In a small study of 16 patients with renal amyloidosis, the 5 patients with AH amyloidosis and the 11 patients with AHL amyloidosis had less frequent concurrent cardiac involvement and better overall survival than 202 patients with renal AL amyloidosis. The hematological response to chemotherapy of the AH and AHL renal amyloidosis patients was comparable to those with renal AL amyloidosis. POEMS syndrome
POEMS syndrome (also known as Crow–Fukase syndrome, Takatsuki disease, or PEP syndrome) is a rare and complex medical syndrome that involves a combination of syndrome-defining signs and symptoms due to the dysfunction of multiple organs. The syndrome is associated with a plasma cell dyscrasia in almost 100% of cases, pathological overexpression of certain cytokines in >95% of cases, and the lymphoproliferative disorder termed Castlemans disease in ~15% of cases. (Rare cases of POEMS have been associated with polyclonal rather than clonal plasma cells; these cases are not plasma cell dyscrasias but rather appear to be caused by the over-activity of non-malignant immune cell responses in chronic infections or autoimmune diseases.) POEMS is an acronym standing for the characteristic signs or symptoms of the syndrome: Polyneuropathy, Organomegaly, Endocrinopathy, Plasma cell disorder (typically, the plasma cell burden is low in POEMS patients), and Skin changes (e.g. hemangioma, hyperpigmentation).
Similarly, selective serotonin reuptake inhibitors can cause mydriasis. Dissociatives such as dextromethorphan (an SSRI and sigma-1 agonist). Certain GABAergic drugs, such as phenibut and GHB. Adrenergic agonists, such as phenylephrine and cyclomydril. Adrenergic agonists may be used if strong mydriasis is needed in surgery. Norepinephrine is a hormone and neurotransmitter that regulates the involuntary muscles of the autonomic nervous system, including dilation of the pupil aperture via the muscles of the iris. Hence adrenergic agonists mimic the activity of norepinephrine, which is how they induce mydriasis.Natural release of the hormone oxytocin can cause mild to moderate mydriasis.Long term effects of drugs can also cause mydriasis, for example opioid withdrawal. Autonomic neuropathy
Parasympathetic fibers travel with cranial nerve III, the oculomotor nerve, to innervate the circular layer of muscle of the eye (sphincter pupillae). Damage to this nerve typically manifests itself as mydriasis, because the sympathetic supply to the pupil, which causes mydriasis, remains unaffected, and therefore unopposed. Multiple central nervous system disorders e.g. epilepsy, stroke, and impending brain herniation are known to lead to temporal mydriasis as well. A brain catastrophe, or a rapidly increasing brain mass, can cause compression of the oculomotor nerve. Trauma
In cases of head injury or orbit trauma (eye injury), the iris sphincter (the muscle responsible for closing the pupil) or the nerves controlling it can be damaged, reducing or eliminating the normal pupillary light reflex. References


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