoxic T-cells and NK-cells lose their ability to kill cells infected with virus or other damaged cells, due to mutation of above mentioned genes, consequently results into uncontroled proliferation of immune system secreting excess quantity of cytokines causing excessive accumulation of Interleukine 1, Interleukine 6, Tumour Necrosis Factor-Alpha, Tumour Necrosis Factor-gamma, Plasminogen Activating Factor, Ferritin etc.

Now excess of IL1,IL6&TNF-alpha leads to fever

TNF-alpha and TNF-gamma in excessive proportion aslo leads to suppression of Heamtopoesis resulting into Cytopenia and inhibition of Lipoprotein Lipase to stimulate Triglyceride Synthesis.

Excess of Plasminogen Activating Factor and Ferritin secreted by activated macrophages leads to Hyperfibrinolysis.


In 70% cases the onset is below one year of age.

  • Fever, nausea, vomitting, weakness, debility
  • Hepatomegaly with fatty infiltration in liver
  • Elevated Liver Enzymes
  • Icterus and rashes
  • Spleenomegaly may also show multiple small granulomas in spleen
  • Lymphomegaly may also show calcified nodes
  • Erythrocytopenia- Reduced Red blood cells
  • Leucocytopenia – Reduced White Blood Cells
  • Thrombocytopenia – Reduced Platelets
  • Reduced Serum Albumin
  • Sphingomyelinase elevated
  • Reduced Fibrinogen
  • Elevated Ferritin especially in children of above 10000 is very sensitive and specific for HLH, but no so in adults.
  • Incresase D-Dimer, CRP and ESR


All patient with Hyperferritinaemia combimed with Cytopenia should be suspected for HLH and soon be considered for further investigations without wasting time.

To be clinically corelated with above mentioned sign and symptom of clinical presentation and investigations and bone marrow biopsy as mentioned below

  • Bone Marrow Aspiration and Imprint may show Hemophagocytosis, Cellular Marrow having Dimorphic Maturation with increased Histiocytes and Megakaryocytes

Other Investigations

  • CBC – reduced RBC, WBC and Platelets
  • CRP elevated
  • ESR elevated
  • D-Dimer elevated
  • Serrum Ferritin elevated
  • Liver function Test – liver enzymes elevated
  • Ultrasonography of whole abdomen – Spleen, Liver and Lymphnodes enlarged

Homeopathic Treatment and Medicines of HLH

Its a life-threatening condition and one should not waste time even in suspected cases and all patient with elevated ferritin along with cytopenia should soon be sent for bone marrow biopsy and other confirmatory supportive tests and be kept under constant medical observation.

Homeopathic prescription for HLH should be strictly derived on basis of symptom similarity basis and the potency of homeopathic medicines and repetition of doses should be as per susceptibiloty of the patient and disease symptom and severity as per homeopathic principles.

Homeopathic Medicines for HLH

Below are few homeopathic medicines that could be theraputically indicated and may proove useful in cases of HLH.

  • Aconitum Nepellus
  • Belladona
  • Arsenicum Album
  • Lycopodium
  • Cholestrinum
  • Crategus Oxyacantha
  • Cinchonna Officinalis
  • Ferrum Phosphoricum
  • Tuberculinum
  • Syphillinum
  • Natrum Muriaticum

Homeopathic medicines for HLH should be strictly dispensed under guidance and observation of homeopathic physician


Autoimmune Hemolytic Anaemia (AIHA) also called Immunohemolytic Anaemia is an autoimmune condition where in there are antibodies driven against our own Red Blood Cells. Due to which there is excessive destruction of RBC reducing oxygen carrying capacity of blood.


Causes of AIHA

Autoimmune Hemolytic Anaemia (AIHA) is believed to be caused due to genetic predisposition and environmental insults on the genome. Still no specific HLA locus has been found which can be related with AIHA in other words, no Human Leucocyte Antigen association has been established yet.

It can be also be secondary to other Autoimmune diseases, Cancers and Infections as mentioned below

1) Autoimmune diseases

  • Systemic Lupus Erythematosus (SLE)
  • Rheumatoid Arthritis(RA)
  • Crohn’s Disease
  • Ulcerative Colitis
  • Scleroderma
  • Autoimmune Hepatitis
  • etc

2) Cancers

  • Chronic Lymphocytic Leukemia
  • Non-Hodgkin’s Lymphoma
  • Other Blood Cancers

3) Infections

  • Mycoplasma infections
  • Cytomegalovirus(CMV)
  • Epstein-Barr Virus
  • Human Immunodeficiency Virus (HIV)
  • Infectious Mononeucleosis
  • Viral Pneumonitis
  • Viral Hepatitis

Differentiation of AIHA

Based on optimal temperature required for reaction of autoantibody of IgG class and autologous erythrocytes AIHA can be differentiated into

  • Warm Autoimmune Hemolytic Anaemia (wAIHA)
  • Cold Autoimmune Hemolytic Anaemia, further classified into i)Cold Aglutinin Disease (CAD) and ii) Paroxysmal Cold Heamoglobinuria(PCT). These both subtypes can be acute or chronic.
  • Mixed Type
  • Atypical (DAT- negative, IgM -wAIHA)
  • Drug Induced

Classification of AIHA

Clinically AIHA can be clasified as Primary or Secondary

Primary AIHA – It is also called Idiopathic AIHA has no known underlying causative factor and presents itself with hemolysis as predominant feature and other complaints are secondary to it. This type can either be cold or warm thermal relation to reaction mention in above differentiation.

Secondary AIHA – It is usually associated with some primary underlying disease condition. This type usually shows cold thermal relation in reaction that is Cold Agglutinin Disease Category.


Autoimmune Hemolytic Anaemia characterises itself by presence of Anti-RBC autoantibodies with or without activation of Complement-Cascade causing excessive destruction of Erythrocytes(RBC).

There are many mechanisms involved in pathogenesis of AIHA. It is a complex scenario with many mechanisms involing Autoantibodies, Phagocytosis, Antibody Dependent Cell-Mediated Cytotoxity, B Lymphocutes and T Lymphocytes, T regs, Cytokines, and Complement System.

Antibody Dependent Cell-Mediated Cytotoxicity (ADCC)

Auto-antibodies are formed by both tissue and circulating self reactive B-Lymphocytes in co-ordination with T-Helper Lymphocytes.IgG sub-classes IgG1 IgG2 IgG3 and IgG4 are involved in ADCC.

Cytotoxic CD8+ T cells and NK cells opsonize the RBC’s with fc portion of IgG for attracting fc receptors on macrophages thus resulting in destruction of RBC by phagocytosis. Occurs in Spleen and lymphoid organs.

Note- Spleenectomy in most cases doesnt have much effect on the disease as in slpeen the erythrolysis is in very lesser proportion in most AIHA cases.

Activation of Final Components of Complement Cascade (Membrane Attack Complex)- DIRECT LYSIS.

IgM dependent- IgM mediated compliment activation results in direct osmotic lysis of RBC, through sequential activation of Membrane attack complex(MAC), in circulation. Also C3b opsonisation of red blood cells by compliment activation results into extracellular erythrolysis by kufper cells of liver, 10 folds more destruction of RBC if compared to ADCC. IgG1 and IgG3 are also responsible in compliment activation to some degree. Majority of erythrolysis is extravascular especially in liver by kufper cells.


Symptoms develop gradually over months with presenting symptoms usually proportionate to degree of anaemia

  • General signs of anaemia depending on degree of anaemia like weakness, lethargy, breathless, etc
  • signs of Red blood cell destruction.
  • Heamoglobinuria
  • Spherocytes in RBC morphology
  • Increased LDH
  • Spleenomegaly
  • Hepatomegaly
  • Reticulocytes in Circulation
  • Hepatoglulin
  • Jaundice which may be mild to moderate or even severe
  • Angina


  • COOMB’s Test
  • DAT test
  • CBC
  • LDH


  • Ferrum Metallicum
  • Ferrum Phosphoricum
  • Calcarea Phosphoricum
  • Calcarea Flourica
  • Ruta
  • Calcarea Carbonica
  • Lycopodium
  • Cinchonna Officinalis
  • Arsenicum Album
  • Lachesis
  • Naja
  • Chelidonium Majus


Anaemia can be defined as decreased haemoglobin counts or reduced red blood cell counts or reduced oxygen carrying capacity of blood, due to “loss of” or “abnormality of” red blood cells or haemoglobin.

Normal Heamoglobin Counts

  • 6 months to 5 years of age > 11g/dl
  • 5 years to 12 years of age > 11.5g/dl
  • 12years to 16 years of age > 12g/dl
  • Adult Females (non-pregnant) > 12g/dl
  • Adult Females (pregnant) > 11gm/dl
  • Adult Males > 13g/dl


  • Blood losss
  • Excessive Red Blood Cell destruction
  • Heamoglobinopathies
  • Hypovitaminosis B12
  • Hypoferremia
  • Anaemia of Chronic diseases
  • Autoimmune haemolytic anaemia
  • Inflamatory bowel diseases
  • Hypervolemia or water retention due to sodium or other salts.
  • Genetic hereditary conditions like Thalasemia
  • Certain cancers
  • Kidney diseases
  • Reduced erythropoetin production
  • Excessive RBC destruction
  • Impaired RBC production
  • Certain infections like malaria which causes RBC destruction.
  • Certain drugs which causes RBC destruction eg. Quinine causes chinchonism.
  • Bone Marrow lesions and pathologies
  • Etc.


There are many types of anaemias. It can be broadly classified into 7 categories depending upon their causes

Anaemia due to

  1. Blood Loss
  2. Hemolysis
  3. Impaired or abnormal Erythropoesis
  4. Hypervolemia
  5. Chronic Diseases
  6. Nutritional deficiency

Based on RBC morphology it can be classified into 3 groups

  • Microcytic
  • Macrocytic
  • Normocytic


  • Iron Deficiency Anaemia
  • Aplastic Anaemia
  • Megaloblastic Anaemia
  • Pernicious Anaemia
  • Sideroblastic Anaemia
  • Autoimmune Hemolytic Anaemia
  • Myelodysplastic Syndrome
  • Thalasemia
  • Fanconi Anaemia
  • Congenital Dyserythropoetic Anaemia
  • Daimond-Blacfan Anaemia
  • Myelopthisis
  • Anaemia of Prematurity
  • Erythroblastopenia or Pure Red Cell Aplasia
  • Hereditary Spherocytosis
  • Hereditary Elliptocytosis


  • Weakness
  • Lethargy
  • In children it affects growth in general
  • Somnolence, Drowziness in day time
  • Disturbed sleep at night
  • Pallor, general pale appearance of skin, mucous membranes and eyes.
  • Dyspnoea on Exertion.
  • Reduced Immunity, tendency to catch infections and slow recovery and healing.
  • Bodyaches
  • Cyanosis in severe cases
  • Palpitations
  • Tachycardia
  • Low blood pressure
  • Chest pain
  • Depression
  • Craving for indigestible things , PICA
  • Cold clammy extremities
  • Oedematous swelling of extremities, dependent oedema
  • Angina or cardiac failure in severe cases
  • Will impact general growth and repair of all the vital organs and tissue of the body.


Depending upon the cause of anaemia and general constitution of the patient, one of the following medicines may be called for duty by a homeopathic physician.

  • Ferrum Metallicum
  • Ferrum Phosphoricum
  • Cinchonna Officinalis
  • Natrum Muriatic um
  • Arsenicum Album
  • Abrotanum
  • Hamamelis Verginiana
  • Pulsatilla Nigricans
  • Janosia Ashoka
  • Crotalus Horridus
  • Lachesis
  • Acidum Phosphoricum


Thalasemia is a genetic disorder where in mutation or deletion in any genes responsible to produce globin chain of haemoglobin results in abnormal haemoglobin production.

Normal adult has Haemoglobin A (HbA). HbA is a hetrotetramer of two α globin chains and two β globin chains. In normal humans there are total 4 genes (2pairs) for production of αglobin chain and 2 genes(1 pair) for production of β globin chain. When there is defect in genes producing α globin or β globin chains of heamoglobin it results into thalasemia.


  • Alpha Thalasemia – Abnormal or dhieficient α globin chain production
  • Beta Thalasemia – Abnormal or deficient β globin chain production.
  • Delta Thalasemia – Abnormal or defective delta chain production.
  • Thalasemia in combimation with other haemoglobinopathies like – Haemoglobin S , Haemoglobin E, Haemoglobin C, Haemoglobin D.

Of the above all types the most common types alpha and beta are discussed below.


Alpha Thalasemia has defective α globulin chain production. Genes responsible to produce α globin chain are situated on chromosome 16. HBA1 and HBA2 genes are responsible for production of α globin chain. Both the genes are acquired from both the parents so total two HBA1 and two HBA2 genes. So, there are two genes acquired from each parent making total 4 genes or two pairs(αα/αα) responsible to produce α globin chain.

Depending upon number of gene deleted the condition is classified into 4 categories

  • α Thalasemia Silent (1 gene deletion)
  • α Thalasemia Trait (2 gene deletion)
  • HbH disease (3 gene deletion)
  • Hb Bart Syndrome (all 4 gene deletion)

Alpha Thalasemia Silent

Any one gene deletion (-α/αα), one of the two allele not received from one parent. Usually there are no sign of anaemia as the remaining three genes produce sufficient alpha globin chains. Althought they dont show symptoms they are the silent carrier and if married to person with one or more α globin making gene deletion then some of their offsprings will have symptoms, probability and severity of the disease in the offsprings will depend on number of gene deletion in the partner.

Alpha Thalasemia Trait

Any two gene deletion, it can be of two genotypes as descussed below, this type shows mild anaemia symptoms.

  1. Two gene deletion – homologous; one of the two allele not received from each parent(-α/-α).
  2. Two gene deletion- heterologous; both the alleles not received from one parent (–/αα).

HbH Disease

Three gene deletion (–/-α) No copy of gene received from one parent and only one of the two copy received from another parent. These causes very low α chain production resulting into excess proportion of β chains causing formation of unstable haemoglobin tetramer made up of 4 β globin chains, instead of two α and two β. This type of haemoglobin with all 4 globin chain of β globin is called HbH which is very unstable. These individuals shows moderate to severe anaemia and other thalasemia related symptoms.

Hb Bart Syndrome

All four gene deletion (–/– )No copy of α chain producing gene received from either of the parent. It is a fatal condition where in there are no α chains produced and results into severe fetal condition called hydrops fetalis. Death ensues soon after birth.


Beta thalasemia has defective β globin chain production. For production of β globin chain there is only one gene acquired from each parent makin it total one pair(β/β) i.e total 2 genes responsible to produce β globin chain. Gene Responsible for production of β globin chain is called HBB and is located on chromosome 11.

Beta Thalasemia Minor

  1. (b/β) One gene received from a parent is altered and the one from other parent is normal.
  2. (-/β) No gene received from a parent and the gene received from another parent is normal.

Beta Thalasemia Intermedia

  1. (b/-) One copy of gene received from a parent altered and one from another parent is absent.
  2. (b/b) Genes received from both the parent are altered.

Beta Thalasemia Major

  • (-/-) No genes producing β globin chain received from either parent.


Symptoms and its severity depends upon the above mentioned severity of genotype the individual has few complaints which patient with this disease condition show are mentioned below.

  • Anaemia
  • Iron Overload
  • Bone deformities
  • Enlarged spleen
  • General growth is slow
  • Ferquent Infections
  • Cardiac complaints


  • Complete blood count
  • Hb Electrophoresis
  • DNA analysis.


  • Cinchonna Officinalis
  • Abrotanum
  • Natrum Muriaticum
  • Phosphorus
  • Calcarea Phosphorica
  • Calcarea Carbonica
  • Calcarea flourica
  • Ruta Graveolens


LYMPHOMA – Malignant neoplasm of lymphoid tissue is called Lymphoma.

They are type of blood cancers where in there is abmormal cell-proliferation of Lymphoid Tissue.

Lymphomas and Leukemias both fall under a broader category “Malignant Neoplasms of Lymphoid and Heamatopoetic Tissue” or cancer of Lymphocytes”. Wherein unlike Leukemias, the term Lymphomas is precisely restricted only to the Tumours of Lymphoid tissue.

Types of Lymphoma

  • Hodgkin’s Lymphoma
  • Non Hodgkin Lymphoma
  • Multiple Myeloma
  • Immunoproliferative diseases


Hodgkin’s Lymphoma

  • Hereditary
  • Epstein Barr Virus Infection

Non Hodgkin’s Lymphoma

  1. Autoimmune Conditions
  2. HIV infection/AIDS
  3. Human T-Lymphotropic Virus Infection
  4. Immunosupressive Medication
  5. Exposure to certain Pesticides
  6. Tobacco Smoking


  • Lymphadenopathy
  • Pel-Ebstein Fever – Intermittent Fever of around 38C lasting for 1-2weeks and relapsing again after days to weeks
  • Weight loss of more than 10% within 6 months.
  • Profuse perspiration especially at night.
  • Anorexia – loss of appetite
  • Weakness and fatigue
  • General Pruritus
  • Dyspnoea on slightest exertion

Ann Arbor Staging System

Principle Stages

  • StageI – Single Lymphnode and surrounding area involved
  • StageII – Two areas involved a lymph node and another area and both are on the same side of daiphram either above or below
  • StageIII – Affected areas on both the sides of daiphram with one organ or region near lymphnode or spleen
  • StageIV – Diffused and disseminated with more than one Extra-Lymphatic organ involved incliding Liver, Bone Marrow, nodular involvement of Lungs.


  • A or B – type symptom – When patient has following three constitutional symptoms then patient is categorised into B-type symptoms 1) Pel-Ebstein Fever. 2) Weight loss and 3)Night Sweats. When there are no above mentioned combination of B-type constitutional symptoms present then patient is categorised into A type.
  • S ” – Disease with Slpeen involvement is denoted with S modifier.
  • ” E” – When disease involves extranodal region that is region surrounding the lymphnodes it is denoted with E modifier.
  • “X” – X is denominated when the largest bulky deposit region is more than 10cm or if more 35% area of chest is occupied by mediastenum on X-Ray.

Nature of Stage

  • Clinical Staging “C.S.” – C.S. Mentioned when staging is done based on clinical examination and test.
  • Pathological Staging “P.S.” – When Staging is done based on pathological findings through invasive techniques like surgical excision etc its Mentioned as P.S.


Biopsy of Lymph node to confirm Lymphoma.

Further to classify Lymphoma:

  • Immunophenotyping
  • Flow Cytometry
  • Fluorescence in-situ Hybridisation.

CT scan and PET scans helps us evaluate extent of spread of the condition and its staging.




Abnormal proliferation of blood cells due to defective medullary heamatopoetic stem cells is called leukemia.

In Layman terms, defective bone-marrow causes uncontrolled multiplication and abnormal growth of cells that are components of blood causing blood cancer.


Based on speed of progression and maturity level of most cells, most of the Leukemia can be categorised into

  • Acute – Fast progressing, takes weeks to few months, most of the cells are blast cells (immature cells), requires immediate treatment, commonly seen in children.
  • Chronic – Relatively slow progressing, takes months to years, has relatively mature cells, patient usually under observation before commencing any aggressive treatment, Common in elderly people.

There are some leukemias which do not follow fixed pattern, even the presentation of symptom may vary in different individual, also there are cases where in they change the classical course and speed of progression.

Based on types of cells involved, most of the Leukemia can be categorised into

  • Lymphoid (Lymphocytic) – Precursors of Lymphocytes are involved. It is further classified as per which lymphocytes are involved wether B-cells or T-cells.
  • Myeloid(Non-Lymphocytic) – Precursors of RBC, Non-Lymphocyte WBC and Platelets are involved.

A Lymphoid or Myeloid leukemia can Either Acute or Chronic as described below

  1. Acute – Lymphoblastic(ALL)
  2. Chronic – Lymphocytic (CLL)
  3. Acute – Myeloid (AML)
  4. Chronic – Myeloid (CML)


Acute Lymphoblastic Leukemia (ALL) –

When there are multiple mutations in the locus that controls cell proliferation, cell maturation and cell death of precursor cells of Lymphocytes, called Lymphoblast, then this results in ALL. ALL can be of T cell type or B cell type.

Genes associated with ALL –

  • KMT2A – Infant ALL – onset before 10yr of age
  • ARID5B
  • CKDN2A
  • CKDN2B
  • TP53
  • GATA3
  • PIP4K2A
  • IKZF1
  • PAX5 – Inherant Autosomal Dominant
  • ETV6 – Inherant Autosomal Dominant

Certain syndromes that increases risk of ALL

  • Down’s Syndrome
  • Bloom Syndrome
  • Fanconi Anaemia
  • X-Linked agamaglobulinaemia
  • Neurofibromatosis Type 1
  • Li-Fraumani Syndrome
  • Paroxysmal Nocturnal Heamoglobinuria
  • Severa Combined Immunodeficiency
  • Costmann Syndrome
  • Ataxia Telangiectasia
  • Schwachmann Daimond Syndrome


  • Precursor B-cell ALL
  • Precursor T-cell ALL
  • Mature B-cell ALL (also called Burkitts Leukemia due to its similarity with Burkitts Lymphoma)
  • Acute Biphenotypic Leukemia.

Acute Myeloid Leukemia (AML)

It is an Acute Non-Lymphocytic type of malignanacy that involves myeloblast cells(precursor of monocytes and granulocytes).

In AML, there are mutations in genes responsible for maturation and differentiation of the myeloblast cell, so the cell freezes in undifferentiated and immature state. When this type of mutations are combined with mutations in genes controlling proliferation in same cell, it results in clonning of immature undifferentiated cells resulting in AML.

Genes associated with AML

Subtypes of AML

Subtypes of AML are classified based on staging of maturation i.e. at which stage the msturation of the cell is arrested and how is the general behaviour of cells and which genes are involved.

  • Undifferentiated Acute Myeloblastic Leukemia
  • Acute Myeloblastic Leukemia with Minimal Maturation
  • Acute Myeloblastic Leukemia with Maturation
  • Acute Pro-Myelocytic Leukemia (APL)
  • Acute Myelomonocytic Leukemia
  • Acute Myelomonocytic Leukemia with Eosinophilia
  • Acute Monocytic Leukemia
  • Acute Erythroid Leukemia
  • Acute Megakaryoblastic Leukemia

Adult T-Cell Leukemia

Blast Crisis of CML


Chronic Lymphocytic Leukemia (CLL)

  • B-cell Pro-Lymphocytic Leukemia(B-PLL)
  • T-Cell Pro-Lymphocytic Leukemia(T-PLL), T-PLL doesnt completely fit into this category.

Hairy-Cell Leukemia(HCL)

Large Granular Lymphocytic Leukemia(LGLL)

Chronic Myeloid Leukemia (CML)

  • Chronic Granulocytic Leukemia
  • Juvenile CML
  • Chronic Neutrophillic Leukemia
  • Chronic Myelo-Monocytic Leukemia(CMML)
  • Atypical CML (aCML)

Chronic Eosinophillic Leukemia

Few other types, preleukemias and syndromes that cannot be classified in above category

  • Clonal Eosinophilia
  • Other Myelodysplastic Syndromes
  • Other Myeloproliferative Syndromes


Leukemia is caused due to mutations in genes that are associated with proliferation, differentiation, growth, maturation and cell death of blood cells. With different types of mutations responsible for different types of leukemia.

These genetic mutations can be inherited or acquired due to multiple reasons of which few known risk factors are

  • Exposure to certain chemicals (e.g. benzene, petrochemicals, hair-dyes, agent orange herbicide, certain insecticides)
  • Radiation – ionising radiations and doubtedly non-ionising radiations too.
  • Smoking and tobacco use.
  • Prior alkylating chemotherapy for some other form of malignancy.
  • Viruses – Human T-cell Lymphotropic Virus – 1 HTLV-1 is associated with Adult T-cell Leukemia and Hepatitis C is associated with CLL
  • Diseases and Syndromes – Down’s Syndrome, Kline Felter syndrome, Fanconi Anaemi, Ataxia-Telangiectasia or Louis-Bar Syndrome, Myelodysplastic syndrom, Myeloproliferation syndrome.

Few of these factor are seen responsible for specific type of cancer (eg HTLV1 causes Adult T-cell Leukemia, Tobacco and Down’s Syndrome increases risk of AML).


Symptoms may vary in different types of leukemia, different individuals and different stages of disease.

  • Tired feeling
  • Paleness due to anaemia
  • Shortness of breath
  • Headache, lethargy, stiffness of neck
  • Loss of appetite
  • Weight loss
  • Tendency to catch infection too frequently
  • Fever usually due to secondary infections
  • Painful long bones
  • (Heamorrhagic diathesis) easily bleeds and frequent ecchymosis and petechiae (bruises).
  • Painless lymphomegaly (Enlarged lymphnodes)
  • Hepatospleenomegaly – can easily palpate liver and spleen due to its increased size.
  • Fibrosis of bone marrow
  • Chloroma or Leukemia Cutis or myeloid sarcoma or granular sarcoma or extramedullary myeloid tumour
  • Swollen painfull and bleeding gums
  • Sweet’s Syndrome
  • Pitting Oedema
  • Enlarged Testis
  • Mediastinal mass
  • Cranial nerve Paralysis if CNS is involved
  • Increased blood cell count , WBC or RBC or Platelets, depending on type with most if the cells immature and lacking differentiation.


  • Complete Blood Count
  • Bone Marrow Biopsy
  • Lymph Node Biopsy


  • Arsenicum Album
  • Phosphorus
  • Hekla lava
  • Lachesis
  • Benzinum
  • Carica Papaya
  • Cinchonna Officinalis
  • X-ray
  • Thuja Occidentalis
  • Syphillinum
  • Baryta Carbonica
  • Calcarea Phosphorica
  • Ruta Graveolens
  • Calcarea Fluorica
  • Calcarea Carbonica
  • Symphytum Officinalis
  • Hyocyamus Niger
  • Medhorrhinum



Mycosis Fungoides is a type of Non-Hogkin Lymphoma. It is the most common type of Cutaneous T-Cell Lymphoma(CTCL).

Mycosis Fungoides is a misnomer which means “Mushroom-like fungal disease” but by no means it is a fungal condition. It is a type of blood cancer caused due to unusual expression of Skin-associated CD4 T-Cells. This cancer affects skin and produces various lesions on skin and rarely metastatise in other tissues.

It is a fatal condition with 10year survival rate of less than 70% which is even less in elderly.

It usually appears in people above 20years of age and is more common after age of 50yrs , males are affected more than females, the disease tends to be more fatal in black race. Survival rate has been found good in married white women.


Causes of Mycosis Fungoides remains unclear

No hereditary or genetic factors have been found associated to the disease.

It is considered to be non-contagious but some studies suggest that Human T-cell Lymphotropic Virus is associated with this condition.


Initially disease shows symptoms that are not distinguishing and in most of the cases it resembles psoriasis or eczema. Even on biopsy it can not be diagnosed easily in early stages. Even in later stages multiple biopies are required to establish diagnosis.

Disease presentation begins from skin as exfoliating, pruritic, erythodermic eruptions resembling to Eczema or Psoriasis and is almost always mistaken initially in most cases. These eruptions tends to appear first on buttocks in vast majority of cases and then spreads throughout the body. Pruritus is present in only 20% of all the cases. In later stages tumourous and ulcerative lesions may also appear. Disease usually in most cases starts appearing at around age of 45-50 and is a slow prohressing condition with and its usually around age of 60+ that mist patient starts presenting symptoms of later stages like tumours, generalised pruritus and erythrodrema and ulceration. Though in many cases it may start as early as age of 20 and rarely before 20yrs of age. The diseases is classified into three stages

Stages of Mycosis Fungoides

Mycosis fungoides is divided into three stages viz.

  1. Pre-Mycotic
  2. Mycotic
  3. Tumourous

Pre Mycotic Stage

It starts appearing on skin at this stage as erythematous, pruritic, exfoliating skin eruptions.

On biopsy it cannot be diagnosed at this stage as histopsthology shows pattern of non specific dermatosis with epidermal psoriasiform changes.

Mycotic Stage

In Mycotic stage Infiltrative Plaques starts appearing as slightly raises or wrinkled spots.

On histopathology polymorphs and few atypical lymphoid cells are seen inflamatory infiltrates in dermis. When this cells are seen lined epidermal basal layer without spongiosis then its confirmatory finding to establish diagnosis of mycosis fungoides.

Tumorous Stage

Nodular overgrowths are seen on skin ranging from few milimeters to centimeters scattered throughout the body along with plaques and patches. Usually it appears on the same place where the plaques and patches are. Also there is erosion of the tumours and ulcerations is seen in many cases over the tumour and plaques.

On histopathology they show medium sized lymphocytes with cerebroid nuclei expands dermis.


Diagnosis is based primarily on histopathological findings of the skin lesions

Clinically patients showing features suggestive of or doubted mycosis fungoides are closely monitored over the time untill biopsy confirms. Multiple boipsies of various lesions might be required at every progressing stage untill confirmed, as its very difficult to estsblish diagnosis in initial stafe wether clinically or histopathologically as it resembles psoriasis or eczema.

On histopathology following findings are required to establish diagnosis of mycosis fungoides

  • Band-like lymphocyte infiltrate in superficial papillary dermis
  • Epidermotropism
    • Cerebroid T-cells in dermal and epidermal infiltrate
  • Pautriers Microabscesses – though not present in most cases but is characteristic finding of mycosis fungoides where in the epidermal infiltrate shows atypical lymphocytes arranged in aggregates of four or more.


  • Thuja Occidentalis
  • Syphillinum
  • Antimonium Crudum
  • Arsenicum Album
  • Ars Sulph Flavum
  • Phosphorus
  • Argentum Nitricum
  • Hepar Sulphuris
  • Sulphur
  • Silicea