i didn't see a specific connection made between niacin or lack thereof and new lesion dev, but fwiw:
Lipid Lowering Agents That Cause Drug-Induced Hepatotoxicity
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2048990/
Niacin
Niacin, or nicotinic acid, is used primarily to increase HDL through a mechanism that is not entirely clear. A reduction in LDL is also seen ... The sustained-released (SR) preparation is easily available over-the-counter and may be used by patients seeking a perceived naturopathic solution to their high cholesterol or by patients seeking a cheaper option to treat themselves. Patients may possibly be using potentially toxic doses without the prior knowledge of their physicians. It is this unsupervised use of the SR formulation that often leads to the dose-related toxicity of niacin and should be discouraged.4,47-49 The onset of hepatotoxicity generally appears anywhere from 1 week to 48 months after the initiation of the drug and usually subsides with discontinuation.50-52 Recovery is usually seen in 1-2 months.48,50 Fulminant hepatic failure has been reported but is very rare.51,53,54 Combination therapy with statins does not increase the incidence of adverse effects of either medication.55
Almost any formulation of niacin can cause hepatotoxicity in doses that exceed 2-3 grams per day, but the sustained-release (SR) formulation is significantly more hepatotoxic.62,63 The immediate-release (IR) formulations of niacin in usual therapeutic doses almost never cause serious liver injury.64,65 The over-the-counter SR formulation of the drug is not FDA approved for the treatment of dyslipidemia but still available to patients for this purpose as a supplement or “neutraceutical”. Half of the patients that take niacin SR develop a symptomatic elevation in transaminases.49,64,66
...
the slower released SR formulation can lead to higher levels of toxic metabolites (Table 5).64,65,67 ... The rapidly-released IR formulation overwhelms the higher affinity amidation pathway and the majority is metabolized using the high-capacity conjugation pathway, leading to a much lower rate of hepatotoxicity.67 Extended-release (ER) niacin has an intermediate rate of dissolution and can be associated with both flushing and hepatotoxicity 64.
62. Capuzzi DM, Guyton JR, Morgan JM, Goldberg AC, Kreisberg RA, Brusco OA, et al. Efficacy and safety of an extended-release niacin (Niaspan): a long-term study. American Journal of Cardiology. 1998;82(12A):74U–81U.
63. Rader JI, Calvert RJ, Hathcock JN.
Hepatic toxicity of unmodified and time-release preparations of niacin. American Journal of Medicine. 1992;92(1):77–81.
Adverse effects on the liver from both unmodified and time-release preparations have been recognized for many years. We reviewed the literature on the hepatic toxicity of both types of niacin preparations.
Adverse reactions in six patients resulted from the exclusive use of unmodified niacin and in two patients from the exclusive use of time-release preparations. In 10 additional patients, adverse reactions developed after an abrupt change from unmodified to time-release preparations. Many of these patients were ingesting time-release niacin at doses well above the usual therapeutic doses currently recommended. Signs of liver toxicity developed in less than 7 days in four of these 10 patients. In doses that achieve equivalent reductions in serum lipids, hepatic toxicity occurred more frequently with time-release preparations than with unmodified preparations. An awareness of toxicity associated with ingestion of high doses of time-release niacin preparations is important because of their widespread availability and the potential for self-prescribed, unmonitored use.
64. Pieper JA. Overview of niacin formulations: differences in pharmacokinetics, efficacy, and safety. American Journal of Health-System Pharmacy. 2003;60(13) 2:S9–14.
65. McKenney J. Niacin for dyslipidemia: considerations in product selection. American Journal of Health-System Pharmacy. 2003;60(10):995–1005.