My parents understood early on in my life that I would likely present them with challenges which might force them to reconsider some of their basic beliefs. What I eventually came to qualify as the Tubercular miasm in myself had found expression in all of my own important life choices. Having emigrated to Russia from the US with my two small children during the turbulent post-perestroika early 90’s, my mother had long ago resigned herself to the possibility that my never-ending search for the sacred homeland would conflict with her desire to have me and my children in close proximity. She had accepted, as well, my vocation as homeopath, even if she couldn’t quite understand what homeopathy is.
And so when she informed me that she had recently been diagnosed with essential thrombocythemia, neither of us doubted that I would insist on treating her with homeopathy. Her physician – a doctor of internal medicine with whom I was well acquainted – had accidentally discovered her platelets to be high on a routine blood test. She had sent her to the oncology department at the local university hospitals and clinics and the diagnosis was confirmed after further testing.
Essential Thrombocythemia (ET) is a chronic myeloproliferative neoplasm (MPN) characterized by an increased number of platelets in the blood. Most commonly diagnosed in women over the age of 50, ET is associated with a proliferation of platelet precursors in the bone marrow and complications frequently include blood clotting and/or bleeding. Less common consequences in the later stages of ET include a transformation to myelofibrosis (marrow scarring) or acute leukemia.
With this disease, as with many others, traditional (allopathic) medicine explains: “No one knows what causes the onset of ET”. One of the greatest contributions to early homeopathic medicine, and certainly one its philosophical foundations, is the understanding of miasms. Miasms don’t point a finger at a single causative agent or a defective gene. Rather they provide an understanding of a specific context, echoed in space and time both within the individual and across generations, that represents latent or explicit expression of form patterns in disease and health. When we grasp the context, the dominant miasm of the individual and the family, we are able to better understand why a particular illness develops in a particular individual. We are also able to make prognoses about potential future illness. And, of course, we then have a far more precise understanding of the nature of the person’s condition. This understanding of the nature of the condition is absolutely essential for effective homeopathic prescribing. Without knowing this we are stabbing at thin air, choosing remedies not based on a totality, but only on surface symptoms.
Allopathic medicine concentrates on the details. It searches for faulty parts and then goes about trying to fix them. Alas, people are not automobiles. Parts don’t have meaning on their own, apart from a totality. Therefore any one symptom, separated from its overall condition, or any one disease entity, separated from the sick person, can’t be understood with any depth of insight. It is an entity floating in space, not attached to anything. This concentration on the parts misleads doctors into making incorrect diagnoses. No disease appears out of thin air. There is a prerequisite inherent in the future patient, a prepared soil. How much wider could traditional medical diagnostics become were it to adopt an understanding of the law of similars!
Having learned of my mother’s diagnosis of ET, the first thing I needed to investigate was the accuracy of the diagnosis. Did it fit into the totality of my mother? Did it represent a particular expression of her dominant miasm, and the family’s miasmatic patterns? Any particular condition has an inherent logic built into it, and that is the logic of the vital force. The vital force always does only what it can with what it has. It can’t be “strong” or “weak”, but it can be forced to go around obstacles. It runs like a river, and rivers can be full of boulders or garbage, beaver dams or boats.
Beyond accurate diagnosis, the homeopath, regardless of his or her medical background, is obligated to study the disease condition in question. We need to understand a disease entity from both the allopathic and homeopathic perspectives. Such an understanding seeks answers to the questions:
- what is the typical course of the disease?
- what are the risk factors of the disease?
- what are the usual treatments? Have there been any documented cases of cure of the disease with homeopathic treatment? What is the experience of treating such a patient with homeopathy?
- what is the mortality rate, with and without regular allopathic treatment?
Familial occurrence of MPNs has long been known. Hereditary predisposition was supported by an epidemiological study from Sweden showing an increased occurrence of these diseases among relatives of MPN patients. Recently, molecular support for these clinical observations was provided by the discovery of an increased frequency of a special haplotype of the JAK2 gene, the 46/1 haplotype, in MPN patients and their first-degree relatives. What allopathic medicine calls “hereditary predisposition”, homeopathy calls miasmatic tendencies. Heredity is more narrow and often involves finding a gene. Miasms are broader and include an entire spectrum of potential disorders.
The WHO diagnostic criteria (as of 2016) for ET include all four of the following:
- Sustained platelet count >450 x 109/L;
- Bone marrow biopsy showing increased number of enlarged, mature megakaryocytic; no significant increase or left-shift of granulopoiesis or erythropoiesis;
- Not meeting WHO criteria for BCR-ABL+CML, PV, PMF, MDS or other myeloid neoplasm;
- Presence of JAK2, CALR or MPL mutation;
- Presence of a clonal marker or absence of evidence for reactive thrombocytosis (for example due to iron-deficiency anaemia).
Risk factors associated with ET include:
- Gender: Women are 1.5 times more likely than men to develop essential thrombocythemia.
- Age: People older than 60 are most likely to develop the condition, although 20% of ET sufferers are under the age of 40.
- JAK2 Mutation: Approximately half of all ET patients have a mutation of the JAK2 gene in their blood-forming cells. This mutation leads to hyperactive JAK (Janus kinase) signaling, causing the body to make the wrong number of blood cells.
- CALR mutation: Nearly a quarter (23.5%) of those diagnosed with MF and ET have a mutation called Calreticulin, or CALR. Discovered in 2013 by two independent laboratories, the identification of the CALR genetic marker has potential implications for treatments and prognosis for those with ET.
The calreticulin gene (CALR) is mutated in about 20-25% of cases of primary myelofibrosis and 20-25% of cases of essential thrombocythemia. The most common mutations (>90%) are caused by either a 52 bp deletion or a 5bp insertion in exon 9 of CALR; both result in a frameshift and premature truncation of the protein. The combination of thrombocytosis and either the JAK2 p.V617F, an MPL exon 10 mutation, or a CALR exon 9 mutation in the absence of bone marrow fibrosis and erythrocytosis may be considered as diagnostic of essential thrombocythemia. Patients with a CALR exon 9 mutation have very high platelet counts but a relatively low risk of thrombosis. Patients with myelofibrosis carrying a CALR exon 9 mutation have an indolent clinical course with better survival than those carrying JAK2 p.V617F or an MPL mutation. The survival is especially superior compared to patients with nonmutated JAK2, CALR, and MPL, who have a very poor prognosis and a particularly high risk of leukemic transformation.
My mother’s test results for the CALR mutation were positive. The lab report reads: A 5 bp insertion, c.1154_1155insTTGTC, or type 2 mutation was detected in the calreticulin gene (CALR), resulting in a frameshift with premature truncation.
ET evolves to myelofibrosis in a minority of cases, whereas transformation to acute leukemia is rare and increases in association with the use of certain therapies. Survival of ET patients does not substantially differ from that of the general population. However, important morbidity is derived from vascular complications, including thrombosis, microvascular disturbances, and bleeding. Because of this, treatment of ET must be aimed at preventing thrombosis and bleeding without increasing the risk of transformation of the disease.
Patients are considered at high risk of thrombosis if they are older than 60 years or have a previous history of thrombosis and at high risk of bleeding if platelet counts are > 1500 × 109/L. Patients with low-risk ET are usually managed with low-dose aspirin, whereas treatment of high-risk ET is based on the use of cytoreductive therapy, with hydroxyurea as the drug of choice and IFN-α being reserved for young patients or pregnant women. For patients resistant or intolerant to hydroxyurea, anagrelide is recommended as second-line therapy. Strict control of coexistent cardiovascular risk factors is mandatory for all patients. The role in ET therapy of new drugs such as pegylated IFN or the JAK2 inhibitors is currently under investigation.
My mother’s oncologist at the university hospitals and clinics in her town was a young woman from India. She immediately prescribed hydroxyurea. This care decision was made despite my mother’s low risk factors. Her platelet count had never exceeded 1,000,000 x 109/L. She never suffered from hypertension and she was not overweight. She did not have diabetes or a history of thrombotic events. These factors alone were sufficient, in my mind, for her doctor to choose an “expectant” path. Yet she was adamant about the chemotherapy.