Hashimoto Thyroiditis/ Chronic Lymphocytic Thyroiditis

Hashimoto's thyroiditis a.k.a. chronic lymphocytic thyroiditis is an autoimmune condition affecting young females. It is sometimes known as Prasad syndrome. It is the most common cause of primary hypothyroidism in North America.

Pathophysiology: Antibodies against thyroid peroxidase and/or thyroglobulin cause gradual destruction of follicles in the thyroid gland. There is infiltration of thyroid tissue by leukocytes, mainly T-lymphocytes. It is associated with non-Hodgkin lymphoma.

Clinical features: Features of hyperthyroidism can be seen initially (and sometimes intermittently), however the predominant feature is hypothyroidism. The thyroid gland is firm and mildly enlarged and sometimes lobulated.

Diagnosis: Hashimoto's thyroiditis is diagnosed by detecting the presence of anti-thyroglobulin antibodies (anti-Tg), anti-thyroid peroxidase antibodies (anti-TPO) and anti-microsomal antibodies.

Differential diagnosis: Depression, cyclothymia, PMS, chronic fatigue syndrome, fibromyalgia and, anxiety disorder.

Treatment: Hypothyroidism is treated with thyroid hormone replacement agents such as levothyroxine. Aim of treatment is to keep TSH levels be kept under 3.

Osteogenesis Imperfecta

The term Osteogenesis imperfecta was coined by Lobstein. The term is some what self explanatory! It is one of the relatively common bone dysplasias (1 in 20000 live births). OI involves all parts of the body that contain type 1 collagen to some extent giving rise to a variety of clinical presentations. Underlying mechanism in simple words is functional or actual decrease in collagen type 1 secondary to mutations in genes (most are inherited in autosomal dominant manner) coding for the same.

Clinical features include blue sclera, triangular facies, macrocephaly, hearing loss, dentition problems, chest deformity, scoliosis, limb deformities, fractures, joint laxity, constipation, sweating and growth retardation. There are several types, some being more severe than others (classified according to Sillence Classification). Type II has the most severe clinical presentation with most babies dying in newborn period. Type I is the mildest and commonest sub-type.

Diagnosis of OI is usually made clinically and confirmed by genetic testing for mutations. Radiological tests are useful and confirmatory in many cases. Findings include: fractures, excessive callus formation and popcorn bones (multiple radiolucent areas with radiodense rims), wormian bones in the skull, enlargement of frontal and mastoid sinuses, deformities of ribs, narrow pelvis. In mild cases dual x-ray absorptiometry (DEXA) scan can be useful and will show decreased bone mineralization.

Treatment is essentially supportive. Bisphosphonates, especially pamidronic acid, are drugs that inhibit osteoclast-induced bone resorption. These are given in a cyclic manner (every few weeks) and have been shown to decrease the fracture rate (especially in type III and IV OI). Side effects of pamidronic acid include hypocalcemia (usually not severe), leukopenia, increase in bone pain (which is typically transient), and scleritis.

Other drugs with unclear roles in the treatment of OI include: Human growth hormone, teriparatide (which is human parathyroid hormone, brand name is Forteo). Bone marrow transplantation and gene therapy are being investigated. Aggressive physical therapy, occupational therapy and education of parents about injury prevention is essential.

Above article also serves as explanation to Quiz 28: 'Femur X-Ray of a 3 year old boy' on the website www.pedsquiz.com

Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is characterized by hyperglycemia, ketonemia and acidemia, with rapid symptom onset.

Most common precipitating cause for DKA is non compliance with insulin regimen. Other precipitating factors include infections, dehydration and other stressful conditions.

Clinical features include weakness, abdominal pain, vomiting, tachycardia, tachypnea (Kussmaul breathing), acidotic breath,  dry mucous membranes, poor skin turgor and hypotension. If cerebral edema has set in there may be altered mental status, seizures and abnormal neurological findings such as brisk knee jerks.

Treatment includes correction of volume depletion and insulin therapy. Special attention should be paid to electrolyte imbalances especially sodium and potassium. Potassium will fall with insulin therapy and will need to be replaced. Sodium will be falsely low in setting of hyperglycemia. Corrected sodium can be calculated as Measured sodium + 0/016x(Current glucose-150). In other words increase sodium by 1.6 for every 100mg/dl of glucose above 100.

End points for treatment:


Plasma glucose less than 200 mg/dL
Serum bicarbonate more than 18 mEq/L
Venous pH more than 7.3
Anion gap more than 10.

No vomiting/pain and able to eat PO

Urine ketones may persist at this point and some physicians will continue patients on IVF while urine has ketones.

Complications of obesity

CVS - Hypertension, coronary artery disease, cor pulmonale, pulmonary hypertension of obesity, obesity related cardiomyopathy, atherosclerosis

CNS - Stroke, Benign intracranial hypertension

Neoplastic - Increased endometrial, prostate, gall bladder, breast and colon cancer

Endocrine - Non Insulin Dependent Diabetes Mellitus(NIDDM), abnormal lipid profile

GIT - cholecystitis, cholelithiasis, nonalcoholic steatohepatitis (NASH), fatty liver, gastro esophageal reflux disease(GERD)

Pulmonary - Obstructive sleep apnea, Pickwickian syndrome(hypoventilation)

Psychosocial -Depression, stigma,

Orthopedic - Osteoarthritis, slipped capital femoral epiphyses, Blount and Legg-Calvé-Perthes disease, backache

Gynecologic - Anovulation and infertility, hyperandrogenism and polycystic ovarian disease

Obstetric - Pregnancy induced hypertension, large baby

Surgical - Deep venous thrombosis, pulmonary embolism