Indian Journal of Research in Homeopathy

: 2020  |  Volume : 14  |  Issue : 1  |  Page : 50--56

Holistic treatment of chronic myeloid leukaemia with adjuvant homoeopathic therapy: A case report

RT Shaji Kumar 
 Central Council for Research in Homoeopathy, New Delhi, India

Correspondence Address:
Dr. R T Shaji Kumar
Central Council for Research in Homoeopathy, New Delhi


Introduction: Chronic myeloid leukaemia (CML) is a clonal myeloproliferative disorder of haematopoietic stem cell. Case Summary: This is a case of a 28-year-old female having CML for 1½ years, on regular allopathic medication. The patient was suffering from ulceration in the oral cavity, frequent offensive loose stools with melena and prolonged menstrual cycle with heavy bleeding for 3 weeks. After analysing the constitutional make-up of the patient, Platinum metallicum 200C was prescribed. Over a period of 3 months, the patient reported improvement in weakness, nausea, sleeplessness, irritability, heavy menstruation, loose black stools and backache. Until the last follow-up while submitting this report, the patient was on the maintenance dose of Imatinib along with homoeopathic medication.

How to cite this article:
Shaji Kumar R T. Holistic treatment of chronic myeloid leukaemia with adjuvant homoeopathic therapy: A case report.Indian J Res Homoeopathy 2020;14:50-56

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Shaji Kumar R T. Holistic treatment of chronic myeloid leukaemia with adjuvant homoeopathic therapy: A case report. Indian J Res Homoeopathy [serial online] 2020 [cited 2020 Jul 12 ];14:50-56
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Chronic myeloid leukaemia (CML) is a clonal myeloproliferative disorder of haematopoietic stem cell (HSC).[1] Multiple haematopoietic cell lineages i.e., erythroid, myeloid, B cells and occasionally T cells express Bcr-Abl protein in most CML patients, indicating the presence of this oncogene in HSCs. The strongest evidence of monoclonality of CML was proved in a female patient with X-chromosome linked heterozygote alleles. CML was demonstrated as a clonal disorder being originating from single-unit multipotent stem cells of bone marrow.[2],[3]

The incidence of CML is 1–2 patients per million per year affecting individuals of all age groups. However, the median age of disease onset is estimated at 45–55 years.[4],[5] CML accounts for 20% of all leukaemias in adult patients. One of the characteristic findings in CML patients is the presence of the Philadelphia chromosome and Bcr-Abl (recombinant protein of human breakpoint cluster region-Abelson murine leukaemia viral oncogene) gene re-arrangement. Philadelphia is the shortened chromosome 22, formed by reciprocal translocation between the long arms of chromosomes 9 and 22.[5],[6] Philadelphia chromosome is found in 95% of CML patients, 5% of children and 15%–30% of adults with acute lymphoid leukaemia. In addition, it is also reported in 2% of diagnosed acute myeloid leukaemia patients.[7]

Reciprocal translocation between the long arms of chromosomes 9 and 22 results in the fusion of Bcr-Abl on Philadelphia chromosome. Bcr-Abl gene expresses protein that effects cell growth, turnover, differentiation, adhesion and apoptosis. Abl (Abelson kinase) gene is located on chromosome 9. Abl gene has 11 exons with a molecular weight of 230 kilo base (kb). The upstream exon 2 is usually the breaking point in Abl gene.[8]

CML has three phases. The chronic phase (CP) is most frequent, followed by the accelerated phase (AP) and blast crisis (BC). CP-CML can easily be managed with great cure rate. Additional genetic aberrations of leukemic stem cells result in its progression to AP-CML and BC-CML which are very difficult to manage. These additional genetic chromosomal aberrations can be identified by cytogenetic analysis. Yet, still other genetic changes do occur in stem cells of patients with CML but are not identifiable with the current laboratory testing.[9]

Patients with CML in CP may be asymptomatic, or symptoms may appear before the treatment due to changes in blood cell counts or splenomegaly may be present. CP-CML may resolve promptly once patients are treated effectively. Complications such as infections and bleeding are uncommon during CP-CML. Once treated successfully, patients with CP-CML are completely normal for performing daily life activities.[10]

AP-CML phase if develops may cause fatigue, lethargy and weight loss. Leucocytes may either be very low or high due to the pooling of blast cells. Platelets usually decrease in number. Blast cell counts increase in the peripheral blood and bone marrow. Splenomegaly may be present; the patients become weak with low haemoglobin (Hb). Bleeding and infections are common in the phase. The general well-being of the patient is lost.[11]

During BC, excessive blast cells are pooled in the peripheral circulation and bone marrow. Red cells, neutrophils and platelets are very low. Severe infections are common, and bleeding tendency occurs. Patients complain of generalised weakness, fatigue, dyspnoea, bone pain, abdominal pain and splenomegaly. BC resembles acute leukaemia regarding clinical signs and symptoms.[12] In 25% of patients, transformation of BC culminates into acute lymphoblastic leukaemia, while in the remaining cases, it progresses to acute myeloid leukaemia. CP-CML is characterised by elevated number of myeloid progenitor and mature cells in the peripheral blood and bone marrow.[13] Quantitative reverse transcriptase-polymerase reaction-mediated detection mRNA of Bcr-Abl and visualisation of Bcr-Abl oncogene by double-fusion fluorescent in situ hybridisation also make the diagnosis definite.[14]

If not treated, CP-CML progresses to AP and BC-CML over 3–5 years of onset.[15] It may take several weeks or months for the transformation of CP-CML into AP and BC-CML20. Differentiation of cells becomes blocked in later stages; blast cells accumulate in the bone marrow and blood; at this stage, it resembles acute leukaemias.[16]

Additional cytogenetic abnormalities appear as disease progresses to BC-CML.[17] BC-CML transformation may be lymphoid, myeloid or both and carries very poor prognosis.[18] The median survival time for patients with acute blast cell crisis in CML is 4–5 months and 12 months, respectively.[19] Imatinib mesylate, a selective Bcr-Abl tyrosine kinase inhibitor introduced in the 1909s, has revolutionised the treatment and prognosis of CML. With long-term follow-up, the solid benefits of Imatinib therapy are sustained; the 7-year estimated incidence of durable cytogenetic response is approximately 70%, the estimated 7-year survival is close to 90% and 94% if only CML-related deaths are counted. Among patients who present with accelerated or blastic-phase CML, or who develop Imatinib resistance, allogenic stem cell transplant, second-generation tyrosine kinase inhibitors and Imatinib combinations are the treatment options.[20] Sporadic literature and case records about the use of Homoeopathy in the treatment of CML are available. However, due to lack of evidence in support of the usefulness of homoeopathic treatment, it is not worth mentioning.

 Case Report


A 28-year-old female (homemaker by occupation), hailing from Kasba, Uttar Pradesh, a known case of CML, was admitted to Delhi State Cancer Institute and Hospital (DSCI) on 6 September 2018 for the complaint of ulceration in the oral cavity, frequent offensive loose stools with melena and prolonged menstrual cycle with heavy bleeding for 3 weeks.

She was asymptomatic before 1½ years. Around this time, she developed hepatomegaly for which symptomatic treatment was taken from DSCI. Consequently, bone marrow aspiration cytology on 4 May 2017 suggested a diagnosis of CML-CP [Figure 1]. She was advised to take tablet Imatinib 400 mg/day. The patient discontinued treatment and consulted All India Institute of Medical Sciences, New Delhi. ABL1-tyrosine kinase domain mutation test conducted on 20 July 2018 was found negative and tablet Imatinib was prescribed as the drug of choice [Figure 2].{Figure 1}{Figure 2}

The patient reported in the allopathic private outpatient department on 20 November, 2018, with severe weakness, retrosternal burning, indigestion, nausea, metrorrhagia, melena and weakness of anal sphincter leading to escape of stool along with urine [Figure 3].

Past history – No history of hypertension, diabetes mellitus and tuberculosisObstetric history – P4L3, youngest child was 2-yearold healthy male childFamily history – No confirmed history of cancer in the familyClinical examination – Appearance – sickly, built – moderate, nutrition – moderately nourished, weight – 48.4 kg, pallor – ++, cyanosis – nil, clubbing – nil, jaundice – nil, oedema – nil, dyspnoea – nil, blood pressure – 110/70 mmHg.

To assess the condition of the patient, she was admitted and the following investigations were performed.

Blood routine – Hb – 7.7 mg/dl, total leucocyte count – 2000/mm 3, platelets – 30,000/mm 3Peripheral blood film – Red blood cell (RBC) – microcytic hypochromic; polychromacia; tear drop cells; 1-2 RBC/100 white blood cellsBone marrow aspiration report – Cellularity: low cellular, megakaryocytes: seen, myelocytes: 4%, metamyelocytes: 8%, neutrophils: 8%, lymphocytes: 8%, blast cells: nil, plasma cells: nil, monocytes: 1%. eosinophils: 1%, erythroid cells: normoblastic 70%. ME ratio ~1:2.3Impression – Hypocellular bone marrow aspirateBone marrow biopsy – Hypocellular bone marrow biopsyUltrasonography dated 10 September 2018 revealed hepatomegalyHIV, HbSAg, HCV – Non-reactive.

The patient was transfused with 6 units of platelet concentrate on 22 November 2018, followed by 4 units on 24 November 2018, 2 units on 27 November 2018 and 2 units on 2 December 2018. She was also given injection tranexa 1 amp. I/V × TDS, injection pantop 40 mg I/V × BD, injection flucanazole 1 amp. I/V × OD, injection metrogyl 1 amp. I/V × BD, injection intabolin I/M stat, tablet bescopan TDS, tablet prednizolone 20 mg × TDS.{Figure 3}

The case was referred by the allopathic consultant to the homoeopathic unit on 29 November 2018 with the presenting complaints of ulceration in the mouth with painful swallowing, weakness, nausea, sleeplessness, irritability, heavy menstruation, loose black stools and backache.

History of presenting illness

The patient complained of colicky pain in the abdomen, resulting in watery, sticky black stools 4–5 times daily with itching in the anal area. Menstrual cycles were heavy with passage of black clotted blood. Occasional intermenstrual bleeding/leucorrhoea was also reported to occur. She had no desire to have food. Though tired, she was not able to sleep more than an hour in the night.


The oral mucosa was hyperemic with ulcers on the mucosa and tongue having yellow pus. The patient looked pale and exhausted.

Mental state of the patient

The patient repeated her complaints and pleaded to do something to save her from death. She told that her children are too young to settle down by themselves. She was not permitting her husband to go home to see their children for the fear of his death on the way. It was also noted that the patient was highly irritable and was verbally abusing her husband when he had attempted to narrate the details of her illness.

When talked to her husband separately, he told that the patient picks fights for trivial reasons and keeps abusing him throughout the day. She never accepts her mistakes and if pointed out, picks a verbal fight. At times, she appears very pleasant and happy but soon becomes angry on silly matters.

Repertorial totality

On analysis of the symptoms, the following rubrics were considered and repertorised using Boericke's Clinical Repertory:[21]

Mind: Death, fatal disease, impending evilMind: Fault finding, finicky, cautiousMind: Haughty, arrogant, proudMind: Hysterical (changeable, vacillatory)Stomach: Heartburn, pyrosisAbdomen: Stools pasty, tenacious adhering to the anusAbdomen: Black stools.

Based on the totality and repertorisation, homoeopathic medicine Platinum metallicum 200C (from a good manufacturing practice-certified pharmaceutical company) one dose was prescribed on 29 November 2018 along with Sacchrum Lactis (SL) 3 pills × TDS × 1 day.

Follow-up and outcomes

[Table 1] shows the details of the follow up from November 2018 to the most recent follow up. The patient said that, “I was in extreme weakness and was passing tarry sticky stools about 3–4 times daily and my periods also were lengthy and heavy. I used to be tense and irritable. After the taking homoeopathic treatment, I feel much relaxed, eating and sleeping well, pleasant and my complaints are far better. I want to continue with Homoeopathic treatment to get rid of my remaining problems”.{Table 1}


Imatinib is a powerful inhibitor of the tyrosine kinase activity of Bcr-Abl, the oncoprotein responsible for CML. The drug shows great efficacy in CP but is less effective in maintaining haematologic remissions in BC patients.[22] Low blood counts, nausea and vomiting, oedema, muscle cramps and bone pain, diarrhoea, haemorrhage, skin rash and fever are the common side effects of Imatinib; the drug of choice in CML. The patient in focus also was on daily dosage of Imatinib 400 mg and was suffering from low blood counts, nausea and vomiting, muscle cramps and bone pain, diarrhoea, haemorrhage and fever. Hepatomegaly, anaemia and blood loss through bowels and uterus were persisting with this drug. Even after repeated transfusion of whole blood and components of blood, the blood picture was not returning to normalcy. To assess the causal attribution to the homoeopathic therapy, modified Naranjo algorithm was applied in this case [Table 2].{Table 2}

The patient was suffering from weakness, retrosternal burning, indigestion, nausea, metrorrhagia, melena, weakness of anal sphincter leading to escape of stool along with urine, frustration causing irritability, anxiety about her family and children's future and fear of death from the time of diagnosis of illness. Unfortunately, no one paid attention to her mental agony and the standard treatment protocol had no place for her ordeal.

Despite 14-unit platelet transfusion between 22 November 2018 and 2 December 2018, the platelet count remained poor as per the blood report on 3 December 2018. Patient was also suffering from persisting weakness, anaemia, loss of appetite and sleep. Introduction of homoeopathic constitutional medicine has improved her general condition by increase in oral intake, reduction on irritability, better sleep and reduction in weakness. From the very next day of the prescription of Platinum metallicum 200C, the patient reported that the colour and stickiness of the stool has changed and there was substantial reduction in weakness. The prescription of Platinum metallicum was finalised mainly on the mental features along with physical symptoms such as black tarry sticky offensive stools and menstrual characters. The patient required infrequent repetition of three doses of Platinum metallicum 200C in a period of 3 months to have relief from the long-standing issues of weakness, anaemia, loss of appetite, retrosternal burning, indigestion, nausea, metrorrhagia, melena, weakness of anal sphincter leading to escape of stool along with urine, irritability, etc., It is also appreciable that the patient did not have any blood transfusion for the last 3 months and no hospitalisation since her vital signs are close to normal and leading a normal routine. The patient was on 400-mg Imatinib on a daily basis from the diagnosis of the illness and is now on maintenance dose of 200 mg from 13 December 2018 along with homoeopathic adjuvant therapy. Therefore, it is observed that, reduction in days of hospitalisation due to CML, side effects of conventional therapy, tapering of conventional therapy and costs involved in the hospitalisation and treatment can be effectively managed through homoeopathic constitutional treatment.


Homoeopathy can play key role in supportive care and as integrative medicine in offering safe, and effective way of managing chronic illness such as CML and to combat the side effects of conventional therapy. It may also be helpful to reduce the days of hospitalisation and can significantly improve therapy outcomes as well as patient's quality of life. Further research in this area is required to ascertain the efficacy of constitutional homoeopathic adjuvant therapy in such cases.

Declaration of patient consent

The author certifies that he has obtained informed verbal consent from patient for her images and other clinical information to be reported in the journal. The patient understands that her name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

None declared.


1American Cancer Society. Cancer Facts and Figures; 2008. Available from: [Last accessed on 2019 Mar 22].
2Barret KE, Barman SM, Boitano S, Brooks H. Ganong's Review of Medical Physiology. 24th ed. McGraw Hill Medical Publishing; 2012. p. 507-8.
3Guyton AC, Hall JE. Textbook of Medical Physiology. 11th ed. Philadelphia, Pennsylvania: Elsevier Saunders; 2012. p. 457-60.
4Hoffbrand AV, Moss PA, Pettit JE. Essential Hematology. 5th ed. USA: Blackwell Publishing; 2012. p. 1435.
5National Cancer Institute's Surveillance, Epidemiology and End Results (SEER); 2011. Available from: [Last accessed 2017 Nov 29].
6Available from: [Last accessed on 2019 Mar 22].
7Blot WJ, Henderson BE, Boice JD Jr. Childhood cancer in relation to cured meat intake: Review of the epidemiological evidence. Nutr Cancer 1999;34:111-8.
8Thompson JR, Gerald PF, Willoughby ML, Armstrong BK. Maternal folate supplementation in pregnancy and protection against acute lymphoblastic leukaemia in childhood: A case-control study. Lancet 2001;358:1935-40.
9Smith DL, Burthem J, Whetton AD. Molecular pathogenesis of chronic myeloid leukaemia. Expert Rev Mol Med 2003;5:1-27.
10Vardiman JW, Harris NL, Brunning RD. The World Health Organization (WHO) classification of the myeloid neoplasms. Blood 2002; 100:2292-302.
11Nowell PC, Hungerford DA. A minute chromosome in human chronic granulocytic leukemia. Science 1960;132:1497.
12Rowley JD. Letter: A new consistent chromosomal abnormality in chronic myelogenous leukaemia identified by quinacrine fluorescence and Giemsa staining. Nature 1973;243:290-3.
13Groffen J, Stephenson JR, Heisterkamp N, Bartram C, de Klein A, Grosveld G. The human c-abl oncogene in the Philadelphia translocation. J Cell Physiol Suppl 1984;3:179-91.
14Elefanty AG, Hariharan IK, Cory S. Bcr-abl, the hallmark of chronic myeloid leukaemia in man, induces multiple haemopoietic neoplasms in mice. EMBO J 1990;9:1069-78.
15Kelliher MA, McLaughlin J, Witte ON, Rosenberg N. Induction of a chronic myelogenous leukemia-like syndrome in mice with v-abl and BCR/ABL. Proc Natl Acad Sci U S A 1990;87:6649-53.
16Pear WS, Miller JP, Xu L, Pui JC, Soffer B, Quackenbush RC, et al. Efficient and rapid induction of a chronic myelogenous leukemia-like myeloproliferative disease in mice receiving P210 bcr/abl-transduced bone marrow. Blood 1998;92:3780-92.
17Reuther GW, Fu H, Cripe LD, Collier RJ, Pendergast AM. Association of the protein kinases c-Bcr and Bcr-Abl with proteins of the 14-3-3 family. Science 1994;266:129-33.
18McWhirter JR, Galasso DL, Wang JY. A coiled-coil oligomerization domain of Bcr is essential for the transforming function of Bcr-Abl oncoproteins. Mol Cell Biol 1993;13:7587-95.
19Pendergast AM, Muller AJ, Havlik MH, Maru Y, Witte ON. BCR sequences essential for transformation by the BCR-ABL oncogene bind to the ABL SH2 regulatory domain in a non-phosphotyrosine-dependent manner. Cell 1991;66:161-71.
20Holland JF, Frei E, Hong WK, Bast RC Jr., Hait WN, Kufe DW, et al. Cancer Medicine. 8th ed. USA: People's Medical Publishing House; 2010. p. 1585.
21Boericke W. New Manual of Homeopathic Materia Medica with Repertory: Third Revised and Augmented Edition Based on Ninth Edition; 2007.
22Available from: [Last accessed on 2019 Mar 19].