Clinical Overview > Condition/ Syndrome > Autoimmune disorders
You are looking at 21 - 23 of 23 items
Search for other papers by M Horsey in
Google Scholar
PubMed
Search for other papers by P Hogan in
Google Scholar
PubMed
Search for other papers by T Oliver in
Google Scholar
PubMed
Summary
A 71-year-old woman with severe right lower leg pain, edema and erythema was presented to the Emergency Department and was found to have an extensive deep vein thrombosis (DVT) confirmed by ultrasound. She underwent an extensive evaluation due to her prior history of malignancy and new hypercoagulable state, but no evidence of recurrent disease was detected. Further investigation revealed pernicious anemia (PA), confirmed by the presence of a macrocytic anemia (MCV=115.8fL/red cell, Hgb=9.0g/dL), decreased serum B12 levels (56pg/mL), with resultant increased methylmalonic acid (5303nmol/L) and hyperhomocysteinemia (131μmol/L), the presumed etiology of the DVT. The patient also suffered from autoimmune thyroid disease (AITD), and both antithyroglobulin and anti-intrinsic factor antibodies were detected. She responded briskly to anticoagulation with heparin and coumadin and treatment of PA with intramuscular vitamin B12 injections. Our case suggests that a DVT secondary to hyperhomocystenemia may represent the first sign of polyglandular autoimmune syndrome III-B (PAS III-B), defined as the coexistent autoimmune conditions AITD and PA. It is important to recognize this clinical entity, as patients may not only require acute treatment with vitamin B12 supplementation and prolonged anticoagulation, as in this patient, but may also harbor other autoimmune diseases.
Learning points
-
A DVT can be the first physical manifestation of a polyglandular autoimmune syndrome.
-
Hyperhomocysteinemia secondary to pernicious anemia should be considered as an etiology of an unprovoked DVT in a euthyroid patient with autoimmune thyroid disease.
-
Patients with DVT secondary to hyperhomocysteinemia should undergo screening for the presence of co-existent autoimmune diseases in addition to treatment with B12 supplementation and anticoagulation to prevent recurrent thromboembolism.
Search for other papers by Luísa Correia Martins in
Google Scholar
PubMed
Search for other papers by Ana Rita Coutinho in
Google Scholar
PubMed
Search for other papers by Mónica Jerónimo in
Google Scholar
PubMed
Search for other papers by Joana Serra Caetano in
Google Scholar
PubMed
Search for other papers by Rita Cardoso in
Google Scholar
PubMed
Search for other papers by Isabel Dinis in
Google Scholar
PubMed
Search for other papers by Alice Mirante in
Google Scholar
PubMed
Summary
Alternating between hyper- and hypo-thyroidism may be explained by the simultaneous presence of both types of TSH receptor autoantibodies (TRAbs) – thyroid stimulating autoantibodies (TSAbs) and TSH blocking autoantibodies (TBAbs). It is a very rare condition, particulary in the pediatric age. The clinical state of these patients is determined by the balance between TSAbs and TBAbs and can change over time. Many mechanisms may be involved in fluctuating thyroid function: hormonal supplementation, antithyroid drugs and levels of TSAbs and TBAbs. Frequent dose adjustments are needed in order to achieve euthyroidism. A definitive therapy may be necessary to avoid switches in thyroid function and frequent need of therapeutic changes. We describe an immune-mediated case of oscillating thyroid function in a 13-year-old adolescent. After a short period of levothyroxine treatment, the patient switched to a hyperthyroid state that was only controlled by adding an antithyroid drug.
Learning points
-
Autoimmune alternating hypo- and hyper-thyroidism is a highly uncommon condition in the pediatric age.
-
It may be due to the simultaneous presence of both TSAbs and TBAbs, whose activity may be estimated in vitro through bioassays.
-
The clinical state of these patients is determined by the balance between TSAbs and TBAbs and can change over time.
-
The management of this condition is challenging, and three therapeutic options could be considered: I-131 ablation, thyroidectomy or pharmacological treatment (single or double therapy).
-
Therapeutic decisions should be taken according to clinical manifestations and thyroid function tests, independent of the bioassays results.
-
A definitive treatment might be considered due to the frequent switches in thyroid function and the need for close monitoring of pharmacological treatment. A definitive treatment might be considered due to the frequent switches in thyroid function and the need for close monitoring of pharmacological treatment.
Search for other papers by Nishant Raizada in
Google Scholar
PubMed
Search for other papers by S H Rahaman in
Google Scholar
PubMed
Search for other papers by D Kandasamy in
Google Scholar
PubMed
Search for other papers by V P Jyotsna in
Google Scholar
PubMed
Summary
Insulin autoimmune syndrome (IAS) is a rare cause of hyperinsulinemic hypoglycaemia, which is known to occur in association with the use of sulfhydryl-containing drugs and autoimmune disorders. We describe a patient with hitherto an unreported association of IAS with ankylosing spondylitis. We have also performed and described a simplified method of polyethylene glycol (PEG) precipitation of an insulin bound antibody in the serum.
Learning points
-
IAS should be considered in differential diagnosis of endogenous hyperinsulinemic hypoglycaemia.
-
Ankylosing spondylitis can be associated with IAS apart from several other autoimmune diseases.
-
Very high serum insulin levels (100–10 000 μU/ml) are frequently seen in IAS.
-
When faced with very high serum insulin before suspecting insulinoma, it is advisable that PEG precipitation of serum be done to identify antibody bound insulin.
-
A clinical suspicion of IAS can avoid expensive imaging and unnecessary surgery in affected patients.
