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Cutaneous Amyloidosis
Published in Charles Theisler, Adjuvant Medical Care, 2023
Primary cutaneous amyloidosis is a form of amyloidosis, where clumps of the abnormal amyloid proteins are deposited in the skin (between the epidermis and dermis), but without associated deposits in internal organs as in other forms of amyloidosis. This gives the skin an abnormal texture or color. There are three types of cutaneous amyloidosis: (1) amyloid type produces symptoms similar to eczema with reddish or brown scaly spots and can be very itchy; (2) macular is less common and less itchy than amyloid but looks very similar; (3) nodular causes red, pink, or brown lumps to form but may not cause any symptoms. Diagnosis is via skin biopsy. Itching is the primary symptom.
Dermoscopy
Published in Dimitris Rigopoulos, Alexander C. Katoulis, Hyperpigmentation, 2017
Teresa Deinlein, Iris Zalaudek
Amyloidosis is a large and heterogeneous group of disorders characterized by extracellular deposits of amyloid in individual organs or tissue. It is either hereditary or acquired. Primary cutaneous amyloidosis is a very rare disease, and therefore just a few cases have been described so far.41–44
Nodular localized primary cutaneous amyloidosis and primary Sjögren’s syndrome
Published in Scandinavian Journal of Rheumatology, 2020
K Davies, A Collins, FG Charlton, W-F Ng
Owing to the nature of the skin lesion, a biopsy was taken. Histology revealed extensive stromal deposition of eosinophilic material which stained positively with Congo Red and was ‘apple green’ under polarized light, consistent with amyloidosis (Figure 2). There was no evidence of mucinosis or immunoglobulin G4 disease. She was referred to the National Amyloidosis Centre at the Royal Free Hospital (London, UK) for review, and immunohistochemical staining for serum amyloid A (SAA) protein and kappa and lambda immunoglobulin light chains was negative. A diagnosis of nodular localized primary cutaneous amyloidosis (NLPCA) was made. She was reviewed by the Royal Free Hospital. No immediate treatment was required but surgical intervention remained an option in the future. At the most recent review, the patient reported that the lesion has slightly grown in size (Figure 1).
Comparing the efficacy of pulsed dye laser, Q-Switched Nd-YAG, CO2, and combined CO2 and Q-Switched Nd-YAG lasers for the treatment of cutaneous macular amyloidosis
Published in Journal of Dermatological Treatment, 2021
Mohammad Radmanesh, Forough Ghanatir, Ramin Radmanesh
The CMA as a subtype of Primary cutaneous amyloidosis (PCA) is not infrequently seen and is a challenging problem in our daily practice. The CMA is characterized by rippled hyperpigmentation of the skin, most commonly seen in the upper back and dorsal aspects of the arms. Many patients suffer from skin discoloration and most commonly are associated with persistent pruritus and subsequently skin lichenification. The disease is developed as a result of dermal extracellular amyloid protein deposition without systemic involvement (1).
Differential expression of MAP3K7 and TROPONIN C proteins and related perturbations in renal amyloidosis
Published in Expert Review of Proteomics, 2020
Nimisha Gupta, Tahreem Sahar, Dinesh Khullar, S.K. Jain, Saima Wajid
Troponin C (cTnC) is a calcium-binding subunit of protein and a part of the troponin complex. The troponin complex consists of 3 regulatory proteins – troponin T, troponin I, and troponin C and is located on the myofibrillar thin (actin) filament of striated (skeletal and cardiac) muscle. cTnC is 18 kDa protein which regulates the activation of the actin filaments [21]. Recently, cTnC was found to be differentially expressed in the primary cutaneous amyloidosis patients [22]. Moreover, an increased level of troponin T was found in patients with end-stage renal diseases (ESRD) and obstructive sleep apnea [23]. Another study has also revealed an elevated level of cardiac troponin in patients with chronic kidney diseases including ESRD. Patients with ESRD have elevated cardiac troponin due to the cardiac injury associated with chronic structural heart diseases. Additionally, we observed that other subunits (cTnT, cTnI) of troponin complex closely interact and are involved in striated muscle contraction pathway. Patients with primary systemic amyloidosis also reported elevated levels of cTnT and cTnI [24]. Bobyleva et al. noticed that MyBP-C, another interactor of troponin C has the potential to form amyloids aggregates in vitro (Figure 4, Supplementary Table 4) [25]. Two different isoforms of human TnC encoded by individual genes have been described, including an isoform exclusively expressed in fast-twitch skeletal tissue and an isoform expressed in both cardiac and slow-twitch skeletal muscle tissue. There is significant homology between the cardiac and TnC isoforms which reduces cardiac specificity; consequently, detection of TnC has limited diagnostic utility in ACS. Significant cardiac involvement is thought to be rare in AA amyloidosis. Cardiac involvement could be the initial presentation of amyloidosis. Cardiac involvement occurs in up to 50% of patients with AL amyloidosis and up to 5% in patients with AA amyloidosis [26]. In the present study, none of the patients was reported to have cardiac amyloidosis. In this study, we found elevated expression of troponin C in RA samples as compared to controls. Hence, the role of troponin C in chronic kidney diseases and amyloidosis may be attributed to the presence and upregulation of cTnC in RA samples.