Sarcoidosis Remission and Aden Protocol
Sarcoidosis, a subacute or chronic inflammatory disease of undetermined etiology, affects the skin, visceral organs, eyes, parotid glands, and lymph nodes. In about 5 of cases, the brain and spinal cord are involved. Clinical features include cranial and peripheral nerve deficits and hypothalamic and pituitary symptoms and signs. The pathology is characterized by a noncaseating granulomatous meningoencephalitis. Grossly, the lepto-meninges are thickened, and the subarachnoid space, mostly at the base of the brain, is filled with a gelatinous exudate. Histologically, noncaseating microgranulomas composed of epithelioid cells, mononuclear cells, and giant cells infiltrate the leptomeninges and underlying parenchyma, the ventricular walls, and the choroid plexus. The brunt of the inflammatory process is at the base, extending into the cranial and peripheral nerve roots.
The eye is frequently involved in sarcoidosis. Involvement usually takes the form of an anterior or posterior uveitis. The choroiditis is more often peripheral and accompanied by inflammatory changes in the retinal veins. Sheathing of the veins can be seen and the vision might be impaired by macular oedema. The inflammatory changes might be similar to those seen in pars planitis. When the diagnosis is suspected, the conjunctiva and skin should be searched for possible nodules, which can be biopsied, and an X-ray of the chest can reveal enlargement of the hilar lymph nodes. The management of the ophthalmological problem might involve treatment with local and systemic steroids but the opinion of a physician specialising in sarcoidosis is essential and should be sought before embarking on treatment.
The categories for granulomatous dermatoses are not absolute and are only useful as a skeletal framework from which to start one's interpretation of a histologic section. For example (i) rarely cutaneous sarcoidosis may demonstrate tuberculoid granulomas or foreign body granulomas (ii) cutaneous infections as tuberculosis or leprosy most commonly present as tuberculoid granulomas but can be sarcoidal or palisading in type (iii) some infectious granuloma can be palisaded (as some fungal, mycobacterial infections and so on) (iv) foreign body granulomata can be nodular (sarcoidal, palisaded, or foreign body) or diffuse and mixed. Therefore, although pattern analysis is a helpful way to begin the evaluation of a slide, often evaluation of a granulomatous dermatitis must exceed routine light microscopy with hematoxylin-eosin staining. 2. If the infiltrate is nodular, is the pattern tuberculoid, sarcoidal, palisaded, or foreign body in type
An underlying problem with these published refractory disease series is the lack of a uniform definition of this entity. Definitions range from progression of disease on upfront therapy to a partial response 3 months posttreatment. Moreover, the inclusion of patients with unconfirmed pathology may result in treatment of patients with aggressive NHL, with a nonmalignant disorder (infection, or sarcoid-like reactions), or with residual radiologic abnormalities but no active HL with an HDT program. These non-HL entities are often strongly positive on gallium or positron emission tomography imaging, thereby making histologic confirmation even more imperative.25-28
Diseases involving the GI tract contribute to delayed gastric emptying (GE) and delayed small-bowel absorption. Such diseases include linitis plastica, pathologies of the small bowel, such as lymphomas, lymphangectasia, sarcoidosis, Whipple's disease, celiac disease, viral enteritis, and haemangiomas of the gut. These processes influence malabsorption by lymphatic infiltration of the mucosal and submucosal tissues. Less obvious aetiologies of delayed GE and malabsorption include cirrhosis, psoriasis, ileitis, and ulcerative colitis 12 . Human studies 13 document the association of gastroparesis and abnormal small-bowel function, which contribute to the malabsorption associated with non-GI tumours, which ultimately leads to malnutrition and cachexia. These GI processes are independent of tumour site, size, or overt constitutional changes 14 , but are clinically manifested in advanced cancer, after weight loss, following chemotherapy or abdominal radiation 14 .
When a modification of the tear film structure occurs, with consequent tear film instability, ocular surface stress will develop, resulting in a clinical condition known as dry eye. The classification of this disorder was carried out in 1995 by the National Eye Institute, dividing dry eye into two different types aqueous layer disorders and tear evaporation disorders (32). This classification is very useful to focus on the main causative factors of the disorder, although the clinical presentation is often a mix of the two pathogenic pathways (i.e., a reduced aqueous production often results in an inadequate lipid layer spreading and in excessive tear film evaporation meibomian gland disease is commonly associated with reduced aqueous secretion by the lacrimal gland). Aqueous layer deficiency is the most common cause of dry eye and is dependent on decreased secretion of the lacrimal glands, although increased evaporation of tears may also be involved. Main causes of tear aqueous...
This refers to a low-grade inflammatory response,which is seen in young adults. It affects both eyes in up to 80 of cases, although the severity can be asymmetrical. There is minimal evidence of anterior uveitis and the patient complains of floating spots in front of the vision. Inspection of the fundus reveals vitreous opacities and careful inspection of the peripheral retina shows whitish exudates in the overlying vitreous. A mild-to-moderate peripheral retinal phlebitis can occur. The condition runs a chronic course and occasionally can be complicated by cataract, cystoid macular oedema and tractional retinal detachment. The cause is unknown in the majority of cases, although there is a known association with sarcoidosis.
The synthesis of calcitriol is usually induced through low serum calcium or inorganic phosphate levels. However, changes in active vitamin D levels occur slower than those in PTH as the 'storage form' of vitamin D, 25-hydroxyvitamin D (calcidiol), needs to be converted into the biologically active form of the hormone, i.e., 1, 25-dihydroxyvitamin D. This conversion activation is achieved through the hydroxylation of 25-hydroxyvitamin D in its C1 position by CYP27B (a-hydroxylase). The activity of the latter enzyme, which is predominantly found in kidney parenchymal cells, is upregulated by PTH, and downregulated by plasma HPO4 levels. Conversely, calcitriol inhibits the secretion of PTH from the parathyroid glands.9 Measurement of serum 25 and 1,25 vitamin D levels may be useful in patients with osteoporosis, vitamin D deficiency, renal disease, hypercalcemia, and sarcoidosis.
The association between HCL and autoimmune disorders such as scleroderma, polymyositis, Raynaud's phenomenon, and various vasculitis, has been described.22 23 Among the vasculopathic syndromes polyarteritis nodosa represents the most frequently associated disorder, with 18 cases reported so far. It has been suggested that a common membrane antigen expressed in leukemia cells and vascular endothelium may lead to a vasculitis by generating cross-reacting antibody.24 Four cases of scleroderma in the setting of HCL have been reported.25-27 It has been postulated that sarcoidosis may be induced directly through hairy
Case 1 Sarcoidosis Case 2 Hypophysitis Case 3 Pituitary Apoplexy Case 4 Metastasis to Pituitary CASE 1 SARCOIDOSIS Case Description This case illustrates many of the difficulties and problems encountered in establishing the diagnosis of hypopituitarism and in defining its etiology. The long duration of symptoms and their nonspecific nature clearly contributed to the delay in diagnosis. The patient had signs and symptoms of, at least, partial hypopituitarism 7 yr before her presentation. In addition, she had histologic findings 3 yr before presentation that were consistent with systemic sarcoidosis. At that time, she had anemia, hyponatremia, and noncaseating granulomas on bone marrow biopsy. She also had clinical features suggestive of adrenal insufficiency (tiredness, fatigue, hypotension, hyponatremia, loss of axillary and pubic hair) as well as hypogonadism (amenorrhea and dyspareunia). Sarcoidosis is a multisystem granulomatous disorder of unknown etiology (1). Its prevalence...
The differential diagnosis includes lymphoma, sarcoidosis, tuberculosis, luetic disease, Wegener's granulomatosis, or several types of vasculitis. Wegener's granulomatosis is a generalized necrotizing vasculitis with ocular involvement in 40 of cases - most often in the form of axial pro-ptosis (with associated scleritis or retinal vasculitis), but also as a form of myositis. Laboratory testing can help to establish the diagnosis of this autoimmune disease, if the c-ANCA (antineutrophile cytoplasmic antibody) shows cytoplasmic staining. The test is often negative in the early stages of the disease and should be repeated periodically, if the diagnosis is strongly suspected.
Can cause disc swelling (dysthyroid optic neuropathy). In both instances, the doctor should be warned that serious consequences might ensue unless prompt treatment is applied. Infiltration of the disc by leukaemia, lymphoma or chronic granulomata (as in sarcoidosis) can also cause disc swelling.
Sarcoid is a multisystem systemic granulomatous disease. Approximately 25 to 33 of the patients demonstrate cutaneous manifestations. The exact etiology of sarcoidosis remains unknown but there is a known association with increased cell-mediated immunity activity and an increase in CD4+ T-helper cells of the Th1 subtype after antigen presentation. Th1 cytokines are increased (including inter-leukin 2 and interferon), which ultimately leads to B-cell stimulation. Granuloma forming T lymphocytes and mono-cytes are in peripheral tissues leading to decreased delayed cellular immunity and lymphopenia with resultant anergy. The antigen responsible for initiating these events is unknown. Sarcoid is considered a diagnosis of exclusion both histologically and clinically. Infections and other systemic diseases must be excluded as the cause of non-caseating granulomas in the skin or other organ systems. However, the identification of a foreign body or infectious agent within the granuloma does...
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