Sarcoidosis Remission and Aden Protocol
CXR shows bilateral symmetrically enlarged hilar and mediastinal lymph nodes. CT (Fig. 11.2) confirms this finding, typical of sarcoidosis. The main differential diagnoses would be lymphoma and tuberculosis, but the lymphadenopathy would then be asymmetrical. Bronchoscopy and transbronchial lung biopsy are positive in 60 of cases, showing non-caseating granulomas and culture negative for tuberculosis and fungus. Blind endobronchial biopsies increase the yield by another 20 but the gold standard is mediastinoscopy. Incidence in people of African origin is ten times higher than in Caucasians.
Fection, sarcoidosis, connective tissue diseases, and neoplastic lesions (basically lymphomas, metastases, and fibrous tumors) (Dalley 1999 Weber et al. 1999). In all these conditions, imaging findings should be carefully matched with clinical information and laboratory tests, as even sophisticated information provided by MR are, in itself, often insufficient to provide the diagnosis. A very limited number of studies in the literature focus on imaging findings of sinonasal sarcoidosis - reflecting the low incidence of this condition. CT and MR findings may consist, in moderate stages, of isolated mucosal thickenings, intrasinusal air-fluid levels, and hypertrophy of turbinates, impossible to differentiate from a mere chronic sinusitis (KrESPi et al. 1995). In advanced stages, submucosal granulomas and bone erosions may be observed, shifting the differential diagnosis towards Wegener granu-lomatosis and cocaine induced midline destructive lesions. MR signal pattern of sarcoid...
Sarcoidosis is a systemic non-caseating granulo-matous disease that mainly involves lungs (80-90 of all patients) (FErgiE et al. 1999) and the upper respiratory tract, including the nasal fossae and paranasal sinuses (Ktespi et al. 1995 DeShazo et al. 1999). Other extra-respiratory localizations are lymph nodes, liver, spleen, eye, skin, bones, brain, salivary and lacrimal glands (DeShazo et al. 1999 MAZZiotti et al. 2001). The etiology of sarcoidosis is still unknown. Some immunological alterations (i.e., depression of T-lym-phocyte function, elevated B-lymphocyte activity and serum levels) are frequently found in affected subjects and are hypothesized to play a relevant role in the onset of the disease. Also infective agents, such as atypical Mycobacteria, are listed among the potential etiologic factors (FErgiE et al. 1999). reports, however, confirmed sinonasal tract involvement in no more than 6 of all cases of sarcoidosis (Marks and GooDmAN et al. 1998 DAmRosE et al. 2000...
Mast cells have been incriminated in such diverse diseases as allergy, asthma, rheumatoid arthritis, atherosclerosis, interstitial cystitis, inflammatory bowel disease, progressive systemic sclerosis, chronic graft-vs-host disease, fibrotic diseases, sarcoidosis, asbestosis, ischemic heart disease, keloid scars, and malignancy (3). The mediators released by mast cells can independently and, in synergy with macrophage- and T-cell-derived cytokines, induce much of the inflammatory pathology observed in inflammation and serve to orchestrate a complex immune response. Histamine, LTB4, LTC4, PAF, and PGD2 may have multiple effects on inflammatory cell recruitment (eosinophils), smooth muscle hyperplasia, and vascular dilatation (80,81). Tryptase, chymase, and TNF-a from mast cells activate fibroblasts, leading to collagen deposition and fibrosis. Mast cell-derived TNF-a regulates NF-KB-dependent induction of endothelial adhesion molecule expression on endothelial cells in vivo (49). Mast...
Sarcoidosis presents as a periarthritis or polyarthritis associated with hilar adenopathy, erythema nodosum, and fever (Lofgren syndrome). A similar disorder can occur without adenopathy and can be due to infections (streptococci, TB, coccy), inflammatory bowel disease, and drug reactions.
Specific types of infections give rise to granulomatous inflammation. These include tuberculosis, sarcoidosis, cat-scratch disease, leprosy, brucellosis, and schistosomiasis (49, 50). A granuloma is identified by its distinctive pattern of inflammatory reaction in which aggregates of epithelial-like macrophages are surrounded by lymphocytes and a few plasma cells. Older granulomas also display an outer layer of fibroblasts and connective tissue. In some cases, fused macrophages, giant cells, are also found (49). Protocol 19 describes the isolation of granuloma macrophages (51) from livers or lungs (52) of infected mice.
The clinical manifestations of the disease were first described in 1888. In 1933, Henrik Sjogren published a monograph describing in great detail the histologic and clinical components of this syndrome, which has often been referred to as Sjogren's syndrome. Confusion later arose between SS and the disease previously reported by Mikulicz in the late 1800s. In 1927, Schaffer and Jacobsen defined two main categories (a) Mikulicz's disease proper, of unknown etiology and following a benign course, and (b) Mikulicz's syndrome, caused by a variety of disorders such as leukemia, lymphosarcoma, tuberculosis, sarcoidosis, and iodide poisoning. Later, Morgan and Castleman concluded, on the basis of pathologic descriptions, that Mikulicz's disease and SS were identical. Much of the interest in SS during the past decade has focused on the opportunity to study the interrelationships among the autoimmune disorders, lymphoproliferative malignancies, and dysproteinemias, all of which may be features...
Isolated angiitis of the central nervous systen is a recently recognized vasculitic disorder primarily involving the
Patients usually have normochromic, normocytic anemia, leukocytosis, thrombocytosis, and an elevated ESR. WG, in contrast to the immune complex vasculitides, is associated with antineutrophil cytoplasmic antibody (ANCA), especially c-ANCA, which has a 98 specificity but a 30 to 99 sensitivity. Titers are usually associated with disease activity consequently, only 30 to 40 of patients with limited WG or generalized WG in remission have c-ANCA positivity. A small minority (5 ) can be positive for p-ANCA also. The limited form of the disease can be difficult to diagnose on clinical grounds, and the presence of c-ANCA may strongly influence the diagnosis. The strongest diagnostic evidence nonetheless comes from biopsy specimens of the involved tissues, which show granulomas. Lymphomatoid granulomatosis and necrotizing sarcoidosis may be confused with WG. The causative agent(s) leading to granuloma formation are unknown.
The CXR shows a right upper lobe ball within a cavity (air crescent sign) patho-gmonic of a mycetoma (also called aspergilloma). A lateral decubitus X-ray may demonstrate the fungal ball shifting position. In this condition, a preformed cavity becomes colonized, usually by the fungus Aspergillus fumigatus. Cavitary disease may be secondary to fibrotic lung disease, e.g. previous tuberculosis, sarcoidosis, or ankylosing spondylitis. Massive hemoptysis can result and bronchial angiogram with embolotherapy (using coils or gel foam) is temporizing. Surgical resection is definitive, but bronchopleural fistula may result. Unfortunately, most patients have insufficient pulmonary reserve to allow surgical resection.
The CXR shows narrowing of the tracheal air column (Fig. 61.2) with calcification of the wall. Tracheal narrowing can be due to malignant causes (lung cancer, lymphoma, metastases) or benign causes (post tuberculosis, posttraumatic, amyloidosis, sarcoidosis, Wegener's, Tracheopathia Osteochondroplastica). Tracheopathia Osteochondroplastica (TO) is an extremely rare condition, characterized by the presence of multiple osseous and or cartilaginous submucosal nodules (Fig. 61.3) protruding into the lumen of the airway. Bronchoscopy is diagnostic but treatment is nonspecific and supportive.
The most common cause of VT is reentry through regions of scar, most commonly an old MI (Fig. 4). Other scar-related VTs occur because of arrhythmogenic right ventricular dysplasia, sarcoidosis, Chagas' disease, and other nonischemic cardiomyopathies. Two features of ventricular scarring lead to reentrant VT (40-42). First, dense scarring creates regions of anatomic conduction block. Second, the scar is not comprised completely of dense fibrotic tissue, but also contains surviving myocyte bundles (43,44). Fibrosis between myocytes and myocyte bundles decreases cell-to-cell connections. The excitation wavefront propagates in a zig-zag manner from myocyte bundle to myocyte bundle, increasing the time for depolarization to procede through the region and thereby causing slow conduction (44). Circulation of an excitation wavefront around an area of block leads to reentry. With slow conduction, each cell in the circuit has sufficient time to recover after each depolarization.
The second patient group has reduced numbers of B cells and defects in the synthesis of IgG and IgM. These patients present with granulomatous disease resembling sarcoid. Granulomata may be found in the spleen, lymph nodes, lungs, skin, and brain. The histology is characteristic ofnoncaseating epithelial granuloma (Spickett et al., 1990).
The CXR shows asymmetric distortion of the mediastinal contour by markedly enlarged lymph nodes overlying the left hilum. This is described as the hilar overlay sign - the normal left pulmonary artery (Fig. 36.2) is seen through the mass (lying at the anterior mediastinum). Other differential diagnoses include chronic lymphocytic leukemia, sarcoidosis, Castleman's disease, and granulomatous disease like tuberculosis or histoplasmosis. The histology from mediastinoscopy in this patient showed Non Hodgkin's lymphoma.
Restrictive cardiomyopathy may be idiopathic or secondary to infiltrative diseases such as amyloidosis, hemochromatosis, hypereosinophilic syndrome and Loeffler endocarditis, sarcoidosis, radiation toxicity, glycogen storage diseases, and Gaucher disease544 (see also Chap. 75). Typical 2D echocardiographic features of these diseases include (1) a diffuse increase of ventricular thickness in the absence of marked ventricular chamber dilation and (2) marked biatrial enlargement509,545-549 (Fig. 13-109). Systolic function is often modestly decreased. As with the other cardiomyopathies, these echocardiographic findings are nonspecific. Doppler
Muscle biopsies in small numbers of sarcoid patients without symptoms of muscle pain or weakness have revealed noncaseating granulomas typical of the disease. The occurrence of asymptomatic muscle involvement has clouded the issue of whether a true sarcoid myopathy exists. Nonetheless, there are sarcoid patients with symptomatic muscle involvement. Muscle pain and tenderness are most often seen in acute sarcoidosis with erythema nodosum. Symmetric proximal muscle weakness can be seen in chronic sarcoid (see Chapters. ).
Aneurysms of the cavernous sinus, as well as infectious (bacterial or fungal abscesses, tuberculosis, and toxoplasmosis) and inflammatory processes (sarcoidosis, giant cell granuloma, lymphocytic hypophysitis, and histiocytosis X) can mimic a pituitary adenoma, causing mass effect and hypothalamic-hypophyseal endocrine dysfunction secondary to infiltration of normal tissue (91).
Pregnancy is the most common condition of altered immunocompetence that has been linked to polyomavirus activation (Coleman et al., 1980 Lecatsas et al., 1981). The onset of virus excretion is related to time of gestation, most often occurring late in the second and during the third trimester. Once established, excretion continues intermittently to term and might even extend into the postpartum period (Coleman et al., 1980 Gardner and Knowles, 1994). Serologic studies revealed that excretion in pregnant women is usually the result of virus activation of a persistent infection. Although activation of infection had no clinical significance (Arthur et al., 1989), women excreting polyomaviruses had more illness before and during pregnancy and may have underlying diseases such as diabetes and sarcoidosis (Gardner and Knowles, 1994). When BKV and JCV viruria were differentiated, BKV excretion rates of 15-25 were observed (Jin et al., 1993 Markowitz et al., 1991). The incidence of JCV...
Pyoderma gangrenosum is frequently associated with ulcerative colitis, Crohn's disease, RA, myeloproliferative disorders, and leukemia. Rarely, it is associated with chronic active hepatitis, myeloma, sarcoidosis, and diabetes mellitus. It begins as a tender pustule that rapidly expands to become a large ulcer many centimeters in diameter with a bluish, undermined border and a necrotic, purulent center. Lesions most frequently occur on the legs and trunk and heal with scar formation. Cutaneous trauma may exacerbate existing ulcers or cause the formation of new lesions.
All cutaneous manifestations of sarcoidosis, except EN and transient maculopapular eruptions, show histologic evidence of sarcoid granulomas on skin biopsy. A. Erythema nodosum is a septal panniculitis that appears as painful, erythematous, slightly raised, rounded lesions symmetrically distributed on the extensor aspect of the extremities, often localized to the shins. Fever and polyarthralgias may occur. When healing, the lesions assume the color of a bruise. Recurrent lesions appear in crops. EN is not specific for sarcoidosis, but the condition is termed Lofgren syndrome when accompanied by bilateral hilar adenopathy. C. Granulomatous cutaneous lesions of sarcoidosis include the following
The diagnosis of LM in general can be difficult to make, since patients may initially have vague complaints and minimal neurologic findings. LM may go on to mimic other disorders, such as tuberculosis or fungal meningitis, CNS sarcoidosis or pseudotumor cerebri.10'31'76 As mentioned in the introduction of this chapter, lymphomatous meningitis and PDLG, primary neoplastic diseases of the leptomeninges, would present a similar picture. The diagnosis of LM for brain tumor patients can also be hampered by the vagueness of the symptoms that may be present, especially since the CNS is already involved with tumor. Occasionally, patients with primary
The training of rhinologists should include the holistic management of patients. This should include not only training in how to communicate with patients but the medical management of patients whose disease is not solely confined to the nose (e.g., asthma, immunosuppression, sarcoid, vasculitis, and ciliary dysmotility). Many rhinologists are aware of the psychological aspects of rhinological symptoms (Homer et al., 2000), yet this subject is not well covered in the medical literature or in teaching and research. Many patients who complain bitterly of postnasal drip or catarrh as primary symptoms describe them as having a much greater effect on their life, or ability to function, than might be expected. One pervading theme for the future is that surgeons should not perceive themselves as being the only people who can help their patients and that a team approach (nurse practitioners, asthma and allergy nurses) involving other disciplines (immunologists, respiratory physicians,...
Cytomegalovirus, HTLV-1, others Fungal (Candida, Aspergillus, others) Non-infectious Involving eye alone Pars planitis Idiopathic vitritis Idiopathic retinal vasculitis Idiopathic multifocal retinochoroiditis Sympathetic ophthalmia White dot syndromes Histoplasmosis-like disease Associated with systemic disease Behfet's disease Sarcoidosis
The CXR shows bilateral infiltrates and calcified nodules in both upper lobes. Differential diagnoses of upper lobe infiltrates include silicosis, tuberculosis, and ankylosing spondylitis. There is also egg-shell calcification of the hilar lymph nodes. The egg-shell calcification plus the upper lobe nodules are typical of silicosis. Differential diagnoses of egg-shell calcification include sarcoidosis, Hodgkin's lymphoma following radiotherapy, and coal-worker's pneumoconiosis.
Teration in refraction that requires the patient to repeatedly blink or wipe their eye. Its prevalence is much more common with aging. It is unusual for intranasal pathology to be responsible, but conditions such as Wegener granulomatosis and sarcoidosis can affect this (Fig. 14.3 a). Nasolacrimal duct obstruction can occur
Otitis externa is generally caused by organisms such as Staphylococcus aureus and Pseudomonas aeruginosa. Malignant otitis externa is almost always due to P. aeruginosa (see Table 1). Only rare cases of malignant otitis externa due to S. aureus (6), Proteus mirabilis (7), and Aspergillus fumigatus (8) have been reported. Rare causes of chronic otitis externa include tuberculosis, fungal infections, syphilis, yaws, leprosy, and sarcoidosis. Fungal otitis externa may be part of a general or local fungal infection Aspergillus spp. are responsible for the most cases (9).
Structural lesions of the hypothalamus and pituitary can lead to an abnormal pattern of GnRH and or gonadotropin secretion (see Chapter 8). Most patients with such tumors have multiple pituitary hormone deficiencies, whereas isolated hypogo-nadotropism is rare (119,120). However, patients with mass lesions can present with hypogonadotropic hypogonadism without adrenal or thyroid hormone deficiency, but GH deficiency with or without hyperprolactimemia is almost always present. Indeed, a mass in the pituitary or hypothalamus is more likely to decrease the secretion of gonadotropins than that of adrenocorticotropic hormone (ACTH) or TSH. Cranio-pharyngioma is the most common tumor resulting in hypogonadotropic hypogo-nadism in childhood. It is often associated with growth retardation, diabetes insipidus, and visual field defects. Prolactinoma is the most frequent tumor causing hypogonadotropic hypogonadism in adult men (121,122). Although rare, infiltrative hypothalamus or pituitary...
Fig. 9.12-lead ECG recording of baseline (left) and VT (right) from a patient with cardiac sarcoidosis. Sarcoid VT frequently originates from the basal left ventricle, producing a RBBB VT morphology with positive concordance across the precordial leads. Sarcoidosis. Sarcoidosis is a chronic, multisystem disorder of unknown etiology characterized by noncaseating granulomas in affected organs. Although 5 of patients with sarcoid have symptomatic cardiac involvement, approx 20 have evidence of cardiac sarcoid at autopsy (50). Cardiac involvement is manifested by myocardial infiltration, CHF, heart block, VT (Fig. 9), and sudden death. Sarcoid granulomas preferentially affect the basal interventricular septum and left ventricular papillary muscles. The right and left ventricular free walls can also be involved. The resting ECG is nonspecific, but frequently abnormal. The mechanism of VT is unclear but ICD therapy has been advocated because sarcoid-related VT is often difficult to control...
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