**4. The thought process of a rheumatologist**

There are deep gaps between the thought process and treatment plans of a rheumatologist versus that of a general internist, family practitioner, ophthalmologist, or orthopedic surgeon or any other practitioner involved in a patient's care.

Rheumatology remains greatly underutilized. This regrettably adds substantial delay to the diagnosis and treatment of a patient. It bears mentioning again that all organ systems may be involved in lupus. Based on this, the all-purpose criteria is preferable to the new SLICC criteria for diagnosis of lupus, as it was far more practical [46]. It also bears mentioning again that no practitioner may diagnose lupus, or any other disease process, based solely on research criteria. Criteria are to be used merely as a guideline. For example, a patient presents to their physician, stating they are "not feeling well". Subsequently, blood studies are ordered that reveal an ANA with a very high titer and upon further perusal, a very high DNA is also discovered, yet the physician fails to recognize that this patient has a forme-fruste of lupus. A rheumatologist would have started the patient on Plaquenil and educated them with regard to their diagnosis, and the physical ramifications to expect in the future.

Two of the most interesting, but also difficult to treat diseases, a physician may encounter include pulmonary renal syndrome, presenting with alveolar hemorrhage, and glomerular nephritis with ANA, DNA, successfully treated with cyclophosphamide [47]. Another rare, but not uncommon complication of lupus, would be TTP with or without the ADAMTS13 gene and ocular inflammation and orbital pseudotumor. Consider the case of a patient who presented with true renal failure, visual hallucinations and movement disorder. At that point the patient was treated with IV Cytoxan and pulse steroids. Therefore, the patient did not have fever; however the patient was anemic and had schistocytes with an elevated reticulocyte count. Thus, the patient did not fulfill all of the criteria for TTP; therefore, a clinical diagnosis was made of the same. The patient responded almost immediately to with all features of the disease disappearing with plasma exchange. This is a wonderful case to recall, when a hematologist says to a patient, "It cannot be TTP because there is no fever", apparently, this hematologist has lost sight of the fact that the high dose steroids likely blunted the fever. They may argue that there are not enough schistocytes [48] to fulfill the bacteria, however when schistocytes should not exist, and anemia cannot be explained, it can only be rationalized that the use of cyclophosphamides and high dose steroids lowered the schistocytes [49, 50]. This is a fantastic example of why research criteria alone, should never be used for diagnostic purposes.

It is very important to understand the mechanism of action for each disease feature, as it will impact a patient's treatment. For the purpose of example, thrombocytopenia will be seen in Sjogren's syndrome and hypersplenism, while in lupus platelet antibodies, both conditions can be present with dry eyes and dry mouth. A salivary gland biopsy may not differentiate, as a positive lymphocyte score of 50 lymphocytes 4mm2 , may presumably be seen in either condition. This may lead to an overlap diagnosis, or based on the mechanism of thrombocytopenia, it may also sway the diagnosis. Pneumonitis, while common in lupus, is seen in other autoimmune diseases, including sarcoidosis. All conditions mentioned may have a positive rheumatoid factor or positive ANA. Even CCP antibodies can be seen in autoimmune diseases with low values [51].
