: Why might lab test results be normal when thyroid nodules are present and there are symptoms of hyperthyroidism? By ultrasound there are many nodules in Thyroid gland but all thyroid tests (TSH,T4,T3, microsomal and thyreoglobulin

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This constellation may result from at least five reasons:

Hypothesis #0 : Both conditions (thyroid nodules and symptoms of
hyperthyroidism) are independent. Hyperthyroid symptoms including
anxiety, hair loss, fatigue and palpitations are unspecific.
Although they are typical for thyrotoxicosis, they may also result
from other conditions, e.g. masked depression or pheochromocytoma.
Hypothesis #1 : The nodules represent fully compensated toxic
adenomas, where somatic mutations lead to constitutive activation of
TSH signaling. Since autonomic production is fully compensated,
concentrations of thyroid hormones remain within their respective
reference ranges. Symptoms of thyrotoxicosis result from deviation
of free T4 concentrations from the personal set point of thyroid
homeostasis. It is well known that the intra-individual variation of
TSH and free T4 concentrations is much smaller than inter-individual
variance (see www.ncbi.nlm.nih.gov/pubmed/11889165 and www.ncbi.nlm.nih.gov/pubmed/25567792 ). This is a consequence
of an individual set point of the pituitary-thyroid feedback control
mechanism, which is encoded as TRH signaling from the hypothalamus.
Deviations of thyroid hormones within the reference range may still
lead to symptoms if they are far from the personal set point. See www.ncbi.nlm.nih.gov/pubmed/26635726 for a review article
discussing this topic and www.ncbi.nlm.nih.gov/pubmed/24480737 for a method for
reconstructing the personal set point.
Hypothesis #2 : This is somewhat similar to hypotheses #1. The
nodules represent fully compensated toxic adenomas (like in
hypothesis #1), but they predominantly produce T3, which results
from intracellular hyperdeiodination (ensuing from constitutive
activation of TSH signaling and consecutive stimulation of the
distal part of the TSH-T3 shunt). T3 concentrations remain within
their reference ranges, but are above the range of concentrations
that are appropriate for the personal receptor sensitivity. See www.ncbi.nlm.nih.gov/pubmed/23339744/ for a discussion of
this topic. It may be helpful to calculate the sum activity of
peripheral deiodinases (SPINA-GD), see also www.ncbi.nlm.nih.gov/pubmed/27375554 for a methodological
overview.
Hypothesis #3: The thyroid nodules produce non-classical thyroid
hormones (e.g. 3,5-T2, a highly active T4 metabolite), which
destabilize the heart rhythm and exert other symptoms of
hyperthyroidism. This is an understudied topic. One of the few
papers discussing this condition is www.ncbi.nlm.nih.gov/pubmed/26279999 .
Hypothesis #4: T3 is secreted episodically from thyroid nodules, so
that it is missed from diagnostic work-up. This is also an
understudied topic. See www.ncbi.nlm.nih.gov/pubmed/2045066 for more details.

It may be beneficial to determine concentrations of free T3 and free T4 (rather than total T3 and total T4) in order to avoid false negative results due to low plasma protein binding.