Clinical Manifestations of Thyroiditis Subtypes

Thyroiditis refers to a group of inflammatory diseases affecting the thyroid gland. With the help of historical information, a physical examination and diagnostic tests, physicians can classify the type of thyroiditis and initiate appropriate treatment.

Subtype	Etiology	Neck pain	RAIU	TSH	T4	Thyroid autoantibodies
Chronic lymphocytic (Hashimoto's disease)	Autoimmune	No	Variable	Variable	Variable	Present
Subacute granulomatous	Viral	Yes	Decreased	Decreased	Increased	Absent
Subacute lymphocytic	Autoimmune	No	Decreased	Decreased	Increased	Present
Microbial inflammatory	Bacterial, fungal, parasitic	Yes	Variable	Normal	Normal	Absent
Hashitoxicosis	Autoimmune	No	Decreased	Decreased	Increased	Present
Invasive fibrous	Unknown	No	Variable	Normal	Normal	Variable

                                   
RAIU = radioactive iodine uptake; TSH = thyroid-stimulating hormone; T4 = thyroxine.

Thyroiditis is a group of inflammatory thyroid disorders. Patients with chronic lymphocytic thyroiditis (also referred to as Hashimoto's thyroiditis) present with hypothyroidism, goiter, or both. Measurement of serum thyroid autoantibodies and thyroglobulin confirms the diagnosis. Subacute granulomatous thyroiditis (sometimes referred to as de Quervain's disease) is a self-limited but painful disorder of the thyroid. Physical examination, elevated erythrocyte sedimentation rate, elevated thyroglobulin level and depressed radioactive iodine uptake (RAIU) confirm the diagnosis. Subacute lymphocytic thyroiditis (silent thyroiditis) is considered autoimmune in origin and commonly occurs in the postpartum period. Symptoms of hyperthyroidism and depressed RAIU predominate. Acute (suppurative) thyroiditis is a rare, infectious thyroid disorder caused by bacteria and other microbes. The rare, invasive fibrous thyroiditis (Riedel's thyroiditis) presents with a slowly enlarging anterior neck mass that is sometimes confused with a malignancy.


References:

1. Slatosky J, Shipton B, Wahba H. Thyroiditis: differential diagnosis and management. Am Fam Physician. 2000 Feb 15;61(4):1047-52 [Medline]
2. Nayak B, Hodak SP. Hyperthyroidism. Endocrinol Metab Clin North Am. 2007 Sep;36(3):617-56 [Medline]

Typical Serologic Course of Hepatitis A Virus (HAV) Infection

Since both clinically and biochemically, acute hepatitis due to HAV cannot be distinguished from that due to the other hepatitis viruses, serologic tests are necessary for a virus-specific diagnosis.

Diagnosis of hepatitis is made by biochemical assessment of liver function (laboratory evaluation of: urine bilirubin and urobilinogen, total and direct serum bilirubin, ALT (SGPT) and/or AST (SGOT), alkaline phosphatase, prothrombin time, total protein, albumin, IgG, IgA, IgM, complete blood count).
The specific routine diagnosis of acute hepatitis A is made by finding anti-HAV IgM in the serum of patients. A second option is the detection of virus and/or antigen in the faeces.
Virus and antibody can be detected by commercially available radioimmunoassay (RIA), enzyme immunoassay (EIA) and enzyme-linked immunosorbent assay (ELISA) kits. These commercially available assays for anti-HAV IgM and total anti-HAV (IgM and IgG) for assessment of immunity to HAV are not influenced by the passive administration of immunoglobulin (IG), because the prophylactic doses are below detection level.
At the onset of disease, the presence of IgG anti-HAV is always accompanied by the presence of IgM anti-HAV. As IgG anti-HAV persists lifelong after acute infection, detection of IgG anti-HAV alone indicates past infection.
Virus may still be present in the absence of detectable HAV antigen, as demonstrated by the use of more sensitive methods.




References:

1. Nainan OV, Xia G, Vaughan G, Margolis HS. Diagnosis of hepatitis a virus infection: a molecular approach. Clin Microbiol Rev. 2006 Jan;19(1):63-79. [Medline]
2. Regev A, Schiff ER. Viral hepatitis A, B, and C. Clin Liver Dis. 2000 Feb;4(1):47-71. [Medline]
3. Advisory Committee on Immunization Practices (ACIP), Fiore AE, Wasley A, Bell BP. Prevention of hepatitis A through active or passive immunization: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Recomm Rep. 2006 May 19;55(RR-7):1-23. [Medline]

Algorithm for Diagnosing Hyperthyroidism

Clinical hyperthyroidism, also called thyrotoxicosis, is caused by the effects of excess thyroid hormone and can be triggered by different disorders. Etiologic diagnosis influences prognosis and therapy.

The most common cause of hyperthyroidism is Graves’ disease. Other common causes include thyroiditis, toxic multinodular goiter, toxic adenomas, and side effects of certain medications. The diagnostic workup begins with a thyroid-stimulating hormone level test. When test results are uncertain, measuring radionuclide uptake helps distinguish among possible causes.

References:

1. Bahn Chair RS, Burch HB, Cooper DS, Garber JR, Greenlee MC, Klein I, Laurberg P, McDougall IR, Montori VM, Rivkees SA, Ross DS, Sosa JA, Stan MN; American Thyroid Association; American Association of Clinical Endocrinologists. Hyperthyroidism and other causes of thyrotoxicosis: management guidelines of the American Thyroid Association and American Association of Clinical Endocrinologists. Thyroid. 2011 Jun;21(6):593-646. [Medline]
2. Pantalone KM, Nasr C. Approach to a low TSH level: patience is a virtue. Cleve Clin J Med. 2010 Nov;77(11):803-11. [Medline]
3. Reid JR, Wheeler SF. Hyperthyroidism: diagnosis and treatment. Am Fam Physician. 2005 Aug 15;72(4):623-30. [Medline]

Diagnostic Criteria for Autistic Disorder

The American Psychiatric Association's Diagnostic and Statistical Manual-IV, Text Revision (DSM-IV-TR) provides standardized criteria to help diagnose Autism Spectrum Disorders (ASDs). 

Diagnostic Criteria for Autistic Disorder
A. Six or more items from (1), (2), and (3), with at least two from (1), and one each from (2) and (3):

1. qualitative impairment in social interaction, as manifested by at least two of the following:

a. marked impairment in the use of multiple nonverbal behaviors such as eye-to-eye gaze, facial expression, body postures, and gestures to regulate social interaction
b. failure to develop peer relationships appropriate to developmental level
c. a lack of spontaneous seeking to share enjoyment, interests, or achievements with other people (e.g., by a lack of showing, bringing, or pointing out objects of interest)
d. lack of social or emotional reciprocity

2. qualitative impairments in communication as manifested by at least one of the following:

a. delay in, or total lack of, the development of spoken language (not accompanied by an attempt to compensate through alternative modes of communication such as gesture or mime)
b. in individuals with adequate speech, marked impairment in the ability to initiate or sustain a conversation with others
c. stereotyped and repetitive use of language or idiosyncratic language
d. lack of varied, spontaneous make-believe play or social imitative play appropriate to developmental level

3. restricted repetitive and stereotyped patterns of behavior, interests, and activities, as manifested by at least one of the following:

a. encompassing preoccupation with one or more stereotyped and restricted patterns of interest that is abnormal either in intensity or focus
b. apparently inflexible adherence to specific, nonfunctional routines or rituals
c. stereotyped and repetitive motor manners (e.g., hand or finger flapping or twisting, or complex whole-body movements)
d. persistent preoccupation with parts of objects

B. Delays or abnormal functioning in at least one of the following areas, with onset prior to age 3 years: (1) social interaction, (2) language as used in social communication, or (3) symbolic or imaginative play.

C. The disturbance is not better accounted for by Rett’s Disorder or Childhood Disintegrative Disorder.


References:

1. Lord C, Risi S, DiLavore PS, Shulman C, Thurm A, Pickles A. Autism from 2 to 9 years of age. Arch Gen Psychiatry. 2006 Jun;63(6):694-701. [Medline]
2. American Psychiatric Association. (2000). Pervasive developmental disorders. In Diagnostic and statistical manual of mental disorders (Fourth edition---text revision (DSM-IV-TR). Washington, DC: American Psychiatric Association, 69-70.

Karnofsky Performance Status (KPS) Scale

The Karnofsky Performance Status Scale (KPS) was designed to measure the level of patient activity and medical care requirements. It is a general measure of patient independence and has been widely used as a general assessment of patient with cancer.

 Karnofsky performance status scale

Value	Level of functional capacity	Definition
100	Normal, no complaints, no evidence of disease	Able to carry on normal activity and to work; no special care needed
90	Able to carry on normal activity, minor signs or symptoms of disease
80	Normal activity with effort, some signs or symptoms of disease
70	Cares for self, unable to carry on normal activity or to do active work	Unable to work; able to live at home and care for most personal needs; various degrees of assistance needed
60	Requires occasional assistance, but is able to care for most needs
50	Requires considerable assistance and frequent medical care
40	Disabled, requires special care and assistance	Unable to care for self; requires equivalent of institutional or hospital care; disease may be progressing rapidly
30	Severely disabled, hospitalization is indicated although death is not imminent
20	Hospitalization is necessary, very sick, active supportive treatment necessary
10	Moribund, fatal processes progressing rapidly
0	Dead

   
The Karnofsky score runs from 100 to 0, where 100 is "perfect" health and 0 is death.
    
References:

1. Yates JW, Chalmer B, McKegney FP. Evaluation of patients with advanced cancer using the Karnofsky performance status. Cancer. 1980 Apr 15;45(8):2220-4. [Medline]
2. Schag CC, Heinrich RL, Ganz PA. Karnofsky performance status revisited: reliability, validity, and guidelines. J Clin Oncol. 1984 Mar;2(3):187-93. [Medline]

Diagnostic Criteria for Diabetic Sensorimotor Polyneuropathy (DSPN)

The Diabetic Sensorimotor Polyneuropathy (DSPN) is a symmetrical, length-dependent sensorimotor polyneuropathy attributable to metabolic and microvessel alterations as a result of chronic hyperglycemia exposure (diabetes) and cardiovascular risk covariates. 

Definitions of minimal criteria for DSPN
1. Possible Clinical DSPNSymptoms or signs of DSPN. Symptoms may include: decreased sensation, positive neuropathic sensory symptoms (e.g. ‘asleep numbness’, ‘prickling’ or ‘stabbing’, ‘burning’ or ‘aching’ pain) predominantly in the toes, feet, or legs. Signs may include: symmetric decrease of distal sensation or unequivocally decreased or absent ankle reflexes.

2. Probable Clinical DSPNA combination of symptoms and signs of distal sensorimotor polyneuropathy with any two or more of the following: neuropathic symptoms, decreased distal sensation, or unequivocally decreased or absent ankle reflexes.

3. Confirmed Clinical DSPNAn abnormal nerve conduction study and a symptom or symptoms or a sign or signs of sensorimotor polyneuropathy. Severity of DSPN can be assessed by staged or continuous approaches described above and by dysfunction and disability scores.

4. Subclinical DSPNNo signs or symptoms of polyneuropathy. Abnormal nerve conduction, as described above, is present.


Dyck's Stages of Severity for DSPN
An alternative approach to estimating severity is to indicate severity by grades:

• Grade 0 = no abnormality of NC, e.g., sum 5 nerve conduction (NC) normal deviates <95th percentile or another suitable NC criterion
• Grade 1a = abnormality of NC, e.g., sum 5 NC normal deviates >/=95th percentile without symptoms or signs
• Grade 1b = NC abnormality of stage 1a plus neurologic signs typical of DSPN but without neuropathy symptoms
• Grade 2a = NC abnormality of stage 1a with or without signs (but if present, <2b) and with typical neuropathic symptoms
• Grade 2b = NC abnormality of stage 1a, a moderate degree of weakness (i.e., 50%) of ankle dorsiflexion with or without neuropathy symptoms.

References:

1. Dyck PJ, Albers JW, Andersen H, Arezzo JC, Biessels GJ, Bril V, Feldman EL, Litchy WJ, O'Brien PC, Russell JW; on behalf of the Toronto Expert Panel on Diabetic Neuropathy. Diabetic Polyneuropathies: Update on Research Definition, Diagnostic Criteria and Estimation of Severity. Diabetes Metab Res Rev. 2011; 27: 620–628. [Medline]
2. Tesfaye S, Boulton AJ, Dyck PJ, Freeman R, Horowitz M, Kempler P, Lauria G, Malik RA, Spallone V, Vinik A, Bernardi L, Valensi P; Toronto Diabetic Neuropathy Expert Group. Diabetic neuropathies: update on definitions, diagnostic criteria, estimation of severity, and treatments. Diabetes Care. 2010 Oct;33(10):2285-93. [Medline]
3. Dyck PJ. Detection, characterization, and staging of polyneuropathy: assessed in diabetics. Muscle Nerve. 1988 Jan;11(1):21-32. [Medline]