Moderate hypercalcaemia is a level of 2.88–3.5 mmol/L (11.5–14 mg/dL) while severe hypercalcaemia is > 3.5 mmol/L (>14 mg/dL). ECG
Abnormal heart rhythms can also result, and ECG findings of a short QT interval suggest hypercalcaemia. Significant hypercalcaemia can cause ECG changes mimicking an acute myocardial infarction. Hypercalcaemia has also been known to cause an ECG finding mimicking hypothermia, known as an Osborn wave. Treatments
The goal of therapy is to treat the hypercalcaemia first and subsequently effort is directed to treat the underlying cause. Fluids and diuretics
Initial therapy:
hydration, increasing salt intake, and forced diuresis. hydration is needed because many patients are dehydrated due to vomiting or kidney defects in concentrating urine. increased salt intake also can increase body fluid volume as well as increasing urine sodium excretion, which further increases urinary calcium excretion. after rehydration, a loop diuretic such as furosemide can be given to permit continued large volume intravenous salt and water replacement while minimizing the risk of blood volume overload and pulmonary oedema. In addition, loop diuretics tend to depress calcium reabsorption by the kidney thereby helping to lower blood calcium levels
can usually decrease serum calcium by 1–3 mg/dL within 24 hours
caution must be taken to prevent potassium or magnesium depletion

Bisphosphonates and calcitonin
Additional therapy:
bisphosphonates are pyrophosphate analogues with high affinity for bone, especially areas of high bone-turnover.
Treatment
There is no known permanent cure or treatment for primary trimethylaminuria, only mitigation of the effects. For secondary trimethylaminuria, it depends on the cause; for precursor overload, reducing the intake of TMA and its precursors will end symptoms. For TMAU caused by hypothetical gut dysbiosis, clinical review by a doctor, a plant based diet and reduced precursor intake should return gut flora to a healthy state.Primary TMAU sufferers generally have some residual FMO3 activity in the liver which processes TMA, however this happens relatively slowly. According to a study by Al-Waiz M TMA filters through to the bladder at half the rate of TMAO, and a healthy functioning person passes 99% of TMAO in urine within 24 hours. Therefore its estimated that the majority of TMA would be filtered out within 48 hours if no additional TMA or precursor is ingested, regardless of liver function. The metabolic and clinical manifestations of TMAU are generally regarded as benign, as there is no associated organ dysfunction. This designation, and the fact that the condition is often unrecognised by doctors, misdiagnosed and can have important ramifications including missed or delayed diagnosis.Affected individuals experience shame and embarrassment, fail to maintain relationships, avoid contact with people who comment on their condition, and are obsessive about masking the odour with hygiene products and even smoking. The malodorous aspect can have serious and destructive effects on schooling, personal life, career and relationships, resulting in social isolation, low self-esteem, depression, paranoid behaviour, and suicide.