A 42-year-old woman with scleroderma+ chronic thyroiditis, 3 normal deliveries, without macrosomia and a mixed connective tissue disease (CTEM) diagnosed in 2000, with small anti-cancer antibodies (mildney disease 51).
One aunt was type 2 diabetic.
She used levothyroxine 50 μg/day, prednisone 7.5 mg daily and MTX 25 mg weekly.
In December 2001, MTX dose was administered at 25 mg every two weeks, with progressive muscle weakness, myalgia and subsequently thirst and polyuria.
Glycemia was 286 mg/dl (always normal previous glycemia), prescribing diet and glibenclamide 5 mg/day.
Three weeks later he consulted in an emergency department for severe thirst.
Blood glucose was 550 mg/dl with ketonemia (-).
Glybenclamide was increased to 10 mg/day, and metformin 850 mg and anaphylaxis were initiated.
A week later, she consulted again for vomiting, thirst, polyuria, myalgia, arthralgia and significant general malaise.
The patient was hospitalized, with emphasis on marked coughing, normotic and polypnea.
BMI: 27.3 kg/mt2.
The skin of the face was reddened, reddened, pigmented, and had a quadroid appearance.
There was no acanthosis nigricans.
Cardiopulmonary and abdominal examination was normal.
There was a lack of strength in the limbs.
Blood glucose was 414 mg/dl, ketonemia (++), glycosylated hemoglobin A1C 12%, there was metabolic acidosis (pH 7.0, bicarbonate 2.9 mEq/L) with normal lactate levels, creatinine 1.3 mg.
She received sodium and potassium bicarbonate.
Infection was ruled out.
Despite the administration of high doses of crystalline insulin, hyperglycemia and ketosis persist.
antisepsis antibodies were determined by an autoimmune mechanism in the genesis of diabetes and insulin antibodies (Clinic Mayo) were requested, which were negative and pancreatic islet antibodies, which were «indeterminate» 640.
Antimicrosomal thyroid antibodies were positive at a titer 1:25.400.
1.
Due to the intensification of osteoarticular symptoms, the prednisone dose was increased to 60 mg daily and the methotrexate dose of 25 mg weekly was restored.
At 16 days of hospitalization, blood glucose levels of 200 mg/dl were obtained and the patient was discharged in good condition, with indications of NPH insulin and crystalline (158 U/day), prednisone 75 mg/dl and le0.4 μg/week.
Conservative treatment began to reduce progressively the amount of prednisone and insulin, until it was suspended after 15 days (used 40 mg of prednisone) due to normalization of blood glucose levels.
One month after discharge, a normal glucose tolerance curve was performed.
Prednisone was replaced to 10 mg/day one month after hospital discharge.
Three months later, due to the absence of osteoarticular and muscular symptoms, the MTX dose was restarted at 25 mg every 2 weeks, with the appearance of postprandial hyperglycemia.
She returned to weekly MTX administration, with normal blood glucose levels.
Six months later, prednisone was restarted. The MTX dose produced new hyperglycemias (180 mg/dl, fasting), so it was decided to maintain the weekly 25 mg injection associated with 10 mg/dl.
Eight months after the episode of ketosis measurement, and being treated with levothyroxine 100 μg/day, prednisone 10 mg/day, calcium, folic acid and MTX 25 mg weekly, the antibodies were repeated.
In her last control, the patient was asymptomatic and normoglycemic with a diet without carbohydrate restriction, using 12.5 mg of MTX weekly.
A new glucose tolerance curve was again normal, with mild hyperinsulinemia detected (fasting 15.11 uU/dl (VN: 3-12.5) and at 2 h 66.63 uU/dl).
It was therefore recommended to restrict the intake of carbohydrates in the diet.
