COMPLEMENTARY TREATMENTS
WHY ?
The objective of the associated treatments is the prevention of possible complications of the disease, hematological, bone, infectious and renal.
INFECTIONS
WHY ?
WHAT TO DO ?
IN PRACTICE...
| Kind | Means |
|---|---|
| Systematics |
|
| Vaccination |
|
| Under treatment if recurrent infections |
|
HYPERCALCEMIA
WHY ?
Myeloma cells produce interleukin 6 (IL-6) and osteoclast-stimulating factors, including OAF ( Osteoclast Activating F actor ). OAF is part of the lymphokine family, including in particular a lymphotoxin, produced by stimulated normal lymphocytes and tumor necrosis factor (TNF), produced by normal monocytes.
These two substances lead to a significant stimulation of osteoclasts.
CALCEMIA
Normal values
The total calcemia varies with the level of proteins in the blood or protidemy. Its level must be corrected according to the albumin level. The formula most often used for this correction is: Corrected serum calcium [mg/l] = measured serum calcium [mg/l] + (40 - serum albumin [g/l]).
Ionized calcium more accurately reflects calcium status, particularly in patients with low serum albumin. The normal concentration of ionized calcium is 1.12 to 1.23 mmol/l (45 to 50 mg/l).
Abnormal values
There is hypercalcemia when the corrected calcemia is greater than 2.58 mmol/l (103 mg/l).
Emergency treatment should be instituted if the value is above 3 mmol/l (120 mg/l).
CLINICAL SIGNS
Mild hypercalcemia may remain asymptomatic.
Moderate to severe poisoning can result in various clinical signs.
The following clinical signs should alert you:
- recent constipation
- Loss of appetite (anorexia)
- Abdominal cramps, nausea or vomiting
- Polyuria, intense thirst (polydipsia), dehydration
- nervous disorders
- Asthenia, muscle weakness
- Heart trouble
It should be noted that the precipitation of calcium in the kidney can lead to acute renal failure.
HOW IS HYPERCALCEMIA TREATED?
The first steps
When the patient becomes symptomatic, treatment should be instituted. It consists of rehydration and the administration of corticosteroids.
Bisphosphonates
Their administration aims to restore bone strength and reduce hypercalcemia, induced by bone destruction.
Clinical studies have demonstrated the effectiveness of zoledronate, pamidronate and clodronate in multiple myeloma in reducing the number of bone events and delaying their onset.
- Clodronate (Clastoban™), active orally at a dose of 1600 mg per day
- Pamidronate (Arédia™), active by injection (IV over two hours) at a dose of 90 mg every month
- Zoledronic acid (Zometa™), active by injection (IV over 15 minutes) at a dose of 4 mg every month
Expected results
Their effectiveness is almost constant, significant drop in calcium from the 2nd day; normalization on the 4-5th day . The duration of action is variable, of the order of 3 weeks. Administered over the long term, these bone resorption inhibitors effectively prevent bone complications of the disease.
The teeth
Before starting the treatment, you will be asked to consult your dentist, and if there is a need for a tooth extraction, this will be carried out before the treatment to avoid osteonecrosis of the jaw.
KIDNEY FAILURE
DEFINITION
We speak of renal failure when the kidneys no longer perform their normal functions of blood purification and urine excretion.
It results in an increase in creatinine in the blood. Better than serum creatinine or uremia, chronic renal failure should be defined by creatinine clearance. The threshold values for defining renal failure are < 60 ml/minute in adults and < 50 ml/minute in the elderly.
WHY ?
There are several possible causes. Kidney failure can result from:
- From the passage of light chains through the glomerulus into the tubule and precipitating there
- From hypercalcemia which induces hypercalciuria, itself toxic for the renal tubule.
- From amyloidosis
- Glomerulopathies with unorganized immunoglobulin deposits, due to a deposition of lambda heavy and/or light chains in the glomerulus
- Kidney infection due to reduced immune defenses
Anuria (absence of urine) is favored by hypercalcemia, hyperuricemia, but above all the urinary elimination of free light chains (Bence-Jones protein) which can precipitate in the tubules in the event of dehydration or injection of iodinated contrast product for an X-ray or a scanner.
THE DEGREE OF KIDNEY DAMAGE
There are three phases in renal failure. First stage of moderate renal failure. It is defined by a serum creatinine level < 20 mg/l and clearance > 40 ml/min, little or no symptoms Second phase of chronic renal failure It is defined by a serum creatinine level < 60 mg/L and a clearance of between 40 and 10ml/min. The clinical manifestations are correlated to the stage of chronic renal failure, but very variable from one patient to another. Third phase of severe chronic renal failure When the clearance of serum creatinine is less than 10ml/min, dialysis or transplantation become necessary.
WHAT TREATMENT?
It is essentially preventive and consists of the introduction of the following measures.
- The maintenance of sufficient hydration and the alkalinization of the urine by taking plenty of drinks: 2 to 3 liters of Vichy water per day.
- The energetic treatment of any dehydration.
- The prudent use of drugs dangerous for the kidney (nephrotoxic)” such as certain chemotherapy drugs (cisplatin), anti-inflammatories (NSAIDs) used to relieve pain or iodinated contrast products, used for medical imaging.
AMYLOIDOSIS
A DEFINITION …
Amylose comes from the Greek amulon which means starch. Its name was given to it in 1854 by Rudolf Virchow, a German doctor born in 1821 in Schivelbein, Prussia and died in 1902 in Berlin.
These are deposits, made up of proteins, called amyloid substance, that is to say resembling starch.
A DISEASE OR DISEASES?
Amyloidosis is not a single disease but a term encompassing a group of diseases that share a common histological characteristic, the extracellular deposition of pathological insoluble fibrillar proteins in organs and tissues.
In the case of myeloma, these are intercellular deposits of amyloid substance formed from light chains (exceptionally heavy chains) of immunoglobulin.
The fibrillar nature of the amyloid substance and its so-called beta-pleated sheet configuration is responsible for the Congo red staining giving an apple green color in polarized light.
These deposits can be seen in several areas of the body. As long as the deposition takes place in a single organ, there are no unfortunate consequences. When it affects several organs, it is responsible for severe alterations. This disease can therefore take on different aspects between these two extreme cases.
SYMPTOMS
The presentation of the disease is highly variable and reflects which organs are predominantly affected.
It is often responsible for renal complications, such as nephrotic or cardiac syndrome, the most serious.
Sometimes it results in the existence of a large tongue or macroglossia.
A carpal tunnel syndrome which is a compression of a nerve of the hand, the median nerve, at the wrist is found in a third of patients. You should know that most carpal tunnel syndromes are not linked to this disease but, nowadays, to intensive use of computer keyboards...
More rarely digestive, hepatic, cutaneous, rheumatological or neurological damage, even haematological (acquired deficiency in coagulation factor X) can be noted.
THE MANAGEMENT OF
Treatment of the consequences of the deposits
This is a symptomatic treatment which aims to treat the consequences of the disease, more particularly renal. In addition, it helps to control cardiovascular, gastrointestinal manifestations and neuropathy.
The elimination of existing deposits
Its objective is to take care of the different facets of the disease. For this, there is currently no standard treatment.
- Dimethyl sulfoxide (DMSO), an organic solvent, and colchicine have been studied
- I-DOX (4'-iodo-4'-deoxidoxorubicin), an anthracycline used against the plasma cell clone interacting with amyloid deposits, has been the subject of clinical research.
- CPHP (4-(4-chlorophenyl)-4-hydroxypiperidine) would allow an elimination of serum of substance P
- Eprodisate, would interact with glycosaminoglycans is under development in primary amyloidosis.
Suppression of the production of amyloidogenic light chains
It is obtained by treating the disease itself, that is to say stopping the clonal proliferation producing amyloidogenic Ig.
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